Download Sleep Disturbances and Psychological Functioning in Respiratory

Sleep Disturbances and Psychological
Functioning in Respiratory Diseases
Daljinder Ritu Virk
January 2010
The thesis is submitted in partial fulfilment of the
requirements for the award of the degree of Doctor of
Philosophy of the University of Portsmouth.
Declaration
No portion of the work referred to in this thesis has been submitted in support of an
application of another degree or qualification of this or any other academic or
professional institution.
2
Abstract
The aims of the present research were to describe in more detail than in previous
investigations the occurrence and nature of self reported sleep problems and
behaviours in individuals diagnosed with respiratory diseases compared to matched
healthy controls and to investigate the psychological associations of these sleep
problems.
The prevalence and range of sleep disorders was investigated using the Basic Nordic
Sleep Questionnaire (BNSQ). Individuals diagnosed with respiratory diseases,
included those with asthma (n=46), Chronic Obstructive Respiratory Disease
(COPD) (n=18), bronchiectasis (n=16) and asbestosis and related conditions (n=11)
and these were compared with healthy matched controls. Individuals with respiratory
diseases were recruited from the Queen Alexandra out-patients Respiratory Service
at Portsmouth Hospitals National Health Service Trust. Healthy matched controls
were recruited through various sources including University of Portsmouth, Queen
Alexandra Hospital and Portsmouth City Council staff.
Overall individuals diagnosed with asthma, COPD, bronchiectasis and asbestosis and
related conditions showed a significantly greater number of self reported sleep
problems and behaviours than the healthy controls. A range of sleep problems and
behaviours were found in the four respiratory disease groups. These were in many of
the categories of sleep disorders as defined by the International Classification of
Sleep Disorders-2 (2005): disorders of initiating and maintaining sleep, features
associated with sleep disordered breathing, other disorders/behaviours occurring
during the sleep and sleep related disorders/behaviours occurring during the day.
Psychological functioning was assessed including quality of life, mental health and
cognitive functioning using validated psychometric assessments. Many significant
differences were found between the individuals with respiratory disease and their
healthy controls on these measures. Significant associations were found between the
sleep disorders and behaviours and measures of psychological functioning.
3
Contents
Declaration
2
Abstract
3
Contents
4-6
List of Figures and Tables
7-9
Abbreviations
10-11
Acknowledgements
12
Dissemination
13
Dedication
14
1
Introduction and outline of the thesis
15-16
2
Literature review
17
2.1 Sleep
2.1.1 Theories of sleep
2.1.2 Physiology of sleep
2.1.3 The classification of sleep disorders
2.1.4 Sleep disorders
2.1.5 Assessments of sleep disorders
2.1.6 Treatments for sleep disorders
2.2 Respiratory Diseases
2.2.1 Asthma
2.2.2 Chronic obstructive respiratory disease
2.2.3 Bronchiectasis
2.2.4 Asbestos related conditions
17-35
36-42
43-47
48-64
65-77
78-84
85-86
87-94
95-103
104-108
109-113
2.3 Studies investigating disturbed sleep and
psychological well-being in patients diagnosed
with respiratory diseases
2.3.1 Sleep studies of respiratory diseases
2.3.2 Psychological studies of respiratory diseases
2.3.3 Psychological functioning in individuals diagnosed
with obstructive sleep apnoea syndrome
114-124
125-132
133-136
2.4 Need and requirements for further research in
individuals living with respiratory diseases
concerning their sleep and psychological functioning 137-138
4
3
A Cross-sectional survey of sleep disturbance and
psychological functioning in individuals with respiratory
diseases and matched healthy controls
141
3.1 Aims
3.2 Method
3.2.1 Design
3.2.2 Procedure
3.2.3 Participant recruitment
3.2.4 Assessments
3.2.5 Ethical Approval
3.2.6 Data analysis
142
142-143
144-146
146-150
150
150
3.3 Results
3.3.1 Demographic characteristics
3.3.2 Sleep disorders and behaviours
3.3.3 Daytime sleepiness
3.3.4 Quality of Life
3.3.5 General Health Questionnaire-12 (GHQ-12)
3.3.6 Beck Depression inventory (BDI)
3.3.7 Cognitive assessments
3.3.8 Associations between sleep disorders and
behaviours, daytime sleepiness, quality of life, mental
health, depression and cognitive functioning
151-159
160-170
171-172
173-178
179-182
183-185
186-191
192-200
201-202
3.4 Summary
5
4
Discussion
203-224
204-207
4.1 Summary
4.2 Main findings and comparison with other studies 207-218
4.3 Evaluation of methodology used and suggestions
for refinements in further studies
218-220
4.4 Feasibility
221
4.5 Future research
221-224
References
225-243
Appendices
244
6
List of Tables and Figures
Table 2. 1. Differences in physiological characteristics of NREM and REM in male
human sleep..........................................................................................................39
Table 2. 2. Terms synonymous with REM and NREM sleep...............................39
Table 3. 1. Total number of individuals diagnosed with respiratory diseases and
healthy matched controls recruited...........................................................................144
Table 3 2. Exclusion and inclusion criteria for selecting individuals………….145
Table 3. 3. General characteristics of all groups. .....................................................151 Table 3. 4. Breakdown of ethnic groups across individuals diagnosed with respiratory
diseases and healthy controls ...................................................................................152 Table 3. 5. Social economic status across all groups. ..............................................153 Table 3. 6. Breakdown of educational qualifications across the groups. .................154 Table 3. 7. Current illnesses or physical disorder that individuals diagnosed with
respiratory diseases and healthy controls have at present or have had in the last 3
months. .....................................................................................................................155 Table 3. 8. Any illness or physical disorder that participants have ever had. ..........157 Table 3. 9. Sleep disturbances in other family members as reported by individuals
diagnosed with respiratory diseases and healthy controls........................................158 Table 3. 10. Mean scores obtained in individuals diagnosed with asthma and healthy
controls. ....................................................................................................................160 Table 3. 11. Mean time required for sleep and sleep duration as reported by
participants within the asthma group........................................................................161 Table 3. 12. Mean scores obtained in individuals diagnosed with COPD and healthy
controls. ....................................................................................................................162 Table 3. 13. Mean time required for sleep and sleep duration as reported by
participants within the COPD group. .......................................................................163 Table 3. 14. Mean scores obtained in individuals diagnosed with bronchiectasis and
healthy controls. .......................................................................................................164 Table 3. 15. Mean time required for sleep and sleep duration as reported by
participants within the bronchiectasis group. ...........................................................165 Table 3. 16. Mean scores obtained in individuals diagnosed with asbestosis related
conditions and healthy controls................................................................................166 Table 3. 17. Mean time required for sleep and sleep duration as reported by
participants within the asbestosis & related conditions group .................................167 Table 3. 18. Mean Epworth Sleepiness Score in individuals diagnosed with asthma
and healthy controls..................................................................................................170 Table 3. 19. Mean Epworth Sleepiness Score in individuals diagnosed with COPD
and healthy controls..................................................................................................170 Table 3. 20. Mean Epworth Sleepiness Score in individuals diagnosed with
bronchiectasis and healthy controls..........................................................................171 Table 3. 21. Mean Epworth Sleepiness Score in individual diagnosed with asbestosis
related conditions and healthy controls. ...................................................................171 Table 3. 22. Mean SF-36 scores in the group with asthma. .....................................173 Table 3. 23. Mean SF-36 scores in the group with COPD.......................................174 Table 3. 24. Mean SF-36 scores in the group with bronchiectasis...........................175 Table 3. 25. Mean SF-36 scores in the group with asbestosis related conditions..........
..................................................................................................................................176 7
Table 3. 26. Mean GHQ-12 scores in the group with asthma ..................................178 Table 3. 27. Mean GHQ-12 scores in the group with COPD...................................179 Table 3. 28. Mean GHQ-12 scores in the group with bronchiectasis ......................179 Table 3. 29. Mean GHQ-12 scores in the group with asbestosis related conditions.. ..
..................................................................................................................................180 Table 3. 30. Global BDI-II scores in the group with asthma ...................................182 Table 3. 31. Global BDI-II scores in the group with COPD ....................................183 Table 3. 32. Global BDI-II scores in the group with bronchiectasis........................183 Table 3. 33. Global BDI-II scores in the group with asbestosis related conditions ......
..................................................................................................................................184 Table 3. 34. Mean Item 1 scores in the group with asthma......................................186 Table 3. 35. Mean Item 1 scores in the group with COPD ......................................186 Table 3. 36. Mean Item 1 scores in the group with bronchiectasis ..........................187 Table 3. 37. Mean Item 1 scores in the group with asbestosis related conditions ........
..................................................................................................................................187 Table 3. 38. Mean Item 2 scores in the group with asthma......................................188 Table 3. 39. Mean Item 2 scores in the group with COPD ......................................188 Table 3. 40. Mean Item 2 scores in the group with bronchiectasis ..........................189 Table 3. 41. Mean Item 2 scores in the group with asbestosis related conditions ........
..................................................................................................................................189 Table 3. 42. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders
during sleep, and other disorders during the day and Epworth Sleepiness score (ESS),
general Health Questionnaire (GHQ-12), physical component score (PCS) and
mental component scpre (MCS), Beck Depression Inventory (BDI) score and
cognitive functioning global score (COG) ...............................................................192 Table 3. 43. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders
during sleep, and other disorders during the day and Epworth Sleepiness score (ESS),
general Health Questio nnaire (GHQ-12), physical component score (PCS) and
mental component scpre (MCS), Beck Depression Inventory (BDI) score and
cognitive functioning global score (COG) ...............................................................194 Table 3. 44. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders
during sleep, and other disorders during the day and Epworth Sleepiness score (ESS),
general Health Question nnaire (GHQ-12), physical component score (PCS) and
mental component scpre (MCS), Beck Depression Inventory (BDI) score and
cognitive functioning global score (COG) ...............................................................195 Table 3. 45. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders
during sleep, and other disorders during the day and Epworth Sleepiness score (ESS),
general Health Question nnaire (GHQ-12), physical component score (PCS) and
mental component scpre (MCS), Beck Depression Inventory (BDI) score and
cognitive functioning global score (COG) ...............................................................197 8
Figure 2. 1. Examples of waveforms that differentiate sleep stages.........................40
Figure 2. 2. The progression of sleep stages across a single night sleep in a normal
adult.......................................................................................................................41
9
Acronyms and Abbreviations
AASM-American Academy of Sleep Medicine
ACQ-Asthma Control Questionnaire
AD-Alzheimer’s Disease
ANS-Autonomic Nervous System
AQLQ-Asthma Quality of life Questionnaire
ATP- Adenosine Triphosphate
ATS-American Thoracic Society
BMI-Body Mass Index
BNSQ-Basic Nordic Sleep Questionnaire
BTS-British Thoracic Society
CABG-Coronary Artery Bypass Grafting
CNS-Central Nervous System
COPD-Chronic Obstructive Pulmonary Disease
CPAP-Continuous Positive Airway Pressure
CT-Computerised Tomography
DIMS-Disorders of Initiating and Maintaining Sleep
DQS-Deep Quiet Sleep
DSM-IV-TR-Diagnostic and Statistical Manual-IV-Text Revision
ECT-Electroconvulsive Therapy
EDS-Excessive Daytime Sleepiness
ER-Emergency Room
ESS-Epworth Sleepiness Scale
FEV1-Forced Expiratory Volume in 1 second
FEV-Forced Expiratory Volume
FVC-Forced Vital capacity
GHQ-General Health Questionnaire
GP-General Practitioner
HRQoL-Health Related Quality of Life.
ICD-9-CM-International Classification of Diseases-9-Clinical Modification
ICD-International Classification of Diseases
ICSD-International Classification of Sleep Disorders
IgE-Immunoglobin class E
LED-Light Emitting Diode
LH-Luteinizing Hormone
LQS-Light Quiet Sleep
LRT-Lower Respiratory Tract Infection
Mini AQLQ-Mini Asthma Quality of Life Questionnaire
MOS-Medical Outcome Study
MSLT-Multiple Sleep Latency Test
NDE-Non Demented Elderly
NHS-National Health Service
NOS-Not Otherwise Specified
NREM-Non Rapid Eye Movement
O2-Oxygen
OSA-Obstructive Sleep Apnoea
OSLER-Oxford Sleep Resistance
PCO2 Partial Pressure of Carbon Dioxide
10
PEF-Peak Expiratory Flow
PH-Power of Hydrogen
PM-Post Meridian
PO2-Partial Pressure of Oxygen
POMS-Profile Of Mood States
PSQI-Pittsburgh Sleep Quality Index
QoL-Quality of Life
REM-Rapid Eye Movement
RLS-Restless Legs Syndrome
RMMA- Rhythmic Masticatory Muscle Activity
SAHS-Sleep Apnoea-Hypopnoea Syndrome
SCL-90-Symptom Checklist-90
SDB-Sleep Disordered Breathing
SGRQ-St Georges Respiratory Questionnaire
SOREMP- Sleep Onset Rapid Eye Movement Period
SRBD-Sleep Related breathing Disorders
SRED-Sleep Related Eating Disorder
SSRI’S- Selective Serotonin Reuptake Inhibitors
SSS-Stanford Sleepiness Scale
SWS-Slow Wave Sleep
TCA-Tricyclic antidepressants
TIB-Time In Bed
TLC-Total Lung Capacity
UK-United Kingdom
UPP- Uvulopalatopharyngoplasty
URT-Upper Respiratory Tract Infection
vs.-versus
α1-Antitrypsin
β2-beta 2
11
Acknowledgements
I would firstly like to thank my parents and my grandparents for their tremendous
support throughout my academic career, their words of encouragement, their
emotional support and believing in me. I would especially like to thank my sister
Aman for the tremendous support she has offered me throughout this PhD.
I would also like to say a big thank you to my dear friends Alex Assimwe and
Heather Mackenzie. I am also eternally grateful to Dr Anthony Fallone, Alison
Hadley, Dr Andrew Sherley-Dale.
I would like to acknowledge all the patients based at Queen Alexandra hospital
without whom this PhD would not have been possible. I am also grateful to staff at
Portsmouth City Council, my friends, family and colleagues who completed my
study questionnaire.
I would like to acknowledge the staff based at the respiratory department at Queen
Alexandra hospital especially Sue Kerley. They have been very patient and
supportive whilst I was recruiting participants from the clinics. I would like to extend
this acknowledgement to Simon Charter in designing the study questionnaire.
I would like to thank my director of studies, Dr Rebecca Stores for her tremendous
support throughout my PhD.
Lastly, thank you to my clinical supervisor, Professor Anoop Chauhan in assisting
with the recruitment of patients from the clinics at Queen Alexandra hospital.
12
Dissemination
Conference presentations
Poster presentation of present study in 2005 and 2006 presented at the following
conferences:
•
The Geographical Health Inequalities Section
•
The Psychoneuroimmunology Section
•
The British Psychology Society annual conference
•
The Southern Allied Health Professions Council annual conference
•
The Psychological Postgraduate Affairs Group annual conference
•
The British Medical Association Winter meeting
•
The British Psychology Society Wessex Branch
•
The British Psychology Society Postgraduate Student conference
13
Dedication
I would like to dedicate this thesis to my late aunt, Iqbal Virk who sadly lost her
battle against cancer on December 8th 2009.
14
1
Introduction and outline of the thesis
The sleep problems and psychological functioning of individuals diagnosed with
respiratory diseases is a much neglected topic despite the fact that there is empirical
evidence of such morbidity found in other chronic conditions which are often severe
and persistent. Observations have been made about the extent of sleep problems in
patients with respiratory diseases. They have highlighted the serious effects of such
phenomena on both the individuals health and their well-being, more specifically
psychological functioning which incorporates quality of life (QoL), mood, memory
and cognitive functioning.
The programme of research to be described focuses upon patients diagnosed with
asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis and
asbestosis and related illnesses. Although these specific groups of patients have
received attention in the literature, the details of the self reported sleep problems
associated with these conditions have not been appropriately defined and the possible
psychological consequences have not been the subject of systematic research.
Clearly, such consequences are potentially serious in patients with these respiratory
diseases as they may add to the overall level of debilitating effect associated with the
conditions. The aims of the present research are to describe, in more detail than
previous investigations, the occurrence and nature of self reported sleep problems
and behaviours in patients with respiratory diseases compared to healthy matched
controls, to investigate their psychological well-being and to explore the
psychological associations of sleep disturbances in these individuals.
This thesis is divided into four parts: Part (1)-Introduction and outline of the thesis;
Part (2)-Literature Review is divided into 4 sections which provide an overview and
discussion of the literature most relevant to the present research; Section 2.1 focuses
on sleep. Section 2.2 includes separate accounts of the four respiratory diseases that
have been investigated within this research, these being asthma, COPD,
bronchiectasis and asbestosis. Section 2.3 focuses on a review of past studies
investigating disturbed sleep and psychological well-being in individual diagnosed
with respiratory diseases, psychological and quality of sleep studies of respiratory
diseases, studies employing both objective and subjective methods to investigate
15
disturbed sleep in individual diagnosed with respiratory diseases and finally studies
investigating psychological functioning in individuals diagnosed with obstructive
sleep apnoea syndrome (OSAS). Section 2.4 is concerned with the need for further
research in patients living with respiratory diseases concerning their sleep and
psychological functioning. This provides the background and rationale to the present
programme of research.
Part (3) describes a cross-sectional survey of sleep disturbances and psychological
functioning in individuals with respiratory diseases and matched healthy controls.
Part (4) is the discussion of the present programme of research. The findings are
discussed and compared with previous studies. Limitations and possible refinements
are also described along with suggestions for future research.
Finally, the references and appendices are presented
16
2
Literature review
2.1 Sleep
2.1.1 Theories of sleep
Definition of sleep
Sleep is an active physiological state that is characterised by dynamic fluctuations in
the central nervous system, (Bae and Foldvary-Schaefer, 2005). The purpose of sleep
has not been fully understood, although it is known that sleep is important in memory
consolidation and repair (Bae and Foldvary-Schaefer, 2005).
Theories of sleep
The three main theories of why humans sleep that will be discussed in this chapter
are as follows: the restoration theory, the evolutionary theory (or ecological theory)
and the neurochemical theory. Each theory will be discussed in turn.
Restoration theory
Oswald (1970, 1976) suggested that both rapid eye movement (REM) and non-rapid
eye movement (NREM) sleep serve the purpose of restoring and replenishing our
bodies and brains. (Rapid eye movement and non-rapid eye movement sleep will be
discussed in section 2.1.2, physiology of sleep). This supposes that we sleep to
restore ourselves physically and psychologically. Oswald (1970) has suggested that
non-rapid eye movement (NREM) is important for restoring bodily processes that
may have deteriorated or may have been worn down during the day. REM sleep has
been described by Oswald (1970) as that which renews brain processes and
replenishes neurochemicals used up in the day; these are regenerated by protein
synthesis.
Evidence that supports the restoration theory
Empirical evidence supports Oswald’s restoration theory (Bentley, 1999). Foetuses
and babies have been shown to sleep with REM and NREM sleep for a greater
proportion of the day than older children or even adults (Bentley, 1999). It is during
these earlier stages of development that the body of a developing foetus or a baby
17
grows faster and neural connections are established. An adult will spend on average
eight hours in sleep (fewer in old age) whereas newborn babies have been shown to
sleep for up to eighteen hours a day. Half of the eighteen hours or so are spent in
REM sleep, whereas adults have been shown to spend about a quarter of their sleep
in REM (Bentley, 1999). The amount of time spent in REM sleep corresponds to the
large amount of activity that occurs in the developing brain, where protein synthesis
is required for cell and synaptic growth (Bentley, 1999). Oswald (1980) states that
physical repair and brain-protein synthesis are both dependant on growth hormone.
Growth hormone is secreted after the first burst of delta activity in slow wave sleep
(slow wave sleep is discussed in section 2.1.2, physiology of sleep).
Further support for the restoration theory is provided by studies in patients who have
incurred damage to their brains from drug overdoses or electroconvulsive therapy
(ECT) and who have been shown to spend an increased time in REM sleep (Crick
and Hitchinson, 1983). It has been suggested that perhaps patients who have had
such damage tend to spend more time in REM sleep so that the brain proteins
required can be synthesized (Bentley, 1999). Blood flow to the brain has been shown
to increase during REM sleep, most likely required to provide extra oxygen, glucose
and nutrients for the protein synthesis (Bentley, 1999). The theories provided here
are speculative, the evidence for them yet to be methodically examined.
Further evidence from a cognitive psychological perspective emerges from studies of
learning, in which REM sleep has been related to learning and consolidation of
memory (Loftus, 1997). A study by Bloch (1976) showed that rats that were given
complex maze-like tasks every day had an increase in REM sleep. This perhaps
shows that learning is related to protein synthesis.
Evidence that does not support the restoration theory
Extensive research into protein synthesis has shown that amino acids (the building
blocks for protein and neurochemicals) are not stored by the body. Since amino acids
only last approximately four hours after a meal within the body. It is likely that
18
protein synthesis might be stopped halfway through the night’s sleep because the
available amino acids are exhausted (Bentley, 1999).
Studies using the sleep deprivation technique have shown that we do not require to
make up for lost sleep but we do appear to need REM sleep or core sleep (core sleep
is discussed in section 2.1.2, physiology of sleep). If the restoration theory proposes
that sleep is required to restore then findings from sleep deprivation studies would be
consistent and this is not the case (Bentley, 1999). It has also been proposed that
some form of recovery and manufacture of biochemicals may also take place during
the day when a person is relaxed (Bentley, 1999).
Another factor which further suggests that sleep may not be seen as a restorative
period is the lack of experimental support for the supposition that the more active an
individual is during the day the more sleep occurs at night. Shapiro et al (1981)
recorded the sleep duration of marathon runners after a race; they showed a decrease
in REM sleep but showed as well more slow-wave sleep. Further agreement with
these results is provided by Horne and Minard (1985) in which participants were
engaged in a number of different physical activities but found no increases in sleep,
although the participants did go to sleep faster. Carlson (1986) has suggested that
perhaps slow-wave sleep is more important for recovery after vigorous activity.
An alternative restoration theory
Professor David Maurice (1998) proposes an alternative point of view of the
restoration theory. Maurice states that REM sleep occurs because during sleep the
fluid inside the eyes would not circulate and the eyes might become short of the
oxygen supply borne by this fluid. Maurice states that moving the eyeballs creates
small currents in this fluid and ensures the delivery of oxygen to the cornea. This
does explain why foetuses have REM sleep and why periods of REM sleep become
longer in adults as the night progresses. However, this alternative theory by Maurice
does not explain why those participants who are experimentally deprived of REM
sleep have no eye problems reported (although, for ethical reasons, perhaps this does
19
not go on long enough for damage to become noticeable) and also have a reported
increased amount of REM sleep when allowed to sleep naturally.
The neurochemical theory
The neurochemical approach suggests that sleep has a particular function within the
brain, a specialised type of restoration theory (Bentley, 1999).
Rapid Eye Movement (REM) Sleep
REM sleep appears to be controlled by a noradrenalin pathway going up through the
brain. Studies have shown that as a feature of depression, sufferers have unusually
large amounts of REM sleep. It has also been found that REM deprivation can
relieve depression (Vogel, 1975). This suggests that there is a link between too much
REM and depression. Some drugs that are used to treat depression such as the
tricyclic
antidepressants
have
also
been
found
to
reduce
REM
sleep
(pharmacological aids for treating sleep disorders are discussed in section 2.5.1).
Tricyclics work by stimulating the noradrenergic pathways and the production of
noradrenalin. Perhaps what the drug is doing is performing the functions of REM
sleep and therefore less sleep is needed and, for whatever reason, the reduced REM
sleep alleviates depression (Bentley, 1999). Parallel experimental studies have also
been performed in non-human species whereby noradrenaline has been reduced in
the brain and thus causing an increase REM sleep. Again, this provides support for
the association between REM and noradrenaline; REM sleep has a neurological
purpose to replenish the brain’s noradrenaline levels that may have been depleted by
daily activities (Bentley, 1999).
Non Rapid Eye Movement (NREM) Sleep
Serotonin, a neurotransmitter, has been shown to be linked with NREM or slowwave sleep. If serotonin is reduced with the use of certain drugs, this has an impact
on the amount of NREM sleep, which is also reduced. This suggests that a serotonin
dependant pathway is required to have NREM sleep, an assertion supported by
studies with depressed patients. Patients with unipolar depression have an inability to
fall asleep: they remain tired but awake every night well into the early hours of the
20
morning and once sleep does come it lasts a very short time (Stern, and Morzane,
1974). Once again, successful treatment of depression using selective serotonin
reuptake inhibitors (SSRIs) such as Prozac increase the activity of serotonin in the
brain, increasing the amount of time the neurotransmitter lingers in the synaptic cleft,
restoring both the sleep patterns and the person’s mood.
Experiments by Greene at Harvard University suggest that sleep is linked to
molecules that appear within all cells. These are the cellular source of energy, what
could be called molecular “torch-batteries” (Holmes, 1997). These molecules are
called adenosine triphosphate (ATP), made up of adenosine (adenosine plays an
important role in biochemical processes, such as energy transfer; it is also an
inhibitory neurotransmitter, believed to play a role in promoting sleep and
suppressing arousal, with levels increasing with each hour an organism is awake).
Adenosine could be the key to why we sleep, as in cats: when adenosine levels rise
above a critical level they get sleepy and sleep longer in both REM and NREM sleep.
As well, during sleep, levels of adenosine fall, to rise again during wakefulness
(Carlson, 1997).
This supports the notion that we have NREM sleep in order to be able to go into
REM sleep and we therefore need REM sleep to deal with the build up of adenosine.
Such a mechanism suggests that sleep is a homeostatic process, to balance various
neurochemicals in our body (Bentley, 1999).
Finally, Hobson (1995) provides a review of the main theories of sleep and puts
forward a three tier analysis:
Behaviourally, sleep conserves energy in situations where it may be required for
example, when foraging for food or for finding a mate when conditions may likely to
be difficult, or when there is a decrease in climatic temperature. This suggests that
sleep is favourable in less hospitable conditions. It is also a time for pair-bonded or
family groups to strengthen relationships by being together either during the period
leading up to sleep as well as when actually sleeping.
21
Developmentally, the brain structures and connections can grow and mature before
they are needed in action, this connects with the restoration theory.
Metabolically, various physiological changes such as alterations in blood pressure
and release of hormones occur during sleep.
Experimental studies of sleep deprivation
Such experiments have been concerned with various types of sleep deprivation: acute
sleep deprivation, chronic sleep deprivation, selective NREM and REM sleep
deprivation and fragmentation of sleep caused by arousals.
Acute sleep deprivation
One of the first published studies of total sleep loss in puppies dates back to 1894
(Manaceine, 1894) and for humans a couple of years later (Patrick and Gilbert,
1896). Manaceine’s observations indicated that sleep loss when prolonged in animals
is fatal; this concept was dismissed until recent findings. The work conducted by
Patrick and Gilbert included a range of variables that looked at physiological and
behavioural measurements and this study remains a model of its kind.
Behaviourally, the effect of sleep loss is sleepiness and this can be extracted from the
subjective reports such as the multiple sleep latency test (MSLT), or the change on
the EEG or in other simpler forms such as looking at the facial expressions of the
participant. Factors that determine the impact of sleep loss can be divided into four
categories, these being sleep and circadian influences, arousal system influences,
subject characteristics and test characteristics. Under the heading of subject
characteristics, the impact of sleep loss on a given individual depends on
characteristics that each participant brings to the sleep loss situation. For example,
age and personality represent differences in physiological or psychological function
that may interact with the sleep loss event.
Changes within mood include increased sleepiness, fatigue, irritability, usually
difficulty in concentrating and disorientation, are commonly reported during periods
of sleep loss. Webb and Levy (1984) reported perceptual distortions and
hallucinations of a visual nature in 80% of the normal individuals in their study but
this also depended on the type of work in which the participants in the study were
22
involved, the visual demands and the length of deprivation. Individuals who have
been diagnosed with schizophrenia also display auditory hallucinations but normal
individuals who undergo sleep loss may also express schizophrenic behaviour, such
as paranoia. A study by Tyler in 1955 reported 2% of three hundred and fifty
participants sleep deprived for 112 hours experienced temporary states resembling
acute paranoid schizophrenia. Some individuals did have some form of
predisposition towards the condition and those that did experienced significant
paranoia during sleep loss and the paranoid behaviour tended to become more
pronounced during the night, with partial recovery during the day and disappearance
after recovery sleep.
Patients who have been known to suffer from depression have also been successfully
treated through sleep deprivation. Sleep deprivation has proven to be a successful
treatment in cases between 40% to 60% of diagnosed patients for the last thirty years
or so (Giedke and Schwarzler, 2002). One theory has proposed that sleep deprivation
is effective in those patients with high levels of activation or high central
noradrenergic activity because it lowers the effects of chronic hyperarousal (WirzJustice and Van den Hoofdakker, 1999); patients did however report feeling tired and
having more energy and improved mood. This study shows that there may be other
individual differences that contribute toward sleep deprivation.
Chronic sleep deprivation
Studies of chronic sleep deprivation have observed increased mood disturbance and
negative mood states and greater effort to perform and decreased motivation during
chronic sleep restriction; however, the significance levels for these reports are small
and unimpressive (Lucas, 1975).
A few studies have also examined the occurrence of self-reported symptoms during
sleep restriction records. A study by Tobler and Borbély (1986) showed how
participants in their study reported an increased incidence of blurry vision, eye
dryness, itching and aching and also an increase in appetite when participants were
gradually restricted in their sleep across six to eight months. A further study by
Tobler, Borbély and Groos (1983) showed how frequent headaches were reported by
23
participants who were restricted to four hours in bed compared to those who were
allowed eight hours.
Selective non rapid eye movement and rapid eye movement sleep deprivation
Studies which examine selective stages of sleep deprivation do so by electively
eliminating one or more stages of sleep while having minimal impact on the other
sleep stages and total sleep time. Originally, such studies were conducted to
determine the significance of REM sleep or SWS and so specific experimental
awakenings or arousals were experimentally induced at the onset of a particular stage
of sleep for one or more night.
Earlier experiments conducted to investigate REM sleep determined that selective
deprivation of REM sleep accomplished by the awakening technique resulted in
increasingly frequent attempts by participants to enter REM sleep. This can be
supported by Agnew, Webb and Williams (1967), who showed how those
participants who were deprived of REM sleep required seventeen awakenings on the
first night, on the fourth night forty two awakenings were needed and sixty eight
awakenings were required on the seventh night to maintain REM sleep deprivation.
Agnew and colleagues also observed large increases in REM sleep amount when
recovery sleep was allowed which was not disturbed.
The EEG data from such studies can be easily replicated but the impact of REM
sleep deprivation psychologically in terms of function and performance has been
difficult to determine (Pearlman, 1982).
There are various theories that attempt to describe the function of REM sleep, such
as the:
•
Drive facilitation hypothesis;
•
Activation synthesis hypothesis;
•
Catecholamine restoration hypothesis;
•
Cortical homeostasis hypothesis;
•
Information-processing hypothesis;
24
•
Neural growth promotion hypothesis;
•
Oculomotor hypothesis;
•
Protein synthesis hypothesis;
•
Sentinel hypothesis.
There are more.
Recent findings have supported the notion that the activation of the brain during
REM sleep is associated with memory consolidation, synthesis of new or adaptive
information or arrangement of information into an internal association framework.
Of the six reviews that have been published since the year 2000, four of the reviews
conclude that REM sleep or sleep in itself is significantly involved with memory
(Maquet, 2001; Stickgold, Hobson and Fosse, 2001; Smith, 2001; Peigneux, Laureys
and Delbeuck, 2001). The remaining two reviews, however, concluded that there was
little evidence to support a role for REM sleep in human memory (Siegel, 2001;
Vertes and Eastman, 2000).
Work by Peigneux, Laureys and Delbeuck (2001) have shown through animal
studies that REM sleep increases after learning and that REM sleep deprivation after
a task that has been learned decreases retention. Studies in humans, however, have
not shown as much support and this could be due to the fact that some of the animal
results may have been secondary to stress or another extraneous variable (Siegel,
2001). Although there is not sufficient evidence to support the role of REM sleep in
declarative memory, there are recent studies in humans which have found an
improvement in perceptual performance after an eight to ten hour training session
and when REM sleep was allowed at intervals (Stickgold, Hobson and Fosse, 2001).
The findings from this study have led to the hypothesis that perceptual learning,
rather than retention of material which has been memorised, is related to REM sleep.
Nevertheless, Siegel (2001) states that these findings do not explain why those
participants whose REM sleep has been eliminated by the use of monoamine oxidase
inhibitors or brainstem injury have no measurable memory deficits.
25
Other studies which have selectively prevented participants from entering stage 4
sleep through continuous arousals have shown that participants would make an
increased effort to enter the stage and had stage 4 rebounds when sleep was not
disturbed (Agnew et al, 1967). Agnew et al (1967) compared the effects of stage 4
and REM sleep deprivation; they found that participants required five to seven times
as many arousals to deprive them of stage 4 sleep than to deprive them of REM sleep
during each night when they were being selectively sleep deprived. The recovery
nights which followed stage 4 increased only on the first recovery night and REM
sleep which was not deprived increased on recovery nights two and three. After the
deprivation of REM sleep, REM sleep increased throughout three recovery nights but
there was no increase of stage 4 sleep on any recovery night.
Sleep fragmentation
Bonnet and Arand (2003) examined the relationship between various schedules of
sleep fragmentation and residual sleepiness on the following day. They showed that
there was a strong relationship between rate of fragmentation and decrease in sleep
latency as measured by the MSLT. A further study supported the fact that increased
sleepiness after sleep fragmentation was also associated with decreased psychomotor
performance on a broad range of tasks with degraded mood (Bonnet, 2005).
Another study by Bonnet (1983) showed how performance loss was the same on a
vigilance test after sleep fragmentation and total sleep deprivation but less on other
problems completed and simple reaction times after sleep fragmentation.
Another study by Series, Roy and Marc (1994) demonstrated patients to have a
significant increase in apnoea/hypopnoea index and it was found that after both sleep
fragmentation and sleep deprivation this increase was actually greater after sleep
deprivation.
The findings from these studies indicate that there is much in common between highfrequency sleep fragmentation and total sleep deprivation. The restorative function of
sleep is severely impaired by high rates of sleep fragmentation. Medical disorders
that are exacerbated by sleep include gastro-oesophageal reflux, nocturnal angina and
asthma.
26
Sleep-deprivation studies
Human participants
In 1960 Dement studied eight volunteers who were monitored during their sleep
throughout the night and woken every time the volunteers went into REM sleep. The
first night the volunteers were woken on average twelve times; by the seventh night
this increased to twenty-six times. This was seen as an indication of the vital nature
of REM sleep, the need for REM sleep growing stronger the more the participants
were deprived of it.
Dement reported that the participants exhibited only minor and temporary behaviour
changes associated with this loss of REM sleep. Dement had expected there to be
disturbed behaviour patterns emerging from volunteers who had been deprived of
REM sleep. The final consequences of sleep deprivation are obviously not shown in
humans compared to non-humans; this is because human participants in experiments
are treated differently to rats or cats (Bentley, 1999).
One of the best signs of stress in humans apart from changes in behaviour during
sleep deprivation is the increase in the output of certain hormones. Under nonstressful conditions cortisol is released in small amounts throughout the day and has
an obvious circadian rhythm. It peaks around the start of wakefulness and troughs at
the beginning of a persons’ daily sleep period. Cortisol production helps mammals
endure stress especially in helpless situations. In the 1950’s, Dr Hans Selye identified
three phases in the cortisol response to stress: alarm, resistance and exhaustion
(Selye, 1976). Exhaustion occurred only when many days would have elapsed.
Selye’s interpretation is said to be too simple an explanation for what is said to be
clearly a complex problem (Horne, 1988). Selye (1976) observed that whilst injury
and illness are major causes for the initial alarm response, it will also occur whenever
the body is pushed to extremes. On an important note, psychological factors such as
“apprehension” and “fear” are also triggers for this hormone (Horne, 1988).
Although animals will show an increase in the release of cortisol during sleep
deprivation this is not however the case in humans. In other words, humans can be
sleepy, irritable and have a great desire to sleep but as long as no harm will come to
us and that we can pull out of the situation if necessary then the deprivation will not
necessarily be stressful and this is true of experimental conditions, too (Horne, 1988).
27
In terms of lifelike and real-world investigations of sleep deprivation in humans,
various military research groups throughout the world mostly using male soldiers and
usually referred to as “Sustained Operation” (“SUSOP”) have carried out various
experiments. The advantages of studying such a group is that some ethical and safety
factors applied to civilian subjects can be put aside and therefore sleep loss of up to
three days of continuous battle can be simulated. Such situations also include heavy
exercise and food restriction (Horne, 1988). Such experiments, although very useful,
do, however, highlight doubts whether the observed effects are due to sleep loss or
other factors (Horne, 1988).
One of the main criticisms of such studies is that civilian subjects can withdraw from
experimental conditions in a laboratory. Soldiers, however, cannot do this easily. The
pressure placed on the individual together with the anxiety caused by the need to
perform well adds to the stress. On a positive note, the continuous stimulation
offered in such conditions will counteract the sleepy state of the soldiers (Horne,
1988).
Case studies in sleep deprivation
There are three classic case studies in severe sleep deprivation that are well
documented and demonstrate various effects of going without sleep for prolonged
periods.
Gulevich (1966) reported a 17-year old young man, Randy Gardner, who was able to
stay awake for 264 hours (11 days). Gardner developed slurred speech and blurred
vision-a combination of perceptual and cognitive faults. Gardner mistook some
objects for people and showed what have been described as symptoms of mild
paranoia: Gardner thought that people were labelling him as stupid because of his
cognitive difficulties. However, Gardner did not experience a complete mental
breakdown and once he was able to sleep he did so for 15 hours on the first night and
made up a total of just one quarter of his lost sleep. Most of this was Stage 4 NREM
and REM sleep. What this may indicate is that Stage 4 NREM and REM sleep may
28
be the most important when the body has been deprived of sleep; nevertheless, it
does not tell us what the important functions are of these stages.
Another case study reported by Dement in 1972 was of a disc jockey named Peter
Tripp who stayed awake for 200 hours as a publicity stunt in New York. Quite severe
paranoid psychosis appeared to develop, with Tripp reporting having been poisoned
by persons unknown. He displayed, too, self-harming behaviour by trying to throw
himself under the wheels of the traffic. Dement described how Tripp’s behaviour and
personality changed drastically subsequent to being deprived of sleep.
Compared to Gardner’s experience of sleep deprivation, the behaviour displayed by
Tripp was very different; this could be due, perhaps, to individual differences or from
differing expectations, as Tripp may have expected to experience strange experiences
and sensations and so on, whereas Gardner may have not (Bentley, 1999).
The final case study, which was of a more clinical or pathological nature, was
observed by Lugaresi (1986). Lugaresi followed the progress of a 52-year-old man
who was unable to sleep. The sudden onset of sleep deprivation happened when the
subject turned 52 and as the sleep deprivation continued, the sufferer became more
and more exhausted which led to the development of a fatal lung infection. Post
mortem analysis revealed lesions in two areas of the thalamus which is linked to
sleep and hormonally controls circadian rhythms. The neurones were found to be
completely destroyed within this area. It can be deduced from this case study that
sleep deprivation alone could have killed this 52-year-old sufferer, however it may
be more likely that the sleep deprivation had major effects including increased stress
that makes the person more susceptible to infection (Bentley, 1999). What was first
described by Lugaresi in 1986 was later (1995) called ‘Fatal Familial Insomnia
(FFI)’ and now is known to be an autosomal dominant prion disease, characterized
by degeneration of the thalamus and impaired control of the sleep-wake cycle,
autonomic and endocrine functions, involving a progressive decrease or complete
absence of sleep activity. Case studies such as these, while it is often said that they
29
are difficult to use to support a hypothesis, can be generalised to a theory, if there
were a good theory about the nature of sleep.
Experimental studies
Experimental studies of sleep deprivation take a more gradualist route of studying
sleep deprivation rather than doing without it altogether. Webb and Bonnet’s (1978)
study of sleep deprivation started with participants being deprived of just 2 hours
sleep; at this point the participants reported feeling well, though it was observed that
they did fall asleep quickly the following night and then slept for longer. The
participants in this experiment were also put on a two-month programme of gradual
sleep reduction from an initial eight hours a night sleep down to a final four hours.
The participants did not report any adverse effects; nevertheless, this is something
that does not indicate that there is an ability to do without sleep if necessary.
In conclusion, the actual amount of sleep per night averages out at about seven to
eight hours in total but there are individual differences. When making up for lost
sleep a need to do so is not shown, just some of it. This is known as the REMrebound effect, as studies have shown that most of the ‘caught-up’ sleep is REM
sleep plus the Stage 4 NREM sleep leading into REM.
Huber-Weidman (1976) collated an overview of the findings of studies that have
investigated sleep deprivation. The symptoms of such deprivation in these studies
were more psychological than physiological for people who had been deprived of
sleep for a few days. It is also important to notice that that many if not most of the
effects were due to REM deprivation alone rather than total sleep deprivation.
Research by Gribbin in 1990 suggested an extra and difficult effect, indicating that
too much sleep can impair performance and perhaps lead to or be part of
psychological disorders. It has been mentioned earlier that increased REM sleep is a
feature of many people with depression; tricyclic antidepressants successfully lift this
disorder, selectively blocking and reducing REM sleep without interfering with
NREM sleep (Gribbin, 1990). Pinel (1993) uses this notion to claim that REM sleep
30
deprivation is not harmful. Speculation by Horne (2006) directs attention to what
have been called ‘ponto-geniculo-occipital spikes’ (PGO spikes) or PGO waves,
which derive from three brain areas: the Pons, the geniculate thalamus and the
occiput. They have been registered on electroencephalographs as coinciding with
REM sleep and both are paralleled with twitches of the fingers and toes. Horne
(2006) theorises that PGO waves are internally generated to bombard the cortex to
simulate exterior stimuli, keeping the brain active while consciousness is ‘switched
off’. In babies in utero this stimulation is especially intense. Such random stimulation
may cause the brain to try to make sense of it by creating dreams.
Evolutionary or ecological theory
Meddis (1975, 1979) put forward an explanation for why we sleep, using an
evolutionary or ecological perspective. This theory proposes that sleep could be a
time of increased safety as animals are immobile and therefore less likely to be
noticed by predators. Meddis suggests that it is better to be still when it is too dark to
see either food or threats, acting as an advantage for some animals.
However, not all species of animals fit the human, primate or mammalian pattern.
Those animals that are nocturnal in habit, such as owls, are specialised to see in low
light conditions and bats, which are not dependant on light to find food or to be
aware of their environment, use sonar mechanisms to find their way around in
conditions where humans are without effective sight. Through evolution these
species have developed sleep patterns that fit in with their way of life, sleeping
during the day in places of safety. Such species’ sleep patterns still agree with
evolutionary theory. There are also those species such as lions that have no predators
(Lloyd et al., 1984). Lions appear to be relatively happy wherever they choose to
sleep and whenever they can.
Another type of creature, which does not fit in with the theory, is grazing animals.
Cows and antelopes spend a majority of their time grazing in herds. For these
animals to remain still in such a wide-open field would pose great danger and
therefore not remaining vigilant could be seriously maladaptive. Given this, as they
31
are constantly at serious risk from predators, this lack of sleep would support
Meddis’ theory concerning safety; conversely it is known that animals which graze
on vegetation gain little nutritional value per kilogram (meat/protein is the highest
energy food) and in order to survive such grazing animals must eat virtually
continuously over any 24 hour period. If they did not and stopped to sleep they
would lack nutrients and energy for the next day (Meddis, 1975).
The evolutionary or ecological theory is based upon the concept that when humans
lived in a truly wild state, when our distant ancestors were evolving, those who were
able to sleep at night survived better as they were less likely to become prey. Energy
had been conserved when it was too dark to see and individuals were successfully
hidden from predators. It was those groups of people who were able to pass on the
characteristic of sleeping through the night who increased the likelihood of survival
for their descendents (Meddis, 1979).
The evolutionary or ecological theory fails to explain why after sleep deprivation
humans sleep longer and fall asleep in daylight. The theory proposes that humans
sleep to preserve themselves. If this were the case it would be found that animals that
are likely to be attacked would sleep rather little. This is generally found to be true:
predators tend to sleep more than those species of animals that are preyed upon
(Bentley, 1999). In addition, it is odd that humans sleep and thus leave themselves in
a poor defensive state, even if in protective social groups where there are others to
act as sentries or night watchmen: 24 hour alertness would clearly enhance survival,
while the sentries always need to sleep in daylight hours to regain their lost sleep.
Generally, being paralysed and senseless for hours does not seem of any value when
animals are faced with various dangers, including predation. It is advantageous being
still and quiet in the dark to avoid danger but being essentially unconscious, unaware
of one’s surroundings shows only vulnerability (Bentley, 1999).
Core sleep
Horne (1988) put forward a model, which acted as a bridge between a theory of sleep
and sleep-deprivation studies. Horne stated that most people have more sleep than is
32
needed. It has been stated and described, in the restoration theory presented earlier,
that people sleep so that their bodies need time to replenish biochemicals that have
been used during the day. Horne pointed out that cell restoration is not just limited to
what goes on during the night, it occurs during the day, too, suggesting that perhaps
only some sleep is necessary, perhaps the early hours. Horne referred to this as being
core sleep. Horne bases this concept on an older study where groups of participants
were allowed six weeks on a fixed amount of sleep per night. One group of
participants slept for four hours nightly, a second group slept for six hours and the
third group for seven-and-a-half hours. Participants were also given cognitive tasks
to complete before and after the experimental sleep period and only those who were
given four hours of sleep showed any deleterious effect on memory. From this Horne
concluded that only about five hours of sleep a night are required; any more has been
termed as optional sleep and could be omitted without any ill effects. Figure 2.2
shows the progression of sleep stages across a single night’s sleep in a normal
human; from this diagram it may be seen that Horne is suggesting that Stage 4
NREM sleep is vital but only about half the average REM sleep is needed (Bentley,
1999). Long-term loss of REM sleep, however, is associated with psychological
dysfunctions such as hallucinations or waking dreams, something that does not
support Horne’s theorising. This theory as a whole is still basically conjecture and it
is difficult to see how empirical evidence could be obtained to support this
hypothesis (Horne, 1992).
Meddis also suggests that babies tend to sleep longer to prevent exhaustion in their
mothers. However this concept does not explain the survival of the non-sleepy trait
in babies, nor the variation in quantities and type of sleep in people of all ages.
Empson (1989) has described Meddis’ theory as a ‘waste of time’ theory, meaning
that it suggests that sleep is a waste of time (Empson, 1989). Empson suggests that
sleep is universal among animals; even the most successful predators; sleep
deprivation can on occasion be fatal, suggesting that sleep has some value.
33
It has been suggested by Horne that sleep may perform different functions in
different species and different sizes of animals, such as aquatic animals, grazing
animals and those with higher intellects (Horne, 1988). There are evolutionary
principles at work when dolphins appear to develop sleep-adaptations specific to
their environment. Sleep must be serving a purpose and each species evolve a means
of sleeping in such a way that does not threaten their survival (Horne, 1988).
Summary
Three of the main theories which propose an explanation for why there is sleep have
been described in this chapter: sleep as restoration and an extension of the restoration
theory in the neurochemical model of sleep and finally sleep as an evolutionary
behaviour.
The restoration theory proposed by Oswald suggests that both REM and NREM
sleep restore and replenishes our brains and bodies. During sleep neurochemicals are
resynthesised and the growth hormone is secreted. There is evidence for and against
this theory. Non-human animal studies show mixed support for this theory.
Hobson proposes a three-tier analysis of sleep which ties together the models
described in this chapter.
Research has shown that detrimental effects occur when various species are denied
sleep. These effects vary from minor, short-term perceptual problems to major and
lasting personality changes. Little is known about the extent that these are
specifically caused by total sleep deprivation or REM deprivation.
The neurochemical theory, states that sleep has a specialised restorative function in
the brain. It has been suggested that REM sleep is associated with a noradrenaline
pathway and replenishes noradrenaline levels in the brain. NREM sleep is associated
with serotonin levels and might require a critical level of serotonin to be switched on.
Sleep is not seen as just one phenomenon but usually several. Sleep can be divided
into two main types, this being REM (rapid eye movement) where dreams occur,
perhaps under the prodding of PGO waves and NREM (non-rapid eye movement)
34
sleep where the eyes are fairly still and we hardly dream. NREM sleep consists of
four stages; each stage is characterised by its own electroencephalographic (EEG)
pattern.
The last theory described in this chapter, the evolutionary or ecological theory
suggests that sleep is a time of inaction so that prey can be safe from predators. Sleep
in babies can be explained using the evolutionary theory. There are, however,
observations which do not fit this model, Horne attempted to overcome these
criticisms by hypothesising that sleep performs different functions in different
species.
The theories and evidence presented within this section attempts to explain the
function of sleep. It can be said that some of the studies do require further
investigation and support. It is also, as usual, quite difficult to extend the evidence
from animal to human studies. All the evidence, human and animal, also as usual,
may be accused of being presented in a rather biased way, according to which
particular school of thought it is attempting to support. This falls short of the ideals
of the scientific method, is characteristic of swathes of human research in every field
but thankfully is not true of all.
35
2.1.2 Physiology of sleep
Although sleep is an altered state of consciousness, it is not a state of
unconsciousness, meaning that even those who are deep sleepers can still be aroused
from their somnolent state. Normal sleep consists of humans sleeping once per day
and within this period of sleep humans will experience a number of different states of
consciousness. Dement and Kleitman’s sleep medicine work has shown that not only
are there two types of sleep but there are, as well, associated brain waves
(electroencephalogram-EEG) (EEG is discussed further in section 2.4.2) patterns.
These two types of sleep alternate in an ultradian rhythm (meaning less than a day,
cycles which occur within a day) and that dreaming is associated much more strongly
with one of those types.
The two types of sleep being referred to here are rapid eye movement or REM sleep
and non-rapid eye movement or NREM sleep, these will be discussed next.
Stages of sleep
As sleep deepens it goes through four separate stages (Bentley, 1999). Each stage of
sleep has its own EEG pattern; there are four stages in NREM sleep (also referred to
as quiet sleep).
Stage 1 NREM
Stage 1 sleep is when sleep begins and this usually takes fifteen minutes. Recordings
show brain waves slow down from the alpha waves of relaxation to even slower and
more irregular theta waves (see figure 2.1). Once these patterns synchronise, typical
characteristics emerge. The parasympathetic nervous system governs this stage; heart
rate slows down and muscles relax. Falling asleep may not be a conscious process
and is a state very similar to deep meditation and relaxation. During this stage
arousal occurs easily and full consciousness can recur quite easily. This first relaxed
stage of sleep is also known as the hypnogogic state and some writers link
hallucinatory images occurring now to creativity.
36
Stage 2 NREM
This stage lasts for approximately twenty minutes, the brain waves get slower and
larger with intermittent little bursts of activity called sleep spindles, electrical activity
(little is understood in terms of its purpose or function), k-complexes, these are tiny
burst of activity which is usually associated with external stimuli which do not
awaken us (environmental stimuli). Physiological changes such as a decrease in heart
rate, blood pressure and body temperature continue and quieter sounds no longer
disturb sleep.
Stage 3 NREM
There is a further decrease in heart and breathing rate and brain waves slow further
and now occur as delta waves. It is usually very difficult to be aroused from this
stage; like stage 2 sleep this stage lasts for only a few minutes.
Stage 4 NREM
This stage is characteristic of the deepest sleep. Metabolic rate is at its lowest and it
is very difficult to waken out of this state – usually only a significant noise can
arouse the person from this stage, such as a baby crying. Brain waves are usually
slow. This stage lasts for thirty to forty minutes and is the bottom of the ‘sleep
staircase’ (Bentley, 1999). Although this stage is the deepest stage of quiet sleep, this
is the stage at which sleepwalking is likely to occur and is not associated with
dreaming (Jacobson and Kales, 1967). Sleep talking also occurs in deep NREM
sleep, although this can happen but less often during REM sleep as well (Arkin,
1970).
REM sleep including dreaming
After half an hour into Stage 4 sleep, the EEG trace speeds up the ‘sleep staircase’
through Stages 3 and 2, thus showing the brain to be suddenly more active, (Bentley,
1999). The once synchronised brain waves become desynchronised and more
complex as well as faster; the brains oxygen and glucose demands also increase. The
eyes will also start to move rapidly under the closed eyelids, this state is known as
REM sleep and the person is most difficult to arouse.
37
Cerebrally there is considerable activity paralleled by physical inactivity; the body
will appear almost paralysed. The heart and lungs will match the brain activity even
though the body is inactive. REM sleep lasts for about ten to fifteen minutes and this
completes the first sleep cycle of the night.
Once REM sleep has elapsed then there is progression through Stages 2 to 4 again
and this cycle repeats about every ninety minutes throughout the night. As the night
continues sleep in Stages 3 and 4 lessens until only Stage 1 and 2 of NREM plus
REM sleep are returned to by the end of the night (see figure 2.2). This ninetyminute cycle is the ultradian rhythm of sleep. Recalling a dream often depends on
which stage a specific awakening occurs.
REM sleep has been called ‘dream sleep’ or the ‘D state’ and some have gone as far
as to call it the ‘third state of existence’. Eighty percent of the time, when sleeping
volunteers are woken during REM sleep, they’ll report that they have been dreaming.
The nature of REM’s reflects the content of the dream.
Other terms for REM sleep
Dement and Kleitman (1957) made observations and noted that REM sleep is
associated with highly active brain activity yet the body is in a paralysed state;
actually, this is called ‘atonia’: ‘without movement’, switched on by a part of the
brain called the locus ceruleus at the commencement of REM sleep and off when it
finishes. Dement and Kleitman coined the term paradoxical sleep to describe this
apparent contradiction, the paradox being that the brain is full of activity while the
body is inactive. Modern researchers would prefer REM sleep to be renamed as
Stage 5 sleep (Bentley, 1999).
Meddis (1979) referred to NREM sleep as quiet sleep and REM sleep as active sleep.
These terms were coined due to the brain activity shown by the EEG traces. Meddis
further subdivided quiet sleep into light quiet sleep (LQS) with synchronised slow
patterns of EEG traces and deep quiet sleep (DQS) which is representative of larger,
regular wave-like EEG traces. Stage 2 sleep would be seen as light quiet sleep and
38
Stage 4 would be seen as deep quiet sleep. Stage 1 and REM sleep would be seen as
Active sleep (AS).
Table 2.1 displays the difference in physiological characteristic of NREM and REM
sleep in humans and Table 2.2 shows the different terms that are used to describe
REM and NREM sleep.
Table 2.1: Differences in Physiological Characteristics of NREM and REM in
Male Humans at/during Sleep
Measurement
NREM Sleep
REM Sleep
Scalp EEG*
Slow waves and spindles
Low voltage, mixed frequency
Hippocampal EEG
Variable
Rhythmic theta activities
Eye movements
None or few slow
movements
Conjugate rapid movements
Chin electromyography
(EMG)*
Decreased from
wakefulness
Almost absent
Body movements
A few gross
movements
Twitches
Respiration
Regular, deep
Variable, shallow
Heart rate
Regular, slow
Variable, rapid
Blood pressure
Below waking level
Variable
Penile erection
Normally absent
Normally present
Mentation
Thought-like, repetitive
Dream-like, dramatic
Galvanic skin response
Frequent
Rare
From: Freemon, (1972) Sleep Research: a critical review. Springfield.
Table 2.2: Terms Synonymous with REM and NREM Sleep
REM
NREM
Dreaming
Paradoxical
Fast
Active
D-sleep
Desynchronised
Nondreaming
Orthodox
Slow
Quiet
S-sleep
Synchronised
From: Anch et al (1988) Sleep: A Scientific Perspective, Prentice Hall, Englewood Cliffs, New
Jersey.
39
Figure 2.1 Examples of waveforms that differentiate sleep stages
Cps - cycles per second. From: www.rtmagazine.com/issues/articles accessed 22nd June 2009.
40
Figure 2.2: The progression of sleep stages across a single night sleep in a normal adult.
From: http://somnience.com/images/sleep_cycle.jpg accessed June 22nd 2009
41
Summary
This section deals with the physiology of sleep. It has highlighted the main stages of
sleep, these being, Stage 1 NREM sleep which lasts for fifteen minutes, Stage 2
NREM sleep which lasts for twenty minutes and brain waves get slower and sleep
spindles begin to emerge. Stage 3 NREM sleep shows a further decrease in heart and
breathing rate leading onto Stage 4 NREM sleep which is also known as deep sleep
where only a significant noise can arouse a person from sleep and finally REM sleep
and dreaming occurs which occurs thirty minutes into Stage 4 NREM sleep, in this
stage the brain has been shown to be more active and a key feature of this stage is
that the eyes will also start to move more rapidly under closed eyelids and the person
is most difficult to arouse.
42
2.1.3 The classification of sleep disorders
Introduction
The last 15 years have seen a major advancement in sleep medicine, the ability to
diagnose, evaluate and treat disorders of sleep and arousal, leading to the discovery
of more than 60 disorders. Sleep disorders are not prevalent in just one particular age
group; they affect all ages. Disorders can be mild or life threatening; these
advancements would not have been made without improved knowledge of the
physiology of sleep, the technological advances which have allowed researchers to
measure the physiological variables affecting sleep.
Historical background
The early 1970’s saw a growing clinical interest in sleep disorders and arousal. As
with any common interest, there was a lack of common terminology and diagnostic
framework for the various disorders. This showed that there was a need for a
classification system that would allow the definition and specification of a disorder.
It is important to note that most medical disorders can still be described using the
phenomenological method, which looks at the effects on certain body systems as
reported by individuals from their subjective experience. Many medical conditions
are classified according to the cause of the disease; such disorders are described as
being infectious, metabolic, neoplastic, and traumatic. The aetiology of sleep and its
disorders remains unknown, thus resulting in the clinician relying upon the
phenomenological method rather than the aetiological classification of sleep
disorders.
Diagnostic Classification of Sleep and Arousal Disorders (1979)
1979 saw the development of the Diagnostic Classification of Sleep and Arousal
Disorders (DCSAD) by The Association of Sleep Disorders Centers (ASDC) and the
Association for the Psychophysiological Study of Sleep (APSS). It was important for
the committee members to produce a diagnostic criterion that had validity and was
standardised too. The production of the manual allowed the various included entities
to be challenged and tested and if proven valid to be revised in future editions.
43
The following table illustrates the main categories of the system:
Table 2.3: The Diagnostic Classification of Sleep and Arousal Disorders
A. Disorders of initiating and maintain sleep (DIMS) (Insomnias)
B. Disorders of excessive somnolence (DOES) (Hypersomnias)
C. Disorders of the sleep-wake cycle
D. Dysfunctions associated with sleep, sleep stages or partial arousal
(Parasomnias)
The International Classification of Sleep Disorders (ICSD) (1990)
The DCSAD was a useful tool and widely used but over the years a number of issues
were highlighted, these being entries included twice, for example, sleep apnoea
which was included in both DIMS and DOES and, as discussed earlier, this was due
to the fact that the classification system was based upon symptoms rather than
aetiology. Other sleep disorders were not classified accordingly and this only became
apparent once the DCSAD had been integrated into the sleep medicine community
and as mentioned previously a new edition would suffice if there were also new sleep
disorders identified.
Due to these issues with the DCSAD, The International classification of sleep
disorders was produced in association with the American Academy of Sleep
Medicine (AASM) with the European Sleep Research Society, the Japanese Society
of Sleep Research and the Latin American Sleep Society in 1985 and was finally
published in 1990; the classification was a revised edition form of the DCSAD.
The ICSD (1990) was based on the formation of a questionnaire survey completed by
sleep specialists. As a result of this survey it was stated that the ICSD would not be
based on symptom but by the physiological manifestations of the presenting sleep
disorder. Due to the advancements made in the last ten years or so since the first
classification manual emerged, it was thought to be possible to be able to do this.
Further evidence and research allowed parasomnias (discussed in section 2.1.4) to be
given subcategories; further diagnostic information was needed through research on
respiratory and neurological disorders.
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The International Classification of Sleep Disorders-2 (2005)
Introduction
The American Academy of Sleep Medicine published the second edition of the
International Classification of Sleep Disorders (ICSD-2) in 2005. The goals of the
ICSD-2 were to scientifically and clinically describe all current sleep and arousal
disorders and that the presentation of the disorders was scientifically valid and
rational and lastly to ensure that the sleep and arousal disorders were compatible with
the ICD-9 and the ICD-10.
Originally it was thought that it would be possible for a common framework in
which sleep disorders could be categorised, this notion had to be abandoned as it
proved to be a impossible task. The ICSD-2 sorts the sleep disorders into eight
categories which appear to be pragmatically and empirically valid (ICSD-2, 2005). In
the ICD-2 some disorders are based on a common complaint (e.g., insomnia or
Hypersomnia), other disorders are based on a basic aetiology, for example biological
clock disturbances for circadian rhythm sleep disorders. Other disorders are based on
depending which organ system the disorder arises from.
The eight categories are:
•
Insomnia
•
Sleep related breathing disorders
•
Hypersomnias of central origin
•
Circadian rhythm sleep disorders
•
Parasomnias
•
Sleep related movement disorders
•
Isolated symptoms and normal variants
•
Other sleep disorders
The members of the sleep committee who revised and updated the ICSD-2
understand that there are probably many cases of sleep pathologies that may not yet
have been adequately documented in the sleep literature. To include a new disorder
within the ICSD-2, it was necessary for the complaint to appear at two different sleep
45
centers, each of which had to have a minimum of two cases and published in specific
reputable journals with a valid evaluation of the new disorder.
With the ICSD-2 there may be a particular sleep disorder which may clearly belong
to a particular sleep category but, for example, cannot be diagnosed as any specific
disorder within that category because it does not satisfy the necessary diagnostic
criteria. As well, if a particular sleep disorder cannot be classified due to the fact that
there is not sufficient detail available to know whether or not all the diagnostic
criteria have been met, then the clinician is required to select “unspecified” or “not
otherwise specified” (NOS) as the appropriate diagnosis. The ICSD-2 can be used to
classify sleep disorders in both adults and children.
Differences between the ICSD-1 and ICSD-2
Although there were a large number of changes that concerned the individual’s sleep
disorder, there were, however, also structural changes which occurred between the
ICSD-1 and the ICSD-2. These are listed below:
•
There is no axial system for the ICSD-2, the ICSD-2 is only concerned with
diagnosing sleep disorders as in axis A in ICSD-1.
•
The ICSD-2 does not contain a list of current procedures that the ICSD-1 did
which were used to diagnose the sleep disorder. The committee felt that the
procedures used in the study of sleep disorders across the world vary and
differ.
•
In order to group the sleep disorders into eight categories it was agreed to
eliminate the terms “intrinsic dyssomnias” and “extrinsic dyssomnias”
•
In the ICSD-2 the category ‘secondary sleep disorders’, for example those
due to mental, neurologic and other medical disorders are not included. The
rules of the ICD stresses that if the underlying mental, neurologic or other
medical disorder is diagnosed then it no longer remains secondary, it
becomes a primary disorder and therefore the category in which it falls under,
for example mental, neurologic or medical are the symptoms.
46
•
In the ICSD-2 there have been modifications made to the text outline used to
describe the individual disorder.
Impact on other classification systems
Impact on ICD-9-CM Classification of sleep disorders within the current
International Classification of Diseases (ICD-9-CM) was revised at the same time
that ICSD-2 was published, in order to establish greater concordance between the
systems. Many sleep disorders are now grouped into a single new series within the
"Diseases of the Nervous System" section of ICD-9-CM, although some remain in
other sections of ICD-9-CM (especially the "Mental Disorders" section).
Limitations of the International Classification of Sleep Disorders-2
One of the key limitations of the ICSD overall is that as one revision is made, newer
sleep disorders, sleep assessment tools and classification systems are being
continually developed due to the advancement in knowledge and extensive research
being conducted and contributing towards the ongoing development within the field
of sleep medicine.
Summary
In summary it is important to see how rapidly the changes have occurred within the
field of sleep medicine; this has been reflected in the way in which sleep disorders
are classified. As advancements in research occur and our knowledge expands so will
the current classification systems continue to develop. The specialists who have
developed the latest edition of the ICSD-2 state that as the classification went to print
there were already newer sleep disorders being discovered. The limitations of the
ICSD-2 have also been discussed.
47
2.1.4 Sleep Disorders
Section 2.2 described the classification systems of sleep disorders. This section will
describe in detail the range of sleep disorders and sleep behaviours that have been
identified using the ICSD-2 and information on the main features is provided.
Section 2.1.5 will describe the range of methods of assessments that are available and
Section 2.1.6 will introduce treatment strategies.
Introduction
Awareness of sleep disorders
Sleep disorders are very common; they also have a very serious health, economic,
social and occupational implication (Dement and Mitler, 1993). Professionally and
educationally it has been shown that sleep medicine training is a neglected area both
in medicine and psychology (Rosen, Rosekind, Rosevear, Cole and Dement, 1993;
Wiggs and Stores, 1996).
Despite sleepiness being a common symptom, those who suffer from sleep problems
maybe reluctant to trouble their general practitioner (GP). Friends and family of the
patient and sometimes the patient themselves are also known to trivialise their
symptoms; for example, a person who snores heavily may have an underlying
disorder such as obstructive sleep apnoea (OSA) so their symptoms will be shrugged
off and the serious respiratory condition is left undetected (Shneerson, 2005).
In the UK, sleep disorders remain amongst the most under-diagnosed and
undertreated group of medical conditions (‘Dead Tired’ Report, 2006).
In humans, sleep occupies approximately 8 hours of each 24-hour cycle but,
according to recent research, much less attention has been paid to the medical
problems associated with it than to those that occur during wakefulness (Shneerson,
2005). Justifications have been put forward to explain this. Patients are often reticent
about events that occur during sleep (Shneerson, 2005). Patients usually regard this
time as a personal and private time and are more reluctant to talk about problems
occurring during sleep than about those occurring during wakefulness. Patients can
also be unaware of any disorders surrounding their sleep at night and may only be
48
informed by a bed partner of disorders that involve irregular movements of limbs and
perhaps obstructive sleep apnoeas. Usually sleep problems are attributed to problems
that occur during the day or everyday life. This can be related to tiredness due to
overwork or age but perhaps it may derive from a sleep disorder.
Sleep disorders and sleep deprivation is on the increase in developed societies but the
awareness of such disorders does not reflect the rate at which this increase is
occurring (Groeger, Zijlstra and Dijk, 2000). Public education is required about the
importance of sleep, its main components and good sleep hygiene. The effects of
shift work and its consequences on sleep should also be made available (Terzano and
Parrino, 2000). Awareness of these issues should be an important influence on those
who have to make decisions regarding, for example, best practices at work, those
who work in educational establishments and those who work in government
establishments and have control over policies and regulations. These could help
those who have to drive for long hours and such decisions can be made on
motorways, on which there is greater risk related to sleepiness (‘Sleep SOS’, 2004).
Medical staff and those who work as health care professionals are also generally less
aware of sleep disorders, the assessment of sleep disorders, management of sleep
disorders and the issues arising during the day with those who have sleep disorders
(‘Sleep SOS’, 2004). Patients who go to see their physician usually do so during the
day whilst they are awake and therefore no diagnosis can be made concerning their
sleep issues. A survey concerning medical schools showed that sleep education was
very minimal throughout undergraduate and postgraduate medical education (Stores
and Crawford, 1998). Overseas, it is a similar story: an American survey of patients
who attended a clinic to complain about their insomnia showed that on average only
2.5 questions were asked concerning the patients sleep complaint throughout the
consultation. This is due to the fact that clinicians are not trained to deal with such
complaints and are unaware of the possible causes and the effects of the symptoms
upon the person (‘Sleep SOS’, 2004). This leads to a lack of any management plan to
help the patient (Shneerson, 2005).
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Costs of sleep disorders
Through research it has been found that the costs of sleep disorders to society are
potentially considerable (‘Sleep SOS’, 2004). Untreated obstructive sleep apnoeas
have been associated with strokes or myocardial infarction, which may be avoided if
the sleep disorder is recognised and dealt with early enough (Sert Kuniyoshi, 2008).
Another factor is that of the reduction in the quality of life (Reimer and Flemons,
2003). Through extensive research into this area it has been found that excessive
daytime sleepiness leads to irritability and difficulties in interpersonal relationships.
This not only impairs social activity but also can reduce and will reduce productivity
at work. Studies involving patients diagnosed with OSA before and after continuous
positive airway pressure treatment have been shown to have a reduced quality of life
before treatment; after treatment QoL improves (McArdle, Kingshott, Engleman,
Mackay and Douglas, 2001). Patients diagnosed with narcolepsy have been shown to
have the same life quality decrease prior to being prescribed modafinil (a drug that
ensures wakefulness) and after treatment show a significant increase. Lastly,
excessive daytime sleepiness impairs work productivity and can lead to accidents
that may have considerable financial consequences, due to those who have to take
time off work. Daytime sleepiness and insomnia appears to be on the increase
(Shneerson, 2005).
These costs can be avoided with better awareness of sleep disorders and the
treatment and advice made available to patients (‘Sleep SOS’, 2004) The cost of
providing facilities whereby such diagnosis and prognosis can be made should be
offset against potential savings (‘Sleep SOS’). Indeed sleep laboratories,
polysomnography and training staff is expensive but surely the cost to society when
lacking in these facilities is more costly. Costs of treatment can be reduced if the
simplest and effective methods are used first rather than the more complex and timeconsuming ones, such as polysomnography. Most drugs that are available to treat
sleep disorders are available at a reduced cost, such as benzodiazepines, hypnotics
and antidepressants. Treatments such as CPAP and light therapy are more expensive.
The intervention of the medical team together with supervision of the patient has to
be balanced against the benefit they provide.
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The ICSD-2
It is important to note that the sleep disorders and behaviours mentioned in this
section are not mutually exclusive. One particular sleep disorder may occur at the
same time as another and one may even have an impact on another. It is also
important to clearly define at this stage certain terms that are associated with sleep,
these being ‘behaviour’, ‘problem’ and ‘disorder’. So, a behaviour associated with
sleep may or may not be a problem, for example night waking is physiologically
normal; it only becomes a problem if the individual or perhaps the individual’s bed
partner is troubled by it (the bed partner may continue to remain awake during the
night because of their partner’s snoring). Laymen tend to equate sleep problems with
sleep behaviour but disorders are when there is something physiologically abnormal
about the individuals sleep. In these terms, the behaviour and the problem associated
with sleep may not be a disorder. In this thesis, ‘sleep disorder’ implies a behaviour
that is a problem, regardless of whether or not it is dependant on abnormal
physiology. Sleep behaviours such as teeth grinding, sleep taking and hypnogogic
jerks are not necessarily a problem.
Insomnia
The ICSD-2 defines insomnia as a “repeated difficulty with sleep initiation, duration,
consolidation, or quality that occurs despite adequate time and opportunity for sleep
and results in some form of daytime impairment” (ICSD-2, 2005).
Adjustment Insomnia (Acute Insomnia)
With adjustment insomnia the essential feature is the presence of insomnia in
association with an identifiable stressor. The sleep disturbance is of short duration
from a few days to a few weeks. The sleep disturbance will resolve once the main
stressor has been dealt with or if the individual is able to cope with the stressor.
Psychophysiological Insomnia
With psychophysiological insomnia the essential feature is heightened arousal and
learned sleep-preventing associations that result in a complaint of insomnia and the
associated decreased functioning during wakefulness.
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Idiopathic Insomnia
With idiopathic insomnia the essential feature it is usually a life-long inability
whereby the patient is unable to obtain adequate sleep and this may perhaps be due to
an abnormal neurologic control of the sleep-wake system; this being a neurochemical
imbalance of either the arousal system or the many sleep-inducing and sleepmaintaining systems.
Insomnia due to Mental Disorder
In insomnia due to mental disorder the essential feature is the occurrence of insomnia
that is caused by an underlying mental disorder. The insomnia usually begins at the
onset of the mental disorder and will usually mirror the disease as it changes.
Inadequate Sleep Hygiene
One of the essential features of inadequate sleep hygiene is that the insomnia is
associated with daily living activities that are inconsistent with the maintenance of
good quality sleep and full daytime alertness. The specific behaviours that are a
common element of this disorder can be classified into two general categories,
behaviours that produce increased arousal and behaviours that are inconsistent with
the principles of sleep organisation.
Insomnia due to Medical Condition
One of the essential features associated with this condition is that it is caused by a
coexisting medical or physiological condition. Usually this particular sleep disorder
is associated with sleep initiation or maintenance and non-restorative and poorquality sleep.
Sleep related Breathing Disorders
The disorders in this sub-group share one common feature: disordered respiration
during sleep.
52
Primary Central Sleep Apnoea
One of the essential features of primary central sleep apnoea (PCSA) is of unknown
aetiology (idiopathic) and is usually characterised in the polysomnogram by
recurrent cessation of respiration during sleep with the apnoea having no associated
ventilatory effort. Usually in patients with CSA ventilation and ventilatory effort
repetitively ceases over the course of the night. This pattern leads to sleep
fragmentation and tends to produce excessive daytime sleepiness and or frequent
nocturnal awakenings.
Cheyne Stokes Breathing Pattern
One of the descriptions of Cheyne Stokes breathing is that it produces recurrent
apnoeas, hypopnoea or both apnoeas and hypopnoeas which can alternate with
prolonged hyperpnoea which leads to the tidal volume to gradually increase and then
decrease, this prolonged increasing and decreasing pattern of hyperpnoea is the
hallmark of Cheyne-Stokes breathing pattern and it also distinguishes it from other
forms of CSA.
Central Sleep Apnoea due to Drug or Substance
Users of long-acting opioids may have central apnoea during sleep. The most
common drug to cause this sleep disorder is methadone, but, time-release morphine
and hydrocodone can also be responsible.
Obstructive Sleep Apnoea Syndromes
Also known as sleep apnoea, sleep apnoea syndrome, obstructive apnoea, mixed
sleep apnoea, sleep-disordered breathing, sleep hypopnoea syndrome and lastly
upper airway obstruction.
Obstructive sleep apnoea (OSA) is characterised by repeated episodes of complete
apnoea or partial hypopnoea in which the upper airway is obstructed during sleep.
OSA often results in reductions in blood oxygen saturation; these events are usually
terminated by brief arousals from sleep. Apnoeic and hypopneic events last by
definition, a minimum of ten seconds; most events last from ten to thirty seconds in
53
duration but can persist for one minute or longer. Apnoeic and hypopneic events can
usually occur in any stage of sleep but are most frequent in stage 1 and 2 NREM and
REM sleep rather than in stage 3 or 4NREM sleep. Events that occur in REM sleep
take longer and associated with more severe decreases in oxygen saturation; this
usually returns to baseline values once normal breathing has resumed. Snoring
usually occurs between apnoeas as reported by bed partners as do episodes of
choking and gasping with frequent movements that disrupt sleep. Symptoms are
exacerbated following the ingestion of alcohol prior to sleep or an increase in body
weight.
Patients report feeling unrefreshed from their sleep upon awakening, symptoms such
as disorientation, unsteadiness, mental dullness, in-coordination, severe dryness of
the mouth and morning headaches.
Sleep-related Hypoventilation/Hypoxemic Syndromes
Sleep-related Non-obstructive Alveolar Hypoventilation, Idiopathic
This sleep disorder is characterised by a decrease in alveolar ventilation; this results
in sleep-related arterial oxygen desaturation in patients with normal mechanical
properties of the lung. When patients present with diurnal as well as nocturnal
hypoventilation without a readily identifiable pulmonary, endocrine, neurological,
ventilatory, muscle or cardiac cause, the condition will be referred to as idiopathic
alveolar hypoventilation. Typically, the sleep-related hypoventilation develops in the
early stages of the condition that is a result of removal of the wakefulness stimulus to
breathe.
Sleep- related Hypoventilation/Hypoxemia due to Lower Airways Obstruction
These disorders are characterised by obstruction or an increase airflow resistance in
the airway below the laryngeal apparatus. Sections 2.9 and 2.10 discuss the nature of
chronic obstructive pulmonary diseases and bronchiectasis, which are both lower
airways diseases respectively.
Hypoxemia is a medical term used to describe insufficient oxygenation of arterial
blood. Patients who are diagnosed with chronic obstructive pulmonary disease and
54
bronchiectasis or other lower airway obstructions are increasingly predisposed to
developing hypoventilation/hypoxaemia as the severity of the underlying lower
airways obstruction increases.
Other Sleep Related Breathing Disorders
Sleep Apnoea/Sleep related breathing disorder, unspecified.
These terms are used for sleep related breathing disorders (SRBD) which cannot be
classified elsewhere or may not neatly fit into one category but are due to respiratory
disturbance in sleep.
Hypersomnias of Central Origin not due to a Circadian Rhythm
Sleep Disorder, Sleep Related Breathing Disorder or other cause of
disturbed Nocturnal Sleep.
Alertness is necessary for well-being and performance in modern society (ICSD-2,
2005). Individuals who experience sleepiness are predisposed to developing serious
performance impairment in a number of areas of function as well as their own
personal and social areas. This section includes a group of disorders in which the
primary complaint is daytime sleepiness but the cause of the primary symptom is not
disturbed nocturnal or misaligned circadian rhythms. Other sleep disorders may be
present and they must be first treated prior to establishing diagnoses within this
category.
Narcolepsy with Cataplexy
This sleep disorder is primarily characterised by excessive daytime sleepiness and
cataplexy. The symptoms associated due to narcolepsy with cataplexy are present
due to an unusual inclination to transition rapidly from wakefulness into REM sleep
and to experience dissociated REM sleep events. One of the most disabling
symptoms of this sleep disorder is excessive daytime sleepiness. Patients with
narcolepsy with cataplexy usually have repeated episodes of lapses into sleep across
the daytime. Patients will usually sleep for a short duration and awaken refreshed but
within two of three hours will begin to feel sleepy again. This pattern is repeated
throughout the day. Sleepiness usually occurs in monotonous situations (a lack of
55
cortical stimulation). Sleep attacks can also occur in unusual situations such as
eating, walking and sleeping. Sleepiness will usually vary in severity and cannot be
easily distinguished whether it is due to insufficient sleep or other sleep disorders.
Cataplexy is usually characterised by a sudden loss of bilateral muscle tone and is
provoked by strong emotions that are usually positive such as laughter, pride, elation
or surprise. Negative emotions such as anger can also be a trigger. Cataplexy can be
localised or can include all skeletal muscle groups. Lower and upper limbs, including
the neck, mouth or eyelids can be affected; those areas that are affected are the knees,
face and neck. Vision can be blurred, respiratory muscles are never affected but
patients may experience a choking sensation if the cataplexy occurs in an awkward
position. The duration of the attack of cataplexy is usually short and can range from a
few seconds to several minutes and recovery is immediate.
Narcolepsy without Cataplexy
One of the key features of narcolepsy without cataplexy is excessive daytime
sleepiness and is associated with naps that are refreshing in nature while nocturnal
sleep is normal or moderately disturbed without prolonged periods of sleep. Other
characteristics that may be present are sleep paralysis, hypnagogic hallucinations or
automatic behaviour. The attacks can last for 3 minutes or so. One of the features
necessary for diagnosis for this sleep disorder is that sleep latency must be less or
equal to eight minutes and two or more sleep onset rapid eye movement periods
(SOREMPs) on a multiple sleep latency test (MSLT) must be present.
Narcolepsy due to Medical Condition
One of the causes for narcolepsy due to a medical condition is a coexisting medical
or neurological disorder. In patients presenting with this condition, the narcolepsy
must be clinically or polysomnographically documented.
The severity of daytime sleepiness is usually varied. Other characteristics such as
sleep paralysis, hypnagogic hallucinations, insomnia or automatic behaviour may or
may not be present.
56
Medical conditions, such as tumours or sarcoidosis of the hypothalamus, multiple
sclerosis plaques that impair the hypothalamus, have been shown to produce genuine
characteristics of secondary narcolepsy with cataplexy.
Recurrent Hypersomnia (including Kleine-Levin syndrome and MenstruationRelated Hypersomnia
A key feature of this sleep disorder is recurrent episodes of hypersomnia, typically
occurring weeks or months apart. Episodes of hypersomnia usually last from a few
days to several weeks and can appear once to ten times a year. Episodes are often
preceded by prodromes such as fatigue or headaches that can last for a few hours
(ICSD-2, 2005).
Idiopathic Hypersomnia with Long Sleep Time
A characteristic feature of this disorder is characterised by severe excessive
sleepiness but with unrefreshing naps of up to three or four hours and a prolonged
major sleep episode and a greater difficulty in waking up either in the morning or at
the end of a nap.
Idiopathic Hypersomnia without Long Sleep Time
The diagnostic feature of this sleep disorder is that patients complain about constant
and severe excessive daytime sleepiness. Such excessive daytime sleepiness usually
results in unintended naps which are generally of an unrefreshing nature.
Behaviourally Induced Insufficient Sleep Syndrome
This sleep disorder often occurs when patients persistently fail to obtain the amount
of sleep usually required to maintain normal levels of alertness and wakefulness.
Patients diagnosed with this sleep disorder often have unintentional chronic sleep
deprivation and upon examining patients this reveals unimpaired or above-average
ability to initiate and maintain sleep.
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Hypersomnias not due to Substance or known Physiological Condition (Nonorganic
Hypersomnia)
A characteristic feature of this disorder is excessive nocturnal sleep, daytime
sleepiness; excessive napping is usually reported. Patients will report their sleep to be
of poor quality and unrefreshing. Patients tend to focus on their hypersomnia and
after episodes of interviews and psychometric testing psychiatric symptoms become
apparent.
Circadian Rhythm Sleep Disorders
Sleep disorders that fall into this subgroup arise when the physical environment is
altered relative to internal circadian timing or the circadian rhythm timing system
that is altered relative to the external environment.
Circadian Rhythm Sleep Disorder, Delayed Sleep Phase Type, (Delayed Sleep-Phase
disorder)
This disorder is marked by the following factors:
1. Sleep-onset and wake times are later than desired.
2. Actual sleep-onset times at nearly the same daily clock hour.
3. There is little or no reported difficulty in maintaining sleep once sleep has
begun.
4. Extreme difficulty in waking up at the desired time in the morning.
5. An inability to advance the sleep phase to earlier hours by ensuring sleep and
wake times.
There is usually no psychopathology present.
58
Circadian Rhythm Sleep Disorder, Advanced Sleep Phase Type, (Advanced SleepPhase disorder)
The advanced sleep-phase disorder is marked by a patient’s chronic inability to delay
the onset of evening sleep, the patient may also sleep later into the morning to
enforce conventional social sleep and wake times.
Circadian Rhythm Sleep Disorder, Irregular-Sleep Wake Type, (Irregular SleepWake Rhythm)
Patients with Irregular Sleep-Wake Rhythm may have a total of 24-hour sleep time
averagely, but the single sleep period is by no means of normal length; there is, too,
unpredictability in the patient being asleep at any particular time of the day.
Circadian Rhythm Sleep Disorder, Shift-Work Type, (Shift Work Disorder)
This disorder arises from irregularly scheduled hours of work during the habitual
hours of sleep; this can be shift work-rotating or permanent shifts, roster work, or
irregular work hours. The patient will report an inability to maintain a normal sleep
duration when the major sleep episode has begun in the morning after a night shift.
There is usually a reduction in sleep length, by one to four hours, which affects REM
and stage 2 sleep (Folkard and Barton, 1993).
Parasomnias
This particular group of sleep disorders are classed as parasomnias and are usually
undesirable physical events or experiences that occur during entry into sleep, within
sleep or during arousals from sleep. These particular events usually manifest through
the central nervous system (CNS) activation transmitted into skeletal muscle and
automatic nervous system channels. Parasomnias involve abnormal sleep related
movements, behaviours, emotions, perceptions, dreaming and automatic nervous
system (ANS) functioning.
59
Disorders of Arousal (from Non-Rapid Eye Movement Sleep)
Confusional Arousals
Patients diagnosed with confusional arousals usually have such symptoms due to
mental confusion or confusional behaviour during or following arousals from sleep,
these arise from slow-wave sleep in the first part of the night, and also when patients
attempt to awaken from their sleep in the morning.
Sleepwalking also known as Somnambulism
Sleepwalking consists of a series of complex behaviours that originate during slow
wave sleep and result in waking during sleep. Patients can either just sit up in bed or
sleepwalk or display frantic attempts to escape. It is usually difficult to wake the
patient and when aroused they are mentally confused. Sleep talking is also present
during sleepwalking.
Sleep Terrors also known as Night terrors
Sleep terrors arise from arousals from slow-wave sleep that can be accompanied by a
cry or a piercing scream and ANS and behavioural manifestations of intense fear.
The person usually sits up in bed and is unresponsive to external stimuli and if the
patient is awakened during the episode they will be confused and disorientated.
Parasomnias usually associated with Rapid Eye Movement Sleep
Rapid Eye Movement Sleep Behaviour Disorder (Including Parasomnia Overlap
Disorder and Status Dissociatus)
REM sleep behaviour disorder (RBD) is characterised by abnormal behaviours that
emerge during REM sleep which can cause injury or sleep disruption. This is
associated with electromyographic (EMG) abnormalities during REM sleep. The
electromyogram will demonstrate an excess of muscle tone or phasic EMG twitch
activity during REM sleep.
Nightmare Disorder
This sleep disorder is often characterised by recurrent nightmares that are disturbing
mental experiences, tending to occur during REM sleep and often resulting in
60
awakening. For patients with this sleep disorder the actual nightmare episode will
appear to be very real and will become increasingly disturbing as the nightmare
unfolds. Anxiety, fear, or terror will usually accompany the episode; however,
emotions such as anger, rage, embarrassment, disgust and other negative feelings are
associated with nightmares.
Other Parasomnias
Sleep Related Dissociative Disorders
These sleep disorders emerge throughout the sleep period during well-established
EEG wakefulness. This can occur at either the transition from wakefulness to sleep
or within several minutes after an awakening from stages 1 or 2 NREM sleep or from
REM sleep. The three categories to date that have been associated with nocturnal
dissociative disorders are dissociative personality disorder (formerly known as
multiple personality disorder), dissociative fugue, and dissociative disorder that has
not been specified.
Sleep Related Eating Disorder
Sleep related eating disorder (SRED) consists of recurrent episodes of involuntary
eating and drinking during arousals from sleep with problematic consequences. They
can occur during partial arousals with partial recall from the patient. Patients usually
cannot be brought to full consciousness during an episode.
Sleep Related Movement Disorders
Sleep related movement disorders are conditions that are primarily characterised by
relatively simple and usually stereotyped movements that disturb sleep or other sleep
related monophasic movement disorders, such as sleep related leg cramps.
Restless Legs Syndrome
Restless legs syndrome (RLS) is a sensorimotor disorder that is characterised by a
complaint of a strong, nearly irresistible, urge to move the legs. The urge to move the
legs is often but not always accompanied by an uncomfortable sensation felt deep
inside the legs or a feeling which is simply difficult or impossible to describe. The
sensations can be painful too. The urge to move usually occurs or is made worse by
61
resting (lying and sitting) and walking or moving the legs often relieves the
sensations. The sensations are worse in the evening and during the night.
Sleep related Leg Cramps
These are usually painful sensations that are caused by sudden and intense
involuntary contractions of muscles or muscle groups. The cramps occur in the calf
or small muscles of the foot and occur during the sleep period and they may arise
from either wakefulness or sleep. The cramps can be sudden or in some cases be
preceded by a less painful warning sensation. The contractions can last for a few
seconds or up to several minutes and then diminish spontaneously. Cramps can be
relieved by intense stretching of the affected limb or by massaging the site.
Sleep Related Bruxism
This is an oral activity characterised by grinding or clenching the teeth during sleep
that is often associated with sleep arousals.
During sleep jaw contraction usually occurs, this contraction can take on two forms,
the first being sustained jaw clenching which are also known as tonic contractions or
a series of repetitive (phasic) muscle contractions termed rhythmic masticatory
muscle activity (RMMA). When the contractions occur during sleep they are very
strong and they tend to produce tooth-grinding sounds and this often referred to as
sleep related bruxism. This often leads to abnormal wear of the teeth and also causes
tooth pain, jaw muscle pain and or temporal headaches. Sleep is often disrupted
during severe episodes of sleep related bruxism.
The disorder is usually brought to the attention of dental or medical professionals
because of the tooth damage which the grinding causes, and the unpleasant sounds
made by the patient with can be disturbing to any bed partner.
Isolated Symptoms and Normal Variants
These are disorders which lie at the borderline between normal and abnormal sleep
or that exist on the continuum of normal to abnormal events in sleep (ICSD-2, 2005).
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Long Sleeper
A long sleeper is a patient who consistently sleeps longer than is considered normal
for his/her age group. Sleep architecture is present and normal. Again there are no
complaints about quality of sleep, daytime sleepiness, or impaired daytime
functioning. Sleep that is more than ten hours per 24 hours is considered unusually
long in young adults. Sleeping less than this amount leads to daytime symptoms of
excessive sleepiness in this group.
Short Sleeper
A short sleeper is a patient who has a shorter sleep episode than is considered normal
with no complaints about the quality of sleep or reduced daytime wakefulness and
functioning. Sleep episodes of less than five hours per 24-hour period is usually
considered short before the age of 60 years.
Snoring
Snoring is a respiratory sound that is generated in the upper airway during sleep that
typically occurs during inspiration but can also occur in expiration. The snoring that
occurs within this subgroup occurs without episodes of apnoea and or
hypoventilation. The intensity of the snoring can vary and will often disturb a bed
partner. This particular type of snoring does not cause daytime sleepiness or
insomnia.
Sleep Talking
This condition consists of utterances of speech/sounds during a sleep episode without
any detailed awareness of the event. Bedpartners and household members may find
that emotional stress is not an underlying cause; however, the episodes may be
frequent; nightly longer speeches occur which can be hostile and aggressive. It can
be spontaneous.
Sleep Starts (Hypnagogic Jerks)
These are sudden, brief, simultaneous contractions of the body or one or more body
segments occurring at sleep onset. Sleep starts consist of a single contraction that
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often affects the body asymmetrically. The jerks can often be spontaneous or brought
on by stimuli. Patients often report a feeling of falling, a sensory flash or a visual
hypnagogic dream or hallucination, and the jerks often occur in a succession.
Other Sleep Disorders
These are sleep disorders that cannot be classified elsewhere in the ICSD-2 and are
listed within this sub-group usually the final diagnosis will have a physiological or
medical related diagnosis
Other Physiological (Organic) Sleep Disorder
This category can also act as a final diagnosis for those disorders that cannot be
diagnosed are also classified here. Sleep disorders not classifiable elsewhere
throughout the ICSD-2 but with a medical, a substance, or a psychiatric aetiology are
classified here.
Other Sleep Disorder not due to Substance Abuse or known Physiological Condition
These disorders usually have a underlying psychiatric or behavioural factor.
Environmental Sleep Disorder
This is a sleep disorder usually caused by sleep disturbances due to a disturbing
environmental factor which causes a complaint of insomnia or daytime fatigue and
somnolence.
Summary
Not every sleep disorder has been discussed in this chapter. The list, while
exhaustive with regard to current knowledge, must be acknowledged to be
perpetually incomplete as there are newer sleep disorders being continuously
discovered. The succeeding editions of the ICSD have been designed to
accommodate these changes as they arrive. Some of the similarities between
disorders, self evident throughout this chapter, derive from underlying behavioural,
physiological and psychiatric factors that are usually present throughout all known
sleep disorders.
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2.1.5 Assessment of Sleep Disorders
To understand what can go wrong during sleep and to assess these problems, it is
important to be able to understand normal sleep. When initially investigating
disordered sleep it is important to obtain a detailed historical account during an
interview with the patient and often with other members of the family. This detailed
account should be supplemented by a physical examination where appropriate
(Shneerson, 2005). Although there are a range of techniques available to assess
disordered sleep, any such examination should only be conducted with clear aims
(Shneerson, 2005). This section assesses the use of the sleep history and examination
and the methods used to assess sleep and its disorders.
History taking
For clinical reasons it is often more difficult to take a patient’s history of a sleep
disorder than it is to enquire about their complaint that occurs during wakefulness.
Obviously, this is because the patient usually has little or no awareness of the
problem and it is often important to obtain the bed partner’s (if any) views of the
events that occur during the sleep episode and during wakefulness (Shneerson,
2005).The aim of this procedure is to be able to establish whether or not there is a
sleep disorder and to assess the relative contribution of psychological, medical and
social factors to the complaint (Shneerson, 2005). The symptoms and the sequence of
the appearance of the complaints should also be recorded, together with when the
complaint started and how it has progressed (Shneerson, 2005).
As part of the investigation process, detailed sleep questionnaires, such as the
Pittsburgh Sleep Quality Index (PSQI) have been developed to cover important
questions that need to be asked during the interview phase. Questionnaires such as
the PSQI supplement a conventional history and can also act as a substitute if the
history is unavailable. Usually a detailed history is preferable and usually the first
step of the diagnostic process is to assess the patient’s complaint or the reason for
seeking attention. It is important to establish whether the presenting problem is
primarily insomnia, excessive daytime sleepiness or abnormal experiences or
movements during sleep. Once this has been established it is important to establish
when the sleep problem began and whether there was any relationship to an external
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factor, which may be physical, such as a head injury, or one more subtle and
psychological in nature.
Factors to consider during history taking
It is often useful to consider the details of events during sleep and wakefulness as a
twenty-four-hour-cycle. Within this twenty-four-hour-cycle the events that should be
examined are as follows:
The sleep-wake patterns of the patient; this includes what time the patient goes to
bed, what time the patient goes to sleep, what time the patient wakes up in the
morning and what time they get out of bed and any events which may occur during
the night.
Events on awakening; does the patient feel refreshed? Are there any symptoms such
as frontal headaches, sometimes an indicator of carbon dioxide retention, caused by
hypoventilation during sleep? Is the patient alert?
It is also important to note daytime activities; for example are naps being taken
during the day and if this is the case, how long are the naps lasting for and how often
are they being taken? Important factors to note within this particular observation are
any sensory symptoms that the patient displays, especially delirium tremens. These
may be indicative of an underlying cause. Are there any memory or concentration
problems? And are there any symptoms related to motor problems?
Excessive daytime sleepiness; firstly, it is important to distinguish between true
hypersomnia and hypersomnolence, the former being based on sleep patterns which
are abnormal in the sense that the subject will sleep for a long period during a
twenty-four-hour-cycle and the latter being the sensation of sleepiness. It is also
important to distinguish between these two symptoms; they should be distinguished
from mental fatigue with poor concentration or motivation, physical weariness or
fatigue that may have an organic cause or may be related to insomnia, and the feeling
of subalertness. The duration, frequency and timing of naps should also be
considered and whether or not these episodes are refreshing.
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Clinicians can usually gauge the severity of daytime sleepiness by its frequency and
the type of situation in which the subject falls asleep. If it is mild, it only occurs
infrequently during periods when sleep would be most expected, for example
between 2 PM and 4 PM or during late evening or during monotonous events.
Cyclical sleepiness may be due to intermittent sleep deprivation. In this case, patients
find themselves sleeping little during the week and tend to catch up on their sleep
debt over the weekend. This then leads to a cycle of sleepiness and recovery. Longer
cycles that occur are usually indicative of other disorders.
Other factors which should also be included in the history taking are factors such as:
pre sleep activities and symptom, other related problems (muscle aches, headaches),
social history, general health, medical history, family history, drug history and a
short physical examination which can be a good indicator for specific disorders.
Factors to consider when examining the patient physically are attitudes of the patient
and any bed partner to the presenting sleep complaint are important. Clinicians may
also want to note the weight and neck circumference and examine the nose and the
pharynx that may suggest obstructive sleep apnoeas. Checking the teeth is also
important, as ground-down teeth are a presenting feature of bruxism. The clinician
will usually perform a detailed examination of the patient presenting with the
complaint to rule out any other underlying disorders.
Objective methods
Polysomnography
Polysomnography, also known as a sleep study, is a multi-parametric test (Carskadon
and Rechtschaffen, 2005). It is used in the study of sleep and as a diagnostic tool in
sleep medicine. The sleep study is a broad recording of the biophysiological changes
that occur in a subject’s sleep. The test is usually performed at night, although some
sleep laboratories do accommodate shift workers or those with circadian rhythm
sleep disorders. The polysomnogram monitors body functions including brain
(electroencephalogram (EEG), eye movements (Electro-oculogram-EOG) and
muscle activity or skeletal muscle activation (Electromyogram) and heart rhythm
(Electrocardiogram) during the patients sleep. Other factors such as respiration
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together with pulse oximetry are also investigated and will be discussed in a later
section.
Polysomnography can be used to diagnose many sleep disorders and eliminate those
that are not present. Disorders such as narcolepsy, restless legs syndrome, REM
behaviour disorder, parasomnias and sleep apnoea can be diagnosed with a
polysomnogram. The polysomnography test is being replaced by actigraphy.
Actigraphy
This is usually a non-invasive method of monitoring human rest/activity cycles. The
patient, to measure gross motor activity, wears a small actigraph unit, also known as
an actimetry sensor. The part of the body whose motor activity is often under test are
wrist movements. Sleep actigraphs are generally watch-shaped and worn on the wrist
of the non-dominant arm. Actigraphs are useful in determining sleep patterns and
circadian rhythms; they can be worn for weeks at a time.
These tests are useful for measuring and assessing daytime sleepiness in situations
where a laboratory or a sleep latency test (discussed later in a different section) is not
appropriate. The actigraphs can be used to clinically evaluate insomnia, circadian
rhythm sleep disorders and excessive sleepiness and restless leg syndrome. The
actigraph can also be used to assess the effectiveness of pharmacologic, behavioural,
phototherapeutic and chronotherapeutic treatments for such disorders.
Actigraphy has not been traditionally used in routine diagnosis of sleep disorders but
is increasingly being used in sleep clinics to replace full polysomnography. The
technique is more extensively used in academic research and is being increasingly
employed in new drug clinical trials where sleep quality is seen as a good indicator
of quality of life (American Academy of Sleep Medicine, 2002).
Actigraph units tend to vary widely in size and features and can be expanded to
include additional measurements. There are a number of limiting factors, however,
such as fastest sample rate, the amount of memory available, battery usage, the
weight of the unit and water resistance qualities so that the actigraph can be worn in
the shower. The actigraph does have some advantages such as watch functionality,
for example making the device more attractive to the user. User input, most
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actigraphs now include a button so the user can indicate a specific event that occurs,
subjective input, to allow surveys at specific times and sensors which monitor
temperature, ambient light, sound levels, parkinsonian tremor, skin resistance and a
full EEG data stream can be included.
Video and audio recording
Video recordings are usually often used together with various other methods of sleep
assessments, providing additional information. Video recordings can reveal
particular parasomnias. Infrared cameras and those sensitive to low light levels
reduce the level of interference with the individual’s sleep. Video and audio
recordings have been used in conjunction with other measures when investigating
sleep related breathing disorders (Stradling, Thomas, Warley, Williams and Freeland,
1990; Ali, Pitson and Stradling, 1993). Vos and Stradling (1991) have developed a
system to automatically process video and audio recordings or movements as a
measure of sleep disturbance and degree of snoring as a measure of disordered
breathing.
Subjective Methods
The above mentioned assessments of sleep and its disorders are very specialised
methods; in some cases such methods may not be available or required. The
following section describes subjective methods of assessments and discusses their
usefulness in research and clinical settings.
Questionnaires
Questionnaires can be a useful method for assessing sleep. Questionnaires can be
designed to assess both children and adults. Questionnaires can be used to obtain
information about a wide range of sleep disorders and behaviours plus their severity.
Questionnaires can be used to assess excessive sleepiness, quality of sleep, sleep
disordered breathing. In this section questionnaires used to assess the quality of sleep
will be discussed. Questionnaires that measure excessive sleepiness and sleep
disordered breathing will be discussed in a different section.
“Sleep quality is an important clinical construct” (quoted from Buysse, Reynolds,
Monk, Berman and Kupfer, 1988). Patients will often complain about their sleep and
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epidemiological studies have shown that fifteen to 35% of the adult population
commonly complain about their quality of sleep. Difficulty in falling asleep and
difficulty maintaining sleep are frequent complaints (Karacan, Thornby, Anch,
Holzler, Warheit, Schivab and Williams, 1976; Karacan, Thornby and Williams,
1983; Lugresi, Cirignotta, Zucconi, Mandini, Lenzi and Coccagna, 1983; Welstein,
Dement, Redington and Guilleminault, 1983 and Mellinger, Balter and Uhlenhuth,
1985). Research has found that sleep quality that is poor can be an important marker
for many sleep and medical disorders (Kripke, Simons, Garfinkiel and Hammond,
1979). Complaints about the quality of patients’ sleep are particularly important in
psychiatry (Buysse et al, 1988). Some of the underlying factors, which contribute to
general complaints about the quality of sleep, are anxiety and stress (Karacan et al,
1983).
Although it is often difficult to define and objectively measure sleep quality (Buysse
et al, 1988), objectively, sleep quality includes quantitative measures such as
duration of sleep, sleep latency, the number of arousals throughout the night, as well
as those aspects of sleep quality which can be subjectively collected, these being
depth of sleep and restfulness of sleep (Buysse et al, 1998). Usually research which
wishes to focus on a person’s sleep quality will often be affected by the type of study
being conducted and the tools used to measure the variable. Usually large population
surveys tend to focus on a few general questions about the individuals quality of
sleep (Bixler, Kale, Soldatos, Kales and Karacan, 1979; Karacan et al, 1983).
Diaries
Sleep diaries or sleep logs are usually kept by the individual when requested to do so
by medical or academic staff. The sleep diary is a record of the individuals sleeping
and waking times with related information; the diary is usually kept over several
weeks. The diary is self-reported or can be used by the caregiver on the patient’s
behalf.
The sleep diary is a tool used by clinicians (Perlis, Jungquist, Smith and Posner,
2005). It is often a useful tool used to diagnose circadian rhythm disorders and in
monitoring whether or not the treatment used for the disorder is useful. Sleep diaries
can often be used together with actigraphy. It is also useful for the patient in order to
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understand what is affecting their sleep. This alone can often help individuals
understand and self-diagnose.
Sleep assessment for sleep-related breathing disorders
Objective methods
It is often important to accurately obtain a careful history to assess disorders of the
upper airways. The issues, however, that should be considered when there is sleep
disturbance, too, are as follows:
What kind of noise is the patient making? This should include factors such as
duration, severity and the type of noise that is being produced and if this noise is
becoming louder and more frequent.
What is the respiratory pattern like when the noise is being generated? Is the bed
partner aware of how the breathing starts and stops, and is there any noise
associated with this sound? The patient may however occasionally awaken during
the night for no apparent reason; this could be due to the noise or due to the
sensation of choking.
Are there any associated symptoms, for example physical restlessness during the
patients sleep?
Does the patient experience excessive daytime sleepiness?
Is there any cause for any upper airway obstruction? Has the patient gained weight
or has their collar size increased? Does the patient have any nasal obstructions? Do
they smoke, drink alcohol, take medication; is there anything wrong with their sleep
hygiene? Is there any aspect of their medical history that the clinician should be
aware of, especially concerning the patients face or nose?
The above questions will usually be asked together with a physical examination; the
clinician will pay particular attention to any weight gain and observe if there is
obesity and if the patient presents with any upper airway abnormalities and
abnormalities of the neck. The patient will usually be observed during a sleep study;
if there is any obstruction during sleep then the patient will usually have either noisy
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breathing or intermittent silences during the apnoeas followed by a snort or similar
noise at their termination. If the apnoea is present, this will also be further supported
by the observation of the chest movement which will be paradoxical.
Once these preliminary tests have been performed, initial assessments will also
include a thyroid function test; tests for arterial blood gases, ECG and an
echocardiogram. A chest x-ray and respiratory function tests are only carried out if
there is a respiratory disorder already present.
Respiratory movements are also measured using inductance, impedance or
magnetometry methods or by using mercury strain gauges. If there are any upper
airway obstructions or airway abnormalities then there may be paradoxical chest
movement.
Respiratory effort can be estimated by measuring oesophageal pressure, which will
reflect the intrapleural pressure. The technique is invasive in that it requires
swallowing a balloon or catheter into the oesophagus.
Pulse Oximetry
Pulse oximetry has become the standard approach for recording blood oxygen
desaturation during overnight sleep studies. Pulse oximeters measure arterial oxygen
saturation; this is measured by using a spectrophotoelectrical technique through a
two-wavelength light transmitter and a receiver placed on either side of a pulsating
arterial vascular bed. Sites that are used are the digits, ear and nasal sites. Usually
any changes detected by the receiver depend upon the change in arterial pulse. The
wavelengths are transmitted through the arterial vascular bed and arterial oxygen
saturation of the arterial haemoglobin. The device is very sensitive and will not
interfere with arterial oxygen saturation measurements. It is important to correctly
align the light transmitter and receiver. If the sensor is applied to a digit then the digit
must be immobilised, this is so that the device can detect a pulsatile flow.
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Assessment of daytime sleepiness
This section describes the techniques used for evaluating self-reported sleepiness.
The Multiple Sleep Latency Test (MSLT), pupillography and ECG approaches are
discussed, along with the Maintenance of Wakefulness Test and vigilance testing are
described. The limitations and advantages of using self-reported sleepiness tests are
also discussed.
Introduction
Excessive sleepiness is a serious condition, which does not just affect the patient but
also his or her colleagues, friends, and family; it can be life-threatening (Mitler,
Carskadon and Hirshkowitz, 2005).
Clinically it is very important to assess daytime sleepiness (Mitler, Carskadon and
Hirshkowitz, 2005). The right tools are required, however, to assess the condition.
There are specific issues relating to measurement, in particular the tools used to
measure daytime sleepiness. The first issue concerns difference between withinsubject comparisons and between-subject comparisons. The second issue concerns
self-report, factors concerning whether the patient is under or over exaggerating can
be a cause for concern (Mitler, Carskadon and Hirshkowitz, 2005). The third issue
concerns clinical testing of sleepiness that usually involves daytime testing.
A traditional and a more conceptualised method for assessing daytime sleepiness was
based on three factors: physiologic sleepiness, manifest sleepiness and introspective
sleepiness (Carskadon and Dement, 1982). This model provides an organisational
method of understanding and measuring sleepiness. Physiological sleepiness is
described as the underlying biological drive to sleep, this being the speed at which
the individual falls asleep. Manifest sleepiness originates from three perspectives,
these being behavioural signs of sleepiness, the individual’s inability to remain
awake and the decline in the performance of psychomotor or cognitive tasks.
Thirdly, introspective sleepiness deals with an individual’s self-assessment of an
internal state.
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Physiological measures of sleepiness
The MSLT is a series of opportunities for the patient to nap (approximately four to
six) that is presented at two-hour intervals and these begin at approximately two
hours after initial morning awakening. Those who undergo the MSLT are often
instructed to allow themselves to fall asleep or not to resist falling asleep. Those who
undergo the MSLT are often tested in standardised conditions and in their street
clothing and do not have to remain in bed between the test sessions. Patients are also
asked not to engage in any vigorous pre-test activity that can alter the outcome of the
test. During test conditions the room is often dark and quiet and electophysiologic
measures are carried out to detect sleep onset and to score sleep stages. Respiratory
flow and sounds in patients who snore will also be recorded.
The MSLT is useful for documenting treatment response (Dement, Carskadon and
Richardson, 1978; Lamphere, Roehrs and Wittig, 1989 and United States; Modafinil
in Narcolepsy Study Group, 1998). The MSLT is also useful in revealing any
residual sleepiness in those patients who no longer report to be feeling sleepy after
treatment (Zorick, Roehrs and Conway, 1983). The MSLT has a direct, objective and
quantitative approach. Prior to undergoing the MSLT the patient will have a full
polysomnogram and will be tested to see if sleepiness is pharmacologically induced.
The American Academy of Sleep Medicine (AASM) Standards of Practice
Committee has published new practice parameters for the clinical use of MSLT
(AASM, 2004). These parameters set by the AASM were developed by the basis of a
comprehensive evidence-based medicine review process.
Other measures of physiological sleepiness
Pupillography
Pupil stability and size are affected by exposure to light and by an individual’s
arousal level. The change in pupil size from pupil constriction to dilation can be
reflected in the autonomic nervous system. Change has been researched as a potential
measure of sleep tendency (Schmidt and Fortin, 1982). Electronic pupillography is
an objective method for monitoring the size of the pupil, but it is difficult to compare
individual’s normative data with one another and the technique has not come into
general use for clinically evaluating sleepiness.
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Electroencephalography
It has long been thought that EEG delta activity can be used to index sleepiness.
Sleep-related EEG delta activity increases in response to experimental sleep
deprivation (Borbely, Baumann and Brandeis, 1981). In essence, the MSLT uses
EEG markers (macroarchitectural features) of sleep onset to quantify sleepiness.
Tests to assess manifest sleepiness
Maintenance of Wakefulness Test
Mitler and colleagues (1997) have stated that the procedures used to conduct the
MWT are similar to those used for the MSLT. The difference between the two tests
is the instruction given to the individual, in this case the individual is asked to remain
awake. In the case of the MWT the assessment focuses on the individual’s capability
of not to be overwhelmed by sleepiness, so in this case the functioning of the
underlying wakefulness system is assessed. In the MWT there is no actual task other
than to remain awake. During this test an individual is monitored for EEG sleep
onset during four to six sessions which is scheduled at two-hour intervals beginning
two hours after awakening from the previous night’s sleep. The MWT will also
include questions on the effect of acute sleep deprivation, age, time of testing and
drugs. The MWT measures often reveal improvement in those patents that have been
treated and who continue to be physiologically sleepy.
Performance and Vigilance Tests
Behavioural or manifest sleepiness can be measured using a variety of performance
tasks. Performance and vigilance tests attempt to measure cognitive slowing, such as
the digit symbol substitution test, whereas others cover changes in attention.
Vigilance tests often tend to mimic the tedious and palling situations of watching for
blips on a radar screen or for ships on a horizon. This test is relevant for those
patients diagnosed with disorders of sleep and arousal. There are a variety of tests
available that measure performance, vigilance and sustained attention. The most
common test used in sleep laboratories is the psychomotor vigilance tests which was
created by Dinges and colleagues (Kribbs, Pack and Kline, 1993; Doran, Van
Dongen and Dinges, 2001). This test employs trials with duration of about tenminutes in which a hand-held computerised display-and-response unit quantifies
75
response latency to multiple light emitting diode (LED) presentations of a stimulus.
Data with this inexpensive method has been validated with the Stanford Sleepiness
Scale (SSS) and the MSLT.
The Oxford Sleep Resistance (OSLER) test is also another performance related test
used in sleep laboratory setting and has been validated with the MWT. The OSLER
test is based on four forty minute long trials during which there are several LED
signal presentations. In this test the patient is asked to respond to each signal with a
simple press of a button. Trials usually last forty minutes or if the patient fails to
respond to a signal, assuming the patient has missed the signal as he or she has not
been able to maintain wakefulness.
Introspective Sleepiness
Profile of Mood States
Although this test is designed to assess mood states it can also be used in sleep
research, (McNair, Lorr and Droppleman, 1992). The profile of mood states (POMS)
test include a dimension assessing sleepiness, however it was removed as it was
found to overlap with other scales. Through extensive research it has been shown
that sleepiness loads several POMS scales in particular vigour, which is negative,
confusion and fatigue. On the other hand, to a lesser extent sleepiness is associated
with increased scores on depression and anger scales.
Stanford Sleepiness Scales
The SSS was the standard measure of sleepiness (Hoddes, Zarcone and Smythe,
1973). Patients who are given the SSS as a measure of their sleepiness are asked to
choose one of seven statements that can describe their self-assessed current state. The
SSS is a momentary assessment scale and can detect sleepiness as it changes over the
course of the day. The SSS is easy to administer and can be taken repeatedly.
Individuals who undergo experimental sleep deprivation score highly on the SSS.
There is no normative data available, however, for the SSS, therefore no clinical
judgements can be made and it is difficult to compare introspective sleepiness
between individuals.
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Epworth Sleepiness Scale
The popularity of the ESS arises from the fact that it is simple to use and the fact that
it is validated through various research studies, has ensured that ESS is one of the
most commonly used self-reported scales used to assess daytime sleepiness. The
problem with the ESS is the question of the usefulness of the test when it is
readministered within a certain brief time interval. It is also not useful in evaluating
circadian rhythm influences on sleepiness, factor such as sensitivity to age, acute
sleep disturbance or deprivation and the reaction to drugs is not known. This
questionnaire has been discussed in section 3.2.4
Summary
This section has provided an overview of the different methods that are used to
assess sleep currently in a clinical setting and in research. Both objective and
subjective tests have been discussed and described. It is important to note that the
choice of the assessments depends entirely on the aim of assessment; for example,
whether it is for research purposes or clinical purposes. This is not to say that other
factors are considered to be unimportant, such as age and presence of any specific
conditions such as underlying disorders.
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2.1.6 Treatments for sleep disorders
This section will provide an overview of the various treatments available for sleep
disorders. Different sleep disorders require different approaches. In this chapter the
three approaches described are: medication, other physical treatments and
psychological approaches. Only treatments for adults are described in this chapter
with emphasis on sleep related breathing disorders because only adults were studied
within this programme of research.
Medication
This section describes the main pharmaceutical treatments used to treat sleep
disorders. One of the most common forms of medication prescribed in clinical
practice is hypnotics.
In the United States, the most frequent clinically used sedatives/hypnotics include
five benzodiazepines (“valium-like” compounds); these are available in both
proprietary forms and generic forms and two non-benzodiazepines (Zolpidem and
Zaleplon) and these are available via prescription. The drugs represent a large market
and tend to involve on average 27 million prescriptions that in 2002 were at a value
of $1.2 billion; in the same year the same number of nonhypnotics were prescribed
for aiding sleep. Trazadone, which is an antidepressant, was one of these drugs
prescribed; this alone accounted for 10 million prescriptions (Mendelson, 2005).
Hypnotics
Hypnotic drugs, also known as soporific drugs, are a class of psychoactives; the
primary function of these drugs is to induce sleep and such drugs are also used in the
treatment of insomnia (Mendelson, 2005) and in surgical anaesthesia. Drugs that fall
within this category are usually dose-dependent and range from anxiolysis to the
production of unconsciousness; collectively they are referred to as sedative-hypnotic
drugs (Mendelson, 2005). Hypnotic drugs are habit forming and the clinician will
usually offer alternatives. If the clinician does prescribe such drugs it is often for a
short time.
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Benzodiazepines
These are the best known and often prescribed hypnotic medications at present.
There are few studies that have researched the effects of drugs such as lorazepam,
nitrazepam and diazepam but those that have studied their uses indicate that they are
effective hypnotics (Mendelson, 2005).
Studies have shown that 10 milligrams of diazepam both decreases sleep latency and
increases total sleep when taken for several days (Mendelson, 2005). There are no
studies that have shown the effects of taking ten milligrams of diazepam for longer
than seven days. Patients have also reported their preference for diazepam over
flurazepam. Diazepam is not officially recognised as a sleeping medication in the
United States.
Flurazepam is better studied than diazepam. Flurazepam is shown to shorten sleep
latency and decrease intermittent awakenings and increases total sleep. It also
decreases slow wave sleep. Thirty milligrams of flurazepam decreases the amount or
percentage of REM sleep; this does not however decrease the REM density.
Nonbenzodiazepines
The nonbenzodiazepines are a class of psychoactive drug whose pharmacological
actions are similar to those of the benzodiazepines; however, the nonbenzodiazepines
are structurally unrelated to the benzodiazepines chemically.
Clinical trials of the use of nonbenzodiazepines in the treatment of sleep disorders
have demonstrated efficacy (Mendelson, 2005). There is some limited evidence,
which suggests that tolerance to nonbenzodiazepines is slower to develop than with
benzodiazepines. These data are limited, however and no conclusions can be drawn
from them. There are also limited data available on the long-term use of
nonbenzodiazepines.
Clinically, there is little understanding of how hypnotics actually work. One
approach suggests that hypnotics work by altering the perception of sleep and
wakefulness (Mendelson, 1990). This arose from the work by Rechtschaffen, who
observed that poor sleepers when experimentally aroused earlier than normal in stage
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2 sleep reported that they had been awake, whereas good sleepers reported that they
had been asleep (Rechtschaffen, 1968). Replication of this work by Mendelson in
1993 and 1995 demonstrated that when doses of triazolam or Zolpidem were
administered, patents that had been diagnosed with insomnia reported to have been
asleep compared to when the same group of patients were given a placebo.
Other Physical Treatments
Positive pressure devices
Nasal Continuous Positive Airway Pressure (CPAP) is the current treatment of
choice for the majority of adults with sleep-related breathing disorders. Nasal CPAP
has proven to be a very successful treatment. 95% of patients can be definitively
treated with this device, including patients with mild disease (Redline, Adams and
Strauss, 1998). Nasal CPAP has been shown to improve many aspects of sleeprelated breathing disorders including daytime sleepiness (daytime sleepiness will be
discussed in greater detail in section 2.4.5) (Engleman, Cheshire and Deary, 1993)
and quality of life (D’Ambrosio, Bowman and Mohsenin, 1999) and patients have
fewer hospital stays (Peker, Hedner, Johansson and Benden, 1997).
One of the biggest disadvantages of using nasal CPAP is that clinicians had to rely
upon the patients report regarding usage. Now, however, CPAP machines contain
timers to measure hours of usage and on average it has been found that the apparatus
is used five hours per night (Engleman, Martin and Douglas, 1994; Reeves-Hoche,
Meck and Zwillich, 1994; Engleman, Asgari-Jirhandeh and Mcleod, 1996).
Behavioural Interventions for OSAS
Apart from medication and physical treatments that are available, good medical care
will also incorporate the patient’s lifestyle. This is necessary to ensure that the
patient’s lifestyle does not complicate the underlying medical problems. There are a
number of lifestyle considerations that need to be considered which can increase the
risk.
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Weight Loss
Obesity can have adverse effects on the upper airway function; this is due to the
mechanical influence of the upper airway geometry (Strollo, Atwood and Sanders,
2005). Animal studies have shown that upper airway resistance is usually influenced
by mass loading of the anterior neck; this may stimulate the clinical scenario of
excessive adipose tissue deposits in this area (Koenig and Thach, 1988). The data
provided from animal studies supports the notion that fat deposits around the neck
area do appear to cause upper airway resistance and this can be seen in patients
diagnosed with obstructive sleep apnoea/hypopnoea syndrome as they have thick
necks and the increased circumference is a predictor of obstructive sleep
apnoea/hypopnoea syndrome.
Smoking cessation
Smoking has damaging effects on sleep. Individuals who smoke tobacco usually
have difficulty in initiating and maintaining sleep and also report daytime sleepiness
(Philips and Danner, 1995). There are a variety of possible explanations for this,
including the impact of nicotine withdrawal. This could be due, as well, to the
predictable association of smoking and sleep disordered breathing (McCardle, Grove
and Devereux, 2000). Smokers are four to five times more likely to suffer from sleep
disordered breathing than non-smokers (McCardle, Grove and Devereux, 2000).
Those who smoke heavily are at a greater risk. Cigarette smoking may cause upper
airway dysfunctions during sleep as it elicits mucosal oedema and increased upper
airway resistance (Strollo, Atwood and Sanders, 2005).
Sleep Hygiene and Sleep Deprivation
We live in a sleep-deprived society (Bonnet and Arand, 1995). The effects of sleep
deprivation were discussed in section 2.6.1. However, repetitive sleep deprivation
may predispose to or worsen symptoms in patients diagnosed with obstructive sleep
apnoea/hypopnoea syndrome.
Patients are also encouraged to maintain good sleep hygiene; sadly, this advice is not
always maintained and could be due to a number of reasons, ranging through
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financial pressure and social pressures. It is important for clinicians to encourage
patients to maintain their sleep hygiene, as poor sleep hygiene can have an impact on
their sleep disorder, which in turn causes their sleep to be of a poor quality.
Body Position
One of the oldest interventions to prevent snoring in patients with obstructive sleep
apnoea/hypopnoea syndrome is for the bed partner to prompt the individual to move
to the lateral recumbent position; those who sleep supine have greater sleep
disordered breathing events (Cartwright, Lloyd, Lilie and Kravitz, 1985; George,
Millar and Kryger, 1988). Upper airway occlusion is increased when sleeping in the
supine position due to the effect of gravity on the tongue.
Body position is also inversely related to obesity (Cartwright, 1984). Patients who
are clinically obese are more likely to suffer from obstructive sleep
apnoea/hypopnoea syndrome regardless of body position (Cartwright, 1984).
Alcohol
Alcohol can increase the chances of upper airway obstruction in individuals who
otherwise only snore and also tends to increase the frequency in patients who have
been diagnosed with obstructive sleep apnoea/hypopnoea syndrome (Issa and
Sullivan, 1982). Alcohol not only increases the frequency of sleep-disordered
breathing but it also increases the duration of these events (Gleeson, Zwillich and
White, 1990). Alcohol can have an effect, as well, on daytime alertness in those
patients diagnosed with obstructive sleep apnoea/hypopnoea syndrome.
Psychological approaches
Psychological and behavioural treatments are readily available for primary insomnia.
Basic sleep hygiene education, psychological and behavioural interventions are one
of the few options that are available for patients diagnosed with insomnia. One of the
main objectives for employing psychological and behavioural approaches is to target
specific factors that perpetuate or exacerbate sleep disturbances. These factors can
include poor sleep habits, irregular sleep-wake schedules, misconceptions and
excessive worrying about sleep and hyperarousal. It is important to deal with these
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factors when dealing with the sleep problems (Spielman and Glovinsky, 1991). One
of the other goals of treatment is to be able to teach patients self-management skills
to cope more adaptively with residual sleep disturbances.
Cognitive Therapy
Cognitive restructuring therapy works by altering dysfunctional cognitions about
sleep. Cognitive therapy works by restructuring the negative thought processes that
the patient holds about their sleep, for example when a person is unable to sleep at
night they will begin to think about the consequences of their lost sleep on their
performance the following day, this then sets off a viscous cycle of insomnia,
emotional distress, and more sleep disturbance. Cognitive therapy is designed to
short-circuit the self-fulfilling nature of this vicious cycle. Cognitive therapy is
useful in the sense to be able to teach patients coping skills to prevent or minimise
recurrence of sleep disturbances after treatment.
Sleep Hygiene Education
This treatment is intended to provide information about the patient’s lifestyle, this
being their diet, exercise and substance use if any and environmental factors such as
light, noise and temperature which can all interfere with or promote better sleep
(Lichstein, Wilson and Johnson, 2000). This treatment includes general sleepfacilitating recommendations, such as teaching the patient to relax before bedtime
and providing the patient with information about maintaining sleep schedule.
Summary
This chapter has shown that there are a wide range of treatments available for those
patients who have been diagnosed with a specific sleep disorder. In this chapter
pharmacological treatments have been discussed, newer drugs are being developed
continuously to improve this form of treatment plan, different drugs behave in
different methods, and clinicians will usually tailor a care package for their patient to
get the most out of treatment. Treatment can involve more than one treatment plan
for example a pharmaceutical intervention along with a behavioural intervention. For
those patients with severe upper respiratory tract obstructions, there are a number of
surgical options available. Lastly psychological and behavioural interventions have
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been discussed and once again there are a range of treatment plans to choose from,
the clinician or the allied health professional will usually adopt the most suitable care
plan for the patient.
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2.2
Respiratory Diseases
Overview
This section deals with the aetiology and pathogenesis of obstructive diseases, in
particular asthma and chronic obstructive pulmonary diseases (COPD) (emphysema
and chronic bronchitis), bronchiectasis and the differential diagnosis of obstructive
diseases, the clinical features and tests of pulmonary function and other diagnostic
procedures.
Introduction
Obstructive diseases of the airways are a diverse group, they have one thing in
common and that is the narrowing of the airway that results in an increase in the
work of breathing. Obstruction can occur in the upper airways as well as the site of
the bronchioles. The mechanisms of airway obstruction involved in obstructive lung
diseases are quite varied, for example the decrease in maximal expiratory air flow in
emphysema is due to the loss of lung elastic recoil secondary to the breakdown of
lung tissue and the enlargement of the alveolar spaces, However in chronic
bronchitis, which is an inflammatory disease of the airway, the narrowing will occur
in the airways themselves. Even so these two diseases are difficult to differentiate
clinically and thus in the past clinicians have pooled these two obstructive diseases
and have given them the common name of COPD.
Another important factor to bear in mind is the difficulty in defining the diseases, for
example, chronic bronchitis is defined clinically by the chronic presence of cough
lasting longer than 1 month and sputum production. Classifying the various
obstructive diseases has its advantages in terms of treatments and prognosis. This is
mainly due to the combination of differences due to the signs and symptoms, the
various tests used for structure and function, the responses to the different treatment
modalities that enable the clinician to deal effectively with the different airway
obstructive disease presented.
It is important to note that the exact cause of most airway diseases is not very well
understood. Research has shown that cigarette smoking is associated with chronic
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bronchitis and emphysema. Researchers are still puzzled by why cigarette smoking
causes lung tissue damage in some people, predominantly chronic bronchitis in
others and yet no detectable illness in most people; the same can be said about
asthma, the pathologic mechanisms still puzzle us. With the case of asthma, often
allergic mechanisms are involved and with many adult asthmatic patients they will
not present with allergic symptoms and it is usually these patients who have severe
asthma.
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2.2.1 Asthma
Definition
Clinically physicians are confident in their ability to recognise the symptoms of
asthma. Nevertheless, agreement on a definition of asthma has proved to be difficult
(Davis, 1996). Difficulty has arisen from the early definitions of the disease and the
overreliance on the characteristics of physiologic abnormality. Definition of any
disease is most satisfactory when it has been derived from the identification of a
discrete single causative agent or from detection of a characteristic pathologic
abnormality (Boushey, Corry and Fahy, 2000). Due to the fact that there has been no
single agent identified which can be a central causal component and no pathologic
feature is unique to asthma, the disease has been more described than defined
(Boushey et al, 2000).
Some of the symptoms of asthma are shared with diseases of other systems.
Even if the symptom of breathlessness is thought to be due to lung disease,
there are numerous relatively common lung diseases and differentiation of
an airway disorder needs to be made from both infections and pulmonary
thromboembolic disease and restrictive lung disorders (Thorax, 2003; p.
13).
The British Guidelines on the Management of Asthma also states within Thorax the
respiratory journal that any features of an airway disorder such as cough, wheeze and
breathlessness should be confirmed where possible by measurement of airflow
limitation. These symptoms could present either due to a localised airway obstruction
for example a foreign body or perhaps a generalised issue such as asthma.
Such attempts to define asthma have been made over a number of years to establish
an unambiguous definition of the disease that is recognised as asthma. An early
definition prior to The British Guidelines on the Management of Asthma was
provided from a Ciba symposium in 1959 and referred to asthma as a condition that
varied spontaneously either with time or in response to therapy (Ciba Guest
Symposium, 1959). The definition applied by Ciba does apply to many patients but it
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raises the question of how much variability is needed before the diagnosis can be
made and what are its acceptable limits. Other attempts to define the disease have
been made as a result of various international symposia and consensus reports
(American College of Chest Physicians/American Thoracic Society, 1975;
International Asthma Management Project, 1982). More recent attempts to date have
incorporated the concept of bronchial hyperactivity; nonetheless, this does appear in
other conditions, too, so it cannot be used as a single entity to define asthma.
From this, a consensus definition for asthma has been developed that recognises this
disorder to be a chronic inflammatory disorder of the airways in which many cells
and cellular elements play a role; those which play a central role are mast cells,
eosinophils, T lymphocytes, neutrophils, and epithelial cells. In individuals who are
susceptible to such a disorder, the inflammation that is present will cause recurrent
episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night
and/or in the early morning. Such episodes of inflammation are present due to the
widespread but variable airflow obstruction that is often reversible either
spontaneously or with treatment. The inflammation also tends to cause an associated
increase in the existing bronchial hyperresponsiveness to a variety of stimuli
(Lemanske et al, 2003).
Risk factors
Those studies conducted with adults have looked at factors weakly associated with
asthma: male gender, low birth weight, prematurity, maternal smoking in pregnancy,
parental smoking, and high intake of salt (Wilfond and Fost, 1990; Barasch et al,
1991). Factors such as family size have also been investigated (Riordan, 1999;
Denning et al, 1992) and consumption of oily fish (Gregory et al, 1991). Work
conducted by Kalin et al (1999) has shown that there is no primary prevention study
that has shown that reduction of any identified risk factor, even house dust mites, did
not significantly reduce asthma prevalence but larger trials are now underway.
There are various factors associated with the onset of asthma; symptoms such as an
ordinary cold often precede asthma exacerbations. Asthma has also been suspected
of having a strong genetic component at least since 1860, when Henry Salter stated
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that he found “distinct traces of inheritance...in two cases out of every five” (Salter,
1864).
What is asthma?
So what exactly is asthma? Asthma is known to be a chronic condition that primarily
tends to affect the air passages in the lungs and at present there is no cure. The
classic symptoms of asthma that a patient presents upon examination are usually
breathlessness, tightness in the chest, cough and wheezing. The airways in the lungs
are usually characterised by inflammation and an increase in irritability, these two
presenting symptoms is what causes the airways to narrow and therefore has a knock
on effect on the other presenting symptoms in asthma. This tends to happen variably
but is maybe worsened by triggers such as infection, exercise and allergens.
Inflammation can reverse spontaneously or in response to treatment, episodes of
asthma attacks can be severe. Death from asthma is uncommon. Airway narrowing
can be due to mucus in the airways of the lungs, swelling of the lining of the airway,
or to spasm of the muscle in the walls of the airways or a combination of all three.
Recognising asthmatic symptoms
Those who live with the disease will usually describe the disease process very
differently to what would be written in a medical textbook. Describing the sensations
experienced with any disease to someone who does not live with it is usually
difficult. Most of the time we are unaware of our breathing except during physical
exertion where even a small amount of shortness of breath can affect the physically
fit. During exercise, breathing is more deep and rapid, there is a certain rawness in
the chest, which occurs due to the drying up the surface of the air passages and this
can be relieved by breathing moist air, this sensation is not however unpleasant,
however, until the point of exhaustion is reached there is usually a feeling of
satisfaction that the breathing is meeting the demands of the body, although this is
not the case with asthma.
When there is bronchial narrowing this slows the movement of air into and out of the
lungs. There is difficulty in breathing in and breathing out. The individual will
require more effort to achieve an adequate airflow, which means greater effort
intrudes itself into the consciousness. The greater the effort is required the more there
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is a sense of difficulty in breathing which is very unpleasant and frightening. The
breathing difficulty experienced by an asthmatic patient is qualitatively different and
therefore requires a different set of descriptive words; common words that are used
to describe such sensations are tightness, congestion and wheezing (Lane, 1987).
Like many words used to describe the symptoms, ‘congestion’ means one thing to
the sufferer and another thing to the clinician. The medical world has a definition for
almost every symptom but congestion to the patient basically means the individuals
chest filling up with phlegm and that it needs to be cleared (Lane, 1987). Patients try
to put into words the sensations of wheezing and distension of their lungs. A New
Zealand physician who had been a lifelong asthmatic remembered describing this
sensation as a child in these words: ‘It’s just as if your chest had been blown up with
a bike pump and then put into an iron clamp.’ (Lane, 1987).
The pattern of asthmatic symptoms
The symptoms that the asthmatic patient presents clinically do not help to recognise
asthma so much as the circumstances in which they occur. Most of the symptoms
that occur in asthma are also present in other chest diseases; in asthma, however,
they occur in seizures. These could be brief episodes of wheezing, which can last up
to an hour or so, merging into a full-blown asthma attack. The asthmatic patient will
also recognise that his/her lungs are sensitive to the weather; this can be apparent
especially during the cold winter months, when there can be tightness and a
momentary shortness of breath. The change from a cold environment to a warm
dwelling can also produce similar sensations. There can be but not necessarily
sensitivity to certain products such as perfume, petrol, wood, smoke and cigarettes.
Violent movements of the chest such as coughing and laughter can also bring on a
sudden paroxysm of wheezing. Such details may demonstrate the extreme sensitivity
of the asthmatic patient’s airways to irritant stimuli. These sensations are not an
attack in itself, just brief episodes. A prolonged episode of wheezing would need to
be triggered by a stronger stimulus, such as exercise.
For all patients with asthma, especially those with adult onset asthma, there is a
history of an extremely rapid progression of symptoms (Wesserfallen et al, 1990;
Benatar, 1986) and a history of anaphylactic sensitivity to certain foods, such as nuts
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and shrimps for certain patients (Sampson et al, 1992; Kemp et al, 1995), ingestion
of aspirin or foods likely to contain sulphites (dried fruits, restaurant salads) as these
can provoke severe life-threatening attacks in patients who otherwise have features
of mild or moderate asthma (Samter and Beers, 1968).
The asthma attack
Aretaeus, an ancient Greek physician who practised in the 1st century CE described
the symptoms of the attack as: ‘The symptoms of its approach are heaviness of the
chest; sluggishness to one’s accustomed work’ (Lane, 1987). There are changes in
mood, irritability that is difficult to rationalise, coupled with depression or
apprehension; there is also a forced gaiety in mood of a few, prior to the
commencement of wheezing, and coughing. The cough is irritating and nonproductive. Skin irritation may also persist in some patients, Lane (1987).
During the height of the attack, psychological symptoms of distress, anxiety will be
experienced, speech is impossible and the patient will usually be gasping for breath,
with beads of sweat forming on the brow which is present in severe cases. Speech is
impossible; feelings of restlessness and fright are also present.
Asthma attacks do sometimes settle spontaneously; during the present time they can
be aborted with medication and there are only a few that persist to the descriptions
set out by Aretaeus: ‘If these symptoms increase, they sometimes produce
suffocation after the form of epilepsy’ (Lane, 1987).
Once the main attack has subsided, the sense of distension is the first to go, breathing
becomes easier, the wheeze remains and there may be an increase in the loudness of
airflow. Secretions are released; the phlegm is clear or white and may contain pellets
or strands which have a branched appearance that may have been trapped in the
smaller bronchi and have been released during the attack.
After the attack the tension is relaxed and mood elevates. The individual will usually
want a drink and have great hunger and want rest. The asthma attack itself is the
hallmark of asthma.
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Pulmonary Function Testing
There are characteristic changes that can be seen once a pulmonary function test has
been performed between attacks or even after long periods of remission. Reductions
in maximal expiratory flow are the easiest to detect Tests of peak flow are dependent
upon effort, however they can be reliable if performed on a cooperative patient and
can be repeatedly measured with any several lightweight, portable and inexpensive
devices which meets the criteria set out by the American Thoracic Society (ATS) for
accuracy (ATS, 1995). The monitoring of ambulatory patients is the best use of peak
flow in such patients; changes in peak flow can serve as a guide to patients for
adjusting treatments (Lahdensuo, 1996). Calculations of peak flow variability are
also a good guide to use to detect abnormal airway lability as an indirect measure of
bronchial responsiveness (Ryan et al, 1982). Peak flow is determined by the diameter
of central airways, it is less sensitive to changes in peripheral airways than are
measurements of flow at lower lung volumes. Such flows contribute to FEV1, which
explains why peak flow underestimates FEV1, by 10% to 20% in 30% to 50% of
asthmatics (Ritchie, 1962; Meltzer et al, 1989).
FEV1 (the volume of air expired in the first second of a forced expiratory manoeuvre
from total lung capacity) is the best-standardised and most widely used test to
measure airflow obstruction. The hallmark of asthma is an improvement in FEV1 of
more than 12% and more than two hundred millilitres after the administration of a
bronchodilator (American Thoracic Society, 1995). Interpretation of scores of an
FEV1 usually requires simultaneous measurement of the forced vital capacity (FVC),
which tests the total volume exhaled from total lung capacity (TLC) to residual
volume; the reduction in FEV1 exceeds the reduction in FVC and therefore the ratio
of FEV1/FVC is low in asthma. This is however not the same in severe asthma,
where the residual volume is increased so that the reduction in FVC is proportional
to the reduction in FEV1. Studies have shown that treatment may reverse the
narrowing of the peripheral airways which will then allow exhalation at a greater
volume before airway closure occurs, therefore allowing the improvement in FVC to
be greater than the improvement in FEV1 (McFadden and Lyons, 1969).
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Other factors which contribute towards the prevalence of asthma
Ethnicity
Ethnic origin plays a major part in the epidemiology of many important chronic
diseases and therefore it is pertinent to consider what effect, if any, it has in asthma.
Within the United Kingdom (UK) work conducted in Blackburn (1987) studied the
clinical situation that asthma admissions among ethnic Asian adults were more
frequent than expected, which concluded that the rise was not due to the readmissions, this was then revisited during the early nineteen nineties when exactly
the same findings were produced. The authors stated that this was perhaps due to the
fact that asthma prevalence was higher in this group or that cultural factors might
explain the observed difference. Work conducted in Southampton during the late
nineteen eighties compared the prevalence of asthma amongst Asian and European
children. It was suggested that differences found amongst the two were due to the
prevalence reported from primary care which might result from either more severe or
less adequately treated asthma among Asians or from a lower threshold for seeking
medical attention in this group. The latter point is supported by data from a study in
London in the early nineteen nineties which highlighted the risk of under-diagnosis
and under-treatment was higher for Asian children. It has been suggested that it
might be more common for foods such as fizzy drinks, fried foods and nuts to act as
a trigger to asthma in Asians; it is unclear whether or not this is due to the fact that
perhaps Asians tend to eat this particular food more frequently than other ethnic
groups.
Summary
Asthma is a chronic long-term condition that affects the airways. Patients who have
been diagnosed with asthma tend to have over-sensitive, narrow and inflamed
airways; this usually makes it difficult for the patient to breathe. Although asthma is
a serious condition, it can be well controlled with the right care plan. Common
symptoms include a cough, wheeze, shortness of breath and tightness in the chest.
The likelihood of a patient being diagnosed with asthma is increased if the symptoms
are variable and unpredictable, intermittent and especially if they are worse at night.
Environmental pollutants and pets, exercise and viral infections and chemical
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pollutants such as chemicals and tobacco smoke can often trigger symptoms.
Diagnosis is usually first made by the patients family GP after a series of tests and
investigations which measure the volume and speed of air that the patients can
breathe, expire and inspire. A patient can be referred to a specialist if the GP cannot
control the patient’s disease. Treatment plans usually include the patient achieving
control of their symptoms. Treatment plans are usually tailored to the patient
according to the patient’s lung function test.
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2.2.2 Chronic Obstructive Pulmonary Disease
Introduction
In the early twentieth century tuberculosis (TB) was the major pulmonary disease
occupying the work of physicians. In the latter part of the twentieth century the two
main pulmonary diseases that have taken over from TB are now carcinoma of the
lung and COPD. The death rate trend of these two conditions is very similar. The
prevalence of COPD, however, including both chronic bronchitis and emphysema
with their symptoms of cough, expectoration, wheezing and laboured breathing is
higher.
Definitions
COPD
According to Snider (2003) it is important to be able to differentiate between the
definition of a disease and its diagnostic criteria. The common properties specifying
the group of abnormal persons are the defining characteristics of a disease and on
whom the description of the disease is based.
A number of expert panels which include The American Thoracic Society (ATS), the
European Respiratory Society (ERS) and The British Thoracic Society have all
defined COPD slightly differently over the last ten years or so (Snider, 2003). The
Global Initiative for Chronic Obstructive Lung Disease (GOLD) and an expert panel
that was joined by the National Heart, Lung and Blood Institute and the World
Health organisation have produced a report and have defined COPD as:
A disease state characterised by airflow limitation that is not fully
reversible. Airflow limitation is usually both progressive and associated
with an abnormal inflammatory response of the lungs to noxious particles
or gases. www.goldcopd.com (Accessed on 20th April, 2007).
Chronic bronchitis and emphysema may occur with or without airflow limitation,
whereas asthma by definition (ATS, 1962) is always associated with discernible
airflow limitation. According to the frequent etiological factors associated with
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chronic bronchitis and emphysema they often occur together (Burrows, 1987). With
asthma, however, which is a disease whose hallmark is reversible airflow limitation,
can lead to fixed airflow limitation (Peat et al, 1987; Lange et al, 1998). Clinically,
these three diseases are often similar physiologically and therefore any precise
classification of the patient’s disease is often difficult. To overcome this problem a
variety of terms have been developed to use synonymously for patients who evidence
one or more of the diseases and these are: chronic obstructive airway disease, chronic
obstructive lung disease and, of course, COPD.
It is difficult to define COPD so it has been agreed that COPD should only be used
for patients who present with airflow limitations that have been ascertained
objectively. According to Higgins (1991) chronic bronchitis and emphysema may
present without much evidence of airflow limitation. The definition of COPD has
evolved over time from one being based on a clinical diagnosis of chronic bronchitis
or anatomical findings of emphysema to one based on the presence of abnormal lung
function (Pauwels et al, 2001; Snider, 2003). The GOLD criterion have been used to
classify the severity of the obstructive lung disease, which has been adopted by the
ATS as well as the ERS. The criteria are classified on the basis of postbronchodilator lung function into various categories, as shown:
The GOLD criteria for classifying obstructive lung disease on the basis of postbronchodilator lung function.
Stage 0 (at risk) FEV1/FVC ≥ 0.70 and FEV1 ≥ 80% predicted and symptoms of
chronic bronchitis,
Stage 1 (mild): FEV1/FVC < 0.70 and FEV1 ≥ 80% predicted,
Stage 2 (moderate): FEV1/FVC < 0.70 and FEV1 < 80% predicted and FEV1 ≥ 50%
predicted,
Stage 3 (severe): FEV1/FVC < 0.70 and FEV1 < 50% predicted and FEV1 ≥ 30%
predicted,
Stage 4 (very severe) : FEV1/FVC < 0.70 and FEV1 < 30% predicted.
Chronic Bronchitis
The American Thoracic Society (ATS) (1962) and the Ciba Foundation Guest
Symposium (1959) have stated that chronic bronchitis should be defined in
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epidemiological terms as the presence of a chronic productive cough for 3 months in
each of 2 successive years in a patient in whom other causes of chronic cough, such
as infection with mycobacterium tuberculosis, carcinoma of the lung, bronchiectasis,
cystic fibrosis and chronic congestive heart failure have been excluded. For the ease
of clinical purposes, chronic bronchitis can simply be defined in a patient who
presents with a chronic productive cough without a medically discernible cause
which may be present for less than 2 years. Although this is a simpler definition to
use clinically there are problems with the fact that patients may present with similar
symptoms if they have a chronic irritation induced by inhaled substances.
Recognising COPD symptoms
History
Cough is the most frequent symptom that is reported by patients who present with
COPD. This particular symptom precedes the onset of dyspnoea and sometimes this
occurs at the same time for most patients. Although patients who are diagnosed with
COPD do manifest cough, expectoration and dyspnoea, it is usually the dyspnoea
that causes them to seek medical attention. The coughing in this case does not
usually interfere with day-to-day activities and usually the patient if often unaware of
the cough. According to Seemungal (1998) the use of a cough suppressant for a
chronic productive cough is believed to lead to retention of secretions; a daily cough
is predictive of frequent exacerbations. With regards to sputum production, this is
usually quite insidious in its onset and in most patients it is ‘scanty’, defined as less
than several tablespoons per day.
Clinically assessing COPD
During a physical examination of some patients with COPD there is little
abnormality revealed, especially during quiet breathing. Although coarse crackles
early in inspiration may be present, this has been usually associated with obstructive
lung disease; other sounds may be present, too. For example rhonchi are more
prevalent in patients who complain of dyspnoea and this is usually presented during
both inspiration and expiration. With regards to wheezing this is not usually a
consistent finding and therefore cannot be related to the severity of the obstruction.
The most objective and consistent finding in patients with symptomatic COPD is the
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prolonged expiratory time; this is best determined by listening over the larynx during
a forced expiratory manoeuvre. If the expiratory phase is longer than the normal 4
seconds than this is indicative of a significant obstruction.
As the severity of the COPD increases, patients begin to demonstrate more apparent
physical changes and signs. These are barrel shaped chest, pursed lip breathing,
emaciation and usually inguinal hernias which may appear in some. Patients will also
display the position of tripodding, which is usually where patients can be observed
sitting forward and leaning on their elbows, or supporting their upper body with
extended arms. This position is usually adopted to maximise intrathoracic volume.
From another perspective, pulmonary hypertension may also be noted with a loud
pulmonary component of the second heart sound; this is due to the fact that heart
sounds maybe displaced to the middle due to hyperinflation.
Computed Tomography (CT)
CT scans can be used to further determine a diagnosis much better than the
traditional chest radiographs. CT scans also be used to quantitate the amount of air
trapping by a comparison of images during inspiration and full expiration (Knudson
et al, 1991).
Pulmonary Function Test
These measurements serve to assess the severity of airflow limitation, which
quantifies the presence of the various abnormalities and to be able to identify and
quantify reversible airflow limitation. Pulmonary function tests are helpful in
documenting the progress of disease and in making a prognosis. With airflow
limitation there is the development of a systemic dysfunction and impairment of gas
exchange and this is one of the most significant functional defects in chronic
bronchitis and emphysema. In emphysema there is a loss of elastic recoil this then
allows the collapse of distal, poorly supported airways at much higher lung volumes
than normal. This leads to the increase in pleural pressure during active expiration by
the patient which then worsens the collapse of the distal airways and may give rise to
dynamic narrowing of the trachea and large bronchi as the gradient between the
extraluminal and intraluminal pressures indent their soft posterior walls (Stevens et
al, 1969; Beck and Heiner, 1981). Peripheral airway narrowing from luminal mucus,
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fibrosis, and inflammation of the walls and from increased smooth muscle is related
to airflow limitation (Cosio et al, 1978). The FEV1 test cannot distinguish between
these lesions. Due to the loss of elastic recoil of the lung which none of the sensitive
parameters of airflow obstruction can be derived from the single-breath nitrogenbreath nitrogen curve, the frequency dependence of compliance, or the density
dependence of maximum expiratory flow, is specific for peripheral airway disease.
Forced Expiratory Spirometry
This is one of the most useful tests of airflow dynamics. According to West (1998)
various indices can be determined from the volume time record, one of the few being
the volume expired in the first second (FEV1), the flow in the first one fourth of the
FVC (FEF0-25) or the middle half of the FVC (FEF25-75), and the peak expiratory flow
(PEF) during forced expiratory effort. The PEF and the FEF0-25 are mostly based on
effort. The FEF25-75 is relatively effort independent. Maximal flow is largely volume
dependant, so therefore when flow limitation is severe, ventilation can be maintained
only by prolongation of expiratory time or increasing the lung volume. Maximal flow
and ventilation are characteristic of COPD. PEF can be measured with peak flow
meters inexpensively whereby patients are usually taught. The other parameters,
FEV1, FVC and PEF rate can be measures by using portable pneumotachographbased spirometers that are now readily available. During exacerbations the PEF rate
and FEV1 cannot necessarily be determined by portable equipment.
The FEV1 has less variation and is more accurately predictable from age, sex and
height than the FEF0-25. The FEV1/FVC ratio is poorly maintained in patients with
obstructive lung disease but can be maintained or increased in those with restrictive
lung disease, making it an important differential point. FEV1 and the FEV1/FVC ratio
tend to fall progressively in patients with COPD and they also tend to have limited
improvement in airflow in response to a bronchodilator although airflow usually does
not normalise. According to Anthonisen et al, (1986) repeated testing increases the
number of patients with reversibility.
Lung Volumes
Total lung volume is increased in emphysema. This is due to the loss of elastic recoil
which permits the inspiratory muscles to stretch the lungs to a greater maximal
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volume. There are variations in the pattern of lung volume abnormality which can be
observed in some patients these patients tend to have a markedly increased total lung
capacity with a relatively well-maintained vital capacity with marked increases in
residual volume. Some patients may reveal a near-normal total lung capacity with
greater decrease in vital capacity and a modest increase in residual volume (Burrows
et al, 1986; Burrows et al, 1989). These differences tend to disappear as the disease
becomes more severe.
Sputum Examination
Those patients diagnosed with bronchitis and who are stable tend to have sputum
which is rather viscid. However during an exacerbation the sputum will become
grossly purulent. There are usually several cultures present upon examination of the
sputum, various tests such as the Gram stain usually shows certain cultures that can
demonstrate the presence of certain organisms. These cultures provide only
qualitative data as they are usually found in the URT. However according to
Chodosh (1985) the number and type of organisms observed in a culture specimen
can help guide physicians in delivering appropriate antibiotic therapy and therefore
selecting the most appropriate drug. Snider et al, (1992) have shown that cultures and
Gram stain are rarely necessary for instituting antimicrobial therapy unless the
patient who is receiving it has had an exacerbation during or soon after receiving a
course of antibiotics.
Treatment
Overview
Patients diagnosed with COPD can be managed in an ambulatory setting except for
when they have experienced an exacerbation that can give rise to the development of
acute respiratory failure. This particular type of therapy can be classified into three
categories; specific, symptomatic, and secondary, the latter is based on whereby the
therapy improves the whole person without affecting lung function.
Specific Therapy
There is little available in the way of directed therapy. Evaluation of occupational
and other environmental inhaled irritants should be evaluated carefully and dealt with
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as circumstances dictate. Those patients aged over 65 years and usually with known
conditions are usually given an annual dose of the influenza vaccine and then a
booster after every 5 years. This then prevents the serious pneumococcal infections
in COPD patients but again this still quite controversial.
Smoking Cessation
Smoking is one of the important cofactors in the cause of COPD and since the
government issued its Smoking Kills White Paper on Tobacco during the late 90’s to
help the population to stop smoking, every effort should be made to help the patient
to stop; this should be particularly important if the airflow is mild to moderate. There
are services that patients’ physicians can utilise to help their patients to quit. Services
of smoking cessation now run within the community in local pharmacies, GP
surgeries and community groups and hospitals.
Development of New Therapeutic Initiatives
The concept that lung function maybe restored after its loss is also undergoing reassessment. All studies that have been designed to improve natural history of COPD
face a common problem, because the progression of the disease is slow, a relatively
long time is needed to demonstrate any reduction of that progression (Auerbach et al,
1972). As well, any changes observed will be relatively small, especially if the
findings are compared to other physiological measures used to assess COPD, such as
Spirometry. Anthonisen et al (1991) has pointed out that due to this if studies were to
be conducted then more than 1000 patients would need to be selected for any
statistical test to have adequate statistical power. This has led to the thought that
more responsive measures of outcome in COPD are needed urgently. Measures such
as a high resolution CT scan, QoL assessments and measures of surrogate markers of
inflammation by histology induced sputum measures and exhaled air analysis. It is
hoped that these measures will help to prevent the progression of emphysema in
those who have the beginnings of the disease but are unable to stop smoking.
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Other factors which contribute towards the prevalence of COPD
Gender, Race and Socioeconomic Status
Sherrill et al, (1990) have reported that most population studies have shown a higher
prevalence of respiratory symptoms in men than in women, even when data have
been controlled for smoking. Burt et al, (1994) additional data became available with
the publication of the Third National Health and Examination Survey. Rates of
mortality in COPD are higher in whites than in nonwhites but this difference is
decreasing over time among men (Higgins et al, 1990). Higgins et al, (1990), Sherrill
et al, (1990) and the US Surgeon General (1984) have reported that morbidity and
mortality rates are related inversely to socio-economic status (SES), measured by the
level of education and income. Generally, it is higher for blue-collar workers than for
white-collar workers. Faling et al, (1993) have stated that COPD may aggregate in
families.
Tobacco Smoking
This has been established as one of the firmest risk factors for COPD. Longitudinal,
cross-sectional and case-control studies have shown that cigarette smokers compared
to non-smokers have higher death rates from chronic bronchitis and emphysema.
Cigarette smokers also have a higher prevalence for, and incidence of, chronic
bronchitis, emphysema and obstructive airways disease and higher frequencies of
respiratory symptoms and lung function abnormalities than non-smokers. Smokers
also have a greater decline annually in FEV1.
Occupation
Population studies that have been based on measures of mortality and morbidity have
suggested that occupations where the atmosphere is polluted with chemical fumes or
non-hazardous dust give rise to an increased prevalence of chronic airflow
obstruction and an increase in the rate of decline of FEV1. Occupations such as
farming or working within dusty occupations are said to increase the risk of
developing chronic bronchitis twofold to threefold; coupled with smoking this
increases to six fold (Frost et al, 1994; Melbostad, 1997). Although being exposed to
some materials may be very hazardous, most studies have shown that cigarette
smoking is still a much greater a risk compared to occupational hazards.
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Summary
COPD is a term used to for a number of chronic airway conditions, these being
chronic bronchitis and emphysema. COPD leads to damaged airways in the lungs
that causes them to become narrower which makes it harder for air to leave and enter
the lungs. One of the most common causes of COPD is smoking; patients who do not
smoke are often advised to quit smoking. There are occupational factors such as coal
dust, genetic factors such as inherited problems and environmental factors such as
pollution that contribute towards COPD. The symptoms of COPD often include
cough, phlegm and shortness of breath. Spirometry can best confirm a firm diagnosis
of COPD. Further tests and referrals can be made available to those patients who are
difficult to diagnose. COPD can contribute towards feelings of anxiety because of
breathlessness. COPD cannot be cured but the treatments available to help relieve the
symptoms include stopping smoking, as mentioned earlier, patients eating a well
balanced diet, remaining mobile, using bronchodilators and sometimes using
antibiotics and steroids. Oxygen therapy is also an option. Other factors that may
contribute towards the severity of the symptoms include occupational factors,
gender, race and the patient’s socio-economic status, too.
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2.2.3 Bronchiectasis
Introduction
The term bronchiectasis is derived from the Greek words broncos, “windpipe,” and
ektasis, “stretching” or “extension” (Baum et al, 1983). This refers to an abnormal
dilation of the proximal medium-sized bronchi greater than 2mm in diameter that has
been caused by destruction of the muscular and elastic components of their walls.
Usually this dilation is associated with chronic bacterial infection and the production
of large amounts of foul smelling sputum. Bronchiectasis is not always associated
with purulent expectoration; sometimes when it involves areas of the lung with
dependent drainage, such as the upper lobes, which are usually involved in patients
with pulmonary tuberculosis (TB). In these cases the bronchiectasis is referred to as
dry, which is to distinguish it from the more common wet or productive variety.
Lander in 1946 showed that bronchial dilation might be temporary, as it occurs in
areas of atelectasis after acute pneumonia. A study by Pontius in 1957 showed that
complete reversal of bronchiectasis after several years is possible. Even so,
bronchiectasis is generally thought to be a persistent if not a permanent pathological
process. Clinicians tend to use the word process to describe bronchiectasis because
they stress that bronchiectasis is not a discrete disease entity unless it is solely caused
by bronchial obstruction or untreated infection. It is usually more commonly referred
to as a pulmonary manifestation of systemic disorders, disorders such as cystic
fibrosis and primary ciliary dyskinesia.
Fraser et al, (1965) have stated that bronchiectasis is a focal process compared to
chronic bronchitis, which is not, as it involves the entire lung. Bronchiectasis can
result from local airway obstruction and infection and therefore may be confined to
one area. This was probably not true prior to the development of antibiotics;
however, because before the advent of antibiotics bronchiectasis was still often
generalised. Patients whom have been diagnosed with chronic bronchitis usually do
still have some bronchial dilation as do patients diagnosed with bronchiectasis may
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show changes pathologically especially if they smoke (Heard et al, 1979). There the
two conditions tend to overlap quite significantly (Mysliwiee, 1999).
Recognising bronchiectasis symptoms
Patients diagnosed with bronchiectasis may display symptoms referable to the
bronchiectatic process alone or to underling disorders. Symptoms include chronic
cough, purulent expectoration, fever, weakness and weight loss. Sputum production
often increases during acute respiratory infections. Bronchiectasis can be classified
into mild, moderate and severe categories developed by Ellis et al, (1981).
Although dyspnoea is not a universal finding, reported only by some patients,
dyspnoea may relate more to those with chronic bronchitis and pulmonary
emphysema than to pure bronchiectasis (Ellis et al, 1981). Breathlessness is also a
common symptom. The effect of cigarette smoking and the presence of severe
airflow obstruction on pulmonary function testing may correlate better with
subjective complaints than with the extent of bronchiectasis.
Baum et al, (1966) highlighted that haemoptysis is also common; it is said to be less
common amongst patients with wet bronchiectasis than amongst those with dry
bronchiectasis, including those patients diagnosed with pulmonary tuberculosis.
Haemoptysis is generally mild and it often consists of the expectoration of purulent
sputum flecked with blood. The bleeding usually originates from bronchialpulmonary anastomoses under systemic pressures.
Clinically assessing bronchiectasis
Diagnosis
The disease maybe suspected on the basis of clinical presentation, especially if the
process involves purulent expectoration and especially if disorders such as
pneumonia, emphysema and lung abscess have been ruled out. The onset of
bronchiectasis may be traced back to a clear-cut aspiration or febrile illness,
especially in those patients with postobstructive or infectious bronchiectasis. In those
patients where bronchiectasis occurs due to underlying disorders such as cystic
fibrosis or primary ciliary dyskinesia is more likely to have an insidious onset but
may be associated with discrete infectious episodes as well.
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Clinically, sputum analysis should reinforce the diagnosis of bronchiectasis. Analysis
of sputum usually include a visual inspection of the expectorated sputum which has
been allowed to settle into the characteristic three layers, an upper frothy and watery
layer, a middle turbid and mucopurulent layer and a bottom layer that is purulent and
opaque (Sepper et al, 1995).
Firm diagnosis of bronchiectasis is usually made by roentgenographic studies. Chest
roentgenograms have not been shown to be useful in distinguishing chronic
bronchiectasis in patients with cystic fibrosis from acute exacerbations of the disease
(Greene et al, 1994).
Bronchography a technique that is now completely obsolete but was once used to
determine the presence of bronchiectasis. This procedure could be performed with
the installation of contrast material via a catheter or bronchoscope. Although
bronchography provides adequate visualisation and it is a safe procedure to use, it
can be dangerous in patients who have respiratory compromise (Richman-Eisenstat
et al, 1993).
Bronchography has been replaced by High Resolution Computed Tomography
(HRCT) scans of the chest, as they involve little discomfort and have few adverse
complications (Lynch et al, 1999).
Bronchoscopy is less helpful than bronchography or HRCT for visualisation of the
entire bronchiectatic segments. Bronchoscopy is usually useful for detecting
aspirated foreign and other obstructing lesions.
Treatment
The introduction of antimicrobial drugs 40 years ago has been the mainstay of
treatment for bronchiectasis. The choice of the drugs is usually dependable upon
sputum, bronchoalveolar lavage fluid culture for aerobes, anaerobes and
mycobacteria whenever possible. If there is mixed flora present then often a broadspectrum antibiotic is given to the patient to identify a specific pathogen (Ramsey et
al, 1996). Most clinicians prefer to give broad-spectrum antimicrobial agents during
acute worsening of the condition; some clinicians tend to prescribe such agents on a
regular basis.
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Other treatments include chest physical therapy with postural drainage, chest
clapping, humidification, the use of mucolytics and other measures have also been
recommended, Mortensen et al (1991). Techniques such as chest clapping can be
administered by family members and is said to be of psychological benefit, however
the physiologic utility has not been well demonstrated, however when a metaanalysis conducted by Thomas et al, (1995) showed that chest physical therapy
resulted in significantly greater sputum expectoration than no treatment, whereas
therapy and exercise were associated with a significant increase in expiratory flow
rates.
A new approach to treat bronchiectasis is anti-inflammatory therapy. Long-term
mechanical ventilation, including that administered by facemask, may be useful in
patients with bronchiectasis and sever chronic respiratory failure (Benhamou et al,
1997). In addition to the above-mentioned therapies there are also specific therapies
that maybe appropriate when the underlying cause of bronchiectasis has been
identified. Although medical management of bronchiectasis should prove to be
successful, consideration should also be given to surgical resection in certain
instances. The first ever, wholly successful surgical resection was carried out in
1901. It should also be mentioned that double-lung and heart-lung transplantation is
also available for some patients who have severe generalised bronchiectasis (Scott et
al, 1988; Whitehead et al, 1991).
Prevention
Prevention involves the administration of vaccines against measles, pertussis,
influenza and other infections that may predispose the person to bronchiectasis. It
also includes the prompt removal of foreign bodies and obstructing lesions in the
airways and aggressive use of antibiotics for further bacterial bronchopulmonary
infections. This also highlights the need for further research into the systemic
disorders which are associated with bronchiectasis in many patients.
Summary
Bronchiectasis is a permanent abnormal dilation in one or more of the bronchioles.
Extra fluid is usually collects in the areas that have been dilated and is prone to
infection. The extent to which damage occurs in the airways in patients diagnosed
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with bronchiectasis is varied. Those areas that are widened are damaged and
inflamed. The cause is often not clear and in almost half the cases. Conditions that
often contribute towards bronchiectasis are diseases such as TB, inherited conditions,
inhaled objects and other inflammatory diseases such as rheumatoid arthritis. Patients
presenting with bronchiectasis usually have symptoms such as sputum production,
feeling tired, poor concentration, wheeziness, breathlessness and recurring chest
infections. Diagnosis is usually confirmed through a CT scan, other tests may be
used if an underlying cause is suspected. Treatments often include antibiotics,
physiotherapy, a steroid inhaler, immunisation, bronchodilators, stopping smoking
and in some cases surgery. There is lack of published research within this area that
considers the psychological symptoms associated with this disease. There is also no
research that has investigated patients sleep quality, QoL, mood or how cognitive
functions can be affected too.
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2.1.4 Asbestos related conditions
Historical background
Asbestos is an ancient mineral exploited by humans from prehistoric times because
of its properties of durability and heat resistance and its fibrous nature, which enable
it to be spun (International Labour Office, 1997; Rom, 1998; Harber et al, 1995). The
Finns used asbestos in the fashioning of pottery as early as 2500 BC; the Vestal
Virgins in Rome used it for the wicks of their oil lamps and Marco Polo was said to
have marvelled at the fire-resisting cloth made by the Chinese during his travels
through Asia. Commercial use of asbestos began in the 19th century, starting in open
pit mining and grew as mechanisation replaced hand cobbing (International Labour
Office, 1997; Rom, 1998) and growth was exponential between the two world wars.
Production peaked at more than 5 million tons per year in 1976 and stabilised at
approximately 4 million tons per year in the early 1980’s, faltering only in the latter
part of that decade when the ill health effects of exposure became a matter of
increasing public concern (International Labour Office, 1997). During the 1980s the
use of asbestos decreased in Europe and North America, the use of substitutes
increasing proportionately (since 1999, the use of asbestos has either been
completely banned or severely restricted). However, on the Asian, African and South
American continents asbestos continues to be in demand as a cheap and durable
material for use in water reticulation and in housing projects.
Asbestos is originally a Greek word meaning “unquenchable” (Harber et al, 1995).
Currently, it is used as a collective term for naturally occurring mineral silicates of
the serpentine and amphibole group. Despite different origins and physical and
chemical properties, these silicates have in common a fibrous habit, that is, they
occur naturally in bundles of parallel, radiating, or interlaced fibres that usually can
be separated readily. The term fibre is of more than pedantic use, because the fibre
particle dimensions are determinants, probably important ones, of biologic potency.
The non neoplastic effects of exposure to asbestos can be classified into:
circumscribed pleural plaques (CPP), diffuse pleural thickening (DPT) and benign
asbestos pleural effusion (BAPE).
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Pleural Plaques
Definitions
Pleural plaques are discrete areas of hyaline or calcified pleural fibrosis, which have
been localised on the parietal pleura of the chest wall, diaphragm and mediastinum.
Diffuse pleural thickening is a condition of more extensive, active and progressive
pleural fibrosis, which involves the visceral pleura. Calcification may also occur in
longstanding DPT.
Diffuse Pleural Thickening
Definition
This pleural thickening appears more closely related to amphibole than chrysotile
exposure (Hussain et al, 1999). In asbestos cement workers, diffuse pleural workers,
diffuse pleural thickening is more common in those with more heavily exposed and
also increases in incidence with increasing time since first exposure (Ribotta et al,
1998). There is also no consistent relationship between smoking status and diffuse
pleural thickening.
Clinically assessing asbestosis related illnesses
The criteria used for diagnosing patients with asbestosis usually depend upon the
purpose for which a diagnosis is required. Clinically, diagnosis depends on
establishing the presence, extent and nature of pulmonary fibrosis and whether there
has been a exposure of a duration and intensity sufficient to put the individual at risk
for developing asbestosis (Jones, 1991). Clinically, the fewer the features, the less
certain the diagnosis and the more trivial the exposure and therefore the less likely
that it is causal. When radiological or lung function changes are marginal, CT or
HRCT often tend to reveal the presence of parenchymal abnormalities usually
associated with pleural thickening or plaques (discussed later in this section). A
biopsy of the lung can also be performed if there is absence of adequate exposure
history. The biopsy is usually conducted to establish the nature of the disease and
establish the presence and burden of asbestos in the lungs.
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The diagnosis of asbestosis for the purpose of legal reasons requires reliable certainty
and the use of criteria that vary accordingly to the legal administrative system
involved (Rom, 1998; Harber et al, 1995; Parkes, 1994; Churg, 1998). Published
papers usually consider histopathological criteria as the best means of establishing
the diagnosis (Harber et al, 1995; Bégin et al, 1989). In the absence of
histopathological criteria the following criteria are proposed: 1) a reliable history of
asbestos exposure; 2) an appropriate lag time between exposure and detection; 3)
there also needs to be evidence of lung fibrosis on the chest radiograph or HRCT
scan; 4) a restrictive pattern of lung function; 5) bilateral fixed inspiratory crackles;
and lastly 6) clubbing of the fingers or toes, or both. Of these history or exposure and
evidence are considered essential and others are regarded as confirmatory (Bégin et
al, 1989).
Clinical Features
Most patients diagnosed with asbestosis are asymptomatic for at least 20 to 30 years
after the initial exposure. Asbestosis has been referred to as a monosymptomatic
disease because of the most distressing symptom, dyspnoea (Selikoff, 1978).
Dyspnoea first occurs after heavy effort and then as the disease progresses it occurs
progressively on diminishing levels of exertion. Clinically, dyspnoea precedes other
evidence of disease and therefore the clinician, because of its subjective nature, may
underrate this. The relationship of dyspnoea to exposure levels in studies of exposed
work forces has been a good reason to take it seriously in any exposed individual
(Becklake et al, 1991). Another symptom, which usually manifests, is a persistent
cough and sputum is also commonly reported (Ernst, 1991; Huuskonen et al, 1978).
The cough is dry, occurs with distressing spasms and has been attributed to the
stimulation of lung receptors. A productive cough is usually associated with
smoking. Chest tightness or pain, or both, is not uncommon and may be caused by
acute asbestos-associated pleural reactions.
Another early distinctive feature of asbestosis is basal crackles which are usually fine
crisp sounds, often heard first over axillary and basal regions and then generally as
the disease advances (International Labour Office, 1997; Parkes, 1994). Other sounds
include coarse crackles and rhonchi that usually reflect airway disease that maybe
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related to cigarette smoking or to dust in the occupational environment (Becklake,
1989). Clubbing of the fingers and occasionally the toes develops in some subjects.
Late manifestations include respiratory and circulatory failure and these, with cancer,
are common causes of death (Huuskonen et al, 1978).
Lung Function
Asbestosis, which has been established, is usually associated with a restrictive lung
function profile. FVC and the diffusing capacity in less advanced radiologic disease
are usually reduced; reduction in flow at low lung volumes is a common finding in
keeping with small airway abnormality (Wright et al, 1992; Bégin et al, 1989; Bégin
et al, 1995; Ernst et al, 1991).
Management, prevention and health monitoring
Clinical management of asbestos-related lung conditions is different from
management when there is no history of asbestos exposure. The clinician is bounded
by law to make the appropriate notification of any case of asbestos-related diseases;
another issue is that the clinician must face how to advise the patient of any future
employments issues; guidance is usually based on the natural history of the disease
processes with or without further exposure (Becklake, 1991; Ernst et al, 1991;
Craighead et al, 1982).
No active treatment measures have been shown to influence the course of asbestosis.
Drugs advocated for interstitial lung diseases prove to be less effective as the active
agent remains in situ in the lungs. Control and prevention of the disease is a public
health issue as discussed earlier. This requires a successful control of the work force
environment, setting and enforcing of standards and pre-employment or in-service
health examination for exposed workers as part of a health-monitoring program.
Quitting cigarette smoking benefits the asbestos-exposed individual (International
Agency for Research in Cancer, 1996).
Summary
Asbestosis is a chronic restrictive lung disease that affects the parenchymal tissue of
the lungs. It often occurs after minimal exposure to asbestos. Patients diagnosed with
asbestosis usually suffer from dyspnoea. One of the primary symptoms of asbestosis
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is the slow onset of shortness of breath upon exertion. Coughing is not a typical
symptom. Most cases of asbestosis do not become apparent until five to ten years
after the initial exposure to the material. Asbestosis is scarring of the lung tissue due
to the inhalation of the asbestos fibres. Here are two types of fibres, amphibole and
serpentine. There is no curative treatment; oxygen therapy is often necessary to
relieve the shortness of breath along with physiotherapy and chest percussion.
Nebulised medication may also be offered. Currently there is no research being
conducted to investigate the psychological consequences of living with asbestosis
and related illnesses and if sleep is disturbed in such a disease.
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2.3 Studies investigating disturbed sleep and psychological
well-being in individuals diagnosed with respiratory
diseases
This chapter provides a review of the literature which has focused upon disturbances
in sleep and psychological well-being in individuals diagnosed with respiratory
diseases. Appendix 1 describes the databases and keyword search terms used for the
literature review.
The review has been grouped into three sections.
•
Firstly, sleep studies of individuals with respiratory diseases using
physiological and questionnaire methodology.
•
Secondly, studies which have focused on the psychological aspects of being
diagnosed with respiratory diseases; these studies have used the questionnaire
method to collect data on psychological functioning and how this affects an
individual’s well-being.
•
Thirdly, studies, which have looked at psychological functioning in
individuals diagnosed with obstructive sleep apnoea syndrome. These studies
have been presented as they have focused on the variables that are being
researched in the present study; these being excessive daytime sleepiness,
mental health, general health, mood and memory, these studies also use
similar methods to the present study and, finally, a conclusion.
Sleep disorders are common in the general population but certain populations such as
older adults, women and individuals with medical conditions (for example,
respiratory diseases) are at greater risk (Zee and Avidan, 2006). This is an area of
research which has been neglected.
2.3.1 Sleep studies of individuals with respiratory diseases
The studies reviewed in this section are concerned with sleep in individuals
diagnosed with respiratory diseases. These studies have investigated disturbed sleep
using physiological studies and the questionnaire method to investigate disrupted
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sleep. Asthma and COPD are the most extensively studied respiratory diseases in
terms of investigating disturbed sleep but the investigation has still been very limited
(Douglas, 1994). Each disease will be discussed in turn in relation to sleep.
Sleep in individuals diagnosed with asthma using objective methods
The number of individual studies with asthma in relation to asthma and sleep are
rather limited, despite the potential importance of such work (Avidan and Zee, 2004).
It is not clear from the sleep literature whether the incidence of asthmatic attacks is
greater or lesser in sleep than during waking hours. Pulmonary disease specialists
state that the incidence of asthmatic attacks is more frequent during the evening
hours and during sleep than during daytime (Avidan and Zee, 2004).
Only a few studies have actually attempted to determine whether asthma is more
likely to occur at one time of the night than another and whether it occurs more often
in one stage of sleep or another (Avidan and Zee, 2004), due to the fact that only
small numbers are involved it is quite difficult to draw a conclusion. However having
said this, the following studies highlight the sleep disturbance in individuals
diagnosed with asthma.
A study by Ravenscroft and Hartmann (1968) studied three individuals diagnosed
with asthma on twenty one subject nights. During this there were thirty seven
asthmatic attacks. The investigators found that twenty attacks occurred during Stage
1 REM sleep. When the asthmatic attack occurred during NREM sleep the
individuals still reported dreaming in 62% of the instances. The investigators
concluded that there is a strong temporal correlation of nocturnal asthma with sleep
stage REM. In NREM, attacks are associated with reports of dreaming, and occur in
Stage 1 or 2. No attacks occurred during Stages 3 and 4. The conclusions of this
study are, however, based on just three individuals diagnosed with chronic asthma.
A further study by Kales, Beall, Bajor, Jacobson, and Kales (1968) monitored twelve
individuals with asthma with continuous all-night recordings of EEG, EOG, EMG
and respiration for a total of thirty five nights. During the sleep study period, ninety
three asthmatic episodes were noted, from these, seventy three occurred during REM
sleep, eighteen in REM sleep, and two after lengthy awake periods. The attacks were
115
scattered throughout the night except for a lower incidence in the first hour of sleep.
The investigators observed no obvious relationship between the asthmatic attacks
and sleep stages, time of night, or both. Individuals with asthma did have disordered
sleep and they also obtained less total sleep time than normal controls because of
frequent awakenings and earlier final awakenings. They also had significantly less
Stage 4 sleep, but REM percent was comparable to the normal controls. It can be said
from this that asthma does disturb sleep and that the attacks are not related to any
particular sleep stage or time of night in adults.
Sleep in individuals diagnosed with asthma using questionnaire studies
This section will present studies concerned with sleep quality and sleep disturbances
in those individuals diagnosed with asthma. These studies have employed
questionnaires as the method to collect their data.
Asthma causes a variety of respiratory symptoms, which can impair the quality of
life and lead to sleep disturbance, and this could persist even in individuals with
hitherto well-controlled asthma by clinical parameters. This is an area that requires
greater study.
Studies of nocturnal asthma (Caterall, Calverley and Brezinova, 1982; Kales, Kales
and Sly, 1968; Kales, Kales and Sly, 1970; Montplaisir, Walsh, Malo, 1982) have
provided some data on sleep in patients diagnosed with asthma but these studies have
been conducted in sleep laboratories which can affect the pattern of sleep due to the
sophisticated instruments that are used to monitor sleep patterns. Recent attempts by
Janson, Gislason and Boman (1990) and Fitzpatrick, Engleman and Whyte (1991)
are the only studies that have attempted to highlight the problem of self-reported
sleep disturbances in patients diagnosed with asthma and the effects that this can
have on daytime functioning. Janson et al (1990) showed that the most common
sleep disturbances amongst asthmatic patients were early morning awakening,
difficulty in maintaining sleep (DMS) and excessive daytime sleepiness coupled with
decreasing asthma control and increased number of acute asthmatic attacks. Patients
also experienced an increase in DMS, nocturnal wakefulness nocturnal breathing
problems and bronchodilator inhalations at night.
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Fitzpatrick’s et al (1991) highlighted the problem of sleep quality and cognitive
functioning in patients diagnosed with nocturnal asthma. Patients with asthma had
poorer average scores for subjective sleep quality, objective overnight sleep quality.
Daytime cognitive functioning was worse in patients with nocturnal asthma and
generally took longer completing cognitive tests, achieved a lower score on the tests
compared to their healthy counterparts. Sharpley (1996) has stated that the impact of
daytime sleepiness in individuals with asthma can have potentially serious effects.
Sleep disturbances in patients with asthma are likely to be under-reported (Van
Keimpema, Ariansz, Nauta and Postmus, 1995) but the problems that patients face
with sleep also include factors that are applicable to the non-asthmatic general
population. These include insufficient or ineffective sleep, circadian rhythm
disturbances and inadequate sleep hygiene. Nevertheless the few studies that have
been conducted in this area have highlighted that asthma per se can disrupt sleep,
these factors being troublesome day-time and nocturnal symptoms, lack of disease
control and contributing psychological reactions of a chronic condition, such as
anxiety, irritability and depression which can further trigger disrupted sleep and
reduced Quality of Life.
It has been estimated that more than 70% of people with asthma are troubled by sleep
disturbances, which leaves them tired and unwell the following day (NAC, 2002). In
a sleep study conducted in 2003 a significant deficit was found in the sleep
‘efficiency’ experienced by people with asthma compared to those without asthma
(Hindmarch, 2003). Those with asthma enjoyed far less of the deep and restful sleep
stages 3 and 4 than those without asthma and spent far more time awake. Many
patients are unaware of the consequences that the lack of sleep brings, a survey of
patients in one particular practice admitted to disturbed sleep because of their
asthma, despite insisting their asthma was well controlled (Crockett, 1998).
Sir John Floyer, who was an asthmatic patient himself, was the first person to give a
clear description of nocturnal asthma in 1698 (Floyer, 1698). The mechanisms of this
particular asthma are still not understood clinically (Douglas, 1985). Previous studies
on nocturnal asthma in sleep laboratories have reported poor quality and shorter
duration of sleep in asthmatic patients (Caterall et al, 1982; Montplaisir et al, 1982).
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A significant feature, which has not received the attention it deserves, is the effect of
asthma on the quality of sleep itself. Some efforts have been made to highlight the
nature of sleep disturbances in asthmatic patients and its effect on daytime
performances (Janson et al, 1990; Fitzpatrick et al, 1991) and Vir et al (in press).
Current opinion indicates that the impact of daytime sleepiness, which has serious
effects, has been underrated (Sharpley, 1996). Epidemiological studies have shown
altered patterns in sleep in patients with obstructive lung diseases (Klink and Quan,
1987). This problem was highlighted by Turner-Warwick (1988) in a study where
7729 asthmatic patients being treated by their GP’s were observed: 74% reported
they woke at least once a week due to symptoms relating to asthma; 64% woke at
least three nights a week and 39% reported doing so every night.
In a study by Janson, Gislason, Boman, Hetta and Roos (1990) sleep complaints and
sleep disturbances was studied prospectively in ninety eight individuals diagnosed
with asthma attending an out-patient clinic, by means of questionnaires and sleep
diaries. The results from the individuals were compared to healthy age and sex
matched group individuals. In individuals diagnosed with asthma early morning
awakening, difficulty in maintaining sleep and daytime sleepiness was most
commonly reported. As the individuals’ control of asthma decreased the disturbance
in sleep increased, this being difficulty in maintaining sleep, nocturnal wakefulness,
nocturnal breathing problems and bronchodilator inhalations at night. Shah et al
(1997) reported that the commonest sleep disturbance observed in their research was
maintaining sleep (60%) and early morning awakening (47%). No gender variation
was reported in sleep disturbances but difficulty in maintaining sleep had a
significant association with daytime naps in asthmatics.
In one study individuals diagnosed with asthma reported more sleep disturbances and
daytime somnolence than healthy controls, although individuals reported decreased
sleep quality, decreased daytime mental fitness and an increase in daytime
somnolence, there was no relationship between lung function and bronchial
hyperactivity or nocturnal asthma (Van Keimpema, Ariaansz, Nauta and Postmus,
1995).
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A random population study of young adults in three European countries aimed to
investigate whether asthma is associated with decreased quality of sleep and
increased daytime sleepiness. Amongst the assessments was a questionnaire on sleep
disturbances, participants also estimated their sleep times and made peak expiratory
flow recordings during a period of one week. Analysis revealed that individuals
diagnosed with asthma reported difficulties inducing sleep, early morning
awakenings and daytime sleepiness compared to healthy participants (Janson,
Backer, Gislason, Plaschke, Björnsson, Hetta, Kristbjarnarson, Vermeire and Boman,
1996).
Excessive daytime sleepiness is one of the most prominent symptoms that have been
associated with obstructive upper airway disorders during sleep (Guilleminault,
1985; Guilleminault, 1994). Consequently excessive daytime sleepiness brings about
significant deterioration in daily performance of patients in psychosocial and
cognitive functions (ATS, 1998), mood swings and emotional distress (Churchill and
Dilsaver, 1990; Jovanovic, 1991; Totterdell et al, 1994; Hill et al, 1996), poor
performance on the job and during leisure activities (Pilcher and Huffcutt, 1996;
Smith-Coggins et al, 1994) and creating a lack of general physical (Theoell et al,
1995) and mental well-being (Kupfer, 1995).
Sleep in individuals diagnosed with COPD using objective methods
Sleep quality is often poor in individuals diagnosed with moderate to severe COPD
(Quan and Zee, 2004). Interrupted sleep can have serious negative consequences for
individuals diagnosed with respiratory diseases, resulting in hypoxemia (Insufficient
oxygenation of arterial blood) and hypercapnia (increase in carbon dioxide in the
blood); these, in turn, can disturb sleep (Mohsenin, 2005). Hypoxemia and
hypercapnia are likely to contribute to the disturbed sleep of individuals diagnosed
with COPD. The worsening of hypoxaemia during sleep in individuals with COPD
has been documented since the early sixties (Trask and Cree, 1962) and has since
been confirmed by polysomnographic studies (Koo, Sax and Snider, 1975; Leitch,
Clancy, Leggett, Tweeddale, Dawson and Evans, 1976). In a sleep study by Fleethan,
West, Mezon, Roth and Kryger (1982) twenty four individuals diagnosed with
COPD were recruited to compare oxygen therapy with air breathing in an attempt to
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gain insight into oxygen desaturation during sleep. Fleethan et al found that during
REM sleep the lowest mean of oxygen saturation occurred; only two individuals had
episodes of sleep apnoea. Less than 23% of the individual’s sleep time was occupied
with oxygen saturation, more than 5% below awake values. Age matched individuals
were shown to have better sleep quality, sleep time, fewer sleep stage changes and
decreased arousal frequency. Those individuals diagnosed with COPD in the study
exhibited increased arousal frequency during reduced arterial oxygen saturation
when they were breathing room air. Since no relief from the high arousal frequency
was obtained with supplemented oxygen, the investigators concluded that hypoxemia
itself was not to blame but hypercapnia.
To further support this view, a study by Ballard, Clover and Suh (1995) assessed the
influence of sleep on respiratory function in five individuals with COPD. Sleep was
monitored during sleep in a horizontal body plethysmograph (a horizontal
plethysmograph designed to accommodate supine subjects). Neither lung volume nor
lower airway resistance changed in association with sleep. The investigators noticed
a change in upper airway resistance during sleep and were highest during REM
sleep, during wakefulness, stages 2, 3-4, respectively. Tidal volume was reported to
decrease during sleep, resulting in a sleep associated decrement in minute ventilation
during wakefulness, stages 2, 3-4, and REM sleep.
The studies mentioned in this section so far have highlighted the respiratory
problems that occur during sleep in individuals diagnosed with COPD. The majority
of the studies have used polysomnography to investigate the disturbance in sleep, a
reliable and objective method for investigating nocturnal disturbances.
Sleep in individuals diagnosed with COPD using questionnaire methods
Sleep quality is often impaired in patients with COPD (Cormick et al, 1986;
Fleetham et al, 1982; Brezinova et al, 1982). During desaturation sleep
fragmentation and arousals frequently occur Sandek et al, 1999). Philip et al (1994)
has shown that fragmented sleep and frequent arousals lead to daytime sleepiness
both in healthy normal adults and in patients with sleep disordered breathing (SDB).
Cormick (1986) and Orr et al (1990) have both revealed that the scarce data available
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regarding daytime sleepiness in patients with COPD are contradictory. A study by
Saaresanta et al (2005) has highlighted that patients with moderate to severe COPD
without acute exacerbations do not complain about excessive daytime sleepiness
(EDS) as much as patients with obstructive sleep apnoea syndrome (OSAS) do.
Many patients with COPD have frequent and prolonged episodes of hypoxemia
during sleep (Flick et al, 1977; Interiano et al, 1972). According to Wynne (1978)
these episodes maybe nocturnal or may occur during daytime naps, Wynne et al,
(1978). Those mechanisms which mediate hypoxemia usually include airway
obstruction, central apnoea, hypoventilation and oxygen desaturation without
apparent breathing abnormalities (Koo et al, 1975). Patients with COPD usually
show a combination of these etiological mechanisms during a single night’s sleep.
There are several studies which have shown that recurrent transient hypoxemia
during sleep is frequent in patients with COPD (Douglas et al, 1981; Becker et al,
1999). As mentioned earlier, hypoxemia is clearly marked in patients with a blue and
bloated clinical phenotype and frequently occurs during REM sleep.
As mentioned in the previous paragraph, symptoms related to sleep disturbances are
common in moderate to severe COPD, as noted in a study by Bellia et al, (2003),
particularly in elderly patients in the form of morning tiredness and early
awakenings. Both depression and arthritis were the most significant independent
correlates for the majority of sleep scores in the elderly population with COPD. In
severe cases, the sleep disturbance is usually related to nocturnal cough, wheezing,
and shortness of breath due to worsening of pulmonary mechanics and gas exchange
during sleep.
In a large survey of patients with COPD, Klink et al, (1994) found that with one
respiratory symptom (cough or wheezing) present, 39% reported insomnia and 12%
excessive daytime sleepiness. With both symptoms present the prevalence of
insomnia and excessive daytime sleepiness were 53% and 23%, respectively. Sleep
studies in COPD conducted by Calverley et al, (1982) and Fleetham et al, (1982)
have shown poor-quality sleep as judged by marked increase in sleep stage changes,
frequent arousals and awakening, and decreased total sleep time (summed Stages 2,
3, 4, and REM) with increased number of arousals. However, in an adult community
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setting and part of the Sleep Heart Health Study, Sanders et al (2003) found that
patients with mild obstructive airway disease (FEV1/FVC 63.8 ± 6.6%, mean ± SD)
did not perceive themselves to have excessive daytime sleepiness and had minimally
altered sleep quality and sleep architecture.
Sleep disturbances are very common in the elderly (Prinz et al, 1990). A progressive
decrease in duration and deterioration in quality of sleep may be assumed as a
hallmark of aging. According to Douglas (1998) and Martin (1993) patients with
COPD and asthma undergo changes in respiration along with other body functions
along with nocturnal sleep. As a knock on effect, nocturnal exacerbations are
frequently recorded in such patients. Banerjee et al, (1998) and Dow (1999) have
illustrated that under-diagnosis in the elderly occurs frequently and the association
between chronic airflow and sleep complaints in the elderly therefore deserve special
attention as the prevalence of this association may be underestimated. As well,
factors such as the role of physical limitation, cognitive decline and depression in
influencing this association have not yet been evaluated.
Although COPD and asthma are two different diseases nevertheless there is a risk of
misdiagnosis in the aged (Ulrik et al, 1999); this is due to the loss of reversibility
which accompanies longstanding asthma, therefore assessing the impact of asthma
and COPD on the type of and severity of sleep impairment may contribute towards
differentiating these conditions in the elderly.
Studies which have used both objective and questionnaire methods to assess sleep
and psychological functioning in respiratory diseases
Within the literature search only one study was found which used both a sleep study
and a survey method to assess sleep quality and daytime sleepiness in individuals
diagnosed with COPD. This rare study, conducted by Saaresranta, Irjala, Aittokallio
and Polo (2005), set out to investigate individuals with COPD who have impaired
sleep quality without excessive daytime sleepiness and analysed the aetiological
factors. Fifteen females with moderate to severe COPD and 20 healthy age matched
women were studied. Individuals with respiratory diseases completed a questionnaire
(BNSQ), had a polysomnography and a blood test. Healthy controls filled in only the
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questionnaire. The average score for individuals diagnosed with COPD versus
controls in terms of sleepiness and insomnia derived from the BNSQ was low.
Although a high proportion of the individuals diagnosed with COPD reported having
never slept well (70%) and sleeping restlessly, only a minority reported feeling tired
in the morning (33%). Healthy controls reported better sleep quality, less tiredness
and sleepiness. With polysomnography the total sleep time was four hours and forty
one minutes ± one hour and twenty minutes in individuals diagnosed with COPD,
sleep was also observed to be fragmented, the proportion of Stage 1 sleep was high
and REM latency was delayed.
It is important to use methods other than objective ones as some patients with good
PEF may still report a poor QoL and vice-versa. Although PEF and QoL are
correlated, this is not usually a strong correlation, as QoL can be affected by many
other factors than PEF. Asthma care is not simply about managing the patient’s
condition and correcting their respiratory function, it is also about maximising the
patient’s QoL (Feeney et al, 1991). Clinicians and investigators have assumed that if
clinical indices improve, then the patient must be feeling better. This may not be the
case; conversely, some patients may experience an improvement in daily functioning
that is not captured by the conventional outcomes (Juniper et al, 1995).
An important factor, which has been highlighted through research investigating QoL
and living with asthma, is that although physical functioning can be improved by
better physiological control, the emotional aspects of asthma are more readily
changed by psychological factors. The management of asthma involves both a
physiological and psychological component. QoL assessments help the health
professional to detect any psychological upset as well as to measure its improvement
following effective patient management. Such measures can reflect the intangible
cost of asthma and can also be a predictor of compliance (Rutten et al, 1995).
COPD is associated with intermittent worsening of symptoms and lung function
impairment. Not only do the exacerbation of symptoms contribute towards mortality
and morbidity but also they considerably affect the QoL experienced by patients
(Murray et al, 1997; Celli et al, 2004). Worsening usually occurs due to bacterial
pathogens that are present in the LRT. Studies by Sethi et al, (2000) and Patel et al,
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(2002) have shown that exposure to certain allergens and pollutants may also worsen
symptoms. Saint et al, (1995) showed that although antibiotics are usually the main
course of treatment for such patients, nevertheless their efficacy is debatable. Some
studies under controlled conditions have shown that they do work and some have
shown that they do not. Kim et al in 2004 have shown that the uncontrolled use of
antibiotics in COPD exacerbations is very expensive and may contribute to the
serious problems of emerging resistance to valuable antibiotics.
Most asthmatic patients are usually treated with theophylline along with inhalers; it
is not however known to what extent theophylline contributes to sleep impairment.
There are reports to suggest that theophylline does contribute to disturbed sleep in
patients who are unaccustomed to this drug, (Janson, Gislason, Almqvist and Boman,
1987). Patients who have been diagnosed with nocturnal asthma tend to benefit from
the drug symptomatically. In a study by Janson and colleagues (1991) asthmatic
patients who received theophylline and had reported sleep problems were given an
alternative form of the drug known as enprofylline (both drugs have the same
properties, the difference being that enprofylline is not a CNS stimulant). It was
found that the difference in the drugs did not improve the quality of sleep in those
patients treated with theophylline, suggesting that there may be some other
underlying biological factors affecting the patients sleep.
A study conducted by Hellgren, Omenaas, Thórarinn, Gíslason, Jögi, Franklin,
Lindberg, Janson Torén on behalf of the RHINE study group (2007) conducted
questionnaire research on a random population sample from North Europe aged
between thirty and fifty four years of age; it was analysed in relation to perennial
non-infectious rhinitis (nasal symptoms such as nasal blockage and secretion in the
absence of common cold). Seventeen percent of the total sample reported perennial
non-infectious rhinitis and this was said to be associated with an increase in having
difficulty in maintaining sleep, early morning awakening and daytime sleepiness.
This study showed that perennial non-infectious rhinitis is an independent risk factor
for sleep disturbances in asthma.
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2.3.2 Psychological studies of respiratory diseases
Psychological well-being
The studies mentioned in this section focus on the psychological well-being of
individuals diagnosed with respiratory diseases.
According to Osler (1903) most clinicians of this era would have agreed that there is
a neurotic element to having been diagnosed with asthma. In 1966, Houston, Joiner
and Trounce confirmed this statement in a popular textbook stating that there is some
form of psychological influence that controls every asthmatic’s anxieties, whether
starting them or maintaining them. The need for scientific support for an established
association between psychological factors and asthma had its roots firmly established
in the first part of the twentieth century. However, post-1990, references to
psychological or psychosocial aspects of living with any respiratory disease,
including asthma, is minuscule (Harrison, 1998). There appears to be a steady
increase amongst academics and clinicians alike in understanding that psychological
factors are associated with asthma (Greaves, Eiser, Seamark and Halpin, 2002). It is
important to state that most studies concerned with psychological well being in
respiratory disease are focused upon individuals diagnosed with asthma and a few
individuals diagnosed with COPD; other areas still remain under researched to date.
Previous studies have usually focused on the aspects of asthma dealing with
morbidity, mortality and compliance in relation to emotional states such as
depression, panic, fear and denial (Adams, Smith and Ruffin, 2000; Adams, Pills and
Jones, 1997; Yellowlees and Ruffin, 1989) and cognitive factors have also been
linked to asthma outcomes (Janson-Bjerklie, Ferketich and Benner, 1993).
Individuals diagnosed with asthma have frequently been associated with having
underlying psychological distress, such as depression and anxiety (Wright,
Rodriguez and Cohen, 1998). In a study cited in Thorax (1997) the psychological
characteristics of individuals with asthma were studied. Although there is no specific
personality profile of individuals diagnosed with asthma (Chetta, Gerra and Foresi,
1998; Michel, 1994) there is, however, evidence of an association between atopic
illnesses and depression (Wamboldt, Hewitt and Schmitz, 2000). A study by Janson,
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Björnsson, Hetta and Boman (1994) has found an association between respiratory
and psychiatric symptoms in healthy participants without respiratory diseases.
In a study by Vamos and Kolbe (1999) levels of psychological distress, social
support factors and emotional adjustment were measured in a sample of individuals
with severe asthma. A sample of eighty individuals was recruited from a hospitalbased asthma clinic designed for individuals with severe asthma. Self-reported
questionnaires were used to measure anxiety, depression, social support, emotional
adjustment to asthma. Vamos and Kolbe found that at least 25% of the sample
population had possible caseness for anxiety while fewer than 11% had caseness for
depression. 25% had inadequate social support in some way. It was concluded that
individuals diagnosed with severe asthma have high levels of distress, particularly
anxiety.
Although asthma is known to be influenced by a variety of physical, psychological
and social parameters, the relationship between such parameters is less well
understood (Jones, Kinsman, Dirks and Dhalem, 1979; Spittle and Sears, 1984;
Nocon and Booth, 1991). In a study by Miles, Garden, Tunnicliffe, Cayton and
Ayres (1997) these variables were further explored using a case control study on
twenty-nine well-characterized brittle and non-brittle asthmatics in the West
Midlands Region to assess their level of psychological morbidity. The GHQ and the
Living with Asthma questionnaire was used and participants’ responses to changes in
asthma symptoms, using the Asthma Symptom Checklist and a taped interview. The
study highlighted the association of brittle asthma with greater psychological
morbidity and altered strategies for coping with deteriorating asthma symptoms.
Further support is provided by Dales, Spitzer, Schechter and Suissa (1988) who
examined the influence of psychological status on respiratory symptoms was
explored. Six hundred healthy subjects were selected from a population of just fewer
than four thousand. Healthy subjects were defined as being between fourteen and
fifty five years of age, having never smoked, had no diagnoses of respiratory
diseases, no heart, kidney, thyroid disease or anaemia and having a normal
spirometry (defined as FEV1 and FVC>eighty percent of predicted). Subjects’ scores
from the American Thoracic Society respiratory symptom questionnaire (ATS-Q)
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and Ilfeld Psychiatric Symptom Index (PSI) scores were compared. Dales and
colleagues found that associations were found between respiratory symptoms (cough,
phlegm, wheeze and dyspnoea) and PSI subscales (anxiety, anger, depression and
cognitive disturbance).
Methodologically, it is difficult to study respiratory symptoms together with
psychological status. For example, it is often difficult to ascertain whether those
individuals with higher levels of anxiety are more aware of their cough symptoms
and whether it is the anxiety which has led to the increased awareness of the cough
or whether if it is the underlying disease which is present which has led to the
increase in anxiety and the increased reporting in the respiratory symptoms (Dales et
al, 1988).
Further studies exploring the relationship between anxiety and depression in relation
to respiratory symptoms and asthma have been investigated by Janson and colleagues
(1994), who further explored the relationship between psychological status and
respiratory health. Seven hundred and fifteen individuals aged between twenty-two
and forty-four took part in the European Commission Respiratory Health Survey.
The study collected various respiratory data alongside a structured interview and
psychological status was assessed using the HADS questionnaire. Significant
correlations were found between anxiety and depression and asthma-related
symptoms. The authors came to the conclusion that there is an association between
reported respiratory symptom and psychological status. This also results in the
indication that it may be valuable to include psychological status indicators in
respiratory symptom questionnaires.
The impact of psychological distress on the health of the population with asthma is
not well described (Adams, Wilson, Taylor, Daly, d’Espaignet, Grande and Ruffin,
2004). In a study by Ware, Kosinski and Keller (1994) of a small sample of
individuals diagnosed with asthma in the Medical Outcomes Study, asthma was
associated with significant negative effects on the Mental Health Component
Summary of the SF-36.
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Quality of Life
These studies focus on quality of life in individuals diagnosed with asthma and
COPD. The relationship between QoL in adults with asthma is believed to be
important but has not been well studied (Archea, Yen, Chen, Eisner, Katz,
Masharani, Yelin, Earnest and Blanc, 2006). Quality of life in asthma is increasingly
recognised as a clinically important health measure, reflecting the effect of disease
from the perspective of the patient (Juniper, 2003).
According to Rutten-Van, Custers, Van Doorslaer (1995), measures used to study
quality of life are increasingly important in evaluating outcomes in asthma care.
Questionnaires used include generic measures such as the SF-36 and respiratory
specific measures such as the St George Respiratory Questionnaire (SGRQ) (Jones,
Quirk, Baveystock, 1991) and the Asthma Quality of Life Questionnaire (AQLQ)
(Juniper, Guyatt, Ferrie, 1993).
There is also little information available in relation to asthma and QoL in elderly
patients. A Medline literature search conducted between 1986 and 1997 using
keywords such as “asthma”, “aged” and “QoL” detected only thirty-seven articles;
most of the studies, however, were only of questionnaire validation studies, including
a small sample of the elderly population (Burr et al, 1979; Burrows et al, 1991).
In a study by Adams and colleagues (2004) a study showing the prevalence of
psychological distress in asthma in the general population and its associations with
QoL showed that psychological distress was more frequent in those with asthma and
a higher proportion with asthma were at higher risk for anxiety or depression. Mental
health conditions were also more common as was frequency of those who sometimes
or always felt a lack of control over their health. People with both asthma and
psychological distress scored significantly lower on the SF-12 physical component
score than those with asthma or distress alone. There was also no difference in scores
amongst individuals with asthma on the mental component score who had
psychological distress.
Although asthma remains one of the most frequently reported chronic respiratory
disorders, if managed effectively, patients can be helped. According to the British
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Thoracic Society, the guidelines for managing asthma indicate that the primary aim
is to restore optimal lung function and to abolish or minimise symptoms and this is
while using minimum medication, this being an objective measures of lung function.
It is well reported that psychological and respiratory symptoms are mutually related.
Work by Dales, Spitzer and Schecter (1989) shows that healthy participants are more
like to report respiratory symptoms, these being cough, phlegm, wheeze and
dyspnoea; the participants diagnosed with having a psychological disorder, such as
anxiety, depression, anger or cognitive disturbances are also often reported.
A study by Janson, Bjornsson and Hetta (1994) demonstrated the association
between respiratory symptoms and psychological status. Patients diagnosed with
asthma were no more anxious or depressed than any other participants with
respiratory symptoms. Work by Cooper, Ryland, and Davies (1997) observed as well
that the same relationship exists between psychological status and morbidity in
patients with severe asthma.
Most studies of asthma are conducted in secondary care as part of a specific study
protocol with tight inclusion and exclusion criteria. Those patients who attended a
secondary care facility using the inclusion and exclusion criteria results in patients
who are not typical of the general population (Rimington, Davies, Lowe and Pearson,
2001).
Insufficient patient knowledge, being able to manage with exacerbations, poor
adherence to treatment and socioeconomic factors all affect the patient who suffers
from asthma (Neville, Gribbein and Harrison, 1991; Padget and Brodsky, 1992; Reed
et al, 1985). Psychological factors have also been suggested: Janson-Bjerklie et al
(1992) suggested that the degree of distress during an asthma attack, perceived
danger from asthma and the all important appraisal of social support were significant
predictors of emergency room (ER) visits. In a study where asthmatic patients were
asked to describe one episode from the previous month, Janson-Bjerklie et al (1992)
concluded that the frequency of ER visits was not only significantly correlated with
perceived and actual severity, suggesting ER visits to be the behavioural
manifestations of the patients appraisal of danger and threat, but it was also found
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that patients reported delaying before seeking help, suggesting that ER visits occur as
a last resort and often after a period of unsuccessful coping with a flare-up.
Psychological, psychosocial and attitudinal factors have been studied as possible
contributory factors to illness and death in a variety of diseases (Watson and
Pennebaker, 1989; Barsky and Wyshak, 1990; Steptoe, 1991; Viinamaki et al, 1993)
as well as asthma (Yellowlees et al, 1988). Hypothesised pathways include effects on
lung function directly (Hyland, 1990), on symptom reporting (Watson and
Pennebaker, 1989; Dirks and Schraa, 1983), on healthcare use (Rea et al, 1986) and
compliance with treatment (Dirks and Kinsman, 1982). In addition to this it has been
shown that socioeconomic and psychological factors act as risk factors for poor
outcome (Rea et al, 1986; Strunk et al, 1985; Miller, 1987).
Studies looking at anxiety, fear and panic have consistently attracted the greatest
interest; it has been shown that panic and fear occur at higher rates in people with
asthma compared to non-asthmatic individuals (Kinsman et al, 1973; Dirks et al,
1973). This is measured as a response to the experience of breathlessness in one
study (Thompson and Thompson, 1985).
In 1989 a study published by Dales and colleagues found a strong positive
association between respiratory symptoms and psychological status. Several studies
have put forward explanations, the first one being that breathlessness is a known
somatic product of anxiety (Bass and Gardner, 1985). As mentioned earlier, those
patients with known psychological symptoms may be more likely to report
respiratory ones (Bass and Gardner, 1985). Other studies have also suggested that
patients diagnosed with bronchial asthma may be more likely to suffer from anxiety
disorders and depression (Lyketsos, Karabetsos, Jordanoglou, Liokis, Armaglanidid,
and Lyketsos, 1984).
Such studies looking at the relationship between psychological and social factors
should be taken into account when plans for the management of asthma are being
devised. In studies that have looked at near-fatal asthma attacks (Sibbald, 1989;
Campbell et al, 1995) the use of the General Health Questionnaire (GHQ) is found.
Both Sibbald and Campbell et al found a prevalence of psychiatric illness of 38%
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and 43% respectively. The scores obtained correlated with days lost from
work/school and the frequency of asthma attacks (Campbell, 1995) which suggest an
association between asthma and morbidity. It has been proposed that perhaps
psychiatric morbidity may decrease an individual’s ability to care for themselves.
Nevertheless, in Sibbald’s study the GHQ scores were not found to be associated
with self-care in acute asthma as judged by the response to a hypothetical attack of
asthma (Sibbald, 1989).
Self-reports that are dependent on the respondents’ perception of physical sensations
may be influenced by psychological factors. Further support has been provided by a
study that reported significant differences in GHQ and living with asthma; this
reinforced the presence of psychological factors in those patients living with asthma
(Miles et al, 1997).
Self-reports, dependent upon the participant’s perception of their own physical
sensations, are inevitably and often importantly influenced by psychological factors.
It follows that psychological factors could reduce bias and the precision of results.
For example, participants who are exposed to atmospheric pollution would be
expected to be more anxious and worried about their health and/or angry about their
working conditions than those who are not exposed (Ware, Ferris, Dockery,
Spengler, Strom and Speizer, 1986; Cotton, Graham, Li KYR, Froh, Barnett and
Dosman, 1983). Another factor which may affect respiratory symptom reporting
could be differences in psychological status which may be associated with
personality characteristics which determine the selection of type of work or area of
residence (Dales, Spitzer, Schechter and Suissa, 1988).
The symptoms of COPD most frequently interfere with various aspects of living such
as work life, family role, socialization daily living activities (Hanson, 1982).
Individuals diagnosed with COPD have also been reported to be severely depressed,
withdrawn, anxious and fearful (Rowlett and Dudley, 1978; Sandhu, 1986).
Impairment in QoL, specifically depression, anxiety, fatigue, social role-functioning
and home management activities were reported to be particular problems compared
to healthy individuals (McSweeny, Grant, Heaton, Adams and Timms, 1982).
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From the literature presented it can be seen that COPD is a progressively debilitating
disease with an insidious onset. The symptoms which manifest in this condition
frequently interfere with various aspects of living, such as work life, family roles,
socialisation and the activities of daily living (Hanson, 1982). Guyatt et al, in 1987
conducted an extensive study that identified dyspnoea and fatigue as major problem
areas in a survey of 100 subjects who were asked how their lives were negatively
affected by COPD. In a study by Rowlett and Dudley (1978) and Sandhu (1986)
factors such as depression, withdrawal, anxiety and feelings of fearfulness were
reported. In a study comparing 203 healthy individuals with those living with COPD
showed that the latter had a greater impairment in QoL. Again, factors such as
depression, anxiety, fatigue, social-role functioning and home management activities
were particular problem areas.
Although assessment of QoL appears to be a particularly strong theme amongst
rehabilitation nursing, from the literature presented so far most studies and most
clinicians tend to heavily rely upon the clinical aspects of the patient’s condition
rather than qualitative aspects of how they are coping with the condition with which
they have to live. QoL has a variety of alternative terms that have been used such as
life satisfaction, well-being, adjustment and self-esteem. QoL can be objectively
measured by observing components such as income, housing, physical functioning
work, SES and support networks and by measuring the subjective components, such
as attitudes, perceptions, aspirations and frustrations (Frank-Stromborg, 1988).
There are several studies that have looked at the QoL of patients living with COPD
(Anderson, 1995; Brown et al, 1981; Guyatt et al, 1987 and Traver, 1988) and
coping (Barstow, 1974; Chalmers, 1984; Post and Collins, 1981; Rowlett and
Dudley, 1978). But none have looked at other factors that too are important and
prevalent in patients whom have been diagnosed with COPD. The symptoms that are
associated with COPD, such as breathlessness, wheezing and coughing, can have
considerable effects on the physical and emotional and social aspects of a patient’s
life.
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2.3.3 Psychological functioning in individuals diagnosed
with obstructive sleep apnoea syndrome
This section has been included as it is the only area within sleep medicine that has
been thoroughly investigated. The studies within this area have focused upon
objectively studying OSAS using polysomnography and using questionnaire
methodology. These studies are included as they closely research many of the
variables that have been studied in the current research, these being; excessive
daytime sleepiness, general health, mood, memory and cognitive functioning using
questionnaires.
Psychologically, secondary depression along with anxiety, irritability, and despair
are associated with OSAS. Individuals with OSAS who have an increase in body
weight will also experience increased severity in their symptoms. In the USA and
other western countries it has been well established that obesity is progressively
increasing (Kuczmarski, Flegal, Campbell and Johnson, 1994; Bjorntorp, 1998). This
finding is important as visceral obesity and body fatness is associated with adverse
health effects such as hypertension, coronary heart disease, stroke, insulin resistance
type 2 diabetes, osteoarthritis and psychological problems (Bjorntorp, 1998).
Nevertheless, there is not much evidence available relating to the respiratory
complications of obesity and reduced exercise capacity, hypoxaemia and
hypoventilation during sleep.
The most common respiratory disturbance is the
development of upper airway obstruction during sleep, which results in OSAS. A
study performed with individuals with severe obesity (mean body mass index (BMI)
> 42.4) showed that more than 50% of individuals without reported sleep-related
disorders had OSAS. Individuals who are clinically obese do report having daytime
sleepiness and fatigue. They have also reported having a lower QoL (Resta, 2001).
Excessive daytime sleepiness has as well been reported to cause social and family
problems (Johns, 1998). Little is known about the sleep-patterns and the sleep-related
symptoms of obese people who do not present with OSAS; however, a study by
Vgontzas, Tsigos, Bixler, Stratakis, Sachman, Kales, Vela-Bueno and Chrousos
(1998) found that obese people without OSAS often report daytime sleepiness and
fatigue. A study by Resta, Caratozzola, Pannaccrulli, Stefano, Giliberti, Carpagnano
133
and De Perzola (2003) showed that individuals with severe obesity, even those who
did not have OSAS, had sleep related disorders and EDS; the authors reported that
these findings could be due to a lower QoL, a higher prevalence of medical
complications and an increased risk of occupational injury and social and family
problems.
Other associated features commonly reported with OSAS are cardiac arrhythmias,
mild hypertension, hypoxemia and blackouts.
Another feature of OSAS is cognitive impairment (Findley, Barth, Powers, Wilhoit,
Boyd and Suratt, 1986; Engleman and Douglas, 2005; Kales and Caldwell, 1985;
Ulfberg, Carter and Talback, 1996; Grunstein et al, 1995; Colt, Haas and Rich, 1991;
Martin, Deary and Douglas, 1996; Roers, Zorick, Wittig, Conway and Roth 1989;
Jennum and Sjol, 1993). In a disease specific inventory, two thirds experienced
memory disturbance and three quarters problems with concentration (Flemons and
Reimer, 1998). In most studies data have suggested an impairment of the so-called
‘executive functions’, a concept initially introduced by Luria (1996) and Lezak
(1982), who defined cognitive functions as planning, programming, regulation and
verification of goal-directed behaviour. Cognitive complaints are also present and
frequent in elderly persons but their clinical significance remains uncertain
(Schofield et al, 1997). For the sake of this thesis, other co-morbidities were taken
into consideration but studies, which have investigated subjective cognitive
complaints and cognitive performance, have given inconclusive results. Some studies
have demonstrated a weak association (Schofield et al, 1997; Jonker et al, 1996)
whereas other studies have failed to show any associations (Jorm et al, 1997; Blazer
et al, 1997; Taylor et al, 1992; O’Connor et al, 1990). Many of these studies,
undermining their usefulness, were based on cross-sectional data or clinical samples
(Schofield et al, 1997; Jonker et al, 1996).
Summary
A review of the literature dealing with sleep and psychological functioning (QoL,
mood and memory) in individuals diagnosed with respiratory diseases has been
presented. The first set of studies presented were those studies that used
physiological sleep studies to investigate the sleep of individuals diagnosed with
134
respiratory diseases. Asthma and COPD are two of the most extensively researched
respiratory diseases in terms of sleep. It has been shown from these studies that sleep
in individuals diagnosed with COPD and asthma is disturbed. Polysomnographic
studies in individuals diagnosed with COPD have revealed disturbed sleep during
REM, wakefulness, Stages 2, 3-4. Disturbed sleep can result in hypoxemia and
hypercapnia but this can also cause the disturbed sleep in individuals diagnosed with
COPD.
Further polysomnographic studies have revealed that individuals diagnosed with
asthma usually have asthmatic attacks during Stage 1 REM sleep, those attacks that
occur during NREM sleep are usually reported as dreams by individuals Asthma
attacks can also occur during Stage 2.
This leads onto studies which have used the questionnaire method to investigate the
psychological functioning, QoL and sleep in individuals diagnosed with respiratory
diseases. Again, asthma and COPD are the only two respiratory diseases that have
been studied extensively in relation to psychological functioning and QoL.
Employing this form of methodology, only sleep in individuals diagnosed with
asthma has been reported. All the studies reported in this area have highlighted the
relationship between anxiety and depression in relation to respiratory symptoms.
QoL is reported low in individuals diagnosed with asthma and COPD and sleep
quality is reported as being poor in individuals diagnosed with asthma. These areas
are still very much under researched and although there are specific areas from a
psychological perspective which have been investigated there isn’t, however,
research being published linking all these factors and understanding how the
patient’s disease and psychological and social well being can contribute towards the
symptoms.
Only a few studies reported to have used both polysomnography and questionnaires
to investigate sleep disturbances in individuals diagnosed with COPD. These
individuals compared to their healthy controls reported to have never slept well, slept
restlessly and had poor quality sleep.
135
The final section dealt with the psychological functioning (QoL, mood and memory)
of individuals diagnosed with OSAS. These studies have been presented because
OSAS has been thoroughly investigated both subjectively and objectively. The
studies within this area have focused upon the variables that have been researched
within the present study using questionnaires. This area has been extensively
researched by both academics and clinicians. There is convincing evidence presented
to suggest that this group of individuals do have poor psychological functioning
(QoL, mood and memory) and disturbed sleep. This hopefully highlights the need for
conducting this project in helping to investigate the disturbed sleep and
psychological functioning in those individuals diagnosed with not just asthma but
COPD, bronchiectasis and asbestosis. The studies within this area have provided a
framework for further concepts to be explored which have not previously been
investigated together using a combination of valid psychometric assessments. The
review has also highlighted the need for further research within specific respiratory
diseases these being; asthma, COPD, bronchiectasis and asbestos and related
conditions. This is further discussed in the next section, 2.4.
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2.4 Need and requirements for further research in
individuals living with respiratory diseases concerning their
sleep and psychological functioning
The following points and issues emerge from the review of the literature that has
been presented in the first part of this thesis.
1. Individuals with respiratory diseases are not a homogeneous group and there
are considerable individual differences that can be identified from the
literature in the introductory chapters. There is very little evidence which
describes sleep disturbances and psychological functioning in patients who
have been diagnosed with respiratory diseases, specifically asthma, COPD,
bronchiectasis and asbestosis. However these studies have shown that
individuals diagnosed with asthma and COPD will have some form of
psychological dysfunction, particularly in their QoL, mood and memory. The
present research conducted has suggested that the individuals symptoms and
the consequences they have on the individuals general health and well-being
adds to the overall anxiety, stress and poor health.
2. The limited amount of research that has been conducted on sleep problems in
chronic illnesses has been difficult to interpret for a variety of reasons.
Firstly, some studies have used a variety of physiological measures to
measure sleep disturbances but have not had clear aims and outcomes for
why sleep was studied and how it has impacted the individual. Secondly,
although disturbed sleep has been reported in a variety of chronic illnesses, it
is difficult to draw any conclusions about chronic illness and sleep
disturbances. Thirdly, researchers have exclusively paid most attention to
excessive daytime sleepiness without reference to other forms of underlying
sleep disorders that may be present. Fourthly, much of the research has been
conducted with individuals who are generally of a retired age; sleep changes
with age and this has not been considered in some of the research. Further
research should also take into account the following points:
137
1. Studies should include groups that have been diagnosed with respiratory
diseases exclusively rather than other cohorts who have other underlying comorbidities, which may interfere with the results.
2. Further research should make comparisons between healthy cohorts and those
with respiratory diseases to indicate the relative size and nature of the sleep
problem and to be able to assess the possibility of characteristic types of sleep
disturbance which may require particular types of management.
3. To be able to assess sleep problems and to take into consideration the wide
range of sleep behaviours and disorders and to be able to use appropriate
methods to study them.
4. Assessments used to study psychological function should be shown to be
psychometrically valid and reliable and relevant to the theoretical issues
involved.
5.
Findings should be representative of similar populations and should only
include appropriate sample populations. The next section deals with the
methodology and data analysis from the present study, describing a survey in
which an attempt was made to meet these requirements. It is the first study of
its type known to the author.
138
3
A cross sectional survey of sleep disturbance and
general well-being in participants with respiratory diseases
and matched healthy controls
To aid the reader, a detailed structure of this section is outlined below:
3.1 Aims
3.2 Method
3.2.1 Design
3.2.2 Procedure
3.2.3 Participant recruitment
3.2.4 Assessments
3.2.5 Ethical Approval
3.2.6 Data analysis
3.3 Results
3.3.1 Demographic characteristics
Demographic characteristics of respiratory and control
Groups
Ethnicity
Occupational status
Highest level of education achieved
Current Illnesses or physical disorder that patients and
participants have at present or have had in the past 3 months
Illnesses or physical disorders that participants have ever
had
Sleep disturbances in other family members
3.3.2 Sleep disorders and behaviours
Asthma and asthma controls
Disorders of initiating and maintaining sleep
Features associated with obstructive sleep apnoea
Other disorders/behaviours occurring during sleep
Sleep related disorders/behaviours occurring during the
day
Time required for sleep and sleep duration
COPD and COPD controls
Disorders of initiating and maintaining sleep
Features associated with obstructive sleep apnoea
Other disorders/behaviours occurring during sleep
Sleep related disorders/behaviours occurring during the
day
Time required for sleep and sleep duration
Bronchiectasis and bronchiectasis controls
Disorders of initiating and maintaining sleep
Features associated with obstructive sleep apnoea
Other disorders/behaviours occurring during sleep
Sleep related disorders/behaviours occurring during the
day
Time required for sleep and sleep duration
Asbestosis related conditions and controls
Disorders of initiating and maintaining sleep
Features associated with obstructive sleep apnoea
139
Other disorders/behaviours occurring during sleep
Sleep related disorders/behaviours occurring during the
day
Time required for sleep and sleep duration
Summary of 3.3.2
3.3.3 Daytime sleepiness
Asthma and asthma controls
COPD and COPD controls
Bronchiectasis and bronchiectasis controls
Asbestosis related conditions and controls
Summary of 3.3.3
3.3.4 Quality of Life (QoL)
Asthma and asthma controls
COPD and COPD controls
Bronchiectasis and bronchiectasis controls
Asbestosis related conditions and controls
Summary of 3.3.4
3.3.5 General Health Questionnaire-12 (GHQ-12)
Asthma and asthma controls
COPD and COPD controls
Bronchiectasis and bronchiectasis controls
Asbestosis related conditions and controls
Summary of 3.3.5
3.3.6 Beck Depression Inventory (BDI)
Asthma and asthma controls
COPD and COPD controls
Bronchiectasis and bronchiectasis controls
Asbestosis related conditions and controls
Summary of 3.3.6
3.3.7 Cognitive assessments
Item 1: Do you suffer from concentration problems, more than
compared to those of your own age?
Item 2: Do you suffer from memory problems, more than compared to
those of your own age?
Asthma and asthma controls
COPD and COPD controls
Bronchiectasis and bronchiectasis controls
Asbestosis related conditions and controls
Summary of 3.3.7
3.3.8 Associations between sleep disorders and behaviours, daytime
Sleepiness, quality of life, mental health, BDI and cognitive
functioning
Summary of 3.3.8
3.4 Summary
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3.1 Aims
The aims of the phase I research were as follows:
To describe the occurrence and nature of self reported sleep disorders and behaviours
in individuals who have been diagnosed with specific respiratory diseases: asthma,
chronic obstructive pulmonary disease (COPD), bronchiectasis and asbestosis &
related conditions and healthy controls
To compare the findings with healthy individuals matched for age and sex on these
measures and measures of excessive daytime sleepiness, quality of life, mental health
and cognitive functioning.
To investigate associations between the sleep problems and self reported daytime
sleepiness, quality of life, mental health and daytime cognitive functioning in the
groups with respiratory disease.
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3.2 Method
3.2.1 Design
This study is a cross-sectional questionnaire survey of individuals with specific
respiratory diseases and age and sex matched healthy controls.
3.2.2 Procedure
Pilot study
A pilot study to check the suitability and acceptability of the assessments (please see
section on assessments 3.2.4) used in the questionnaire was conducted. Specialist
respiratory clinics based at Queen Alexandra Portsmouth Hospital held throughout
the week were attended.
Initially a total of 60 individuals, 10 from each from each of the following respiratory
groups Asthma, Chronic Obstructive Pulmonary Disease (COPD), Bronchiectasis,
Asbestosis, Asbestos Pleural Plaques, Asbestos Pleural Thickening were recruited
via a database containing information concerning patients who were attendees of the
respiratory clinics held at Queen Alexandra Hospital.
Individuals were posted a pack containing a patient invite letter (appendix 2), the
patient information sheet (appendix 3), a consent form (appendix 2), the study
questionnaire (appendix 4), along with a stamped addressed envelope for the
individuals to return their completed questionnaire.
Main study – Individuals diagnosed with respiratory diseases.
As with the pilot study, individuals diagnosed with asthma, COPD, bronchiectasis,
asbestosis were recruited from the outpatient Respiratory Service at Portsmouth
Hospitals NHS Trust under the supervision of the respiratory specialist.
Recruitment during clinics
Recruitment took place during clinic times. Individuals were approached and asked
whether they would like to take part in a study and briefed on what the study
involved. Individuals who expressed an interest were provided with a information
sheet, once the information sheet had been read by the individual and they still
expressed an interest to take part they were then given an invite letter along with a
142
consent slip. Individuals had the opportunity to take the information sheet and the
invite letter away with them to carefully consider taking part rather than feeling
hurried. Once consent had been given, the individual was given the questionnaire to
complete either whilst waiting for their appointment or alternatively complete the
questionnaire in the comfort of their own homes and return the completed
questionnaire in the stamped addressed envelope which was given to the individual.
Individuals who were not approached during clinic times were then approached by
postal means. A letter of invite, a consent slip, the questionnaire booklet along with
the patient information sheet and a stamped addressed envelope was posted to the
individuals.
Matched controls
An attempt was made to recruit matched controls through staff based at University of
Portsmouth, Queen Alexandra Hospital NHS Trust and Portsmouth City Council.
The same packs of information were sent to the control participants as described
above, the only difference being that the Invite letter (Appendix 5) along with the
participant information sheet (Appendix 6) was tailored to those who did not have a
diagnosis of respiratory diseases.
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3.2.3 Participant recruitment
Individuals diagnosed with respiratory diseases.
Individuals recruited through the respiratory clinics were professionally diagnosed by
specialist consultants in respiratory medicine at Portsmouth Hospitals NHS Trust,
Queen Alexandra Hospital, using the current guidelines in respiratory management to
care for individuals diagnosed with asthma, COPD, bronchiectasis and asbestosis &
related conditions.
The diagnosis of asthma, COPD and bronchiectasis is made by clinicians using the
National Institute for Health and Clinical Excellence (NICE) guidelines and lung
function tests. For further information on diagnosing asthma, COPD, bronchiectasis
conditions can be accessed from: http://www.nice.org.uk
Table 3.1 shows the total number of individuals diagnosed with respiratory diseases
and healthy matched controls recruited into the study with respiratory diseases.
Table 3. 1. Total number of individuals diagnosed with respiratory diseases and
healthy matched controls recruited.
Diagnosis
Individuals diagnosed
Healthy Matched
with respiratory diseases
Controls*
Asthma
46
46
Chronic Obstructive
18
18
Bronchiectasis
16
16
Asbestos related
11
11
Pulmonary Disease
(COPD)
conditions
*Matched for age and sex.
Individuals diagnosed with respiratory diseases were recruited through QA Hospital
outpatient’s respiratory clinic. These individuals had already had their diagnosis
confirmed by a respiratory specialist and were under the care of the specialist and
144
seen at specific clinics. All individuals diagnosed with respiratory diseases who
attended the outpatient’s clinic were approached by the researcher and invited to
participate in the study. The individuals medical files were accessed to ensure that
they did not have any significant co-morbidity that would interfere with the results.
Any individual who did take part and was found to have a significant co-morbidity,
their questionnaire was not included for analysis.
Individuals diagnosed with respiratory diseases and healthy controls were matched
for age and sex. A healthy control was matched to only one individual in a particular
category.
Exclusion and inclusion criteria for selecting individuals
Table 3.2 shows the various factors that were taken into consideration to exclude and
include individuals with respiratory diseases into the study.
Table 3. 2. Exclusion and inclusion criteria for selecting individuals
Principal inclusion criteria
Specific respiratory diseases:
Exclusion criteria
<18- to give informed consent
Significant co-morbidities
Asthma
Bronchiectasis
COPD
Asbestos related conditions
Current/ex-smokers >10 pack year smoking
history
Clinically significant cardiopulmonary
clinically significant neurological, renal,
endocrine, gastrointestinal, hepatic,
haematological abnormalities uncontrolled
with standard treatment.
Alcohol and recreational drug abuse.
Treatment with immunodilators
Non-English speaking individuals were excluded on the grounds that translation may
have affected the reliability and validity of the measurement tools. Individuals were
also able to exclude themselves if they felt they were unable to complete the
145
questionnaires. This included individuals who could not understand the instructions
or the questionnaire due to having a poor understanding of English.
Individuals who attended the outpatients respiratory clinic at QA Hospital did so
through a referral process by their GP in primary care. Usually this involves the
individuals GP contacting a specialist clinician and requesting an appointment to be
sent out to the individual to be seen by the specialist.
Healthy controls
Criteria for selecting control individuals
The research team ensured that healthy control individuals did not have any
diagnosed respiratory diseases and other contra-indications. This was done by
administering two screening questions to exclude such cases (Please see appendix 4).
Diseases and contra-indications such as clinically significant cardiopulmonary
abnormalities, clinically significant neurological, renal, endocrine, gastrointestinal,
hepatic, or haematological abnormalities uncontrolled with standard treatment,
alcohol and recreational drug abuse, treatment with any other immunomodulators
which might interfere with the outcome of the assessments.
Response rates
A total of 290 questionnaires were sent to individuals diagnosed with respiratory
diseases. Of the 290 questionnaires, 203 fully completed questionnaires that fulfilled
the inclusion/exclusion criteria were used. This is a 70 % response rate.
A total of 105 questionnaires were sent to healthy controls, all 105 questionnaires
were fully completed and returned and used for the study. This was a 100 % response
rate from the health controls. The matching process involved selecting an individual
diagnosed with a respiratory disease from each category (asthma, COPD,
bronchiectasis and asbestos and related conditions) and matching them to an
individual healthy person. Individuals were matched according to exact age and sex.
3.2.3 Assessments
This section describes the questionnaires used in the present study measuring sleep
disturbances, daytime sleepiness, QoL, mood and memory.
146
Sleep disorders
Basic Nordic Sleep Questionnaire (BNSQ) (Partinen and Gislason, 1995)
The BNSQ is based on a five-point (scale from 1; never or less than once per month
to 5 Daily or almost daily) quantitative scale. It has 27 different items in 21 main
questions. The questionnaire is designed to question the patients sleeping habits and
disorders for the past three months. This is a self-administered questionnaire. The
BNSQ has been used widely in a variety of studies performed in Nordic countries
during the last several years, and it has proven to be a valid tool (Partinen and
Gislason, 1995).
The BNSQ assesses the following areas:
1. Dysomnias – which consist of disorders of initiating and maintaining sleep
(insomnias), disorders of excessive daytime sleepiness (hypersomnias) and circadian
rhythm sleep disorders.
2. Parasomnias – which are disorders and behaviours occurring during sleep or made
worse by sleep.
3. Medical/Psychiatric sleep disorders – Psychiatric disorders that impede sleep and
therefore affect the person’s ability to sleep.
4. Proposed sleep disorders – most newly described sleep disorders fall into this
category until replicated data is available in the literature.
Individuals with respiratory diseases and healthy controls were also given the
opportunity to write down anything they thought was important to the quality of their
sleep.
The BNSQ has served as a basis in many epidemiological studies preformed in the
Nordic and also in other countries. In Finland and Iceland the questions from the
BNSQ have also been adopted to routine clinical patient questionnaires in hospitals.
Daytime Sleepiness
The Epworth Sleepiness Scale (ESS) (Johns, 1991).
The ESS is an eight-item questionnaire that has been proposed as a simple method
for measuring daytime sleepiness in adults. The ESS is designed to measure sleep
147
propensity in a simple yet standardized way. The ESS is based on questions referring
to eight situations; some known to be very soporific, others less so. The scale covers
the whole range of sleep propensities from the highest to the lowest. The
questionnaire is self-administered. The questionnaire has a high level of internal
consistency as measured by Cronbach’s alpha (0.88). Comparisons between the ESS
responses of 87 students on two separate occasions, 5 months apart, enabled an
estimate to be made of the test-retest reliability of the questionnaire (Johns, 1992).
The ESS is a simple and reliable method for measuring persistent daytime sleepiness
in adults (Hardinge, Pitson and Stradling, 1995).
Quality of Life
The 36-item Short-Form Health Survey (SF-36) (Ware and Sherbourne, 1992).
The 36-item short-form (SF-36) was constructed to survey health status and QoL in
the Medical Outcomes Study. The SF-36 is designed for use in clinical practice and
research, health policy evaluations and general population surveys. The SF-36
includes one multi-item scale that assesses eight health concepts. These are:
Physical functioning, Role limitations due to physical problems, Social functioning,
Bodily pain, General mental health, Role limitations due to emotional problems,
Vitality, General health perceptions. The SF-36 is designed to be self-administered.
Mental Health
The General Health Questionnaire (GHQ-12) (Goldberg, 1978).
The general health questionnaire (GHQ-12) is designed to detect psychiatric
disorders among respondents in community settings and non-psychiatric clinical
settings, such as primary care or among general medical outpatients. It is aimed at
detecting those forms of psychiatric disorder that may have relevance to a patient
attending an outpatient clinic, therefore the focus of the general health questionnaire
is of psychological components of ill-health. In construction of the GHQ-12, the
items selected were to cover four main areas and these being depression, anxiety,
social performance, somatic complaints and on occasion sleep disturbance over the
last four weeks.
The questionnaire comprises twelve questions, asking informants about their general
level of happiness, experience of depressive and anxiety symptoms, and sleep
148
disturbance over the last four weeks. Interpretation of the answers is based on a four
point response scale scored using a bimodal method. The GHQ12 is designed to be
self-administered.
The Beck Depression Inventory (The BDI) (Beck, Ward, Mendelson, Mock and
Erbaugh, 1961).
The items in this inventory were primarily clinically derived. The instrument was
designed to measure the behavioural manifestations of depression. The inventory is
composed of 21 categories of symptoms and attitudes. The symptom-attitude
categories are as follows: 1. Mood, 2. Pessimism, 3. Sense of failure, 4. Lack of
satisfaction, 5. Guilty feelings, 6. Sense of punishment, 7. Self-hate, 8. Self
accusations, 9. Self punitive wishes, 10. Crying spells, 11. Irritability, 12. Social
withdrawal, 13. Indecisiveness, 14. Body image, 15. Work inhibition, 16. Sleep
disturbance, 17. Fatigability, 18. Loss of appetite, 19. Weight loss, 20. Somatic preoccupation, 21. Loss of libido. Each category describes a specific behavioural
manifestation of depression and consists of a graded series of 4 to 5 self-evaluative
statements. The statements are ranked to reflect the range of severity of the symptom
from neutral to maximal severity. Numerical values from 0-3 are assigned to each
statement to indicate the degree of severity. This is self-administered questionnaire.
Studies of the internal consistency and stability of the instrument indicate a high
degree of reliability, (Beck, Ward, Mendelson, Mock and Erbaugh, 1961).
Comparisons between the scores on the inventory and the clinical judgements by the
diagnosticians indicate a high degree of validity.
Concentration and memory problems
Cognitive items (Jennum and Sjol, 1994).
Authors Jennum and Sjol (1994) originally conducted an epidemiological study of
1504 females and males aged between 30-60 years, which is known as the DanMONICA II Study (Dan-MONitoring trends in CArdiovasuclar diseases) to highlight
the fact that patients with obstructive sleep apnoea syndrome often complain that
they have concentration and memory disturbances. Jennum and Sjol found that
concentration and memory problems were associated with a tendency to morning
depression, insomnia and partly with unintended sleepiness. Concentration problem
149
showed a positive correlation to habitual snoring and sleep apnoea, but memory
problems did not show such correlations.
Classification of cognitive complaints:
Concentration problems: This was assessed by using the following phrase: ‘Do you
suffer from concentration problems?
Memory problems: This was assessed by using the following phrase: ‘Do you suffer
from memory problems, more than compared to those of your own age?’
The responses for both sets of items were:
Not at all, slightly, moderately, quite a bit and very much.
Demographic information
Additional information was collected to complete the questionnaire booklet, this
included demographic details (name, address, date of birth, height, weight, smoking
history, occupation, qualifications, ethnicity, gender) and whether the participants
had previous illnesses, previous medications had been taken, current medication
taken and current diagnosed illnesses and if they know of anyone who suffers from a
diagnosed sleep disorder (mother, father, siblings, husband, wife).
3.2.4 Ethical approval
Ethical Approval was gained from the Local Research Ethics Committee for the
Portsmouth and Isle of Wight Healthcare Authority (this can be found in appendix
7a). The Portsmouth NHS R and D Consortium also gave approval (this can be found
in appendix 7b).
3.3.5 Data analysis
The information collated from clinics was compiled into an Excel spreadsheet. The
questionnaire data was coded and analysis was carried out using SPSS version 16. A
range of statistical tests were used. Details of the analyses are given in the
appropriate sections.
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3.3 Results
Introduction
The results section is divided into 8 main sections: Demographic characteristics of
respiratory and control groups, sleep disorders and behaviours, daytime sleepiness,
QoL, and general health and well-being, mental health, depression and anxiety and
cognitive functioning: memory and concentration problems. Participants (healthy and
respiratory) were matched according to age and sex.
3.3.1 Demographic characteristics
Demographic characteristics of respiratory and control Groups
Table 3.3 shows a breakdown of the demographic characteristics; age, number of
males and females, height and weight and body mass index (BMI).
Table 3. 3. General characteristics of all groups.
Group
(N)
Age
(Years)
Mean
S.D.
Minimum
Maximum
Gender
Male
(%)
Females
(%)
Weight
(KG’s)
Mean
Minimum
Maximum
Height
(CM’s)
Mean
Minimum
Maximum
Body Mass
Index*
(BMI)
Mean
Asthma
(n=46)
Asthma
Ctrl
(n=46)
COPD
(n=18)
COPD
Ctrl
(n=18)
Bronc
(n=16)
Bronc ctrl
(n=16)
Asbestos
related
conditions
(n=11)
Asbestos ctrl
(n=11)
53
15
22
79
53
15
22
76
66
10
52
77
66
10
52
78
56
14
35
78
56
14
34
78
67
9
53
76
67
9
53
79
18
(39)
18
(39)
7
(39)
7
(39)
5
(31)
5
(31)
9
(82)
9
(82)
28
(61)
28
(61)
11
(61)
11
(61)
11
(69)
11
(69)
2
(18)
2
(18)
77
39
140
74
44
108
73
45
106
71
46
99
72
48
121
73
59
102
84
67
95
78
64
95
168
147
188
169
152
188
167
155
183
170
152
193
166
150
182
168
157
180
176
165
183
174
157
188
27
26
26
25
26
26
27
26
*BMI Less than 20 — Under Weight, BMI 20-25 — Normal Weight
BMI 25-30 — Over Weight, BMI 30-40 — Obese, BMI Over 40 — Severely Obese
Individuals with respiratory diseases and healthy controls were broadly similar with
respect to their height, weight and BMI.
151
Ethnicity
The following shows the ethnic background of individuals with respiratory disease
and their healthy controls.
Table 3. 4. Breakdown of ethnic groups across individuals diagnosed with
respiratory diseases and healthy controls
Ethnicity
Asthma
(n=46)
N (%)
Asthma
ctrl
(n=46)
N (%)
COPD
(n=18)
N (%)
COPD
Ctrl
(n=18)
N (%)
Bronchiectasis
(n=16)
N (%)
Bronc
ctrl
(n=16)
N (%)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
ctrl
(n=11)
N (%)
White
British
English
Asian
Indian
27 (59)
37 (82)
17 (95)
16 (89)
14 (87)
12 (75)
10(91)
9 (82)
5(11)
1(5)
Asian
other
Other
Missing
1(6)
19 (41)
3 (7)
2(13)
1 (6)
1 (6)
1(9)
1(9)
2 (12)
1 (6)
1(9)
The majority of participants were British English; there were, however, a small
minority of patients from different ethnic backgrounds representing different groups
across the UK. Individuals diagnosed with asthma show a more diverse range of
patients recruited into the study.
The other category was collapsed due to small numbers, this category consists of
Scottish, Welsh, Irish, Other White, Mixed White & Black Caribbean, Mixed White
& Black Africans and Mixed White & Asians.
152
Occupational status
This section displays information relating to the individuals diagnosed with
respiratory diseases and healthy controls (social and economic status). This
information
was
extracted
from
The
National
Statistics
Socio-economic
Classification User Manual (Office for National Statistics 2005 Edition (Appendix
8). For the study participants were asked to state their main occupation; these data
were then coded into the categories below according to The National Statistics Socioeconomic Classification User Manual.
Table 3.5 shows the breakdown of the different employment background that the
individuals diagnosed with respiratory diseases and healthy controls stated in the
questionnaire.
Table 3. 5. Social and economic status across all groups.
*Socioeconomic
scale
Asthma
(n= 46)
N (%)
Asthma
ctrl
(n=46)
N (%)
COPD
(n=18)
N (%)
COPD
Ctrl
(n=18)
N (%)
Unemployed
5(11)
5(11)
1(6)
6(33)
Employees in
large
organisation
15(32)
20(44)
Lower
professional
and higher
technical
occupations
5(11)
1(2)
Routine
occupations
5(11)
4(9)
13(72)
Retired
9(20)
8(17)
4(22)
Other
7 (15)
8 (17)
Bronchiectasis
(n=16)
N (%)
3(17)
Bronc
ctrl
(n=16)
N (%)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
ctrl
(n=11)
N (%)
3(19)
1(9)
2(18)
5(32)
7(44)
3(27)
2(12)
1(6)
1(9)
1(5)
4(25)
1(6)
4(36)
7(39)
4(25)
3(19)
4(36)
1 (6)
1 (6)
1 (6)
1 (9)
1(9)
5(46)
There are no major differences in SES between the asthma, bronchiectasis and
asbestosis respiratory groups and their healthy controls. Within the COPD group a
greater number of healthy controls were unemployed compared to the individuals’
diagnosed COPD group. Another major difference is the number of COPD patients
reporting to work in routine occupations.
The other category has been collapsed to include intermediate occupations,
employers in small organisations and lower supervisory occupations due to small
numbers.
153
Highest level of education achieved
Table 3.6 shows the highest level of education that the participants have reported.
Table 3. 5. Breakdown of educational qualifications across the groups.
Educational
level
Asthma
(n=46)
N (%)
Asthma
ctrl
(n=46)
N (%)
COPD
(n=18)
N (%)
COPD
Ctrl
(n=18)
N (%)
Bronchiectasis
(n=16)
N (%)
N
(%)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
ctrl
(n=11)
N (%)
3(19)
5(46)
4(36)
Bronc
ctrl
(n=16)
No
qualifications
10(22)
7(15)
9(50)
6(34)
2(13)
O’Level/GCSE
5(11)
7(15)
4(21)
1(5)
2(13)
A’ Level/GCE
8(17)
4(9)
2(11)
1(5)
1(6)
1(6)
1(9)
Degree or
equivalent
8(17)
9(20)
1(6)
5(28)
6(37)
3(18)
3(27)
Postgraduate
qualification
4(9)
12(26)
1(6)
1(5)
1(6)
4(25)
Other
qualifications
10(22)
5(11)
1(5)
4(25)
2(13)
Missing data
1(2)
2(4)
1(6)
3(18)
1(9)
2(19)
2(18)
3(19)
4(36)
Within the asthma group and their healthy controls there are no major differences
except for the amount of participants within the asthma control group have reported
to achieve more postgraduate qualifications compared to participants diagnosed with
asthma.
Within the COPD group again there are no major differences other than healthy
controls reporting to have gained higher educational qualifications. There are no
major differences reported within the bronchiectasis and asbestosis group.
154
Current Illnesses or physical disorder that patients and participants
have at present or have had in the past 3 months
Information for this section was extracted from the British National Formulary, BNF
53, March 2007. Participants were asked to state “Current illnesses or physical
disorders that they may have at present or have had in the past 3 months” and “any
illness or physical disorder that participants have ever had.” This data was then
coded into the categories displayed below. A brief description of each category can
be found in appendix 9. Not all categories have been displayed, only those that
represented the illnesses/disorders that the patients and participants have stated in the
study questionnaire.
The following table shows the breakdown of the various disorders that the
individuals diagnosed with respiratory diseases and matched controls have stated in
the last 3 months.
Table 3. 6. Current illnesses or physical disorder that individuals diagnosed
with respiratory diseases and healthy controls have at present or have had in
the last 3 months.
*Category
Name any
illness or
physical
disorder you
have at present
or have had in
the last 3
months
Cardiovascular
disorders
Gastrointestinal
system
disorders
Obstetrics,
gynaecology
and urinary
tract disorders
Musculoskeletal
and joint
diseases
disorders
Endocrine
system
disorders
Other
None stated
Missing
Asthma
(n=46)
N (%)
7(15)
2(4)
Asthma
ctrl
(n=46)
N (%)
1(2)
1(2)
COPD
Ctrl
(n=18)
N (%)
Bronchiectasis
(n=16)
N (%)
Bronc ctrl
(n=16)
N (%)
1(6)
2(11)
4(25)
1(6)
1(6)
1(6)
1(6)
1(9)
2(11)
1(6)
2(18)
1(9)
1(6)
1(6)
6(55)
2(18)
1(6)
2(13)
7 (44)
3 (18)
7(45)
2(18)
2 (18)
6(55)
2(5)
6(13)
3(7)
22 (47)
2(5)
4(9)
7(15)
3(6)
7 (15)
25(55)
5(26)
4(22)
1(6)
9 (50)
1 (6)
8(44)
1(6)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
ctrl
(n=11)
N (%)
COPD
(n=18)
N (%)
3(19)
There are no major differences observed within the asthma, COPD, bronchiectasis
and asbestosis group and their healthy controls.
155
The other category consisted of skin disorders, ear, nose, oropharynx disorders,
central nervous system disorders, psychiatric disorders and lastly respiratory
disorders.
156
Illnesses or physical disorders that participants have ever had.
Table 3.8 shows the number of participants who have reported to have ever had any
of the physical disorders as listed in the table below.
Table 3.7. Any illness or physical disorder that participants have ever had.
*Category
Name any
illness or
physical
disorder that
you have ever
had
Skin disorders
Asthma
(n=46)
N (%)
Asthma
ctrl (n=46)
N (%)
3 (7)
1(2)
Cardiovascula
r disorders
Musculoskelet
al and joint
diseases
disorders
Endocrine
system
disorders
Childhood
illnesses
disorders
Other
None stated
Missing
2(4)
5(11)
1(2)
1(2)
5(11)
17(37)
4 (8)
COPD
(n=18)
N (%)
2(11)
COPD
Ctrl
(n=18)
N (%)
1(6)
Bronchiect
asis
(n=16)
N (%)
Bronc ctrl
(n=16)
N (%)
1(6)
1(6)
1(6)
1(6)
1(6)
1(6)
2(11)
1(6)
3(19)
4(9)
3(16)
(6)
8 (17)
25(55)
2 (12)
6 (32)
8(43)
16(35)
9(50)
8(50)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
is ctrl
(n=11)
N (%)
1(9)
2(18)
1(9)
1(6)
5(46)
1(9)
2 (13)
7(44)
2 (18)
2(18)
2 (18)
6(55)
6(38)
Generally no major differences can be observed between the asthma and COPD
group and their healthy controls. Individuals diagnosed with bronchiectasis and
asbestosis have reported to have had more childhood related disorders.
The other category consists of
collapsed categories due to small numbers, the
disorders which are included in this category are; ear, nose, oropharynx disorders,
gastro-intestinal system disorders, Obstetrics, gynaecology and urinary tract
disorders, central nervous system disorders, psychiatric disorders and lastly
respiratory disorders.
157
Sleep disturbances in other family members
Individuals diagnosed with respiratory diseases and healthy controls were asked to
report any sleep disturbances or disorders within their immediate family that they
may be aware of.
Table 3.9 show the different family members who have been observed with sleep
disturbances or sleep disorders by the individuals diagnosed with respiratory diseases
and healthy controls.
Table 3.8. Sleep disturbances in other family members as reported by
individuals diagnosed with respiratory diseases and healthy controls
Does
anybody in
your family
suffer from
a sleep
problem?
Who and
what is the
problem?
No
Asthma
(n=46)
N (%)
Asthma
ctrl
(n=46)
N (%)
COPD
(n=18)
N (%)
COPD
Ctrl
(n=18)
N (%)
Bronchiectasis
(n=16)
N (%)
Bronc
ctrl
(n=16)
N (%)
Asbestos
related
conditions
(n=11)
N (%)
Asbestos
ctrl
(n=11)
N (%)
12(26)
40(88)
1(6)
16(90)
6(38)
11(69)
9(82)
9(91)
Mother
25(55)
1(2)
13(72)
1(5)
5(31)
1(6)
Father
3(7)
2(4)
2(13)
1(6)
Sibling
1(2)
2(4)
Other
4 (8)
1 (2)
1 (6)
1(6)
No
response
1(2)
2(12)
2(13)
1(9)
1(5)
1 (9)
4(22)
Missing
1(9)
Major differences can be observed within the asthma, COPD and bronchiectasis
group, healthy controls and those diagnosed with a respiratory disorder, specifically
those who have reported their mother as having family problems.
The other category has been collapsed due to small numbers to include wife,
grandparents, husband and other.
158
3.3.2 Sleep disorders and behaviours
For a detailed and quantitative comparison of the matched groups, a score of either 0,
1, 2, 3, 4 was awarded for each participant depending on whether they reported the
sleep problem or behaviour,
never or less than once per month; 0,
less than once per week; 1,
on 1-2 days per week; 2,
on 3-5 days per week; 3,
daily or almost daily; 4,
A mean score for each sleep problem or behaviour was then calculated for each
group.
As the data were measured on a scale that had an underlying continuous distribution
and therefore met the assumptions of the parametric paired samples t-test, this was
used to test for statistical significance between groups for each sleep problem and
behaviour. As a more conservative analysis 2-tailed tests were used to test the data
and no previous research has been conducted to suggest a definite direction of
difference.
Each of the respiratory groups and their healthy counterparts are described in turn.
159
Asthma and asthma controls
The following table shows the mean scores in individuals diagnosed with asthma and
their healthy controls.
Table 3. 9. Mean scores obtained in individuals diagnosed with asthma and
healthy controls.
Sleep problem/behaviour
Asthma
Control
mean
(n=46)
t-test
P
(2 tailed)
1.72
3.20
2.00
2.33
1.124
2.89
1.62
1.35
1.702
1.591
2.275
4.151
.096
.119
.028*
<.0001***
2.05
1.54
.95
1.51
.90
.19
1.573
2.274
3.072
.123
.028*
.004**
.60
.68
.32
.44
0
.02
.78
.44
.04
.05
.29
.05
.00
.12
0
0
.52
.42
0
0
1.334
3.455
2.201
2.149
0
1.000
1.372
-.121
1.431
1.000
.189
.001**
.033*
.037*
0
.323
.177
.904
.160
.323
2.27
2.16
.70
1.43
1.59
1.18
1.40
.38
.73
1.22
3.379
2.591
1.231
2.356
1.318
.002**
.013*
.226
.023*
.194
Asthma
mean
(n=46)
Disorders of initiating and maintaining sleep
Difficulties falling asleep
Waking during the night
Occurrence of waking during the night
Early waking
Features associated with sleep disordered breathing
Snoring
Quality of snoring
Breathing pauses
Other disorders/behaviours occurring during sleep
Narcolepsy
Cataplexy
Sleep paralysis
Sleep talking
Sleep walking
Bed wetting
Nightmares
Teeth grinding
Night screaming
Rocking at night
Sleep related disorders/behaviours occurring during the day
Excessive sleepiness after awakening
Excessive sleepiness during the day
Excessive sleepiness during work
Excessive sleepiness during leisure
Daytime naps
*P<0.05 **p<0.01 ***p<0.001 (2-tailed)
Significant differences were found across all of the categories of sleep disorders and
behaviours.
Within the category of disorders of initiating and maintaining sleep the individuals
with asthma reported significantly more waking during the night and early waking
than the healthy controls.
Within the category of features associated with sleep disordered breathing,
individuals with asthma reported significantly poorer quality of snoring and
breathing pauses than the healthy controls.
160
Within the category of other disorders/behaviours occurring during the day, the
individuals diagnosed with asthma reported significantly more episodes of cataplexy,
sleep paralysis, and sleep talking than the healthy controls.
Within the category of sleep related disorders/behaviours occurring during the day,
the individuals diagnosed with asthma reported significantly more excessive
sleepiness after awakening, excessive daytime sleepiness during the day and
excessive sleepiness during leisure than the healthy controls.
Duration of sleep, daytime naps and years of snoring
The following table shows the mean time (hours/minutes) for time required for sleep
and sleep duration by participants within the asthma group and healthy controls.
Table 3. 10. Mean time required for sleep and sleep duration as reported by
participants within the asthma group and healthy controls.
Sleep problem/behaviour
Asthma
mean
(n=46)
Asthma
Control
mean
(n=46)
t-test
P
(2
tailed)
24.11
20.17
.789
.436
21.50
18.76
.776
.443
6
63.90
20.70
26
7
20.70
8.40
33
-2.103
3.884
3.960
-1.948
.041*
.001**
.003**
.109
Time required for sleep and sleep duration
How many minutes do you stay awake in bed before you
fall asleep (during working days)
How many minutes do you stay awake in bed before you
fall asleep (during free time)
Sleep duration (hours)
Duration of naps (minutes)
Years of snoring (years)
Age of onset of snoring (age)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Within the category time required for sleep and sleep duration the individuals with
asthma reported sleeping significantly less hours than the healthy controls.
Individuals with asthma reported napping for significantly longer periods and
reported that they had been snoring for a significantly longer duration of years
compared to the healthy controls.
161
COPD and COPD controls
The following table shows the mean scores in individuals diagnosed with COPD and
their healthy controls.
Table 3. 11. Mean scores obtained in individuals diagnosed with COPD and
their healthy controls.
Sleep problem/behaviour
COPD
mean
(n=18)
COPD
Control
mean
(n=18)
t-test
P
(2
Tailed)
Disorders of initiating and maintaining sleep
Difficulties falling asleep
Waking during the night
Occurrence of waking during the night
Early waking
2.00
3.50
2.59
2.47
1.67
2.78
2.06
1.71
.537
2.247
1.376
1.641
.598
.038*
.188
.120
.86
.64
.44
2.00
.93
.31
2.280
-.806
.460
.040*
.435
.652
Narcolepsy
Cataplexy
Sleep paralysis
Sleep talking
Sleep walking
Bed wetting
Nightmares
Teeth grinding
Night screaming
Rocking at night
Sleep related disorders/behaviours occurring during
the day
.71
1.35
.25
.31
0
0
.75
1.07
0
0
.24
.35
0
.44
0
0
.69
.60
0
0
1.224
2.062
1.732
-6.20
0
0
.187
.767
0
0
.239
.056
.104
.544
0
0
.855
.456
0
0
Excessive sleepiness after awakening
Excessive sleepiness during the day
Excessive sleepiness during work
Excessive sleepiness during leisure
Daytime naps
1.94
3.06
.55
2.11
3.11
1.22
2.06
.82
1.28
1.72
1.146
2.637
-1.000
1.667
3.571
.268
.017*
.341
.114
.002**
Features associated with SDB
Snoring
Quality of snoring
Breathing pauses
Other disorders/behaviours occurring during sleep
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found in three categories of sleep disorders and
behaviours.
Within the category of disorders of initiating and maintaining sleep, the individuals
diagnosed with COPD reported significantly more waking during the night compared
to healthy controls.
162
Within the category of features associated with sleep disordered breathing, healthy
controls reported significantly more episodes of snoring compared to individuals
diagnosed with COPD.
Within the category of sleep related disorders/behaviours occurring during the
night, the individuals with COPD reported significantly more excessive sleepiness
during the day and longer daytime naps compared to healthy controls.
Duration of sleep, daytime naps and years of snoring
The following table shows the mean time (hours/minutes) for time required for sleep
and sleep duration by participants within the COPD group and healthy controls.
Table 3. 12. Mean time required for sleep and sleep duration as reported by
participants within the COPD group.
Sleep problem/behaviour
Time required for sleep and sleep duration
How many minutes do you stay awake in bed before you
fall asleep (during working days)
How many minutes do you stay awake in bed before you fall
asleep (during free time)
Sleep duration (hours)
Duration of naps (minutes)
Years of snoring (years)
Age of onset of snoring (age)
COPD
mean
(n=18)
COPD
Control
mean
(n=18)
t-test
P
(2
tailed)
76.08
21.67
4.082
.002**
38.79
24.29
1.001
.335
6
52.86
25.00
50.00
6.5
28.57
40.00
30.00
-.153
1.642
0
0
.881
.124
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found in this category.
The individuals with COPD reported staying awake significantly longer in bed
before falling asleep than the healthy controls.
163
Bronchiectasis and bronchiectasis controls
The following table shows the mean scores of individuals diagnosed with
bronchiectasis and their healthy controls.
Table 3.13. Mean scores obtained in individuals diagnosed with bronchiectasis
and their healthy controls.
Sleep problem/behaviour
Bronc
mean
(n=16)
Bronc
Control
Mean
(n=16)
t-test
P
(2
tailed)
1.06
2.81
1.50
1.38
.81
2.62
1.56
.88
.522
.284
-.148
1.035
.609
.780
.884
.317
Snoring
Quality of snoring
Breathing pauses
Years of snoring
Age of onset of snoring
Other disorders/behaviours occurring during sleep
1.64
1.93
.15
16.25
33.00
1.14
.50
.00
15.75
32.00
.959
3.069
1.477
.110
.167
.355
.009**
.165
.920
.883
Narcolepsy
Cataplexy
Sleep paralysis
Sleep talking
Sleep walking
Bed wetting
Nightmares
Teeth grinding
Night screaming
Rocking at night
Sleep related disorders/behaviours occurring during the
day
.25
.25
.06
.44
.06
0
.75
.06
0
0
.50
.25
0
.25
.06
0
.25
.56
0
0
-.808
0
1.000
.716
0
0
2.449
1.519
0
0
.432
1.000
.333
.485
1.000
0
.027*
.150
0
0
1.88
2.00
.43
1.12
1.31
.88
1.00
.29
.62
1.12
2.449
2.284
.520
1.225
.387
.027*
.037*
.612
.240
.704
Disorders of initiating and maintaining sleep
Difficulties falling asleep
Waking during the night
Occurrence of waking during the night
Early waking
Features associated with SDB
Excessive sleepiness after awakening
Excessive sleepiness during the day
Excessive sleepiness during work
Excessive sleepiness during leisure
Daytime naps
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found in 3 of the categories of sleep disorders and
behaviours.
Within the category of features associated with sleep disordered breathing, the
individuals with bronchiectasis reported significantly more poorer quality in their
snoring compared to healthy controls.
164
Within the category of other disorders/behaviours occurring during sleep, the
individuals with bronchiectasis reported experiencing significantly more episodes of
nightmares than the healthy controls.
Within the category of sleep related disorders/behaviours occurring during the day,
the individuals with bronchiectasis reported significantly more excessive sleepiness
after awakening and during the day than the healthy controls.
Duration of sleep, daytime naps and years of snoring
The following table shows the mean time (hours/minutes) for time required for sleep
and sleep duration by participants within the bronchiectasis group and healthy
controls.
Table 3. 14. Mean time required for sleep and sleep duration as reported by
participants within the bronchiectasis group and healthy controls group.
Sleep problem/behaviour
Bronc
mean
(n=16)
Bronc
Control
mean
(n=16)
t-test
P
(2
tailed)
16.30
32.00
-.770
.461
22.75
15.33
.880
.398
6.5
35.83
16.25
33
7
22.67
15.75
32
1.750
1.164
.110
.167
.102
.297
.920
.883
Time required for sleep and sleep duration
How many minutes do you stay awake in bed before you fall
asleep (during working days)
How many minutes do you stay awake in bed before you fall
asleep (during free time)
Sleep duration (hours)
Duration of naps (age)
Years of snoring (years)
Age of onset of snoring (age)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Within the category of time required to sleep and sleep duration, no significant
differences were found between the individuals with bronchiectasis and healthy
controls.
165
Asbestos related conditions and controls
The following table shows the mean scores in individuals diagnosed with asbestos
and related conditions and their healthy controls.
Table 3. 15. Mean scores obtained in individuals diagnosed with asbestosis and
healthy controls
Sleep problem/behaviour
Asbestos
related
conditions
mean
(n=11)
Asbestos
Control
mean
(n=11)
t-test
P
(2
tailed)
1.45
3.27
1.91
2.64
1.82
2.91
2.00
2.45
-.599
.614
.000
1.104
.563
.553
1.000
.295
1.57
1.71
.00
2.00
.71
.38
-.441
1.528
1.426
.675
.177
.197
Narcolepsy
Cataplexy
Sleep paralysis
Sleep talking
Sleep walking
Bed wetting
Nightmares
Teeth grinding
Night screaming
Rocking at night
Sleep related disorders/behaviours occurring during
the day
1.00
.50
.36
.09
0
0
.45
0
0
0
.90
.10
0
.18
0
0
.73
.36
0
0
.133
1.000
1.000
-.430
0
0
-.582
1.000
0
0
.897
.343
.341
.676
0
0
.574
.341
0
0
Excessive sleepiness after awakening
Excessive sleepiness during the day
Excessive sleepiness during work
Excessive sleepiness during leisure
Daytime naps
1.55
2.27
.60
2.30
2.44
1.73
2.27
.00
1.50
2.22
-.209
.000
1.500
1.238
.300
.839
1.000
.208
.247
.772
Disorders of initiating and maintaining sleep
Difficulties falling asleep
Waking during the night
Occurrence of waking during the night
Early waking
Features associated with SDB
Snoring
Quality of snoring
Breathing pauses
Other disorders/behaviours occurring during sleep
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
There were no significant differences observed across the four categories of sleep
disorders and behaviours.
166
Duration of sleep, daytime naps and years of snoring
The following table shows the mean time (hours/minutes) for time required for sleep
and sleep duration by participants within the asbestos & related conditions group
and healthy controls.
Table 3.16. Mean time required for sleep and sleep duration as reported by
participants within the asbestos & related conditions group and healthy controls
Sleep problem/behaviour
Asbestos
& related
conditions
mean
(n=11)
Asbestos
Control
mean
(n=11)
t-test
P
(2
tailed)
13.33
40.33
1.335
.314
18.12
16.50
.207
.842
6.1
64
11
42
6
13
14
27
2.500
2.796
-.273
5.084
.047*
.049*
.830
.001**
Time required for sleep and sleep duration
How many minutes do you stay awake in bed before you
fall asleep (during working days)
How many minutes do you stay awake in bed before you
fall asleep (during free time)
Sleep duration (hours)
Duration of naps (minutes)
Years of snoring (years)
Age of onset of snoring (age)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found in this category.
The individuals with asbestos & related conditions reported sleeping significantly
longer and having significantly longer naps compared to healthy controls.
Healthy controls reported to snore at a significantly earlier age compared to
individuals diagnosed with asbestosis.
167
Summary of 3.3.2 Sleep disorders and behaviours
In nearly all the items, individuals with respiratory diseases scored higher than
healthy controls.
Asthma and asthma controls
In this group significant differences were observed;
•
Individuals with asthma reported; significantly more waking during the night,
awoke earlier, and had significantly poorer quality of snoring and
significantly more episodes of breathing pauses, significantly more episodes
of cataplexy, sleep paralysis and sleep talking. They also reported
significantly more excessive sleepiness after awakening, during the day and
during leisure compared to healthy controls.
•
Individuals with asthma also significantly reported sleeping less, had
significantly longer naps and had been snoring significantly a great deal
longer compared to healthy controls.
COPD and COPD controls
In this group significant differences were observed;
•
Individuals with COPD reported waking significantly more during the night,
significantly more excessive sleepiness during the day and having
significantly longer daytime naps compared to healthy controls and staying
awake significantly longer in bed before falling asleep compared to healthy
controls.
•
Healthy controls significantly reported snoring on more nights compared to
individuals diagnosed with COPD.
Bronchiectasis and bronchiectasis control
In this group significant differences were observed;
•
Individuals with bronchiectasis significantly reported poorer quality of
snoring, significantly more episodes of nightmares, significantly more
excessive sleepiness after awakening and significantly more excessive
sleepiness during the day.
Asbestos related conditions and controls
In this group significant differences were observed;
168
•
Individuals with asbestosis significantly reported longer duration of sleep and
significantly more naps.
•
Healthy controls significantly reported to be snoring at a younger age
compared to individuals diagnosed with asbestosis.
169
3.3.3 Daytime sleepiness
Tables 3.18 to 3.21 provide the mean Epworth Sleepiness Score for each respiratory
group.
Asthma and asthma controls
Table 3.18. Mean Epworth Sleepiness Score in individuals diagnosed with
asthma and healthy controls.
Asthma
Asthma control
Mean (Std Dev)
Mean (Std Dev)
(n=46)
(n=46)
8.37(5.24)
6.59(4.99)
t
P (2 tailed)
1.594
.118
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
No significant difference was observed between the individuals diagnosed with
asthma and healthy controls although the individuals with asthma scored higher.
COPD and COPD controls
Table 3.19. Mean Epworth Sleepiness Score in individuals diagnosed with
COPD and healthy controls.
COPD
COPD control
Mean (Std Dev)
Mean (Std Dev)
(n=18)
(n=18)
8.25(4.13)
6.06(3.91)
t
P (2 tailed)
1.441
.169
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
No significant differences were found between individuals diagnosed with COPD
and healthy controls although individuals with COPD scored higher.
170
Bronchiectasis and bronchiectasis controls
Table 3.20. Mean Epworth Sleepiness Score in individuals diagnosed with
bronchiectasis and healthy controls.
Bronchiectasis
Bronchiectasis
control
t
P (2 tailed)
2.585
.021*
Mean (Std Dev)
Mean (Std Dev)
(n=16)
(n=16)
8.88(5.60)
5.12(2.94)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between individuals diagnosed with
bronchiectasis and healthy controls in the mean score of ESS. Individuals diagnosed
with bronchiectasis scored significantly higher than healthy controls.
Asbestos related conditions and controls
Table 3.21. Mean Epworth Sleepiness Score in individual diagnosed with
asbestos & related conditions and healthy controls.
Asbestos related
conditions
Mean (Std Dev)
Asbestos control
t
P (2 tailed)
.886
.397
Mean (Std Dev)
(n=11)
(n=11)
8.82(5.75)
6.64(3,41)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
No significant difference was found between individuals diagnosed with asbestosis
and healthy controls, although individuals diagnosed with asbestosis scored higher
on the ESS compared to healthy controls.
Summary of 3.3.3 Daytime sleepiness
Generally in all groups, the groups with respiratory disease scored higher then their
healthy counterparts. A significant difference was only found within the
bronchiectasis group.
171
3.3.4 Quality of Life
The following section describes scores for the Short-Form 36 (SF-36) for individuals
diagnosed with respiratory diseases and healthy controls. The SF-36 assesses quality
of life across nine health concepts. These are: physical functioning, role limitations
due to physical problems, role limitations due to emotional problems, social
functioning, general mental health, energy/vitality, bodily pain, general health
perceptions and change in health.
In addition; transformed physical (PCS) and transformed mental (MCS), can be
calculated (details of the procedure can be found in appendix 12).
These health concepts were considered separately.
Tables 3.22 to 3.25 shows the mean scores for the SF-36 subscales and transformed
physical and transformed mental health concepts across all groups.
A lower score relates to lower QoL.
172
Asthma and asthma controls
Table 3.22. Mean SF-36 scores in the group with asthma and healthy controls.
Category
Physical
function
Role physical
Role emotional
Social
functioning
Mental health
Energy/Vitality
Pain
General health
perception
Change in health
Transformed
physical
Transformed
mental
Asthma
Mean/Std Dev
(n=46)
62.33/28.63
Asthma ctrl
Mean/Std Dev
(n=46)
86.74/35.57
Paired t-test
P (2 tailed)
-3.330
.002**
53.12/41.28
70.00/39.07
52.02/28.63
85.62/31.46
85.83/30.08
90.40/17.37
-5.025
-2.383
-7.342
<.0001***
.022*
<.0001***
63.27/17.72
48.11/18.89
59.01/29.75
47.58/17.64
74.81/15.66
62.44/21.83
66.41/23.02
73.60/21.03
-4.255
-3.629
-1.395
-6.394
<.0001***
.001**
.170
<.0001***
41.84/26.38
48.59/11.68
55.97/19.84
51.63/7.44
-2.818
-1.531
.007**
.135
26.60/7.53
51.35/10.68
-13.367
<.0001***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found across most of the SF-36 scales.
Individuals with asthma scored significantly less than the healthy controls on the
following SF-36 subscales (indicating a lower perceived QoL) these were;
Physical function, role physical, role emotional, social functioning, mental health,
energy and vitality, general health perception and finally change in health.
A significant difference was also reported between individuals diagnosed with
asthma who scored significantly lower compared to healthy controls in transformed
mental health.
173
COPD and COPD controls
Table 3.23. Mean SF-36 scores in the group with COPD and healthy controls.
Category
Physical
function
Role physical
Role emotional
Social
functioning
Mental health
Energy/Vitality
Pain
General health
perception
Change in health
Transformed
physical
Transformed
mental
COPD
Mean/Std Dev
(n=18)
18.82/13.63
COPD ctrl
Mean/Std Dev
(n=18)
73.83/20.83
Paired t-test
P (2 tailed)
-8.898
<.0001***
9.37/25.61
33.33/44.09
59.47/21.85
67.18/45.38
73.33/42.16
84.96/18.40
-3.529
-3.141
-3.251
.004**
.008**
.005**
53.55/17.14
50.55/20.92
45.09/26.48
38.46/16.82
71.05/16.40
56.47/20.52
59.87/22.91
64.52/23.99
-2.682
-1.107
-1.432
-3.968
.016*
.285
.171
.001**
27.77/29.56
27.95/7.82
54.16/23.08
45.93/9.17
-3.124
-4.04
.006**
.002**
43.59/9.29
50.37/10.62
-1.576
.146
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found across most of the SF-36 scales.
Individuals with COPD scored significantly less than the healthy controls on the
following SF-36 subscales (indicating a lower QoL) these were;
Physical function, role physical, role emotional, social functioning, mental health,
general health perception, and change in health.
Individual diagnosed with COPD also scored significantly lower than healthy
controls on transformed physical health.
174
Bronchiectasis and bronchiectasis controls
Table 3.24. Mean SF-36 scores in the group with bronchiectasis
Category
Bronchiectasis
Mean/Std Dev
(n=16)
Physical
function
Role physical
Role emotional
Social
functioning
Mental health
Energy/Vitality
Pain
General health
perception
Change in health
Transformed
physical
Transformed
mental
Paired t-test
P (2 tailed)
72.33/33.90
Bronchiectasis
ctrl
Mean/Std Dev
(n=16)
131.87/23.37
-6.095
<.0001***
59.37/45.52
50.00/35.35
56.25/28.24
86.66/35.18
83.33/34.42
115.27/12.08
-2.168
2.988
-7.020
.048*
.009**
<.0001***
72.25/14.12
43.50/14.37
57.63/30.14
51.66/20.34
105.00/15.91
70.00/19.23
69.44/22.03
78.50/23.93
-6.988
-4.171
-1.407
-3.652
<.0001***
.001**
.180
.003**
46.66/18.58
35.97/7.39
48.43/17.00
56.29/7.04
-.250
-9.226
.003**
<.0001***
43.29/8.07
59.38/7.56
4.853
.000***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found across most of the SF-36 scales.
Individuals with bronchiectasis scored significantly less than the healthy controls on
the SF-36 subscales (indicating a lower perceived QoL), these were;
Physical function, role physical, role emotional, social functioning, mental health,
energy/vitality, general health perception and change in health.
Individuals diagnosed with bronchiectasis also scored significantly lower in
transformed physical and transformed mental component scores compared to healthy
controls.
175
Asbestos related conditions and controls.
Table 3.25. Mean SF-36 scores in the group with asbestos & related conditions
and healthy controls.
Category
Physical
function
Role physical
Role emotional
Social
functioning
Mental health
Energy/Vitality
Pain
General health
perception
Change in health
Transformed
physical
Transformed
mental
Asbestos related
conditions
Mean/Std Dev
(n=11)
38.13/24.04
Asbestos ctrl
Mean/Std Dev
(n=11)
t
P (2 tailed)
116.87/24.19
-6.251
<.0001***
34.37/49.88
18.29/18.24
57.57/25.73
62.50/51.75
87.50/35.35
106.06/17.47
-1.116
6.012
-8.281
.301
.001**
<.0001***
69.09/14.76
39.27/13.24
43.33/19.20
35.90/13.92
95.90/16.25
55.45/18.36
66.66/21.59
66.50/26.12
-4.403
-3.619
-2.739
-3.396
.001**
.005**
.023*
.008**
31.81/16.16
22.33/12.93
50.00/22.36
52.43/10.50
2.667
-3.359
.024*
.020*
44.11/9.16
55.51/6.96
2.883
.034*
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Significant differences were found across most of the SF-36 scales.
Individuals with asbestosis related conditions scored significantly less than the
healthy controls on the following SF-36 scales (indicating a lower perceived QoL),
these were;
Physical function, role emotional, social functioning, mental health, energy/vitality,
pain, general health perception and change in health.
Individuals diagnosed with asbestosis & related conditions also scored significantly
lower in transformed physical and transformed mental component scores compared
to healthy controls.
176
Summary of 3.3.4 Quality of Life
Significant differences were observed in all the groups.
Asthma and asthma controls
•
Individuals diagnosed with asthma scored significantly lower scores across
the following SF-36 scales; Physical function, role physical, role emotional,
social functioning, mental health, energy and vitality, general health
perception, change in health and finally transformed mental health compared
to healthy controls indicating significantly lower QoL.
COPD and COPD controls
•
Individuals diagnosed with COPD scored significantly lower scores across
the following SF-36 scales; physical function, role physical, role emotional,
social functioning, mental health, general health perception, change in health
and finally transformed physical health compared to healthy controls
indicating significantly lower QoL.
Bronchiectasis and bronchiectasis controls
• Individuals diagnosed with bronchiectasis scored significantly lower on the
following SF-36 scales; Physical function, role physical, role emotional,
social functioning, mental health, energy/vitality, general health perception,
change in health, and finally transformed physical and transformed mental
component scores compared to healthy controls indicating a significantly
lower QoL.
Asbestos related conditions and controls
• Individuals diagnosed with asbestos related conditions scored significantly
lower on the following SF-36 scales; physical function, role emotional, social
functioning, mental health, energy/vitality, pain, general health perception,
change in health and finally transformed physical and transformed mental
component scores compared to healthy controls indicating a significantly
lower QoL.
177
3.3.5 General Health Questionnaire-12 (GHQ-12)
This section describes the findings of the GHQ-12 questionnaire.
The Likert scale (0, 1, 2, 3) was used to score the responses of the questionnaire
which gave an overall individual global score of 0 to 36. Caseness can be obtained
from the overall individual global score. Further information can be obtained from:
http://www.gl-assessment.co.uk
Tables 3.26 to 3.29 show the mean scores, standard deviations, t-test analysis and p
values (2 tailed) for individuals diagnosed with respiratory diseases and healthy
controls
Asthma compared to Asthma control
Table 3.26. Mean GHQ-12 scores in the group with asthma and healthy controls
Asthma
Asthma control
t
P (2 tailed)
Mean (Std Dev)
Mean (Std Dev)
(n=46)
(n=46)
14.61(7.52)
10.02(3.89)
3.469
.001**
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the individuals with asthma and healthy
controls. Individuals with asthma scored significantly higher on the GHQ-12. 83 %
of individuals with asthma scored above the threshold score compared to 50
% of healthy controls.
178
COPD and COPD controls
Table 3.27. Mean GHQ-12 scores in the group with COPD and healthy controls
COPD
COPD control
t
P (2 tailed)
Mean (Std Dev)
Mean (Std Dev)
(n=18)
(n=18)
17.78(6.44)
9.72(3.96)
4.070
.001**
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the individuals with COPD and healthy
controls. Individuals scored significantly higher on the GHQ-12. 39 % of individuals
with COPD scored above the threshold score compared to 17 % of healthy controls.
Bronchiectasis and bronchiectasis controls
Table 3.28. Mean GHQ-12 scores in the group with bronchiectasis and healthy
controls
Bronchiectasis
Bronchiectasis
t
P (2 tailed)
Mean (Std Dev)
control
(n=16)
Mean (Std Dev)
(n=16)
11.75(5.10)
9.25(4.28)
1.768
.097
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
No significant difference was found within this group, individuals diagnosed with
bronchiectasis did however score highly on the GHQ-12 compared to healthy
controls. 25 % of individuals diagnosed with COPD scored above the threshold score
compared to 20% of healthy controls.
179
Asbestos related conditions and controls
Table 3.29. Mean GHQ-12 scores in the group with asbestos & related
conditions
t
P (2 tailed)
Asbestos related
Asbestos control
conditions
Mean (Std Dev)
Mean (Std Dev)
(n=11)
(n=11)
14.45(4.90)
9.27(4.31)
3.866
.397
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
No significant difference was reported between this group. 25 % of individuals
diagnosed with asbestosis & related conditions scored above the threshold score
compared to 12% of healthy controls.
180
Summary of 3.3.5 General Health Questionnaire (GHQ-12)
Asthma and asthma controls
•
Individuals diagnosed with asthma scored significantly higher on the GHQ12 compared to healthy controls. 83 % of individuals scored above the
threshold score compared to 50 % of healthy controls.
COPD and COPD controls
•
Individuals diagnosed with COPD scored significantly higher than healthy
controls. 39 % of individuals diagnosed with COPD scored above the
threshold score compared to 17 % of healthy controls.
Bronchiectasis and bronchiectasis controls
•
No significant difference was reported between this group. Individuals
diagnosed with bronchiectasis did however still score highly on the GHQ-12
compared to healthy controls. 25 % of individuals diagnosed with COPD
scored above the threshold score compared to 20 % of healthy controls.
Asbestos related conditions and controls
•
No significant difference was reported between this group. Individuals
diagnosed with asbestosis related conditions did however still score highly on
the GHQ-12 compared to healthy controls. 25 % of individuals diagnosed
with asbestosis & related conditions scored above the threshold score
compared to 12 % healthy controls.
181
3.3.6 Beck Depression Inventory (BDI)
This section describes the findings on the Beck Depression Inventory (BDI) in each
group. The BDI consists of 21 items and assesses the symptoms which may
correspond to the criteria for diagnosing depressive disorders as listed in the
American psychiatric Association’s Diagnostic and Statistical Manual of Mental
Disorders-Fourth editions (DSM-IV; 1994). The case scores, which include the
means and standard deviations of the BDI-II scores by sample and diagnostic groups,
can be found in appendix 19. The items have been considered separately.
Tables 3.30 to 3.33 shows the global score for the BDI-II across all groups.
Asthma and asthma controls
Table 3. 30. Global BDI-II scores in the group with asthma
Asthma
Asthma control
Mean (Std Dev)
Mean (Std Dev)
(n=46)
(n=46)
15.67(13.10)
5.76(7.41)
t
P (2 tailed)
4.776
<.0001***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Individuals diagnosed with asthma scored significantly higher on the BDI compared
to the healthy controls.
182
COPD and COPD controls
Table 3.31. Global BDI-II scores in the group with COPD and healthy controls
COPD
COPD control
Mean (Std Dev)
Mean (Std Dev)
(n=18)
(n=18)
19.83(7.83)
7.00(7.82)
t
P (2 tailed)
4.081
<.0001***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Individuals diagnosed with COPD scored significantly higher on the BDI compared
to healthy controls.
Bronchiectasis and bronchiectasis controls
Table 3.32. Global BDI-II scores in the group with bronchiectasis and healthy
controls
Bronchiectasis
Bronchiectasis
control
t
P (2 tailed)
2.384
.015*
Mean (Std Dev)
Mean (Std Dev)
(n=16)
(n=16)
7.56(6.30)
3.63(3.93)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Individuals diagnosed with bronchiectasis scored significantly higher on the BDI
compared to healthy controls.
183
Asbestos related condition and controls
Table 3.33. Global BDI-II scores in the group with asbestos & related conditions
and healthy controls
Asbestos related
conditions
Asbestos control
Mean (Std Dev)
Mean (Std Dev)
(n=11)
(n=11)
12.18(6.36)
5.36(3.58)
t
P (2 tailed)
3.858
.003**
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
Individuals diagnosed with asbestosis scored significantly higher on the BDI
compared to healthy controls.
Summary of 3.3.6 Beck Depression Inventory (BDI)
Significant differences were found across all groups diagnosed with respiratory
diseases compared to the healthy controls.
184
3.3.7 Cognitive assessments
Cognitive function was assessed using two items to measure memory and
concentration problems. These have been adapted from the study by Jennum and Sjol
(1994). The comparison for assessing whether individuals diagnosed with respiratory
diseases have memory and concentration problems has been derived from the DanMONICA (MONItoring trends in cardiovascular diseases) data to evaluate the
relation between snoring, sleep apnoea and cognitive complaints in adults.
Those diagnosed with sleep apnoea in the Dan-MONICA study, scored a mean of
3.53 (concentration item) and 1.51 (memory item).
Tables 3.34 to 3.41 show the mean scores of individuals with respiratory disease and
healthy controls in these items:
Classification of cognitive complaints:
Concentration problems: This was assessed by using the following phrase: ‘Do you
suffer from concentration problems more than compared to those of your own age?’
Memory problems: This was assessed by using the following phrase: ‘Do you
suffer from memory problems, more than compared to those of your own age?’
The 2 items were considered separately.
185
Concentration problems
Item 1: Do you suffer from concentration problems, more than compared to those
of your own age?’
Asthma and asthma controls
Table 3. 34. Mean Item 1 scores in the group with asthma and healthy controls
Asthma
Asthma control
Mean (Std Dev)
Mean (Std Dev)
(n=46)
(n=46)
1.96(1.11)
.54(.808)
t
P (2 tailed)
7.416
<.0001***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two samples. The mean score for
individuals with asthma was significantly higher than the healthy controls indicating
more self-reported problems with concentration.
COPD and COPD controls
Table 3.35. Mean Item 1 scores in the group with COPD and healthy controls
COPD
COPD control
Mean (Std Dev)
Mean (Std Dev)
(n=18)
(n=18)
2.00(.966)
.81(.655)
t
P (2 tailed)
3.884
.001**
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two samples. Individuals diagnosed
with COPD scored significantly higher on the concentration items compared to
healthy controls indicating more self-reported problems with concentration.
186
Bronchiectasis and bronchiectasis controls
Table 3.36. Mean Item 1 scores in the group with bronchiectasis
Bronchiectasis
Bronchiectasis
control
t
P (2 tailed)
5.196
<.0001***
Mean (Std Dev)
Mean (Std Dev)
(n=16)
(n=16)
1.19(.403)
.44(.629)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two groups. Individuals diagnosed
with bronchiectasis scored significantly higher on the concentration item compared
to healthy controls indicating more self-reported problems with concentration.
Asbestos related conditions and controls
Table 3.37. Mean Item 1 scores in the group with asbestos & related conditions
and healthy controls
Asbestos related
conditions
Asbestos control
t
P (2 tailed)
3.105
.011*
Mean (Std Dev)
Mean (Std Dev)
(n=11)
(n=11)
1.55(.934)
.73(.647)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A Significant difference was found between the two samples. Individuals with
asbestosis related conditions scored significantly higher on the concentration item
compared to healthy controls indicating more self-reported problems with
concentration.
187
Memory problems
Item 2: Do you suffer from memory problems, more than compared to those of
your own age?
Asthma and asthma controls
Table 3. 38. Mean Item 2 scores in the group with asthma and healthy controls
Asthma
Asthma control
Mean (Std Dev)
Mean (Std Dev)
(n=46)
(n=46)
1.78(1.22)
.59(.77)
t
P (2 tailed)
5.574
<.0001***
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A Significant difference was found between the two groups. Individuals diagnosed
with asthma were significantly more likely to report memory problems than their
healthy controls.
COPD and COPD controls
Table 3.39. Mean Item 2 scores in the group with COPD and healthy controls
COPD
COPD control
Mean (Std Dev)
Mean (Std Dev)
(n=18)
(n=18)
1.94(1.12)
.69(.87)
t
P (2 tailed)
2.887
.011*
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two groups. Individuals diagnosed
with COPD were significantly more likely to report memory problems than their
healthy controls.
188
Bronchiectasis and bronchiectasis controls
Table 3.40. Mean Item 2 scores in the group with bronchiectasis and healthy
controls
Bronchiectasis
Bronchiectasis
control
t
P (2 tailed)
3.576
.003**
Mean (Std Dev)
Mean (Std Dev)
(n=16)
(n=16)
1.12(.342)
.56(.814)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two groups. Individuals diagnosed
with bronchiectasis were significantly more likely to report memory problems than
their healthy controls.
Asbestos related conditions and controls
Table 3.41. Mean Item 2 scores in the group with asbestos & related conditions
and healthy controls
Asbestos related
conditions
Asbestos control
t
P (2 tailed)
1.550
.011*
Mean (Std Dev)
Mean (Std Dev)
(n=11)
(n=11)
1.64(1.02)
1.00(.894)
*P<0.05 **p<0.01 ***p<0.001 (2 tailed)
A significant difference was found between the two groups. Individuals diagnosed
with asbestosis & related conditions were significantly more likely to report memory
problems than their healthy controls.
189
Summary of 3.3.7 cognitive assessments
Concentration problems
The mean score for individuals diagnosed with respiratory diseases was significantly
higher than the healthy controls indicating more self-reported problems with
concentration.
Memory problems
The mean score for individuals diagnosed with respiratory diseases was significantly
higher than the healthy controls , individuals diagnosed with respiratory diseases
were significantly more likely to report memory problems than their healthy controls.
190
3.3.8 Associations between sleep disorders and behaviours, daytime
sleepiness, quality of life, GHQ-12, BDI and cognitive functioning
Associations between sleep disorders and behaviours, daytime sleepiness, quality of
life, mental health, depression and cognitive functioning were investigated in each of
the respiratory groups.
In order to investigate these associations, additional sleep scores were computed for
each individual with respiratory disease.
These sleep scores were based on the intuitive groupings of disorders of initiating
and maintaining sleep (difficulties falling asleep, waking during the night,
occurrence of waking during the night, early waking), features associated with sleep
disordered breathing (snoring, quality of snoring, breathing pauses), other sleep
disorders and behaviours occurring during sleep (narcolepsy, cataplexy, sleep
paralysis, sleep talking, sleep walking, bed wetting, nightmares, teeth grinding, night
screaming and rocking at night), sleep related disorders and behaviours occurring
during the day (excessive sleepiness after awakening, excessive sleepiness during the
day, excessive sleepiness during work, excessive sleepiness during leisure and
daytime naps).
For each of the sleep scores, the individuals score for each item in that particular
group was summed to produce a composite score.
Pearson correlation coefficients were then calculated between each sleep score and
the daytime sleepiness score (ESS), quality of life (SF-36), mental health (GHQ),
depression (BDI) and cognitive functioning (summed 2 items). This was carried out
separately for each of the respiratory groups. The results are shown in tables 3.42 to
3.45.
191
Asthma
Table 3.42. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders during
sleep, and other disorders during the day,
and Epworth Sleepiness score (ESS), General Health Questionnaire score (GHQ-12),
physical component score (PCS) and mental component score (MCS), Beck depression
Inventory (BDI) score and cognitive functioning global score (Cog).
ESS
GHQ-12
PCS
MCS
BDI
COG
Daytime
sleepiness
General
health
Physical
component
score
Mental
component
score
depression
Cognitive
functioning
Asthma
Asthma
Asthma
Asthma
Asthma
Asthma
DIMS score
-.047
.254
-.473**
.008
.337*
.085
SDB
.252
.211
-.414**
.128
.240
.121
Other
disorders
during sleep
.395**
.386**
-.393*
-.202
.459**
.190
Other
disorders
during day
.635**
.491**
-.524**
.142
.472**
.274
Score
*p<0.05 **p<0.01 ***p<0.001 (p=2-tailed)
Individuals diagnosed with asthma
Significant associations were observed within this group.
A significant negative correlation was found between the DIMS and PCS showing
higher scores on DIMS subscale was associated with lower quality of life relating to
perceived physical component score.
A significant correlation was found between the DIMS score and BDI score, showing
higher scores on DIMS subscale was associated with higher levels of depression
relating to the BDI scores
A significant negative correlation was found between the SDB score and the PCS
showing higher scores on SDB subscale was associated with lower quality of life
relating to perceived physical component score.
192
Significant correlations were found between the other disorders during sleep score
and the ESS, GHQ-12 and BDI. Higher scores on other disorders during sleep
subscale were associated with higher scores on the ESS, GHQ-12, and the BDI.
A significant negative correlation was found between the other disorders during sleep
score and PCS showing higher scores on the other disorders during sleep subscale
was associated with lower quality of life relating to perceived physical component
score.
Significant correlations were found between other disorders during day and ESS,
GHQ-12 and BDI scores showing higher scores on other disorders during day
subscale was associated with higher scores on the ESS, GHQ-12 and BDI.
A significant negative correlation was found between other disorders during the day
and PCS, showing higher scores on other disorders during the day subscale was
associated with lower quality of life relating to perceived physical component score.
193
COPD
Table 3.43. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders during
sleep, and other disorders during the day,
and Epworth Sleepiness score (ESS), General Health Questionnaire score (GHQ-12),
physical component score (PCS) and mental component score (MCS), Beck depression
Inventory (BDI) score and cognitive functioning global score (Cog).
ESS
GHQ
PCS
MCS
BDI
COG
Daytime
sleepiness
General
health
Physical
component
score
Mental
component
score
Depression
Cognitive
functioning
COPD
COPD
COPD
COPD
COPD
COPD
DIMS score
-.415
.085
.518
-.132
.137
.805**
SDB
.319
.073
.245
-.433
.272
.047
Other
disorders
during sleep
.288
.333
-.017
-.199
.416
.498*
Other
disorders
during day
.139
-.198
.529
-.159
-.062
.215
Score
*p<0.05 **p<0.01 ***p<0.001 (p=2-tailed)
Individuals diagnosed with COPD
Significant associations were observed within this group.
A significant correlation was found between the DIMS score and cognitive
functioning score showing higher scores on DIMS subscale was associated with
greater problems with cognitive functioning.
A significant correlation was found between other disorders during sleep and
cognitive functioning score showing higher scores on other disorders during sleep
subscale was associated with greater problems with cognitive functioning.
194
Bronchiectasis
Table 3.44. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders during
sleep, and other disorders during the day,
and Epworth Sleepiness score (ESS), General Health Questionnaire score (GHQ-12),
physical component score (PCS) and mental component score (MCS), Beck depression
Inventory (BDI) score and cognitive functioning global score (Cog).
ESS
GHQ
PCS
MCS
BDI
COG
Daytime
sleepiness
General
health
Physical
component
score
Mental
component
score
Depression
Cognitive
functioning
Bronc
Bronc
Bronc
Bronc
Bronc
Bronc
DIMS score
.064
.004
-.244
.140
.153
.400
SDB
-.145
-.518*
-.490
.393
-.551*
.011
.319
.582*
.064
-.688**
.657**
.560*
.698**
.466
-.043
-.441
.555*
.310
Score
Other
disorders
during sleep
Other
disorders
during day
*p<0.05 **p<0.01 ***p<0.001 (p=2-tailed)
Individuals diagnosed with bronchiectasis
Significant associations were observed within this group.
Significant negative correlations were found between the SDB score and the GHQ12 score and BDI scores showing higher scores on SDB subscale was associated with
lower scores on the GHQ-12 and lower scores on the BDI scores.
Significant associations were found between the other disorders during sleep and
GHQ-12, BDI and cognitive functioning scores showing higher scores on other
disorders during sleep was associated with higher scores on GHQ-12, BDI and
cognitive functioning score.
195
A significant negative correlation was found between other disorders during sleep
and MCS showing higher scores on other disorders during sleep subscale was
associated with lower quality of life relating to mental health component score
Significant correlations were found between other disorders during sleep and ESS
and BDI scores showing higher scores on other disorders during sleep subscale was
associated with higher scores the ESS and BDI scores.
196
Asbestos related conditions
Table 3.45. Pearson Correlation Coefficients for the Disorders of Initiating and
Maintaining Sleep (DIMS), Sleep Disordered Breathing (SDB), other disorders during
sleep, and other disorders during the day,
and Epworth Sleepiness score (ESS), General Health Questionnaire score (GHQ-12),
physical component score (PCS) and mental component score (MCS), Beck depression
Inventory (BDI) score and cognitive functioning global score (Cog).
ESS
GHQ
PCS
MCS
BDI
COG
Daytime
sleepiness
General
health
Physical
component
score
Mental
component
score
Depression
Cognitive
functioning
Asbestos
& related
condition
Asbestos
& related
condition
Asbestos &
related
condition
Asbestos
& related
condition
DIMS score
.124
-.173
.044
-.148
.068
.240
SDB
-.091
-.069
.280
-.040
-.026
.234
.397
.448
.201
-.300
.427
.224
.549
-.305
-.618
.038
-.165
.230
Asbestos
& related
condition
Asbestos &
related
condition
Score
Other
disorders
during sleep
Other
disorders
during day
*p<0.05 **p<0.01 ***p<0.001 (p=2-tailed)
Individuals diagnosed with asbestosis related conditions
There were no significant associations found between any of the sleep scores and the
individual items on the various questionnaires.
197
Summary of 3.3.8 Associations between sleep disorders and
behaviours, daytime sleepiness, quality of life, mental health,
depression and cognitive functioning
Associations between sleep disorders and daytime behaviour problems
Asthma
• Generally, significant associations were found between sleep disorders and
measures of psychological functions. As sleep problems increased in DIMS,
quality of life associated with physical component score was lowered,
however, depression scores increased. As SDB scores increased, quality of
life associated with physical component score was lowered. Other disorders
during sleep and other disorders during day increased so did the problems
associated with daytime sleepiness, general health, physical functioning and
higher scores of depression.
COPD
• Generally significant associations were found between sleep disorders and
problems related to cognitive functioning. As sleep problems associated with
DIMS and other disorders during sleep increased individuals diagnosed with
COPD
reported
increased
problems
associated
with
memory
and
concentration.
Bronchiectasis
• Significant association were found between sleep disorders and problems
related to daytime behaviour problems. As sleep problems associated with
SDB increased, general health deteriorated along with increased feelings of
depression. As sleep problems associated with other disorders during sleep
increased poorer scores in general health, depression and cognitive
functioning was reported, mental health deteriorated too. Individuals also
reported increased daytime sleepiness and feeling more depressed as sleep
problems associated with other disorders during day increased.
198
Asbestos related conditions
• No significant associations were observed within this group between sleep
disorders and daytime behaviour problems.
199
3.4 Summary of survey
Differences between groups - sleep disorders
•
Significant differences were reported between individuals diagnosed with
respiratory diseases compared to healthy controls across the sleep disorders
and behaviours.
Daytime sleepiness
•
A significant difference was found within the bronchiectasis group compared
to healthy controls. No other significant differences were observed between
the asthma, COPD and asbestosis group compared to healthy controls.
Quality of life
•
Significant differences were observed in all the groups. Individuals diagnosed
with respiratory diseases scored significantly lower on the SF-36 scales
compared to healthy controls including the two component scores.
General Health Questionnaire-12
•
Individuals diagnosed with asthma, COPD and bronchiectasis scored
significantly higher on the GHQ-12 questionnaire compared to healthy
controls.
•
A greater proportion of individuals with respiratory diseases scored above the
threshold score compared to healthy controls.
Beck Depression Inventory
•
Individuals diagnosed with respiratory diseases scored significantly higher on
the BDI compared to healthy controls.
Cognitive assessments
•
Individuals diagnosed with respiratory diseases reported greater concentration
problems compared to healthy controls. Significant differences were also
200
observed between individuals diagnosed with respiratory diseases compared
to healthy controls in terms of memory problems.
Associations between sleep disorders and daytime behaviour problems
•
Significant associations were found sleep disorders and measures of
psychological function problems in individuals diagnosed with asthma,
COPD and bronchiectasis.
201
4 Discussion
Overview
The reason for undertaking the present series of surveys was that they were
concerned with topics of clinical importance to the care of individuals who have been
diagnosed with respiratory diseases, more specifically asthma, COPD, bronchiectasis
and asbestosis. It is evident from the literature review that there has been little
previous work conducted within this area. Previous studies that have tried to address
the issues raised within this study have been informative and of great importance.
The findings from these studies have indicated a need for further research on the
many points that they raise.
The present research programme has a number of individual features that
distinguishes it from previous research, which has been conducted in individuals
diagnosed with respiratory diseases. These are as follows:
1. Investigation of a population based sample of such adults rather than adults
whom have been referred for investigation to specialised sleep centres.
2. Comparison with a matched control group from the general population to
assess the relative frequency and nature of the sleep problems.
3. Examination of the comparative profiles of sleep problems in adults
diagnosed with specific respiratory diseases.
4. Comprehensive assessment of self-reported sleep disorders and behaviours of
these adults as reported through the use of validated questionnaire.
5. Investigations of associations between sleep disorders, daytime behaviour
problems, excessive daytime sleepiness and psychological functioning in
adults diagnosed with respiratory diseases.
The main aims were, firstly, to describe the occurrence and nature of self reported
sleep problems in individuals who have been diagnosed with specific respiratory
diseases namely asthma, chronic obstructive pulmonary disease (COPD), asbestosis,
and bronchiectasis; secondly, compare the findings with those matched for age and
202
sex and finally investigate associations between the sleep problems and self reported
daytime sleepiness, quality of life, mental health and daytime cognitive functioning
in the groups with respiratory disease.
4.1 Summary of findings
The data extracted from the BNSQ questionnaire measuring sleep behaviours and
disorders
The data analysed from the BNSQ questionnaire revealed those individuals
diagnosed with asthma reported significantly greater problems related to sleep.
Individuals diagnosed with asthma in this group reported more episodes of waking
during the night, waking earlier than normal, exacerbated snoring, greater number of
breathing pauses, greater number of episodes of cataplexy, sleep paralysis and sleep
talking. They also reported feeling excessively sleepy after awakening during the day
and during free time. Individuals diagnosed with asthma reported sleeping less but
also reported longer episodes of napping during the day and snoring for a lot longer
compared to healthy controls.
Although individuals diagnosed with COPD also reported significantly greater
problems related to sleep, these individuals revealed that they woke during the night
a great deal more often compared to healthy controls. They also snored a lot more,
felt excessively sleepy during the day, had a greater number of daytime naps and
reported staying awake longer in bed before falling asleep, compared to healthy
controls.
Individuals diagnosed with bronchiectasis reported significantly worse snoring,
experienced a greater number of nightmare episodes, reported feeling excessively
sleepy after arousing and during the day, compared to healthy controls.
The data analysed for individuals diagnosed with asbestosis revealed that these
individuals slept significantly longer, napped for longer and started to snore at a
much later age compared to their healthy counterparts.
203
The Epworth Sleepiness Scale data measuring daytime sleepiness
The data analysed for daytime sleepiness revealed a significant difference between
individuals diagnosed with bronchiectasis and healthy controls. No significant
differences were found between individuals diagnosed with asthma, COPD and
asbestosis compared to their healthy counterparts. These results will be discussed in
greater detail in the next section.
SF-36 scale and the physical and mental component score measuring QoL.
Individuals diagnosed with asthma revealed significantly reduced QoL. These
individuals were perceived to have reduced physical functioning, reduced emotional
well being, reduced social functioning, reduced social functioning, reduced mental
health, less energy and vitality in relation to quality of life. They generally thought,
as well, that they had reduced health and that their health would either remain the
same or be further reduced in the near future. The transformed mental component
score was also significantly lower compared to healthy controls.
Individuals diagnosed with COPD revealed a similar picture. These individuals
reported reduced quality of life relating to physical component score, were perceived
to have poor health, perceived to feel more emotionally withdrawn, have reduced
social functioning, poor mental health and reduced general health. These individuals
reported remaining the same or worse in the near future. The transformed physical
component score was also significantly lower compared to their healthy counterparts.
Individuals diagnosed with bronchiectasis reported significantly reduced QoL
compared to their healthy counterparts. These individuals scored lower on all but the
pain scale on the SF-36. Both the component scores for mental and physical health
were significantly lower compared to their healthy counterparts.
Individuals diagnosed with asbestosis reported significantly lower on the QoL SF-36
scales compared to their healthy counterparts. These individuals scored significantly
lower on all but the role physical scale of the SF-36. Both the transformed physical
and mental component scores were significantly lower than their healthy
counterparts.
204
The GHQ-12 questionnaire data measuring mental health
Individuals diagnosed with asthma reported significantly higher on the GHQ-12
compared to healthy controls. 83 % of these individuals revealed a psychiatric
disorder similar to that of individuals attending an out-patient clinic compared to 50
% healthy controls. The psychiatric disorder revealed using the GHQ-12 are
depression, anxiety, social performance, somatic complaints and occasionally sleep
disturbances over a 4-week period.
Individuals diagnosed with COPD scored significantly higher than healthy controls
on the GHQ-12. 39 % of individuals with COPD scored above the threshold score to
detect caseness, in those individuals who attended an outpatient clinic over a 4-week
period compared to 17 % healthy controls.
Although no significant differences were found in this group, individuals diagnosed
with bronchiectasis did score highly on the GHQ-12. 25 % of these individuals
scored above the threshold, revealing that some of the individuals appeared to have
underlying psychiatric problems, according to this questionnaire, compared with
patients attending an outpatient clinic compared to 20 % healthy controls.
No significant difference was found between individuals diagnosed with asbestosis
compared to their healthy counterparts. However, interestingly 25 % of these
individuals did score above the threshold score, revealing that a minority of the
individuals, according to this questionnaire, appear to have psychiatric problems
compared to 12 % healthy controls.
The Beck Depression Inventory measuring depression
Individuals diagnosed with asthma, COPD, bronchiectasis and asbestosis revealed
significantly greater episodes of depression compared to their healthy counterparts.
Cognitive assessments – 2 items derived from the Dan-MONICA data: concentration
and memory problems
Individuals diagnosed with asthma, COPD, bronchiectasis and asbestosis were
significantly more likely to report concentration problems compared to their healthy
counterparts. These individuals did not however obtain a mean score greater than the
comparison score in the Dan-MONICA study.
205
Individuals diagnosed with asthma, COPD and asbestosis were significantly more
likely to have greater memory problems compared to their healthy counterparts.
These individuals also scored above the threshold core as revealed in the DanMONICA study. Individuals diagnosed with asbestosis were shown to have
significantly greater memory problems but scored below the threshold score.
Associations between sleep disorders and behaviours, daytime sleepiness, quality of
life, mental health, depression and cognitive functioning.
Significant associations were observed across all four respiratory groups, both
positive and negative.
Individuals diagnosed with asthma revealed that as their self-reported sleep problems
increased so did the score on their daytime sleepiness and General Health
Questionnaire-12. Their QoL was lower and their feelings of depression increased,
too.
Individuals diagnosed with COPD revealed that as their sleep problem (DIMS and
other disorders during sleep) increased, their self-reported cognitive complaints were
greater, too.
Individuals diagnosed with bronchiectasis revealed that as their sleep problems
(SDB, other disorders during sleep and other disorders during the day) increased,
their score in general health increased, they reported higher on the BDI. Their QoL
was reduced and they had reduced cognitive functioning.
There were no significant associations found in the groups of individuals diagnosed
with asbestosis.
4.2.1Main findings and comparisons with other studies
This section discusses the main findings and compares them to the studies that have
been discussed in the literature review. The section will be arranged in terms of the
data analysis where by sleep problems and sleep disorders will be discussed first,
followed by daytime sleepiness, QoL, General health Questionnaire-12 and Beck
Depression Inventory and finally cognitive functioning, for each respiratory group.
206
Asthma
Sleep problems and sleep disorders
In this study, individuals diagnosed with asthma reported greater sleep problems
compared to healthy controls. Asthma causes a variety of respiratory problems which
can impair the QoL and lead to sleep disturbances. The individuals diagnosed with
asthma in this study reported problems with disorders of initiating and maintain
sleep; sleep associated with disordered breathing, sleep related disorders/behaviours
occurring during the day and time required for sleep and sleep duration. These results
are supported by Janson et al (1990) and Shah et al (1997) who reported that the
most common sleep disturbances amongst asthmatic patients were early morning
awakening, difficulty in maintaining sleep, excessive daytime sleepiness, nocturnal
wakefulness and nocturnal breathing problems.
The fact that individuals reported waking during the night in this study could be due
to the fact that the individual’s asthma woke them due to their symptoms relating to
asthma. This problem has been explored by Turner-Warwick (1988) who showed
that individuals diagnosed with asthma reported they woke at least once a week due
to their symptoms and woke frequently throughout the week.
Individuals diagnosed with asthma in the present study reported poor sleep quality
Caterall et al (1982); Montplaisir et al (1982); Fitzpatrick et al 1991) highlighted the
problem of sleep quality in those individuals diagnosed with asthma. Asthma per se
can disrupt sleep, these factors being troublesome day-time and nocturnal symptoms.
Sleep quality maybe further reduced especially if the individual experiences an
asthma attack during stages 1 and 2 and NREM sleep. Individuals will often report
feeling unrefreshed and fatigued in the morning and will experience excessive
sleepiness in the morning after awakening; this is supported by the work of
Ravenscroft and Hartmann (1968).
In this study individuals also reported staying awake in bed before they fell asleep;
this may be because those with asthma enjoy far less of the deep and restful sleep
stages 3 and 4 than those without asthma and spend far more time awake
(Hindmarch, 2003).
207
Daytime sleepiness
Although non-significant scores were observed in this group, individuals diagnosed
with asthma did obtain a mean score that was greater than their healthy controls.
These individuals also bordered on showing similar ESS scores classified with mild
OSAS according to the ESS normative scores (appendix 11). These individuals did
report, however, being significantly sleepier during the day and leisure time on the
BNSQ. Further analysis of the data also revealed significant associations between
other sleep disorders during the day and during sleeping and excessive daytime
sleepiness. Excessive sleepiness is a serious condition, which does not just affect the
individual but also his or her colleagues, friends and family; it can be life-threatening
in a variety of conditions from work, to driving and to developing other co
morbidities (Mitler et al, 2005). Some efforts have been made to highlight the nature
of sleep disturbances in individuals diagnosed with asthma and its effects on daytime
performances (Janson et al; Fitzpatrick et al, 1991) and Vir et al (in press). The
effects of daytime sleepiness are underrated in such individuals (Sharpley, 1996).
The effects that daytime sleepiness has upon the individual are detrimental in the
sense that they affect the daily performance of individuals diagnosed with asthma in
psychosocial performances and cognitive functions (which will be discussed later in
this section), mood swings and emotional distress and reduced leisure activities thus
resulting in reduced physical and mental well-being.
QoL
The relationship between asthma and QoL in adults is believed to be important but
has not been well studied, according to Archea et al (2006).
In this study, individuals diagnosed with asthma reported reduced QoL on all but the
pain scale of the SF-36. Perhaps the reasons for such low scores could be that
psychological distress is more frequent in those with asthma and thus at risk of being
anxious and more likely to feel depressed. The transformed mental health component
score was also significantly lower than healthy controls and the reason for this could
be that such individuals always feel a lack of control over their health; such
208
individuals have been shown to score significantly lower on the SF-12 scales, too, as
shown by Adams et al (2004).
Further analysis of the data in this group revealed significant associations between
the selected sleep categories and the two SF-36 component scores, thus providing
further support for the knowledge that as the various sleep problems increase in an
individual this can then have a knock on effect on the individuals physical and
mental QoL.
General Health Questionnaire-12 and Beck Depression Inventory
In individuals diagnosed with asthma, mental health was reported significantly lower
in relation to healthy controls both on the SF-36 and the GHQ-12. The reasons for
this occurring could be due to several factors. Individuals diagnosed with asthma
often report feelings of anxiety and depression, as shown by Janson et al (1994). It is
important to note that the severity of the asthma status was not monitored but studies
have shown that those with severe asthma do also display the same relationship
between psychological status and morbidity (Cooper et al, 1997). Individuals may
also report feeling mentally worse and more depressed because of the distress that
perhaps the individual experiences during an attack. Individuals may also have
insufficient knowledge, unable to manage exacerbations and have poor adherence to
treatment which can also cause great anxiety; these issues have been briefly explored
by Neville et al (1991), Padget and Brodsky (1992) and Reed et al (1985).
Further studies have shown that panic and fear occur at higher rates in people with
asthma compared to non-asthmatic individuals, as shown by Kinsman et al (1973)
and Dirks et al (1973). Suggestions to explain why individuals diagnosed with
asthma have been shown to have higher rates of panic and fear is firstly the feeling of
breathlessness (Bass and Gardner, 1985), individuals who are predisposed to anxiety
and depression (Bass and Gardner, 1985) and those diagnosed with bronchial asthma
have shown to report greater feelings associated with anxiety and fear (Lyketsos et
al, 1984).
In the present study, 83% of individuals with asthma scored above the threshold
score in the GHQ-12 and 50 % of healthy controls scored above the threshold score,
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these individuals who scored 83% above the threshold score help towards the
explanation of the association between asthma and morbidity in terms of poor social
functioning (Sibbald, 1989; Campbell et al, 1995) and it has been proposed that
perhaps psychiatric morbidity may decrease an individual’s ability to care for
themselves, as shown by Sibbald (1989). Further studies which support this is the
work conducted by Vamos and Kolbe (1999) who found that 25% of their sample
had possible caseness for anxiety, lower than the present study and 11% had caseness
for depression. The associations conducted on the data in the present study revealed
that as other disorders during sleep and other disorders during the day increased so
did the score on the BDI.
Cognitive functioning
Individuals diagnosed with asthma reported greater concentration and memory
problems compared to healthy controls. Reasons why individuals may experience
greater memory and concentration problems have been explored by a few published
studies. Individuals who report greater sleep disturbances associated with DIMS also
report excessive daytime sleepiness which has an impact on cognitive functioning.
Daytime cognitive functioning is worse in individuals diagnosed with asthma and
usually shown to take longer to complete cognitive tasks (Fitzpatrick et al, 1991;
Janson et al, 1990). The ATS (1998) has further supported this by studying the
consequences of excessive daytime sleepiness and the significant deterioration that it
brings in daily performance in individuals diagnosed with asthma, thus having a
knock on effect on occupational performance and during leisure activities (Pilcher
and Huffcutt, 1996; Smith-Coggins et al, 1994). The associations conducted on the
data in the present study did not reveal any significant correlations between any of
the sleep subscales and cognitive functioning.
COPD
Sleep problems, sleep disorders and daytime sleepiness.
In the present study, individuals diagnosed with COPD reported significant sleep
problems and behaviours compared to healthy controls. Sleep quality is often
impaired in individuals diagnosed with COPD (Cormick et al, 1986; Fleetham et al,
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1982; Brezinova et al, 1982). Individuals in the present study reported waking during
the night and snoring more often than their healthy counterparts; these individuals
also reported excessive sleepiness during the day and increased daytime napping and
staying awake longer in bed before falling asleep. A study by Saaresranta et al
(2005) who used the BNSQ to assess sleep problems and behaviours in individuals
diagnosed with COPD, showed that those with COPD reported never sleeping well,
slept restlessly and feeling tired in the morning.
In terms of excessive daytime sleepiness although significant findings were not
reported, it did however reveal that individuals diagnosed with COPD reported
greater excessive sleepiness, the current data are contradictory in the sense that a
study by Saaresanta et al (2005) revealed that individuals with mild to moderate
COPD without acute exacerbations do not complain about excessive sleepiness as
much as individuals diagnosed with OSAS do. Bellia et al, (2003) has reported,
however, that elderly individuals diagnosed with COPD complain more of morning
tiredness and early awakenings.
Sleep disturbances in individuals diagnosed with COPD is usually related to
nocturnal cough, wheezing and shortness of breath due to the worsening of
pulmonary mechanics and gas exchange during sleep. This is further supported by
Klink et al (1994), who showed where one respiratory symptom was present, such as
cough or wheeze, 12% of the sample population reported excessive daytime
sleepiness and 39% reported insomnia. With both symptoms present, 23 % reported
feeling excessively sleepy during the day and 53% reported episodes of insomnia.
Poor quality sleep can be further explained by marked increases in sleep stage
changes, frequent arousals and awakening and decreased total sleep time. It is also
important to note that individuals with poor quality sleep will not necessarily
perceive themselves as having poor sleep, despite that sleep studies in individuals
diagnosed with COPD have been shown to have excessive daytime sleepiness,
minimally altered sleep quality and sleep architecture (Sanders et al, 2003). One
factor that has not been considered but is important to mention is that age related
sleep changes can also occur in this group of individuals and studies have shown that
sleep quality does deteriorate in the elderly population.
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A further explanation why these individuals may experience such sleep behaviours is
that hypoxemia and hypercapnia are both factors that are likely to contribute to the
disturbed sleep of such individuals. The worsening of hypoxemia during sleep in
individuals diagnosed with COPD has been documented since the early sixties (Trask
and Cree, 1962). This notion of hypoxemia and hypercapnia contributing to disturbed
sleep is further supported in a study by Fleethan et al (1982) who showed that
individuals exhibited increased arousal frequency during reduced arterial oxygen
saturation when they were breathing room air. This also showed that hypoxemia
alone does not cause sleep arousals but so does hypercapnia. Further evidence
suggests that a change in upper airway resistance during sleep is highest during REM
sleep, during wakefulness, stages 2, 3-4 respectively (Ballard et al, 1995).
QoL
COPD is a progressively debilitating disease. This has been further supported with
the results obtained from the SF-36 QoL sub scales. The symptoms which manifest
in this condition frequently interfere with various aspects of living, such as work,
family roles, socialisation and the general daily activities. The studies mentioned in
part 2 briefly touch upon the consequences of living with such a debilitating
condition. A survey of individuals diagnosed with COPD showed how COPD is
associated with intermittent worsening of symptoms and lung function impairment
(Murray et al, 1997; Celli et al, 2004). Not only do the exacerbations of symptoms
contribute towards mortality and morbidity but also they considerably affect the QoL
experiences by such individuals (Murray et al, 1997; Celli et al, 2004). Another
factor which may explain the poor QoL in such individuals is that the symptoms
associated with COPD, such as breathlessness, wheezing and coughing can have
considerable effects on the physical and emotional and social aspects of a
individual’s life.
General Health Questionnaire-12, Beck Depression Inventory and cognitive
functioning.
In the present study, individuals diagnosed with COPD reported significantly
reduced mental health and greater feelings of depression; individuals also reported
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increased concentration and memory problems, compared to healthy controls. In part
2 it has been stated that factors such as cognitive decline and depression influencing
sleep disturbances and vice versa have not been evaluated in this condition.
It is known that disturbed sleep does lead to poor daytime functioning. Disturbed
sleep can affect daytime activities, have a negative impact on QoL, have a negative
impact on mental health, increase feelings of depression and cause impairment in
cognitive functioning. Again, although age was a factor that was not studied, it is
also important to consider the age factor of these groups of individuals. Generally,
elderly individuals will naturally show a decline in these areas regardless of
matching individuals for age and sex.
In the present study individuals revealed that as their self reported sleep problems
concerning DIMS and other disorders during sleep increased, they reported
experiencing greater problems concerning cognitive functioning.
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Bronchiectasis
Sleep behaviours, sleep disorders and daytime sleepiness
Individuals in this group reported worsened snoring, frequent nightmares and
excessive sleepiness after awakening and during the day. Although there is no
empirical evidence available to support and explain the findings of the present study
but from the studies presented in part 2 of this thesis it can be said that the symptoms
of bronchiectasis (sputum production, wheeziness, breathlessness and recurring chest
infections) can cause nocturnal arousals and can disrupt sleep. Sleep quality maybe
be further reduced, especially if the individual experiences respiratory distress during
stages 1 and 2 and NREM sleep (Ballard et al, 1995). Individuals will often report
feeling unrefreshed and fatigued in the morning and will experience excessive
sleepiness in the morning after awakening. This can be further supported by the
results of the present study whereby the associations revealed that as an individual’s
score on sleep behaviours and problems increased so did their score for excessive
sleepiness on the ESS.
QoL
The QoL reported in the present study was shown to be significantly reduced in
individuals diagnosed with bronchiectasis. Studies investigating QoL in relation to
individuals diagnosed with asthma and COPD have shown the detrimental effects
that disturbed sleep can have on a person’s QoL and how this can affect not only
their physical and mental functioning but also relationships with friends, family and
perhaps colleagues, too. Further analysis of the present data revealed that as the sleep
problems increased so did the individual’s negative perception of their mental health.
Poor QoL can also have a knock on effect on the individual’s mood and memory,
too. Another reason for why these individuals will report poorly on the QoL
assessments is that they feel they do not have any control over their illness and
therefore the disease itself controls the individual and dictates what they can do and
when.
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General Health Questionnaire, Beck Depression Inventory and cognitive functioning
Individuals diagnosed with bronchiectasis showed that their self-reported sleep
problems increased their feelings of depression and caseness for psychiatric
problems increased, too, together with poor cognitive functioning.
Although there is not an individual study to support these facts, there are, however,
particular studies that have researched specific psychological concepts in relation to
respiratory diseases (asthma and COPD) and sleep disturbances. This clearly shows
the lack of research published in this area to try to fully understand how individuals
diagnosed with respiratory diseases cope with their condition on a day-to-day basis
and more importantly how the condition affects their sleep and the psychological
consequences for their daily life.
An important finding from the GHQ-12 showed that 25 % of individuals in this
group diagnosed with bronchiectasis showed caseness for psychiatric problems in the
present study and 20 % of healthy controls. According to the GHQ-12, caseness
detects psychiatric impairment and is relevant to those attending outpatient clinics.
The present study, however, did not examine this concept. The fact that caseness is
present for the other 3 respiratory conditions is evidence that this is not something
that may be present in just those attending an outpatient clinic but perhaps the
disease itself may also manifest these psychiatric problems. Poor cognitive
functioning is often present where disturbed sleep is reported. Poor sleep can usually
have an impact on the cognitive functioning of the individual.
Asbestos related conditions
Sleep behaviour, sleep disorders and daytime sleepiness
The results obtained within this group were interesting and it is important to note the
sample size of the group was small. Individuals diagnosed with asbestosis did not
report any significant sleep problems, sleep disorders and daytime sleepiness,
compared to their healthy counterparts that would suggest that their condition was
perhaps causing these disturbances. The sleep problems that these individuals did
report were that they slept slightly longer, took longer naps and started snoring at a
215
later age compared to their healthy counterparts, which is nothing unusual in this
group specifically in terms of age.
These sleep problems could be age related rather than related to the individual’s
disease. Clinically, most individuals diagnosed with asbestosis are asymptomatic for
at least 20 to 30 years after the initial exposure. Asbestosis has been referred to as a
monosymptomatic disease because of the most distressing symptom, dyspnoea.
Dyspnoea is terrifying to the individual and the attack itself can cause sleep
disturbances and leave the individual feeling excessively sleepy during the day.
QoL
In the present study, individuals had reduced QoL compared to their healthy
counterparts. A number of reasons can be put forward why these individuals reported
poor QoL; firstly, age is a factor, although not explored, which could have had a
significant impact on both the physical and mental elements of the individual SF-36
scales. Socio-economic factors were not analysed in the present study but can also
have an impact on individual QoL. The group of people who were of a retired age
showed that such an impact can cause poorer QoL. The disease itself is an important
factor; dyspnoea itself is a very distressing symptom and may cause the individual to
feel that they are not in control of their symptoms and an attack can occur at anytime.
Asbestosis causes persistent cough and sputum, the cough is usually dry; chest
tightness and pains are not uncommon.
General Health Questionnaire-12, Beck Depression Inventory and cognitive
functioning
Although individuals diagnosed with asbestosis did not report significant differences
in general health compared to healthy controls, 25% of individuals diagnosed with
asbestosis did, however, score above the threshold for the GHQ-12 and had caseness
for psychiatric problems and 12 % healthy controls. These psychiatric problems are
reflected in the BDI scores, whereby significant differences were observed and these
individuals did report greater feelings of depression compared to their healthy
counterparts. Due to the fact that there are no previous data available to explain why
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these individuals experience elevated levels of depression and poor mental health this
may be because living with the disease has a negative impact on the person.
In terms of poor cognitive functioning, this may be due to age related cognitive
decline rather than specific sleep disturbances, which were not observed in this
group. Further analysis of the data in this group revealed no significant associations
between the sleep disorders and behaviours, daytime sleepiness, quality of life,
mental health, depression and cognitive functioning.
4.3 Evaluation of methodology and suggestions for
refinements in further studies
The return rates (70%) of the sample of individuals diagnosed with respiratory
diseases were relatively high and those of the healthy participants recruited into the
study. Individuals and healthy participants were informed of the importance of
returning completed questionnaires, individuals and healthy participants were willing
to participate and return questionnaires, most probably due to the nature of the
research and an opportunity to discuss their sleep problems. This is suggestive of the
fact that those who had problems with their sleep were more likely to respond,
compared to those individuals and participants who felt that they did not have
problems with their sleep. As well, the composition of the samples of the participants
and healthy controls in terms of sex and age allowed direct comparisons of the
different groups.
In terms of questionnaire studies there are a number of limitations in general, mainly
regarding the subjectivity of the data collected and the possibility of bias in the
responses of the participants. In the current study there is no reason to assume that
individuals and participants would be motivated to provide misleading and false
information concerning their sleep, QoL and psychological functioning. The author’s
main concern, however, in terms of responding to the individual items is to the
content of specific questions, particularly concerning mental health and depression.
The results suggest that individuals and healthy participants would not report
misleading information concerning their mental health.
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Another problem concerning a survey design is in the interpretation of some of the
individual items or particular questionnaires. The main concern was possible
vagueness of item wording or ambiguity, regardless of attempts by the original
author of the questionnaire to make it readily understandable and acceptable by those
completing it. This was particularly the case in the interpretation of the BNSQ
questionnaire. There were no specific instructions how to score the individual items
in the questionnaire. This lack posed the problem of whether or not the items on
sleep had been interpreted and scored appropriately. Although individuals who had
participated in the survey had scored highly in some areas of the BNSQ,
nevertheless, in order to further clarify any specific sleep disorders, clinical
evaluation was needed to usefully diagnose sleep disorders.
Within the BSNQ was a free response question for which the participants
(individuals and healthy counterparts) could voice their own personal problems
concerning sleep. The author feels that this information could have been utilised,
perhaps by using qualitative methods of analysis to gain a deeper understanding of
the patient’s perspective.
The data collected from the questionnaires can be viewed to be useful for preliminary
screening purposes only; these data can further lead to a more detailed enquiry
including objectively measuring sleep. This is most certainly the case where
individuals reported disturbed sleep due to SDB and sleep disorders occurring during
the night, e.g., bruxism, nightmares and sleep talking; these need a careful special
investigation to justify a definite diagnosis.
Data was also collected on whether individuals diagnosed with respiratory diseases
had any other co-morbidity. Although there was a specific set of exclusion and
inclusion criteria followed by the researcher, individuals did, however, report having
other disorders and or diseases that may have impacted on their responses to some of
the questionnaires. The data collected resulted from asking whether or not
individuals had any current illnesses or physical disorders or have had such in the
past 3 months and any illness or physical disorder that participants have ever had.
These, when the participants answered ‘yes’, could have been associated with sleep
disturbances and many of the other responses on the assessments concerned with
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mental health, QoL, depression and cognitive functioning. It would be interesting to
evaluate the relative contribution such factors make to the existence of sleep
problems in these individuals. Taking these factors into account, however, in the
detail that some of them would have required would have meant going beyond the
time and the resources available to the author.
Further data on height, weight, BMI, smoking status, ethnicity, education and
occupation was collected. During the systematic review of the literature, it was noted
that there were studies that dealt with some of these factors in relation to respiratory
diseases (asthma and ethnicity, smoking and occupation). It would have been
interesting to see how these factors (occupation and education) contribute towards
the individuals QoL, mental health and depression. Further data was also collected
on whether or not an individual was aware of any family member (mother, father,
sibling, partner, grandparents) who were known to have experienced sleep
disturbances.
The issue concerning the statistical tests used to analyse the data is also important.
Although the findings from the tests of differences and associations appear to be
meaningful it would be interesting to see whether the same pattern of results emerge
with a larger sample of individuals. In addition, some type 1 errors may have
occurred due to the large number of comparisons conducted within the phase 1 data.
Having said this, the majority of the comparisons were significant at the 1% level or
greater.
The findings show the importance of considering individuals sleep, QoL and
psychological well-being as well as acknowledging their clinical diagnosis. It has
been suggested by research that individuals do tend to under-report their disturbed
sleep (Van Keimpema, Ariansz, Nauta and Postmus, 1995). In clinical practice,
administering a simple sleep questionnaire should become routine as part of the
clinical assessment of the patient’s disease. Considering the patient’s sleep problem
will also help in improving the patient’s overall condition.
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4.4 Feasibility
In general, the questionnaires used were shown to have face validity and were
acceptable to the individuals diagnosed with respiratory diseases and the healthy
controls. The questionnaires themselves were initially piloted to confirm that they
were user friendly. One of the main problems, however, that did arise from the study
was that individuals complained about the size of the questionnaire booklet
(appendix 2). Generally the questionnaire was accepted and the author assisted those
individuals who did not wish to complete the questionnaires themselves. Another
problem that did arise, however, was that a minority of the individuals approached in
clinics were illiterate and refused to take part; the author was not aware of this prior
to collecting the data but the matter was discussed and to overcome this problem,
individuals who refused to take part were asked whether they wouldn’t mind
responding while the questionnaire was completed for them but not pressured. Every
effort was made to ensure that no bias from the author found its way into these
dictated responses. Individuals were also offered the opportunity to complete the
questionnaire in their own time but many chose to complete the questionnaire in
clinic and so could ask any questions which may have arisen during the study phase.
It is accepted that as a result of the diverse contexts in which these data were
collected some uncontrolled variations may be present, perhaps having an effect on
which comparisons were found to be significant and which were not.
4.5 Future research
It is expected that in research such as that described in this thesis, which is concerned
with a relatively unexplored field, that many issues will arise which need further
investigation. A number of research possibilities have already been identified and
many more could be suggested regarding sleep disorders in general, and those related
to disturbed sleep in individuals diagnosed with respiratory diseases.
Basic topics which need to be investigated by specialist respiratory clinicians
include:
•
What is the range of sleep disorders in respiratory disease? What are their
effects on the management of individuals diagnosed with respiratory
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diseases? Tests of associations showed that individuals diagnosed with
respiratory diseases complained of increased excessive daytime sleepiness as
their sleep problems during the night and during the day worsened. How can
excessive daytime sleepiness be diagnosed and monitored in such
individuals?
•
How can clinicians ensure that the individual’s disturbed sleep is not due to
their disease but a factor that has been present prior to the onset of the
disease?
•
Can certain treatments have negative consequences on the individual’s
quality of sleep?
•
Sleep studies to monitor when respiratory attacks occur and how these impact
the individuals day-to-day functioning. How can these nocturnal attacks be
managed? Are there any triggers which cause these attacks?
•
How do the individual’s diseases impact their mental health, QoL, feelings of
anxiety and depression and cognitive functioning? Are there specific tests
which can be performed to gauge what the individual has scored before and
after treatment?
Other topics for research of a non-respiratory nature include:
•
The QoL of individuals diagnosed with respiratory disease using
qualitative methods to gain a deeper understanding of how the disease
impacts them as an individual.
•
Age related comparative studies of individuals diagnosed with asbestosis
and other respiratory diseases to understand the normal age related
cognitive decline, sleep decline and physical functioning decline in
comparison to those diagnosed with asbestosis.
•
To further explore the impact of living with asbestosis and bronchiectasis
and use both objective and subjective methods to explore sleep quality.
221
•
To further explore variables related to depression and the disease and
whether these impact sleep quality.
•
Whether or not ethnicity, occupation and education are associated with
specific sleep behaviours and problems and the impact on the
psychological functioning of specific respiratory groups.
Some of the suggestions made would require the expertise of both a respiratory
physician and psychologist with a special interest in sleep medicine to work together.
Assessments of the severity of the sleep problems in general and also treatment
evaluations have to take into account cognitive and behavioural aspects (not just
physical considerations) because they are what matter most to the individual’s wellbeing. Skills relating to psychological functioning are essential in preventative and
treatment programmes for the sleep disorders which are not physical in origin and
also in aspects of management of those which are, these being counselling and being
able to manage anxiety in such individuals. The present findings confirm the high
levels of anxiety felt by such individuals. It is also important to state that the standard
measures of lung function do not necessarily relate to the severity of psychological
functioning.
The psychologist’s role is also particularly important in the investigation of the
relationship between sleep disturbances and physical functioning. One of the basic
problems with certain sleep problems is whether sleep disturbances cause daytime
problems or whether the sleep problem is caused by behaviour that is already
disturbed. When the sleep problem is behavioural in nature this issue may be settled
by careful developmental studies of the sequence of events by treating one problem
to see the effect it has on another.
It is important to take note of these possibilities and to understand that the present
study has only scratched the surface and highlighted the importance of understanding
and acknowledging that individuals diagnosed with respiratory diseases do have
disturbed sleep in many of the areas highlighted by the BNSQ. Disturbed sleep is
also very detrimental to the individual’s psychological well-being, in particular their
general health, mood, QoL and cognitive functioning. Future research needs to
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include objective measures to further explore the disturbed sleep patterns of such
individuals and to collect normative data which would be highly useful in exploring
these factors and how they may affect the individuals sleep and psychological
functioning.
************************************
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224
Acknowledgement of the limitations in both the literature review and methodology.
Limitations in the literature review
A more thorough search of the literature may have identified additional relevant
research. Additional strategies which could have been used include: searching
additional databases, using additional search terms including additional Mesh and
Thesaurus terms, and searching for grey literature by contacting experts. Further
attempts at refining the search strategy as the literature search progressed would have
helped identify all relevant studies. In addition, further assessment of the quality of
the articles selected for the literature review could have been more rigorous including
utilisation of the Critical Appraisal Skills Programme (CASP) checklists. This
combined with more rigorous use of inclusion and exclusion criteria of studies would
have been useful in producing a higher quality review of the literature.
Limitations in the methodology
General strengths and weaknesses of the questionnaire method will be discussed first
and then strengths and weaknesses of the specific questionnaires used in the present
study.
Advantages of using a questionnaire method
•
Responses are gathered in a standard way, so questionnaires are more
objective, certainly more so than interviews. A study information sheet was
provided to the participants with the questionnaire so that they understood
what was expected of them.
•
Generally it is relatively quick to collect information using a questionnaire.
However, in some situations they can take a long time not only to design but
also to apply and analyse (Biemer & Lars, 2003).
•
Potentially information can be collected from a relatively large sample. This
potential is not often realised, as returns from questionnaires are usually low,
(Biemer & Lars, 2003). However return rates can be dramatically improved if
the questionnaire is delivered and responded to perhaps with stamped
addressed envelopes, (Biemer & Lars, 2003).
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Disadvantages of using a questionnaire method
•
Questionnaires are usually used to obtain information retrospectively, so are
dependent on accurate recall by participants. The Basic Nordic Sleep
Questionnaire, Epworth Sleepiness Scale, General Health Questionnaire-12,
The Short form-36, Beck Depression Inventory and the 2 items from the
Jennum and Sjol study all required the participants to recall information about
their sleep, health, and quality of life, mood and memory over a certain
period of time. Along with this, most of the participants were elderly too and
studies have shown that there is generally a cognitive decline in the elderly
which may affect the recall of items in the questionnaire, (Fowler & Cannell,
1996).
•
Questionnaires are standardised so it is not possible to explain any points in
the questions that participants might misinterpret. This could be partially
solved by piloting the questionnaire with the particular group of participants
recruited for the study. For the present study the questionnaire was initially
piloted with a group of 60 participants from Portsmouth Hospitals NHS Trust
to ensure that the questionnaire itself was adequate to administer in such a
population.
•
Open-ended questions can generate large amounts of data that can take a long
time to process and analyse. One way of limiting this could be to limit the
space available to participants so their responses are concise or to sample the
participants and survey only a portion of them. In the present study
participants generally ticked boxes and had the opportunity to speak of their
concerns regarding their sleep for just one question.
•
Respondents may not be willing to answer the questions. They might not
wish to reveal the information or they might think that they will not benefit
from responding perhaps even be penalised by giving their real opinion.
Participants should be told why the information is being collected and how
the results will be beneficial. Those participants who did participate in the
present study did complete the questionnaire fully and were more than happy
to discuss their problems during clinic times with the primary researcher.
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Specific questionnaires used in the present study
Sleep related questionnaires:
In the present study the Basic Nordic Sleep Questionnaire (BNSQ) was used to
collect data on sleep from the participants. This questionnaire is designed to question
the participants sleeping habits and disorders for the past three months. It is a selfadministered questionnaire and has been used widely in a variety of studies
performed in Nordic countries during the last several years and has proved to be a
valid tool (Partinen & Gislason, 1995). However, although the BNSQ has served as a
basis in many epidemiological studies performed in the Nordic and other countries,
one of the disadvantages of using the BNSQ is that it questions the participants
sleeping habits over the last 3 months which could be considered to be a relatively
long recall period.
The Pittsburgh Sleep Quality Index (PSQI) may have been a more appropriate choice
of sleep questionnaire. The PSQI is also a self-rated questionnaire but assesses the
participant’s sleep over the last month rather than 3 months in the base of the BNSQ.
The BNSQ assess four main areas of sleep (dysomnias, parasomnias,
medical/psychiatric and proposed sleep disorders) and gives an overall score where
as the PSQI generates seven component scores (sleep quality, sleep latency, sleep
duration, habitual sleep efficiency, sleep disturbances, use of sleep medication and
daytime function) and the seven components yield one global score.
Other questionnaires:
In the current study the author did not select a disease specific questionnaire to
measure the severity of respiratory diseases. Perhaps, in hindsight this would have
been an appropriate addition to understand the severity of the diseases of
participants. However, it was important not to overburden participants with too many
questionnaires.
A useful additional questionnaire to assess the severity of symptoms in participants
living with a respiratory disease specifically asthma, COPD, bronchiectasis and
asbestosis and related illnesses would have been the St George’s Respiratory
227
Questionnaire (Jones, Quirk & Baveystock, 1991). The questionnaire is designed to
cover the participant’s recollection of their symptoms over a preceding period that
may range from one month to one year. It is not designed to be an accurate
epidemiological tool; its purpose is to assess that participant’s perception of their
recent respiratory problems. It also addresses the participant’s current state. The
usefulness of collecting this data would have meant a greater insight into how the
individual copes with their condition and how it directly affects their sleep, QoL,
mood and memory.
In the current study the Beck Depression Inventory (BDI) and the General Health
Questionnaire (GHQ) have been used to collect data relating to mood. A more
suitable alternative to these two questionnaires could have been the Hospital Anxiety
and Depression scale (HADS) developed by Zigmond and Snaith (1983). The HADS
may have been better suited because it is a reliable instrument for screening for
clinically significant anxiety and depression in participants attending a general
medical clinic, therefore the researchers would have had a better understanding of
whether anxiety and depression was due to the lack of sleep, coping with the
condition or generally having to attend regular clinic appointments concerning their
condition as the HADS would have highlighted this. The HADS has also been shown
to be a valid measure of the severity of these disorders of mood. In comparison the
BDI measures the behavioural manifestations of depression but some of the
questions in the BDI maybe viewed as inappropriate in an already anxious and
depressed population because there are questions which are sensitive and may cause
participants to alter their responses. The GHQ is also designed to detect psychiatric
disorders among participants in community settings and non-psychiatric clinical
settings such as primary care or among general medical outpatients. In the present
study participants were recruited from an outpatient’s clinic and with no psychiatric
illnesses.
A further change could be implemented by replacing the two cognitive items by
Jennum and Sjol with the Cognitive Failures Questionnaire (CFQ) developed by
Broadbent, Cooper, Fitzgerald and Parkes, (1982). This is a self-reported assessment
designed to measure failures in perception, memory and motor function. The
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questions are based on the participant’s experiences in the last six months. In
comparison to the two items from the Jennum and Sjol study that were used to
collect data on memory and concentration in the present study the CFQ has 25
individual items and provides a more comprehensive picture.
Further points to consider in this section is that firstly the author acknowledges the
limitations of the questionnaire studies, specific aspects to consider are subjectivity
of interpreting the items and scoring items, researcher bias when administering the
questionnaire. The current questionnaires used to collect the data in the present study
had varying time periods to which collect the data from, for example the BNSQ is
designed to question the patients sleeping habits and disorders for the past three
months. Both the SF-36 and GHQ is used to question the QoL of patients over the
last 4 weeks. It is important for all the questionnaires to have the same time period
for which the data needs to be collected.
Alternative methods to implement into a future study.
A further method which would have been useful to incorporate into the study if there
had been funding made available during the project was the actigraph. The actigraph
could have been deployed as a tool for investigating whether participants who
reported disturbed sleep through the BNSQ were also shown to have disturbed sleep
using an objective measure. It is a non-invasive method of monitoring human
rest/activity cycles and is worn in the shape of a watch on the wrist of the nondominant arm.
Actigraph are useful in determining sleep patterns and circadian rhythms; they can
also be worn for weeks at a time. There are several factors that would need to be
considered when using an actigraph in a study, these being the element of cost, the
type of device to be used with the study population, for example the size and weight
of the device, durability and water resistance, the flexibility of the device, for
example the sleep parameters measured, the features of the device and validating the
device in the prospective study population. As there was also a relatively large
sample recruited across the four respiratory groups, this would be very costly too.
229
A sleep diary would also be needed to ensure that the actigraph data corresponds to
the diary times and vice versa. These tests are useful for measuring and assessing
daytime sleepiness in situations where a laboratory or a sleep latency test is not
appropriate. The actigraphs can be used to clinically evaluate insomnia, circadian
rhythm sleep disorders and excessive sleepiness and restless legs syndrome. Adding
a sleep diary would have provided further data on the individuals sleep and this could
have been used to closely
analyse the BNSQ and see whether the individuals
comments in their sleep diary match up to those in the BNSQ.
Actigraphy has not been traditionally used in routine diagnosis of sleep disorders but
is increasingly being used in sleep clinics to replace full polysomnograpghy. There
are limitations for using the actigraph such as battery usage, the weight of the unit
and water resistance qualities. The advantages being that it has watch like
functionalities so that the device is more attractive to the user, user input so the
wearer is in control of the device. Some of the individuals within the present study
may not have consented to using an actigraph as they would have felt it is something
else that they need to consider on top of managing their condition.
230
The following table highlights the advantages and disadvantages of the questionnaire
method versus the actigraph.
Table 1: The advantages and disadvantages of the questionnaire method versus the
actigraph.
Actigraph
Questionnaire method
Advantages
Accurate indicator of physical activity
Standardised therefore objective
Low burden in the participant
Quick to collect data
Non-invasive technique
Can collect large amounts of data
Provides feedback
Easy to administer
Less reactivity – influence behaviour
Disadvantages
Moderate cost.
Participants may forget important events
Difficult to assess large samples.
Due to standardisation-not possible to explain any
Water activities and static activities may be a
problem to engage in.
points to participants.
Open ended questions can generate large volumes
Non-criteria for what equations and/or cut off
of data.
points to use.
Lengthy time to code, analyse data.
Worn for at least 10-14 hours per day.
Superficial answers.
Charge and download data.
Responder bias.
Another important factor to consider is the sample size of the current study. The
author acknowledges the small sample size within the bronchiectasis and asbestosis
and related conditions group in the present study. Collecting larger sample sizes may
have yielded different results and therefore different interpretations of the data.
231
Larger sample sizes may have provided more reliable findings within the clinical
population.
Furthermore, the following factors could have been incorporated into the study;
•
Analysis between groups with respiratory diseases could have been built into
the design of the study
•
Predictions into the direction of results could have been made in places
•
Discussion of alternative scoring methods of some questionnaires
•
Possible type 1 errors and correcting for multiple comparisons.
2. Explicit synthesis of her results in the discussion and within the wider
literature
Sleep
Generally individuals diagnosed with respiratory diseases specifically asthma, COPD
and bronchiectasis reported greater problems associated with sleep in comparison to
their healthy counterparts.
All four respiratory groups also reported excessive daytime sleepiness in comparison
to their healthy counterparts.
Psychological functioning
All four respiratory disease groups (asthma, COPD, bronchiectasis and asbestosis
and related illnesses) reported to have poorer psychological functioning across all the
psychological assessments (SF-36, GHQ-12, BDI and the two cognitive items) thus
reporting lower QoL scores, lower mood and poorer self reported memory and
concentration compared to their healthy controls.
Associations between sleep and psychological functioning
Generally significant associations were found between sleep disorders and measures
of psychological functions. Individuals diagnosed with asthma, COPD and
bronchiectasis reported to have significant associations between sleep disorders and
behaviours, daytime sleepiness, QoL, mental health, depression and cognitive
232
functioning. No significant associations were observed with individuals diagnosed
with asbestosis and related illnesses between sleep disorders and daytime behaviour
problems. One of the explanations for this is that the sample size for this particular
group was relatively small compared to the other three respiratory disease groups.
In summary, the present study supports the literature presented in this thesis
highlighting the fact that those individuals diagnosed with respiratory diseases
especially asthma, COPD and bronchiectasis are more likely to suffer from sleep
disturbances and poor psychological functioning compared to their healthy
counterparts. The studies presented within the literature review were limited as the
author could only find those which represented asthma and COPD, however they do
provide a great insight into how individuals living with such conditions may have
poor sleep and how this can affect them the individual on a clinical basis but also
from a psychological process in terms of poor QoL, poor general health, low mood
and generally poor cognitive functioning. The studies in the literature review also
provided greater insight into the various methods that have been used to collect such
data in such a clinical sample population and draws upon the various methods that
have been used to collect data. The current study plays an important part in bridging
the gap between studies which focus upon the clinical aspects of living with a
respiratory diseases and the consequences that this may have on the individuals sleep
whereas the present study focuses upon these factors too but from a subjective point
of view.
So how does the present study help in terms of clinical care?
The findings from the present study highlight several factors these being: the need
for further research; the need for further management of symptoms in acute and
chronic conditions, the need for a screening tool to measure whether individuals with
a specific diagnosis especially respiratory diseases have disturbed sleep; the need for
further training of medical and allied health care staff in managing such conditions;
wide use of referring individuals to specialists sleep clinics; understanding the
individuals subjective needs as well as clinical needs, for example the implications of
being diagnosed with a specific disorder and how this can affect a person’s day-today functioning especially adhering and complying to medication usage and
233
understanding of their diagnosis. The implications of the findings from the present
study will be discussed in the next section.
3. Clear conclusions showing how they are directly informed by the results
In conclusion, in general, individuals diagnosed with respiratory diseases showed a
significantly greater number of sleep problems then their matched controls from the
general population.
From a psychological perspective individuals diagnosed with respiratory diseases
across all four groups reported greater reduced psychological functioning (QoL,
mental health, mood and cognitive function) compared to their healthy controls.
Significant associations between sleep disorders/behaviours and psychological
functioning were found in individuals diagnosed with asthma, COPD and
bronchiectasis but no significant association were found in the group diagnosed with
asbestosis and related illnesses.
Implications of findings:
The need for further study
It is important to further investigate this area as highlighted in the thesis. There are
factors which have not been considered which have been mentioned earlier, for
example collecting further lifestyle factors to include in the analysis and to ensure
that previous episodes of clinical sleep disturbances are also noted. Addition of
different disease specific questionnaires can also be included to measure the severity
of the disease.
The need for further management of symptoms in acute and chronic conditions
It is important for clinicians and allied health care staff to be able to manage the
individuals condition. This is not only from a clinical perspective for example
monitoring the individuals diagnosis and prognosis but, also from a subjective
perspective for example, understanding what the individual must be going through
outside of the clinical setting and how the diagnosis is affecting their psychological
well-being. Both Clinical staff and allied health care staff should be able to offer
234
advice and a suitable referral should the need arise to visit a health psychologist who
has been trained to work with individuals living with acute and chronic conditions.
The need for a screening tool to measure whether individuals with specific diagnosis
especially respiratory diseases have disturbed sleep.
The present study has highlighted the need for a tool within clinical practice to
measure an individual’s sleep regardless of their condition to screen for any sleep
problems. Within respiratory medicine, most patients who may have OSA are usually
given the ESS which is quick and easy to administer and score by the clinician to use
within the diagnosis process. The author believes that a sleep specific test regardless
of the patient’s condition should be incorporated into clinical practice so that not
only the individual’s condition is managed but also their sleep disturbances too from
the onset.
The need for further training of medical and allied health care staff in managing
such conditions.
Generally within the UK, respiratory medicine is the only branch of medicine which
considers sleep medicine as a sub speciality and it is only emerging as an important
branch in recent years. Various authors generally from a psychological background
have conducted research highlighting the need for further training and understanding
the importance of sleep generally as well as in the disease process.
Referral of individuals to specialist sleep clinics.
Sleep clinics within the UK have been relatively rare until recent times but are
slowly emerging in both private and clinical settings. General Practitioners who now
see individuals with suspected sleep problems can be referred on to specialists either
privately or through the National Health Service by their General Practitioner.
It is also important to ensure correct diagnosis of the individual’s condition and have
suitable treatments set in place and then to see if the individual is still reporting
disturbed sleep.
235
Understanding the individual’s subjective needs such as psychological well-being,
quality of life, mood and memory as well as clinical needs such as managing and
treating the diagnosis.
The present study has highlighted the importance of understanding the individual’s
subjective needs which are considered to be of importance to the individual as well
as the clinical needs of their respiratory condition. The individual should be able to
inform their clinician or allied health care staff of their psychological well-being and
how they are coping with their condition and the affects that their condition is having
on their well-being in general.
The implications of being diagnosed with a specific disorder, how this can affect a
person’s day-to-day functioning especially adhering and complying to medication
usage and understanding of their diagnosis.
The present study has highlighted the fact that poor sleep, excessive daytime
sleepiness, may be associated to the individuals QoL which results in poor QoL, poor
general health, anxiety and low mood which affects the individual’s memory and
concentration. These factors can also affect the way in which the individual copes
with their condition, for example the individual may not be able to recall how to
manage their symptoms if a respiratory attack was to occur, how to take their
medication because they were too tired to understand and listen.
Furthermore those individuals with psychological problems will need specialist care
to be able to manage their psychological symptoms appropriately. It is important to
note that further research is highly recommended to develop this area of research
fully to gain a better understanding.
236
References
Ciba Foundation Guest Symposium. (1959). Terminology, definitions and classifications of chronic
pulmonary emphysema and related conditions. Thorax, 14, 286-299.
American Thoracic Society: Chronic bronchitis, asthma and pulmonary emphysema. (1962). A
statement by the committee on diagnostic standards for nontuberculosis respiratory diseases. Am Rev
Respir Dis, 85, 762-768.
Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2005). Global strategy for the
diagnosis, management, and prevention of chronic obstructive lung disease: Executive summary 2005.
www.goldcopd.com (Accessed on April 20th, 2007).
Aaron T. Beck, Robert A. Steer and Gregory K. Brown. (1996). BDI-II Beck Depression Inventory
Manual. San Antonio, The Psychological Corporation.
Adams, R. J, Smith, B.J, & Ruffin, R.E. (2000). Factors associated with hospital admissions and
repeat emergency department visits for adults with asthma. Thorax, 55, 566-573.
Adams, R. J, Wilson, D.H, Taylor, A.W, Daly, A, Tursan d'Espaignet, E, Dal Grande, E, & Ruffin,
R.E. (2004). Psychological factors and asthma quality of life: a population based study. Thorax, 59,
930-935.
Adams, S, Pill, R, & Jones, A. (1997). Medication, chronic illness and identity: the perspective of
people with asthma. Soc Sci Med, 45, 189-201.
Agnew, H. W. J, Webb, W.B, & Williams, R.L. (1967). Comparison of stage 4 and 1-REM sleep
deprivation. Percept Mot Skills, 24, 851-858.
Akerstedt, T. a. T, L. (1985). Napping in Shift Work. Sleep, 8, 105-109.
Alliance, S. (2004). Sleep SOS Report.
Anch, A. M, Browman, C.P, Mitler, M.M, & Walsh, J.K. (1988). Sleep: A Scientific Perspective
Englewood Cliffs, New Jersey, Prentice Hall.
Anderson, K. (1995). The effect of chronic obstructive pulmonary disease on quality of life. Research
in Nursing & Health, 18, 547-556.
Anthonisen, N. R, Wright, E, & Group, I.T. (1986). Bronchodilator response in COPD. Am Rev Respir
Dis, 133, 814-819.
Archea, C, Yen, I.H, Chen, H, Eisner, M.D, Katz, P.P, Masharani, U, Yelin, E.H, Earnest, G, &
Blanc, P.D. (2006). Negative life events and quality of life in adults with asthma. Thorax, 62, 139146.
American Thoracic society/American Sleep Disorders Association (1998). Statement on health
outcomes research in sleep apnea. Am J Respir Crit Care Med, 157, 335-341.
Avidan, A. Y, & Zee, P.C. (2006). Handbook of sleep medicine. Philadelphia, Lippincott Williams &
Wilkins.
Baiardini, I, Braido, F, Cauglia, S, and Canonica, G.W. (2006). Sleep disturbances in allergic diseases.
Allergy, 6, 1259-1267.
Baillie, M. (1799). A series of Engravings, Accompanied with Explanations Which are Intended to
Illustrate the Morbid Anatomy of Some of the most Important Parts of the Human Body, Divided into
10 Fasciculi. London, W. Bulmer and Co.
237
Baillie, M. (1808). The Morbid Anatomy of Some of the Most Important Parts of the Human Body.
Brattleborough, W. Fessenden.
Ballard, R. D, Wyant, C.C, & Suh, B.Y. (1995). Influence of sleep on respiratory function in
emphysema. Am J Respir Crit Car Med, 151, 945-951.
Banarjee, D. K, Lee, G.S, & Malik, S.K. (1987). Underdiagnosis of asthma in the elderly. Br J Dis
Chest, 81, 23-29.
Barsky, A. J, & Wyshak, G. (1990). Hypochondriasis and somatosensory amplification. British
Journal of Psychiatry, 157, 404-409.
Barstow, R. (1974). Coping with emphysema. Nursing Clinics of North America, 9(1), 137-145.
Bass, C, & Gardner, W.N, (1985). Emotional influences on breathing and breathlessness. J.
Psychosom Res, 29, 599-609.
Bass, C, & Gardner, W.N, (1985). Respiratory and psychiatric abnormalities in chronic symptomatic
hyperventilation. BMJ, 290: 1387-1390.
Baum, G. L, & Wolinsky, E. (1983). Textbook of pulmonary medicine. Boston, Little Brown.
Beck, A. T, Ward, C.H, Mendelson, M, Mock, J, and Erbaugh, J. (1961). An Inventory for Measuring
Depression. Archives of General Psychiatry, 4, 561-571.
Beck, C, Heiner, DC. (1981). Selective immunoglobin G4 deficiency and recurrent infections of the
respiratory tract. Am Rev Respir Dis, 124, 94-96.
Becker, H. F, Piper, A.J, & Flynn, W.E. (1999). Breathing during sleep in patients with nocturnal
desaturation. Am J Med, 159, 112-118.
Becklake, M. R. (1976). Asbestos-related diseaes of the lung and other organs: their epidemiology and
implications for clinical practice. Am Rev Respir Dis, 114, 187-227.
Becklake, M. R. (1989). Occupational exposures: Evidence for a causal association with COPD. . Am
Rev Respir Dis, 140, (Supplement): S85-S89.
Becklake, M. R. (1991). Asbestos and other fiber-related diseases of the lungs and pleura:
Distributions and determinants in exposed populations. Chest, 100, 248-254.
Becklake, M. R. (1991). Asbestosis. Mineral Fibers and Health. D. Liddell, & Miller, K. Boca Raton:
CRC Press.
Bellia, V, Catalano, F, & Scichilone, N. (2003). Sleep disorders in the elderly with and without
chronic airflow obstruction SARA study. Sleep, 26, 318-323.
Benatar, S. R. (1986). Medical Progress: fatal asthma. N Engl J Med, 314, 423-429.
Bentley, E. (1999). Awareness: Biorhythms, Sleep & Dreaming, Routledge.
Beutler, L. E, Ware, C, Karacan, I, & Thornby, J.I. (1981). Differentiating psychological
characteristics of patients with sleep apnea and narcolepsy. Sleep, 4(1), 39-47.
Biemer, P. & Lyberg, G. (2003). Introduction to Survey Quality. Wiley Inter science.
Bjorntop, P. (1998). Obesity: a chronic disease with alarming prevalence and consequences. J. Intern
Med, 244, 267-269.
Blazer, D. G, Hays, J.C, & Fillenbaum, G.G. (1997). Memory complaints as a predictor of cognitive
decline: A comparison of African American and White elders. . J Aging Health, 9, 171-184.
238
Bonnet, M. H. (1986). Performance and sleepiness as a function of frequency and placement of sleep
disruption. Psychophysiology, 23, 263-271.
Bonnet, M. H. (1993). Cognitive effects of sleep and sleep apnea. Sleep, 16, S68-S70.
Bonnet, M. H, & Arand, D.I. (1995). 24-Hour metabolic rate in insomniacs and matched normal
sleepers. Sleep, 19, 581-588.
Bonnet, M. H. (2005). Sleep fragmentation. Sleep deprivation: Basic science, Physiology, and
Behvaiour. C. A. Kushida. New York, Marcel Dekker. 192 Lung Biology in Health and Disease.: 103120.
Bonnet, M. H. A, D.L. (2003). Clinical effects of sleep fragmentation versus sleep deprivation. Sleep
Med Rev, 7, 297-310.
Brewis, R. A. L, Ed. (1990). Classic papers in asthma volume one. London, Science Press Limited.
Brezinova, V, Catterall, J.R, Douglas, N.J, & Flenley, D.C. (1982). Night sleep of patients with
chronic ventilatory failure and age matched controls: number and duration of the EEG episodes of
intervening wakefulness and drowsiness. Sleep, 5, 123-130.
Broadbent, D.E., Cooper, P.F., FitzGerald, P., & Parkes, K.R. (1982). The Cognitive Failures
Questionnaire (CFQ) and its correlates. British Journal of Clinical Psychology, 21, 1–16.
Brown, J, Rawlinson, M, & Hilles, N. (1981). Life satisfaction and chronic disease: Exploration of a
theoretical model. Medical Care, 39, 1136-1146.
Buist, A, Ducic, S. (1978). Smoking. Evaluation of studies which have demonstrated pulmonary
function changes. The Lung in Transition Between Health and Disease. M. P. P. S. New York, Marcel
Dekker: 271-286.
Burney, P. (1988). Why study the epidemiology of asthma? Thorax, 43, 425-428.
Burney, P. (1993). Epidemiology of asthma. Allergy, 48, 17-21.
Burney, P. G. L, Luczynska, C.M, Chinn, S, & Jarvis, D. (1994). The European Community
Respiratory Health Survey. Eur Respir J, 7, 954-960.
Burr, M. L, Charles, T.J, Roy, K, & Seaton, A. (1979). Asthma in the elderly: an epidemiological
survey. BMJ, 1, 1041-1044.
Burrows, B, Lebowitz, M.D, Camilli, A.E, & Knudson, R.J, (1986). Longitudinal changes in forced
expiratory volume in one second in adults: methodologic considerations and findings in healthy
nonsmokers. Am Rev Respir Dis, 133, 974-980.
Burrows, B, Bloom, JW, Traver, GA et al (1987). The course and prognosis of different forma of
chronic airways obstruction in a sample from the general population. N Engl J Med, (317), 1309-1314.
Burrows, B, Martinez, F.D, Halonen, M, Barbee, R.A, & Cline, M.G. (1989). Association of asthma
with scrum IgE levels and skin-test reactivity to allergens. N Engl J Med, 320, 271-277.
Burrows, B, Barbee, R.A, Cline, M.G, & Knudson, R.J. (1991). Characteristics of asthma among
elderly adults in a sample of the general population. Ches,t 100, 935-942.
Burt, V. L, & Harris, T. (1994). The third national healthand nutrition examination survey:
contributing data on aging and health. Gerontologist, 34, 486-490.
Buysse, D. J, Reynolds, C.F, Monk, T.F, Berman, S.R, & Kupfer, D.J. (1989). The Pittsburgh Sleep
Quality Index (PSQI): A new instrument for psychiatric research and practice. Psychiatry Research,
28(2), 193-213.
239
Calverley, P. M. A, Brezinova, V, Douglas, N.J, Catterall, J.R, & Flenley, D.C. (1982). The effect of
oxygenation on sleep quality, bronchitis and emphysema. Am Rev Respir Dis, 126, 206-210.
Calverley, P. M. A, MacNee, W, Pride, N.B. & Rennard, S.I. (2003). Chronic Obstructive Pulmonary
Disease. London, Arnold.
Carskadon, M. A, & Brown, E.D, & Dement, W,C. (1982). Sleep fragmentation in the elderly:
relationship to daytime sleep tendency. Neurobiol Aging, 3, 321-327.
Caterall, J. R, Calverley, P. M. A, Brezinova, V. (1982). Irregular breathing and hypoxemia during
sleep in chronic stable asthma. Lancet, 1, 301-304.
Caterall, J. R, Calverley, P. M. A, Brezinova, V. (1982). Irregular breathing and hypoxemia during
sleep in chronic stable asthma. Lancet, 88, 425-434.
Celli, B. R, & MacNee, W. and committee members. (2004). Standards for the diagnosis and
treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J, 23, 932946.
Chalmers, K. (1984). A closer look at how people cope with chronic airflow obstruction. Canadian
Nurse, 80, 35-38.
Cheshire, K, Engleman, H, & Deary, I. (1992). Factors impairing daytime performance in patients
with sleep apnea/hypopnea syndrome. Arch Intern Med, 152, 538-541.
Chetta, A, Gerra, G, & Foresi, A. (1998). Personality profiles and breathlessness perception in
outpatients with different gradings of asthma. . Am J Respir Crit Car Med, 157, 116-122.
Chodosh, S. (1985). Why, when, how and by whom. Current topics in the management of respiratory
diseases. J. S. Brody, & Snider, G.L. New York, Churchill Livingston.
Churchill, C. M, & Dilsalver, S.C. (1990). Partial sleep deprivation to prevent 48-hour mood cycles.
Acta Psychiatr Scand, 81(4), 398-399.
Churg, A, & Green, F.H.Y. (1998). Pathology of occupational lung disease. Baltimore, Williams &
Wilkins.
Cohen, J. (1988). Statistical power analysis for the behavioural sciences New Jersey, Erlbaum.
Coleman, R. M. (1983). Diagnosis, treatment and follow-up of about 8,000 sleep-wake disorder
patients. In C. Guilleminault & E. Lugaresi (Eds.), Sleep-Wake Disorders: Natural History,
Epidemiology, and Long-Term Evolution. New York, Raven.
Colt, H. G, Haas, H, & Rich, G.B. (1991). Hypoxemia Vs. sleep fragmentation as cause of excesive
daytime sleepiness in obstructive sleep apnea. Chest, 100, 1542-1548.
Connor, J, Norton, R, Ameratunga, S, Robinson, E, Civil, I, and Dunn, R. (2002). Driver sleepiness
and risk of serious injury to car occupants: population based case control study. BMJ, 324, 1125.
Coolican, H. (2004). Research Methods and Statistics in Psychology. Oxon, Hodder & Stoughton.
Cooper, A, Ryland, I, & Davies, L. (1997). Anxiety and depression among chronic severe asthmatics.
Eur Respir J, 10(25), 1274.
Cormick, W, Olson, L.G, Hensley, M.J, & Saunders, N.A. (1986). Nocturnal hypoxaemia and quality
of sleep in patients with chronic obstructive lung disease. Thorax, 41, 846-854.
Cosio, M, Ghezzo, H, Hogg JC. (1978). The relations between structural changes in small airways and
pulmonary function tests. N Engl J Med, 298, 1277-1281.
240
Cotton, D. J, Graham, B.C, Li, K.Y.R, Froh, F, Barnet, G.D, & Dosman, J.A. (1983). Effects of grain
dust exposure and smoking on respiratory symptoms and lung function. J Occup Med, 25, 135-140.
Craighead, J. E, Abraham, J.L. & Churg, A. (1982). The pathology of asbestos assocuated diseases of
the lungs and pleural cavities: Diagnostic criteria and proposed grading schema. Arch Pathol Lab
Med, 106, 544-596.
Crockett, A. (1998). Elm Tree Surgery survey 1998. . Respiratory College pre-BTS meeting.
D.E. Broadbent, P. F. C, P. Fitzgerald and K.R. Parkes (1982). The Cognitive Failures Questionnaire
(CFQ) and its correlates. British Journal of Cognitive Psychology, 21, 1-16.
Dales, R. E, Spitzer, W.O, Schechter, M.T, & Suissa, S. (1989). The influence of psychological status
on respiratory symptom reporting. Am Rev Respir Dis, 139, 1459-1463.
D'Ambrosio, C, Bowman, T, & Mohsenin, V. (1999). Quality of life in patients with obstructive sleep
apnea: effect of nasal continuous positive airway pressure-a prospective study. Chest, 115, 123-129.
Daniel J. Buysse, C. F. R. I, Timothy H. Monk, Susan R. Berman and David J. Kupfer (1989). The
Pittsburgh Sleep Quality Index: A New Instrument for Psychiatric Practice and Research. Psychiatry
Research, 28, 193-213.
David Moher, K. F. S. a. D. G. A. (2001). The CONSORT statement: revised recommendations for
improving the quality of reports of parallel group randomized trials. BMC Medical Research
Methodology, 1(2),
Dinges, D. F, Pack, F, Williams, K, Gillen, K.A, Powell, J.W, and Ott, G.E. (1997). Cumulative
sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of
sleep restricted to 4-5 hours per night. Sleep, 20, 267.
Dirks, J. F, & Kinsman, R.A, Staudenmayer, H, Kleiger, J.H. (1973). Panic-fear in asthma: a
symptomatology as an index of signal anxiety and personality as an index of ego resources. Journal of
Nervous and Mental Disease. 167, 615-619.
Dirks, J. F, & Kinsman, R.A. (1982). Bayesian prediction of noncompliance : as-needed (PRN)
medication usage patterns and the battery of asthma illness behaviour. Journal of Asthma 19: 25-31.
Douglas, N. (1998). Sleep in patients with chronic obstructive pulmonary disease. Clin Chest Med, 19,
115-126.
Douglas, N. J. (1983). Nocturnal hypoxemia in patients with chronic obstructive pulmonary disease.
Clin Chest Med, 13, 523-532.
Douglas, N. J. (1985). Asthma at night. Clin Chest Med, 6, 663-674.
Douglas, N. J. (1994). Breathing during sleep in patients with chronic obstructive pulmonary disease. .
Philadelphia, WB Saunders.
Dow, L. (1994). The diagnosis of asthma in older people. Clin Exp Allergy Review, 24, 156-159.
Ellis, B. W, Johns, M.W. & Lancaster, R. (1981). The St Mary's Hospital Sleep Questionnaire: A
study of reliability. Sleep, 4, 93-97.
Empson, J. (1993). Sleep and Dreaming. Hemel Hempstead, Harvester Wheatsheaf.
Empson, J. (2001). Sleep and Dreaming. Hemel Hempstead, Harvester Wheatsheaf.
Engleman, H. M, and Douglas, N.J. (2004). Sleep 4: Sleepiness, cognitive function , and quality of
life in obstructive sleep apnoea/hypopnoea syndrome. Thorax, 59, 618-622.
241
Ernst, P, & Zejda, J. (1991). Pleural and airways disease associated with mineral fibers. Mineral
Fibers and Health. D. Liddell, & Miller, K. Boca Raton: CRC Press.
F.M Hardinge, D. J. P. a. J. R. S. (1995). Use of the Epworth sleepiness Scale to demonstrate response
to treatment with nasal continuous positive airways pressure in patients with obstructive sleep apnoea.
Respiratory Medicine, 89, 617-620.
Findley, L, Barth, J.T, Powers, D.C, Wilhoit, S.C, Boyd, D.G, & Suratt, P.M. (1986). Cognitive
impairment in patients with obstructive sleep apnea and associated hypoxemia. Chest, 90, 686-690.
Fitzpatrick, M. F, Engleman, H, Whyte, K. F. (1991). Morbidity in nocturnal asthma: sleep quality
and daytime cognitive performance. Thorax, 46, 569-573.
Fitzpatrick, M. F, Martin, K, Fossey, E, Shapiro, C.M, Elton, R.A & Douglas, N.J. (1993). Snoring,
asthma and sleep disturbance in Britain: a community-based survey. Eur Respir J, 6, 531-535.
Fleetham, J, West, P, Mezon, B, Conway, W, Roth, T, & Kryger, m. (1982). Sleep, arousals, and
oxygen desaturation in chronic obstructive pulmonary disease. The effect of oxygen therapy. .Am Rev
Respir Dis, 126, 429-433.
Fleethan, J, West, P, Mezon, B, Conway, W, Roth, T, & Kryger, M. (1982). Sleep, arousals, and
oxygen desaturation in chronic obstructive pulmonary disease. The effect of oxygen therapy. Am Rev
Respir Dis, 126, 429-433.
Flemons, W. W, & Reimer, M.A. (1998). Development of a disease-specific health-related quality of
life questionnaire for sleep apnea. Am J Respir Crit Car Med, 158, 494-503.
Flick, M. R, & Block, A.J. (1977). Continuous in vivo monitoring of arterial oxygenation in chronic
obstructive lung disease. Ann Intern Med, 86, 725-730.
Floyer, J. A. (1698). Treatise of the asthma. London, Wilkin.
Folkard, S, & Barton, J. (1993). Does the forbidden zone for sleep onset influence morning shift sleep
duration? Ergonomics, 36, 85-92.
Foresman, B. H. (2000). Sleep and breathing disorders: the genesis of obstructive sleep apnea. J. Am
Osteopath Assoc, 8, S1-S8.
Formulary, B. N, Ed. (2009). BNF 57. London, BMJ Group.
Foundation, B. L. Lung Report III-Casting a shadow over the nation's health.
Fowler, F. J., & Cannell, C. F. (1996). Using behavioral coding to identify cognitive problems with
survey questions. In N. Schwarz & S. Sudman (Eds.), Answering questions. Methodology for
determining cognitive and communicative processes in survey research (pp. 15-36). San Francisco:
Jossey-Bass.
Frank-Stromborg, M. (1988). Instruments for clinical nursing research. Norwalk, CT: Appleton &
Lange.
Fraser, R. G, Macklem, P.T, & Brown, W.G. (1965). Airway dynamics in bronchiectasis. A combined
cinefluorographic-manometric study. Am J Roentgenol, 93, 821-835.
Freemon, F. R. (1972). Sleep research: a critical review. Sprignfield, Charles C Thomas.
Giedke, H, & Schwarzler, F. (2002). Therapeutic use of sleep deprivation in depression. Sleep Med
Rev, 6, 361-377.
242
Gislason, T, & Almqvist, M. (1987). Somatic diseases and sleep complaints. Acta Med Scand, 222,
475-481.
Gough, J, & Wentworth, JW. (1949). The use of thin sections of entire organs in morbid anatomical
studies. J R Microsc Soc, 69, 231-235.
Gough, J. (1952). Discussion on the dignosis of pulmonary emphysema. The pathological diagnosis of
emphysema. Proc R Soc Med, 45, 576-577.
Greaves, C. J, Eiser, C, Seamark, D, & Halpin, D.M.G. (2002). Attack context: an important mediator
of the relationship between psychological status and asthma outcomes. Thorax, 57, 217-221.
Groeger, J. A, Zijlstra, F.R.H, Dijk, D-J. (2004). Sleep quantity, sleep difficulties and their perceived
consequences in a representative sample of some 2000 British adults. J. Sleep Res, 13, 359-371.
Gross, R. (2005). Psychology The Science of Mind and Behaviour, Hodder Education.
Grunstein, R. R, Stenlof, J.A, & Hedner, J.A. (1995). Impact of self-reported breathing disturbances
on psychosocial performance in the Swedish obese subjects (SOS) study. Sleep, 18, 635-643.
Guerrien, A. (1994). Paradoxical sleep and memory process in humans. Acta Psychiatr Belg, 94, 7587.
Guilleminault, C. (1985). Disorders of excessive sleepiness. Ann Clin Res, 17, 209-219.
Guilleminault, C. (1994). Clinical features and evaluation of obstructive sleep apneas. In: Kryger,
M.H, Roth, T, & Dement, W.C. Principles and practice of sleep medicine. Philadelphia, WB
Saunders.
Guyatt, G, Townsend, M, Berman, L, & Pugsley, S. (1987). Quality of life in patients with chronic
airflow limitation. British Journal of Diseases of the Chest, 81(1), 45-54.
Hanson, I. (1982). Effects of chronic lung disease on life in general and on sexuality: Perceptions of
adult patients. Heart and Lung, 11, 435-441.
Harber, P, Schenker, M.B, & Balmes, J.R. (1995). Occupational and environmental respiratory
disease. St.Louis: Mosby.
Hardinge, F. M. P, D.J, and Stradling, J.R. (1995). Use of the Epworth Sleepiness Scale to
demonstrate response to treatment with nasal continuous positive airways pressure in patients with
obstructive sleep apnoea. Respiratory Medicine, 89, 617-620.
Harrison, B. D. W. (1998). Psychosocial aspects of asthma in adults. Thorax, 53, 519-525.
Heard, B. E, Khatchatourov, V, & Otto, H. (1979). The morphology of emphysema, chronic
bronchitis, and bronchiectasis: Definition, nomenclature, and classification. J. Clin Pathol, 32, 882892.
Hellgren, J, Omenaas, E, Gíslason, T, Jögi, R, Franklin, K.A, Lindberg, E, Janson, C, & Torén, K, on
behalf of the RHINE study group, North Europe (2007). Perennial non-infectious rhinitis-an
independant risk factor for sleep disturbances in asthma. Respiratory Medicine, 101, 1015-1020.
Higgins, M. (1991). Risk factors associated with chronic obstructive lung disease. Ann NY Acad Sci,
(624), 7-17.
Higgins, M. W. (1990). Incidence, prevalence and mortality: intra- and inter- country differences.
Clinical epidemiology of COPD. M. J. S. Hensley, N.A. New York, Marcel Dekker.
Hill, D. W, Welch, J.E, Godfrey III, J.A. (1996). Influence of locus of control on mood state
disturbance after short-term sleep deprivation. Sleep, 19(1).
243
Hindmarch, I. (2003). The effects of asthma on sleep. HPRI Medical Research Centre. Guildford,
University of Surrey.
Hobson, J. A. (1995). Sleeping and dreaming. London, Longman.
Hoddes, E, Zarcone, V, Smythe, H, Phillips, R, & Dement, W.C. (1973). Quantification of sleepiness:
a new approach. Psychophysiology, 10, 431-436.
Horne, J. (1988). Why We Sleep: The Function of Sleep in Humans and Other Mammals. Oxford,
Oxford University Press.
Horne, J. A. (1978). A review of the biological effects of total sleep deprivation in man. Biol Psychol,
7, 55-102.
Horne, J. A. (1988). Why We Sleep. The Functions of Sleep in Humans and other Mammals. Oxford,
Oxford University Press.
Houston, J. C, Joiner, C.L, & Trounce, J.R. (1966). A short textbook of medicine, English University
Press.
Hyland, M. E. ((1990)). The mood-peak flow relationship in adult asthmatics: a pilot study of
individual differences and direction of causality. British Journal of Medical Psychology, 63, 379-384.
Interiano, B, Perkins, P.T, & Fuleihan, F. (1972). Changes in arterial blood gases during sleep in
patients with cardiopulmonary disease. . Am Rev Respir Dis, 105, 980.
Janson, C, Gislason, T, Almqvist, M, & Boman, G. (1989). Theophylline disturbs sleep mainly in
caffeine-sensitive persons. Pulm Pharmaol, 2, 125-129.
Janson, C, Gislason, T, Boman, G, (1990). Sleep disturbances in patient with asthma. Respir Med, 84,
37-42.
Janson, C, Gislason, T, Laxmyr, L, Boman, G, & Persson, C. (1991). Sleep disturbances in asthma:
Theophylline Versus Enoprofylline. Upsala J Med Sci, 96, 119-127.
Janson, C, Bjornsson, E, Hetta, J, & Boman, G. (1994). Anxiety and depression in relation to
respiratory symptoms and asthma. Am J Respir Crit Car Med 149: 930-934.
Janson, C, Gislason, T, De Backer, W. (1995). Prevalence of sleep disturbances among young adults
in three European countries. Sleep, 18, 589-597.
Janson, C, De Backer, W, Gislason, T, Plaschke, P, Bjornsson, E, Hetta, J, Kristbjarnarson, P,
Vermeire, P, & Boman, G. (1996). Increased prevalence of sleep disturbances and daytime sleepiness
in subjects with bronchial asthma: a population study of young adults in three European countries. Eur
Respir J, 9, 2132-2138.
Janson, C, Chinn, S, Jarvis, D, and Bumey, P. on behalf of the European Community Respiratory
Health Survey. (1997). Physician-diagnosed asthma and drug utilization in the European Community
Respiratory Health Survey. Eur Respir J, 10, 1795-1802.
Janson-Bjerklie, S, Ferketich, S, & Benner, P. (1993). Predicting the outcomes of living with asthma
with asthma. Res Nurs Health, 16, 241-250.
Jennum, P, and Sjol, Anette. (1994). Self-assessed cognitive function in norers and sleep apneics: An
epidemiological study of 1.504 females and males aged 30-60 years: The Dan-MONICA II Study. Eur
Neurol, 34, 204-208.
Johns, M. (1998). Rethinking the assessment of sleepiness. Sleep Med Rev, 2, 3-15.
Johns, M. W. (1991). A New Method for Measuring Daytime Sleepiness: The Epworth Sleepiness
Scale. Sleep, 14(6), 540-545.
244
Johns, M. W. (1992). Reliability and Factor Analysis of the Epworth Sleepiness Scale. Sleep, 15(4),
376-381.
Johns, W, Murray. (1992). Reliability and Factor Analysis of the Epworth Sleepiness Scale. Sleep,
15(4), 376-381.
Johns, W, Murray. (1993). Daytime sleepiness, snoring, and obstructive sleep apnea. the Epworth
Sleepiness Scale. Chest, 103(1), 30-36.
Jones, N. F, Kinsman, R.A, Dirks, J.F, & Dhalem, N.W. (1979). Psychological contributions to
chronicity in asthma: patient response styles influencing medical treatment and its outcome. Med
Care, 17, 1103-1118.
Jones PW, Quirk FH, Baveystock CM. The St George's Respiratory Questionnaire. Respir Med
1991;85 (Suppl B): 25-31.
Jonker, C, Launer, L.J, & Hooijer, C. (1996). Memory complaints and memory impairment in older
individuals. J Am Geriatr Soc, 44, 44-49.
Jorm, A. F, Christensen, H, Korten, A.E. (1997). Do cognitive complaints either predict future
cognitive decline or reflect past cognitive decline? Psychol Med, 27, 91-98.
Jovanovic, U. J. (1991). General considerations of sleep and sleep deprivation. Epilepsy Res Suppl, 2,
205-215.
Juniper, E. (1994). Asthma Quality of Life Questionnaire (AQLQ). Interviewer-administered United
Kingdom Version. Q.T. Ltd. Bosham.
Juniper, E. (1994). Asthma Quality of Life Questionnaire (AQLQ) Self administered United Kingdom
Version QOL Technologies.
Juniper, E. (1997). Asthma Control Diary. United Kingdom Version. Q. T. Ltd. Boshma.
Juniper, E. (1998). Asthma Quality of Life Questionnaire with Standardised Activities (AQLQ(S)).
Self-administered United Kingdom Version. Q. T. Ltd. Bosham.
Juniper, E. (2002). Asthma Quality of Life Questionnaire with Standardised Activities. Selfadministered United Kingdom version (>12 years). Q. T. Ltd.
Juniper, E. (2005) Asthma Quality of Life Questionnaire (AQLQ, AQLQ(S), Mini AQLQ and Acute
AQLQ.
Juniper, E. F, Guyatt, G.H, & Ferrie, P.J. (1993). Measuring quality of life in asthma. Am Rev Respir
Dis 147, 832-838.
Juniper, E. F, Johnston, P.R, Borkhoff, C.M, Guyatt, G.H, Boulet, L-P, & Haukioja, A. (1995).
Quality of life in asthma clinical trials: comparison of Salmeterol and Salbutamol. Am J Respir Crit
Car Med 151, 66-70.
Juniper, E. F. (2000). Mini Asthma Quality of Life Questionnaire (Mini AQLQ). Self-administered
United Kingdom Version. Q. T. Ltd. Bosham.
Juniper, E. F. (2003). Interpreting quality of life data: should we listen to the patient or the clinician?
Ann Allergy Asthma Immunol 91, 115-116.
Juniper, E. F, Cox, G, F.M, Ferrie, P.J, and King, D.R. (1999). Development and Validation of the
Mini Asthma Quality of Life Questionnaire. Eur Respir J, 14, 32-38.
Juniper. E. F, Epstein, Robert S, Ferrie. Penelope J, Jaeschke. Roman, Hiller, Thomas K. (1992).
Evaluation of impairment of health related quality of life in asthma: development of a questionnaire
for use in clinical data. Journal of the British Thoracic Society, 47(2), 76-83.
245
Juniper, E.F, William. Andrew, and Griffith, Lauren E. (1993). Measuring Quality of Life in Asthma.
Am Rev Respir Dis, 147, 832-838.
Juniper, E.F, William. Andrew, and Griffith, Lauren E. (1994). Determining a Minimal Important
Change in a Disease-Specific Quality of Life Questionnaire. Journal of Clinical Epidemiology, 47(1),
81-87.
Juniper, E. F, Cox, G, F.M, Ferrie, P.J, and King, D.R. (1999). Validation of a Standardized Version
of the Asthma Quality of Life Questionnaire. Chest, 115, 1265-1270.
Kales, A, Beall, G. N, Bajor, G. F, (1968). Sleep studies in asthmatic adults: relationship of attacks to
sleep stage and time of night. . J Allergy 41, 164-173.
Kales, A, Kales, J, D, Sly, R. M. (1970). Sleep patterns of asthmatic children: all night
electroencephalographic studies. J Allergy 46, 300-308.
Kapur, V. K, Redline, S, Nieto, F.J, Young, T.B, Newman, A.B, and Henderson, J.A. (2002). Sleep
Health Research Group. The relationship between chronically disrupted sleep and healthcare use.
Sleep 25, 289-296.
Kim, S, Emerman, C.H, Cydulka, R.K. (2004). Prospective multicenter study of relapse following
emergency department treatment of COPD exacerbation. Chest 125, 473-481.
Kinnear, W, & Tattersfield, AE. (1990). Emphysematous bullae: Surgery is best for large bullae and
moderately impaired lung function. BMJ, 300, 208-209.
Kinsman, R. A, Luparello, T, O'Banion, K, & Spector, S. (1973). Multidimensional analysis of the
subjective symptomatology of asthma. Psychosomatic Medicine, 35, 250-267.
Kleitman, N. (1927). Studies on the Physiology of Sleep; V; Some Experiments on Puppies. American
Journal of Physiology, 84, 386-395.
Klink, M. E, Dodge, R, & Quan, S.F. (1994). The relation of sleep complaints to respiratory
symptoms in a general population. Chest, 105(1), 151-154.
Klink, M. Q, S.F. (1987). Prevalence of reported sleep disturbances in a general adult population and
their relationship to obstructive airways disease. Chest, 91, 540-546.
Knudson, R, Standen, JR, & Kaltenborn, WT. (1991). Expiratory computed tomography for
assessment of suspected pulmonary emphysema. Chest, 99, 1357-1366.
Koo, K. W, Sax, D.S, & Snider, G.L. (1975). Arterial blood gases and pH during sleep in chronic
obstructive pulmonary disease. Am J Med, 58, 663-670.
Kryger, M. H, Roth, T, & Dement, W.C. (2005). Principles and Practice of Sleep Medicine.
Philadelphia, Elseiver Saunders.
Kuczmarski, R. J, Flegal, D.M, Campbell, S.M, & Johnson, C.L. (1994). Increasing prevalence of
overnight among US adults. JAMA, 272, 205-211.
Kupfer, D. J, Ulrich, R.F, Coble, P.A, Jarrett, D.B, Grochocinski, V.J, Doman, J, Matthews, G, &
Borbely, A.A. (1984). The application of automated REM and slow-wave sleep analysis (normal’s
and depressives). Psychiatric Research, 13, 325-334.
Kupfer, D. J. (1995). Sleep research in depressive illness: Clinical: implications-a tasting menu. Biol
Psychiatry, 38(6), 391-403.
Laennec, R. (1819). De L'Auscultation Mediate, ou traite du diagnostic des maladies des poumons et
du coeur. Paris, Tome Premier.
246
Laennec, R. (1835). A Treatise on the Diseases of the Chest and on Mediate Auscultation.
Philadelphia, Thomas & Co.
Lahdensuo, A, Haathela, T, Herrala, J. (1996). Randomised comparison of guided self management
and traditional treatment of asthma over one year. 312: 748-752.
Lamphere, J, Roehrs, T, & Wittig, R. (1989). Recovery of alertness after CPAP in apnea. Chest, 96,
1364-1367.
Lander, F. P. L. (1946). Bronchiectasis and Atelectasis: temporary and permanent changes. Thorax, 1,
198-210.
Lane, D. J. (1987). Asthma. Oxford, Oxford University Press.
Lane, D. J. (1996). Asthma. Oxford, Oxford University Press.
Lange P, P. J, Vestbo J et al (1998). A 15 year old follow-up study of ventilatory function in adults
with asthma. N Engl J Med, (339), 1194-1200.
Leger, D, Poursain, B. (2005). An international survey of insomnia: under-recognition and undertreatment of a polysymptomatic condition. Curr Med Res Opin, 21, 1785-1792.
Leitch, A. G, Clancy, L.J, Leggett, R.J.E, Tweeddale, P, Dawson, P, & Evans, J.J. (1976). Arterial
blood gas tensions, hydrogen ion, and electroencephalogram during sleep in patients with chronic
ventilatory failure. . Thorax, 31, 730-735.
Lemanske, R. F, & Busse, W.W. (2003). Asthma. J Allergy Clin Immuno, 111(2), S502-S519.
Leopold, J, & Gough, J. (1957). The centrilobular form of hypertrophic emphysema and its relation to
chronic bronchitis. Thorax, 12, 219-235.
Lewis, A, David. (1999). Sleep in patients with respiratory disease. Respiratory Care Clinics of
North-America. 5(3), 447-460.
Lezak, M. D. (1982). The problems of assessing executive functions. Int J Psychol, 17, 281-297.
Lichstein, K. L, Wilson, N.M, & Johnson, C.T. (2000). Psychological treatment of secondary
insomnia. Psychol Aging, 15, 232-240.
Lojander, J, Kajaste, S, Maasilta, P, & Partinen, M. (1999). Cognitive function and treatment of
obstructive sleep apnea syndrome. J. Sleep Re. 8, 71-76.
Luria, A. R, Ed. (1966). Higher cortical functions in man. London, Tavistock.
Lyketsos, G. C, Karabetsos, A, Jordanoglou, J, Liokis, T, Armagianidis, A, & Lyketsos, C.G. (1984).
Personality characteristics and dysthymic states in bronchial asthma. Psychother Psychosom, 41, 177185.
Manaceine, M. (1894). Quelques observations experimentals sur l'influence de l'insomnie absolue.
Arch Ital Biol, 21, 322-325.
Mann, C, J, Ed. (1950). Hippocrates. Airs, Waters, Places. In: Hippocratic Writings. Oxford,
Blackwell.
Maquet, P. (2001). The role of sleep in learning and memory. Science, 294, 1048-1052.
Martin, R. (1993). Nocturnal asthma: an overview. In: Martin, R. Nocturnal asthma, mechanisms and
treatment. Mount Kisco, NY, Futura Publishing.
Martin, S, Engleman, H, Deary, I, and Douglas, N. (1996). The effect of sleep fragmentation on
daytime function. Am J. Respir Crit Care Med, 153, 1328-1332.
247
McArdle, N, Kingshott, R, Engleman, H.M, Mackay, T.W, Douglas, N.J. (2001). Partners of patients
with sleep apnoea/hypopnea syndrome: effect of CPAP treatment on sleep quality and quality of life.
Thorax, 56, 513-518.
McFadden, E. R, & Lyons, H.A. (1969). Serial studies of factors influencing airway dynamics during
recovery from acute asthma attacks. J Appl Physiol, 452-459.
Meddis, R. (1975). The Sleep Instinct. London, RKP.
Medicine, A. A. o. S. (2005). The Intrenational Classification of Sleep Disorders, 2nd edition,
Diagnostic and ocidng manual. Westchester, Illinois.
Meltzer, A. A, Smolensky, M.H, & D'Alonzo, G.E. (1989). An assessment of peak flow as a surrogate
measurement of FEV1in stable asthmatic children. Chest, 96, 329-333.
Meltzer, E. O. (2002). Does rhinitis compromise sleep and daytime productivity? Clin Exp Allergy
Review 2, 67-72.
Mendelson, W. B. (1990). Clinical neuropharmacology of sleep. Sleep Hypnosis, 8, 154-162.
Mendelson, W. B. (1993). Pharmacologic alteration of the perception of being awake or asleep. Sleep,
16(16), 641-646.
Mendelson, W. B. (1995). The effects of Flurazepam and Zolpiderm on the perception of sleep in
insomniacs. Sleep, 18, 92-96.
Mendelson, W. B. (2005). Hypnotic medications: Mechanisms of action and pharmocologic effects.
Principles and practice of sleep medicine. M. H. Kryger, Roth, T, & Dement, W.C. Philadelphia,
Elsevier Saunders: 444.
Michael E. Hyland, S. F. a. S. H. I. (1991). A Scale for Assessing Quality of Life in Adult Asthma
Sufferers. Journal of Psychosomatic Medicine, 35(1), 99-110.
Michel, F. B. (1994). Psychology of the allergic patient. Allergy, 49, 28-30.
Miles, J. F, Garden, G.M.F, Tunnicliffe, R.M, Cayton, R.M, & Ayres, J.G. (1997). Psychological
morbidity and coping skills in patients with brittle and non-brittle asthma: a case-control study.
Clinical and Experimental Allergy, 27, 1151-1159.
Miller, B. D. (1987). Depression and asthma: a potentially lethal mixture. Journal of Allergy and
Clinical Immunology, 80, 481-486.
Mills, R. S. B. a. G. H. (2004). Sleep disruption in critically ill patients-pharmacological
considerations. Anaesthesia, 59, 374-384.
Mohsenin, V. (2005). Sleep in chronic obstructive pulmonary disease. Semin Respir Crit Care Med,
26(1), 109-116.
Montplaisir, J, Walsh, J, Malo, J. L, (1982). Nocturnal asthma: features of attacks, sleep and breathing
patterns. Am Rev Respir Dis 125, 18-22.
Murray, C. J. L, & Lopez, A.D. (1997). Mortality by cause for eight regions of the world: Global
Burden of Disease Study. Lancet, 349, 1269-1276.
Mysliwiee, V, & Pina, J.S, (1999). Bronchiectasis: the other obstructive lung disease. Postgrad Med,
106, 123-126.
National Heart, L. A. B. I, National Institutes of Health (March 1995). Global Strategy for Asthma
Management and Prevention. NHLBI/WHO Workshop Report. 95: 6.
248
Nicola Brace, R. K, Rosemary Snelgar (2000). SPSS for Psychologist versions 12 and 13. Hampshire,
Palgrave Macmillan.
Nocon, A, & Booth, T. (1991). The social impact of asthma. Fam Prac, 8, 37-41.
O'Connor, D. W, Pollitt, P.A, Roth, M. (1990). Memory complaints and impairment in normal,
depressed, and demented elderly persons identified in a community survey. Arch Gen Psychiatry, 47,
224-227.
Office, I. L. (1997). Encyclopedia of occupational health and safety. Geneva, ILO.
Ohayon, M. M, Carskadon, M.A, Guilleminault, C, Vitiello, M.V. (2004). Meta-analysis of
quantitative sleep parameters from childhood to old age in healthy individuals: developing normative
sleep values across the human lifespan. Sleep, 27, 1255-1273.
Orr, W. C, hamma-Othman, Z, Levin, D, Othma, J, & Rundell, O.H. (1990). Persistent hypoxaemia
and excessive daytime sleepiness in chronic obstructive pulmonary disease. Chest, 97, 583-585.
Orsos, F. (1907). Uber das elastiche Gerauust der normalen und der emphysematosen Lunge. Pathol
Anat, 41, 95-121.
Osler, W. (1903). The principles and practice of medicine.
Oswald, I. (1966). Sleep. Harmondsworth, Penguin.
Oswald, I. (1974). Sleep. Harmondsworth, Penguin.
P.M.A. Calverley, W. M, N.B. Pride, S.I. Rennard, Ed. (2003). Chronic Obstructive Pulmonary
Disease. London, Arnold.
Palomaki, H, Partninen, M, Juvela, S, and Kaste, M. (1989). Snoring as a risk factor for sleep-related
brain infarction. Stroke, 20, 1311-1315.
Parkes, W. R. (1994). Occupational lung disorders. London, Butterworth.
Parthasarathy, S. T, M.J, (2002). Effect of ventilator mode on sleep quality in critically ill patients. Am
J Respir Crit Care Med, 166, 1423-1429.
Partinen, M. a. G, Thorarinn. (1995). Basic Nordic Sleep Questionnaire (BNSQ): a quantitated
measure of subjective sleep complaints. J. Sleep Res. 4(1), 150-155.
Patel, I. S, Seemungal, T.A, Wilks, M. (2002). Relationship between bacterial colonisation and the
frequency, character, and severity of COPD exacerbation. Thorax 57, 759-776.
Patrick, G. T. W, & Gilbert, J.A. (1896). On the effect of loss oF sleep. Psychol Rev, 3, 469-483.
Pauwels, R. A, Buist, A.S, & Calverley, P.M. (2001). Global strategy for the diagnosis, management,
and prevention of Chronic Obstructive Pulmonary Disease. NHLBI/WHO Global Initiative for
Chronic Obstructive Pulmonary Disease (GOLD) workshop summary. Am J Respir Crit Car Med 163,
1256-1276.
Pearlman, C. A. (1982). Sleep structure variation and performance. Biological rhythms, sleep, and
performance. W. B. Webb. New York, John Wiley & Sons: 143-173.
Peat JK, W, AJ, Cullen, K (1987). Rate of decline of lung fucntion in subjects with asthma. Eur J
Respir Dis, (70), 171-179.
Peigneux, P, Laureys, S, & Delbeuck, X. (2001). Sleeping brain: Learning brain: The role of sleep for
memory systems. 12: A111-A124.
249
Philip, P, Stoohs, R, & Guilleminault, C. (1994). Sleep fragmentation in normals: a model of
sleepiness associated with upper airway resistance syndrome. Sleep, 17, 242-247.
Pilcher, J. J. a. H, A.L. (1996). Effects of sleep deprivation on performance: a meta-analysis. Sleep,
19, 318-326.
Pinel, J. P. J. (1993). Biopsychology. Boston, Allyn & Bacon.
Pontius, J. R, & Jacobs, L.G. (1957). The reversal of advanced bronchiectasis. Radiology, 68, 204207.
Post, L, & Collins, C. (1981). The poorly coping COPD patient: a psychotherapeutic perspective.
International Journal of Psychiatry in Medicine, 11(2), 173-182.
Prinz, P, Vitiello, M, Raskind, M. (1990). Geriatrics: sleep disorders and aging. N Engl J Med, 323,
520-526.
Quan, S. F, & Zee, P. (2004). Evaluating the effects of medical disorders on sleep in the older patient.
. Geriatrics, 59(3), 37-42.
Rabe, K. F, Vermeire, P.A, Soriano, J.B, and Maier, W.C. (2000). Clinical management of asthma in
1999: the Asthma Insights and Reality in Europe (AIRE) study. Eur Respir J, 16, 802-807.
Ravinder Vir, R. B. a. A. S. (1997). Sleep disturbances in clinically stable young asthmatic adults
Ann Allergy Asthma Immunol, 79, 251-255.
Rechtschaffen, A. (1968). Polygraphic aspects of insomnia. The abnormalities of sleep in man. H.
Gastaut, Lugaresi, L, Berti, G, & Coccagano, C. Bologna, Italy, Gaggi: 109-125.
Rechtschaffen, A, Bergman, B.M, Everson, C.A, Kushida, C.A. & Gilliland, M.A. (1989a). Sleep
deprivation in the rat: 1. Conceptual issues. Sleep, 12, 1-4.
Rechtschaffen, A, Bergman, B.M, Everson, C.A, Kushida, C.A. & Gilliland, M.A. (1989b). Sleep
deprivation in the rat: X. Integration and discussion of the findings. Sleep, 12(68-87).
Redline, S, Strauss, M.E, & Adams, N. (1997). Neuropsychological function in mild sleep-disordered
breathing. Sleep, 20, (160-7).
Reimer, M. A. F, W,W,. (2003). Quality of life in sleep disorders. Sleep Med Rev, 7(4), 335-349.
Resta, O, & Foschino-Barbaro, M.P. (2001). Sleep-related breathing disorders, loud snoring and
excessive daytime sleepiness in obese subjects. Int J Obes, 25: 1-7.
Resta, O, Fochino-Barbaro, M.P, Bonfitto, P, Giliberti, T, Depalo, A, Pannacciulli, N, & De Pergola,
G. (2003). Low sleep quality and daytime sleepiness in obese patients without obstructive sleep
apnoea syndrome. Journal of Internal Medicine, 253, 536-543.
Reynolds, C. F, Kupfer, D.J, Taska, L.S, Hoch, C.C, Sewitch, D.E, & Grochocinski, V.J. (1885). Slow
wave sleep in elderly depressed, demented, and healthy subjects. Sleep, 8, 155-159.
Rimington, L. D, Davies, D.H, Lowe, D, & Pearson, M.G. (2001). Relationship between anxiety,
depression, and morbidity in adult asthma patients. Thorax, 56, 266-271.
Ritchie, B. (1962). A comparison of forced expiratory volume and peak flow in clinical practice.
Lancet, 2, 271-273.
Roers, T, Zorick, F, Wittig, R, Conway, W, & Roth, T. (1989). Predictors of objective level of
daytime sleepiness in patients with sleep-related breathing disorders. Chest, 95, 1202-1206.
Rom, W. N. (1998). Environmental and occupational medicine. Philadelphia, Lippincott-R.
250
Rowlett, D, & Dudley, D. (1978). COPD: Psychosocial and psychophysiological issues.
Psychosomatics, 19, 273-279.
Rutten-Van Molken, M. P. M. H, Cuters, F, & Van Doorslaer, E.K.A. (1995). Comparison of
performance of four instruments in evaluating the effects of Salmeterol on asthma quality of life. Eur
Respir J, 8, 888-898.
Ruysch, F. (1691). Observationem Anatomico-Chirurgicarum. Amsterdam, Henricum Boom.
Ryan, G, Latimer, K.M, & Dolovich, J. (1982). Bronchial responsiveness to histamine: Relationship
to diurnal variation of peak flow rate, improvement after bronchodilator, and airway calibre. Thorax,
37, 423-429.
Saaresranta, T, Irjala, K, Aittokallio, T, & Polo, O. (2005). Sleep quality, daytime sleepiness and
fasting insulin levels in women with cjronic obstructive pulmonary disease. Respiratory Medicine, 99,
856-863.
Salter, H. H. (1864). On asthma: its pathology and treatment. Philadelphia, Blanchard & Lea.
Sandek, K, Andersson, T, Bratel, T, Hellstrom, G, & Lagerstrand, L. (1999). Sleep quality, carbon
dioxide responsiveness and hypoxaemic patterns in nocturnal hypoxaemia due to chronic obstructive
pulmonary disease (COPD) without daytime hypoxaemia. Respir Med, 93, 79-87.
Sanders, M. H, Newman, A.B, & Haggerty, C.L. (2003). Sleep and sleep-disordered breathing in
adults with predontal obstructive airway disease. Am J Respir Crit Car Med, 167, 7-14.
Scadding, J. G, Ed. (1983). Definition and clinical categories of asthma. Asthma. London, Chapman
& Hall.
Schofield, P. W, Jacobs, D, Marder, K. (1997). The validity of new memory complaints in the elderly.
Arch Neurol, 54,756-759.
Sears, M. (1998). Epidemiology. Asthma: Basic mechanisms and clinical management.
Seemungal, T, Donaldosn, GC, & Paul, EA. (1998). Effect of exacerbations on quality of life in
patents with chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 157, 1418-1422.
Series, F, Roy, N, & Marc, I. (1994). Effects of sleep deprivation and sleep fragmentation on upper
airway collapsibility in normal subjects. Am Respir Crit Care Med, 150, 481-485.
Sethi, S. (2000). Infectitious etiology of acute exacerbations of chronic bronchitis. Chest, 117, S380385.
Shah, A. (1997). Bronchial Asthma and Sleep Disturbances. Indian J Chest Dis Allied Sci, 39, 77-79.
Sharpley, A. (1996). Impact of daytime sleepiness underrated. Lancet, 348, 71.
Sherrill, D, Lebowitz, M, & Burrows, B. (1990). Epidemiology of COPD. Clin Chest Med 11, 375387.
Shneerson, I. E. S. a. J. M. (1995). Is the SF-36 sensitive to sleep disruption? A study in subjects with
sleep apnoea. J. Sleep Res, 4, 183-188.
Shneerson, J. M. (2005). Sleep medicine: a guide to sleep and its disorders. Massachusettes, USA,
Blackwell Publishing.
Siegel, J. M. (2001). The REM sleep-memory consolidation hypothesis. Science 294, 1058-1063.
Simon, G. E, VonKorff, M. (1997). Prevalence, burden, and treatment of insomniain primary care. Am
J Psychiatry 154, 1417-1423.
251
Sjol, P. J. A. (1994). Self-Assessed Cognitive Function in Snorers and Sleep Apneics. Eur Neurol,
(34), 204-208.
Smith, C. (2001). Sleep states and memory proceses in humans: procedural versus declarative
memory systems. Sleep Med Rev, 5, 491-506.
Smith-Coggins, R, Rosekind, M.R, Hurd, S, Buccino, K.R. (1994). Relationship of day versus night
sleep to physician performance and mood. Ann Emerg Med 24(5), 928-934.
Snaith, A. S. Z. a. R. P. (1983). The Hospital Anxiety and Depression Scale. Acta Psychiatry Scand,
67, 361-370.
Snider, G. L, Stone, P.J, & Lucey, E.C. (1992). Development and evaluation of antiproteases as drugs
for preventing emphysema. Biochemistry of pulmonary emphysema. C. Grassi, Travis, J, & Casali, L.
Verona, Bi and Bi Publishers.
Snider, G. L. (2003). Nosology for our day: its applications to chronic obstructive pulmonary disease.
Am J Respir Crit Car Med, 167, 678-683.
Society, A. t. (1991). Lung Function testing: Selection of reference values and interpretive strategies.
Am Rev Respir Dis, 144, 1202-1216.
Society, A. T. (1995). Standardization of Spiromtery update. Am J Respir Crit Car Med, 152, 11071136.
Society, B. T. (1997). The British guidelines on asthma management: 1995 review and position
statement. Thorax, 52(1), S1-21.
Society, B. T. (2004). British Guidelines on the Management of Asthma: a national clinical guideline.
B. T. S. S. I. G. Network.
Spittle, B. J, & Sears, M.R. (1984). Bronchial asthma: lack of relationships between allergic factors,
illness severity and psychological variables in adult patients attending an asthma clinic. Psychol Med,
14, 847-852.
Steptoe, A. (1991). The links between stress and illness. Journal of Psychosomatic Research, 35, 633644.
Stevens, P, Orman, BF, Graves, G. (1969). Contribution of lung recoil and airway resistance to forced
expiratory flow limitation. Am Rev Respir Dis, 100, 54-62.
Stickgold, R, Hobson, J.A, & Fosse, R. (2001). Sleep, learning, and dreams: off-line memory
reprocessing. Science, 294, 1052-1057.
Stores, G, & Crawford, C. (1998). Medical student education in sleep and its disorders. J R Coll
Physicians Lond, 32(2), 149-153.
Stores, G, Ellis, A.J, Wiggs, L, Crawford, C, & Thomson, A. (1998). Sleep and psychological
disturbance in nocturnal asthma. Arch Dis Child 78,413-419.
Stores, G. Crawford, C. (1998). Medical student education in sleep and its disorders. J R Coll Phys 32,
149-153.
Stradling, J. R, & Crosby, J.H. (1991). Predictors and prevalence of obstructive sleep apnoea and
snoring in 1001 middle aged men. Thorax 46: 85-90.
Strollo, P. J, Atwood, C.W. Jr, & Sanders, M.H. (2005). Medical therapy for obstructive sleep apneahypopnea syndrome. In: Principles and practice of sleep medicine. M. H. Kryger, Roth, T, & Dement,
W.C. Philadelphia, Elsevier Saunders.
252
Strunk, R. C, Mrazek, D.A, Furrmann, G.S.W, & LaBrecque, J.F. (1985). Physiologica and
psychological characteristics associated with deaths due to asthma in childhood: a case-controlled
study. JAMA, 254, 1193-1198.
Survey, E. C. R. H. (1996). Variations in the prevalence of respiratory symptoms, self-reported
asthma attacks, and use of asthma medication in the European Community Respiratory Health Survey
(ECRHS). Eur Respir, J 9, 687-695.
Symposium, C. G. (1959). Terminology, definitions and classification of chronic pulmonary
emphysema and related problems. Thorax 14, 286-299.
Taylor, J. L, Miller, T.P, Tinklenberg, J.R. (1992). Correlates of memory decline: A 4-year
longitudinal study of older adults with memory complaints. Psychol Aging, 7, 185-193.
Terzano, M. G, Parrino, L. (2000). Origin and significance of the cyclic alternating pattern (CAP).
Sleep Med Rev, 4(1), 101-123.
Theoell, T, Schuldt, C, Ekholm, J, Michelsen, H. (1995). Physical strength and endurance in relation
to perceived psychosocial work environment, sleep disturbnace and coping strategies in men. Scand J
Rehabil Med, 27(2) 67-71.
Thompson, W. L, & Thompson, T.L. (1985). Psychiatric aspects of asthma in adults. Advances in
Psychosomatic Medicine, 14, 33-47.
Thorax (1997). Asthma in adults and schoolchildren. Thorax, S2, S2-S8.
Thorax (2003). British Guidelines on the Management of Asthma. Thorax, 58(S1).
Totterdel, D, P, Parkinson, S, Reynolds, and Briner, R.B. (1994). Associations of sleep with everyday
mood minor symptoms and social interaction experience. Sleep, 17, 466-475.
Totterdell, P, Reynolds, S, Parkinson, B, & Briner, R.B. (1994). Associations of sleep with everyday
mood, minor symptoms and social interaction experience. Sleep, 17(5), 466-475.
Trask, C. H, & Cree, E.M. (1962). Oximeter studies on patients with chronic obstructive emphysema,
awake and during sleep. N Engl J Med, 266, 639-642.
Traver, G. (1988). Measures of symptoms and life quality to predict emergent use of institutional
health care resources in chronic obstructive airways disease. Heart & Lung, 17, 689-697.
Turner-Warwick, M. (1988). Epidemiology of nocturnal asthma. Am J Med, 85 (Suppl 1B), 6-8.
Tyler, D. B. (1955). Psychological changes during experimental sleep deprivation. Dis Nerv Syst 16,
293-299.
Ulfberg, J, Carter, N, Talback, M, & Edling, C. (1996). Excessive daytime sleepiness at work and
subjective work performance in the general population and among heavy snorers and patients with
obstructive sleep apnea. Chest, 110(3), 659-663.
Ulrik, C. S, & Backer, V. (1999). Non reversible airlfow obstruction in life-long nonsmokers with
moderate to severe asthma. Eur Respir J, 14, 892-896.
V Swanson, S. W, KG Power, B Duncan, J Morgan, E Turner and D Gordon, (2000). The Impact of a
Structured Porgramme of Asthma Care in General practice. IJCP, 54(9), 573-580.
Vamos, M, & Kolbe, J. (1999). Psychological factors in severe chronic asthma. Australian and New
Zealand Journal of Psychiatry, 33, 538-544.
van Keimpema, A. R. J, Ariaansz, M, Nauta, J.J.P, & Postmus, P.E. (1995). Subjective sleep quality
and mental fitness in asthmatic patients. Journal of Asthma, 32(1), 69-74.
253
Venables, K. M, Burge, P.S, Davison, A.G, and Newman-Taylor, A.J. (1984). Peak flow rate records
in surveys: reproducibility of observers' reports. Thorax, 39, 828-832.
Vertes, R. P, & Eastman, K.F. (2000). The case against memory consolidation in REM sleep. Behav
Brain Sci, 23, 867-876.
Vgontzas, A. N, Bixler, E.O, Tan, T.L, Kantner, D, Martin, L.F, & Kales, A. (1998). Obesity without
sleep apnea is associated with daytime sleepiness. Arch Intern Med, 158, 1333-1337.
Viinamaki, H, Niskanen, L, Korhonen, T, & Tahka, V. (1993). The patient-doctor relationship and
metabolic control in patients with Type I (insulin dependent) diabetes mellitus. International Journal
of Psychiatry in Medicine, 23, 265-274.
Vir, R, Bhagat, R, Shah, A. (In press). Sleep disturbances in clinically stable young asthmatic adults.
Ann Allergy Asthma Immunol.
Wamboldt, M. Z, Hewitt, J.K, & Schmitz, S. (2000). Familial association between allergic disorders
and depression in adult Finnish twins. Am J Med Genet, 96, 146-153.
Ware, E, John, and Sherbourne, D, Cathy. (1992). The MOS 36-Item Short-Form Health Survey (SF36). Medical Care, 30(6), 473-481.
Ware, J. E. (1993). Measuring patients' views: the optimum outcome measure. SF-36, a valid, reliable
assessment of health from the patient's point of view. BMJ, 306, 1429-1430.
Ware, J. E, Kosinski, M, & Keller, M. (1994). SF-36 physical and mental health summary scales: a
users manual. Boston, MA, The Health Institute, New England Medical Centre.
Ware, J. H, Ferris, B.G. Jr, Dockery, D.W, Spengler, J.D, Strom, D.C, & Speizer, F.E. (1986). Effects
of ambient sulfur oxides and suspended particles on respiratory health of preadolescent children. . Am
Rev Respir Dis, 133, 834-842.
Watson, D, & Pennebaker, J.W, (1989). Health complaints, stress, and distress: exploring he central
role of negative affectivity. Psychological Review, 96, 976-983.
Webb, W. B. (1975). Sleep: The Gentle Tyrant. New Jersey, Prentice-Hall.
Webb, W. B, & Levy, W.B. (1984). Effects of spaced and repeated total sleep deprivation.
Ergonomics, 27, 45-58.
West, J. B. (1998). Pulmonary pathophysiology: the essentials. Baltimore, Williams & Wilkins.
Williams, D. G. a. P. (2004). A User's Guide to the General Health Questionnaire GHQ. London,
nferNelson
Williams, R. L, Karacen, I, & Moore, C.A. (1988). Sleep Disorders diagnosis and treatment. New
York, John Wiley & Sons.
Williamson, D. G. a. P. (2004). A user' guide to the General Health Questionnaire GHQ. London,
nferNelson.
Wirz-Justice, A, & Van den Hoofdakker, R.H. (1999). Sleep deprivation in depression: What do we
know? where do we go? Biol Psychiatry 6, 361-377.
Wright, J. L, Cagle, P, & Churg, A. (1992). Diseases of the small airways. Am Rev Respir Dis, 146,
240-262.
Wynne, J. W, Block, A.J, & Hunt, L.A. (1978). Disordered breathing and oxygen desaturation during
daytime naps. John Hopkins Med, J. 143, 3-7.
254
Wynne, J. W, Block, A.J, & Hemenway, J. (1978). Disordered breathing and oxygen desaturation
during sleep in patients with chronic obstructive pulmonary disease. Chest, 73S, 301S-303S.
Yellowlees, P. M, Haynes, S, Potts, N, & Ruffin, R.E. (1988). Psychiatric morbidity in patients with
life-threatening asthma: initial report of a controlled study. Med J Aust, 149, 246-249.
Yellowlees, P. M, & Ruffin, R.E. (1989). Psychological defences and coping styles in patients
following a life threatening attack of asthma. Chest, 95, 1298-1303.
Zigmond, A.S., Snaith, R.P. 1983, "The Hospital Anxiety and Depression Scale". Acta Psychiatrica
Scandinavica, vol. 67, pp. 361-370.
255
Appendices
Appendix 1:
Key terms and databases used for the literature review.
Appendix 2:
Patient invite letter with consent form for individuals
Appendix 3:
Patient information sheet for individuals
Appendix 4:
Study questionnaire
Appendix 5:
Participant invite letter with consent form for healthy participants
Appendix 6:
Participant information sheet for healthy participants
Appendix 7:
Ethics Letters
Appendix 8:
The National Statistics Socio-economic classification: user manual
Appendix 9:
Legend for diseases listed in results section
Appendix 10: The British guidelines for asthma management
Appendix 11: ESS normative scores
Appendix 12: SF-36 normative scores and Z-score calculations
Appendix 13: GHQ-12 normative scores
Appendix 14: BDI normative scores
Appendix 15: Phase 1 raw data SPSS sheet
256
Appendix 1: Key terms and databases used for the
literature review.
Databases and keyword search terms used for the literature review.
Databases used for literature review:
Key terms used to gather data:
Medline
Sleep disturbances.
Sleep disturbances & QoL.
Sleep Disturbances & Cognitive functioning.
Sleep Disturbances & daytime functioning.
Daytime functioning, cognitive functioning &
QoL.
All above combined.
Psycinfo-Psyclit
Problematic sleep.
Sleep disturbances.
Sleep and breathing.
Sleep and respiratory diseases.
Respiratory diseases.
All 6 of the respiratory conditions and sleep
individually.
Sleep apnoeas.
Respiratory diseases & QoL.
Respiratory diseases & cognition.
CINAHL
Combination of the above key words were used.
The Cochrane Library
Asthma.
Asthma & Sleep.
Asthma, Sleep & QoL.
COPD & Asthma.
SCOPUS
Sleep and respiration.
Sleep and daytime functioning.
Impaired sleep and daytime function.
Quality of sleep
257
Appendix 2: Phase 1 patient invite letter with consent
form for patients
Respiratory Centre Miss D R Virk
PhD Research Student
Telephone: 023 9284 5235
[email protected]
Trafalgar Building
Queen Alexandra Hospital
Southwick Hill
Cosham PO6 3LY
3rd November 2006.
Dear
Re: “Sleep Disturbance and General Well-Being in Respiratory Diseases.”
We know that you may recently have attended the Respiratory Clinic either at Queen
Alexandra or St Mary’s Hospitals.
We would be grateful if you would consider helping us in a study to investigate
whether sleep disorders occur in individuals with respiratory problems, and whether
sleep disorders are associated with daytime sleepiness, reduced quality of life and
general mood, memory and concentration disturbance. Information will also be
obtained from individuals who do not have respiratory problems. You would be
required to either complete a questionnaire and return it by post; or complete it at a
visit to the clinic.
Before you decide about taking part, please read the enclosed patient information
sheet. If you are willing then please complete the slip below along with the
completed questionnaire and return it to us in the enclosed pre-paid envelope.
Alternatively, if you are given this letter in the clinic, please still complete the slip
below along with the completed questionnaire and either return it to us in the
enclosed pre-paid envelope, or hand it to one of the investigators in the clinic.
If you require further information, please do not hesitate to contact us at the
addresses on the information sheet.
Yours sincerely
Miss D R Virk
PhD Research Student
………………………………………………………………………………………
258
Please tear off this slip and tick one of the following boxes and return in the envelope
provided, thank you.
I agree to take part in the study (“Sleep Disturbances and General Well-Being in
Respiratory Diseases”)
I do not wish to take part in the study (“Sleep Disturbances and General Well-Being
in Respiratory Diseases”)
Name…………………………………………………………………………………
Address………………………………………………………………………………
259
Appendix 3 Phase 1 Patient information sheet for
individuals
STUDY INFORMATION SHEET
Sleep Disturbance and general well-being in respiratory diseases.
You are being invited to take part in a research study. Before you decide it is
important for you to understand why the research is being done and what it will
involve. Please take time to read the following information carefully and discuss it
with others if you wish. Ask us if there is anything that is not clear or if you would
like more information. Take time to decide whether or not you wish to take part.
Thank you for reading this.
What is the purpose of the study?
Sleep disturbance is a common complaint in various respiratory diseases and can
affect an individual’s ability to function properly during the day. Little research has
been done in this area.
The purpose of this study is to investigate whether sleep problems occur in
individuals with respiratory diseases and whether they are associated with daytime
sleepiness, reduced quality of life and general mood and memory and concentration
difficulties.
Information will also be obtained from individuals who do not have respiratory
diseases.
Why have I been chosen?
You have been chosen to take part in the study as you have attended the Respiratory
Clinic at Queen Alexandra or St Mary’s Hospital. Many individuals who have
attended this clinic will be asked to participate.
Do I have to take part?
It is up to you to decide whether or not to take part. If you do decide to
take part you will be given this information sheet. If you decide to take
part you are still free to withdraw at any time and without giving a
reason. A decision to withdraw at any time, or a decision not to take part,
will not affect the standard of care you receive.
What will happen if I take part?
If you decide to take part, you will be asked to complete a questionnaire asking about
different aspects of any sleep disturbance and daytime sleepiness you may
experience, how you rate your quality of life and your general mood and any
memory and concentration difficulties you may have. You will then be asked to send
260
the completed questionnaires back to us in a stamped addressed envelope, or return it
to the investigating team at your clinic appointment if you completed it on the day.
Will my taking part in this study be kept confidential?
All information that is collected about you during the study will be kept confidential.
Any information about you used for analysis will have your name and address
removed so that you cannot be recognised from it.
What will happen to the results of the study?
It is likely the results of the study will be published in a scientific journal for health
professionals. Participants will not be identified in any report or publication. A
summary of the results will be made available to all interested participants at the end
of the study.
Who is organising and funding the research?
The research is being conducted jointly by staff at the Respiratory Service,
Portsmouth Hospital NHS Trust and The School of Health Sciences and Social Work
(SHSSW) University of Portsmouth.
Who has reviewed the study?
The study had been reviewed by the Isle of Wight, Portsmouth and South East
Hampshire NHS Local Research Ethics Committee and the Portsmouth NHS Trust.
Thank you for reading this.
Contacts for Further Information:
Ms Dally Virk
Dr A J Chauhan
School of Health Sciences and Social Consultant Respiratory Physician
Work
Trafalgar Building
Room 0.302
Queen Alexandra Hospital
James Watson Hall
Cosham
2 King Richard First Road
PO6 3LY
Portsmouth
PO1 2FR
023 9284 4434
023 9228 6000 ext 1386
[email protected]
[email protected]
261
Appendix 4:
Phase 1 questionnaire
262
263
264
265
266
267
268
269
270
271
272
273
274
275
276
277
278
279
280
281
282
283
284
285
Appendix 5: Phase 1 participant invite letter with
consent form for healthy participants
Respiratory Centre Miss D R Virk
PhD Research Student
Secretary:
023 92 845235
[email protected]
Trafalgar Building
Queen Alexandra Hospital
Southwick Hill
Cosham PO6 3LY
3rd November 2006
Dear
Re: “Sleep Disturbance and General Well-Being in Respiratory Diseases.”
We would be grateful if you would consider helping us in a study to investigate
whether sleep disorders occur in individuals with respiratory problems, and whether
they are associated with daytime sleepiness, reduced quality of life and general
mood, memory and concentration disturbance.
Information will also be obtained from individuals known to have respiratory
diseases.
Before you decide about taking part, please read the enclosed patient information
sheet. If you are willing then please complete the slip below along with the
completed questionnaire and return it to us in the enclosed pre-paid envelope.
If you require further information, please do not hesitate to contact us at the
addresses on the information sheet.
Yours sincerely
Miss D.R. Virk
PhD Research Student.
286
Please tear off this slip and tick one of the following boxes and return in the envelope
provided, thank you.
I agree to take part in the study (“Sleep Disturbances and General Well-Being in
Respiratory Diseases”)
I do not wish to take part in the study (“Sleep Disturbances and General Well-Being
in Respiratory Diseases”)
Name…………………………………………………………………………………
Address………………………………………………………………………………
287
Appendix 6: Phase 1 participant information sheet for
healthy participants
STUDY INFORMATION SHEET
Sleep Disturbance and general well-being in respiratory diseases.
You are being invited to take part in a research study. Before you decide it is
important for you to understand why the research is being done and what it will
involve. Please take time to read the following information carefully and discuss it
with others if you wish. Ask us if there is anything that is not clear or if you would
like more information. Take time to decide whether or not you wish to take part.
Thank you for reading this.
What is the purpose of the study?
Sleep disturbance is a common complaint in various respiratory diseases and can
affect an individual’s ability to function properly during the day. There is very little
research in this area.
The purpose of this study is to investigate whether sleep problems occur in
individuals with respiratory diseases and whether they are associated with daytime
sleepiness, reduced quality of life and general mood, memory and concentration
difficulties.
Information will also be obtained from individuals who do have respiratory diseases.
Why have I been chosen?
It is important to compare the findings from those with respiratory diseases and those
who do not have respiratory diseases. Once the data has been collected from both
groups we shall be able to see how those who live with respiratory diseases are
affected in terms of their quality of life, general mood, memory and concentration
and whether their respiratory disease has an impact upon their quality of sleep. We
will only be able to do this once we have collected data from those without
respiratory diseases and compared the findings.
Do I have to take part?
It is up to you to decide whether or not to take part. If you do decide to
take part you will be given this information sheet. If you decide to take
part you are still free to withdraw at any time and without giving a
reason. A decision to withdraw at any time, or a decision not to take part,
will not affect the standard of care you receive.
What will happen if I take part?
288
If you decide to take part, you will be asked to complete a questionnaire asking about
different aspects of any sleep disturbance and daytime sleepiness you may
experience, how you rate your quality of life and your general mood and any
memory and concentration difficulties you may have. You will then be asked to send
the completed questionnaires back to us in a stamped addressed envelope.
Will my taking part in this study be kept confidential?
All information that is collected about you during the study will be kept confidential.
Any information about you used for analysis will have your name and address
removed so that you cannot be recognised from it.
What will happen to the results of the study?
It is likely the results of the study will be published in a scientific journal for health
professionals. Participants will not be identified in any report or publication. A
summary of the results will be made available to all interested participants at the end
of the study.
Who is organising and funding the research?
The research is being conducted jointly by staff at the Respiratory Service,
Portsmouth Hospital NHS Trust and the School of Health Sciences and Social Work
(SHSSW) University of Portsmouth.
Who has reviewed the study?
The study had been reviewed by the Isle of Wight, Portsmouth and South East
Hampshire NHS Local Research Ethics Committee and the Portsmouth NHS Trust.
Thank you for reading this.
Contacts for Further Information:
Ms Dally Virk
Dr A J Chauhan
School of Health Sciences and Social Consultant Respiratory Physician
Work
Trafalgar Building
Room 0.302
Queen Alexandra Hospital
James Watson Hall
Cosham
2 King Richard First Road
PO6 3LY
Portsmouth
PO1 2FR
023 9284 4434
023 9228 6000 ext 1386
[email protected]
[email protected]
289
Appendix 7:
of study
Letters from ethics committee for approval
290
291
Appendix 8: The National
classification: user manual
292
Statistics
Socio-economic
Appendix 9:
Legend for diseases listed in results section
Skin:
• For example eczema, psoriasis, acne, rosacea, warts, calluses, candidiasis, crab lice,
dermatophytoses, head lice, hirsutism, nappy rash, photodamage, pityriasis versicolor and
scabies.
Ear, Nose and oropharynx:
• For example allergic rhinitis, nasal polyps, oropharyngeal infections and peridontitis.
Cardiovascular:
• Angina, arrhythmias, cardiovascular disease risk, heart failure, hypertension, myocardial
infarction and phaeochromocytoma.
Gastro-intestinal system:
• Antibiotic-associated colitis, constipation, crohn’s disease, diverticular disease, food allergy,
helicobacter pylori infection, irritable bowel syndrome, NSAID-associated ulcers,
ulcerative colitis.
Obstetrics, gynaecology and urinary tract disorders:
• Nocturnal enuresis, premature labour, prevention and treatment of post-partum haemorrhage
and priapism.
Musculoskeletal and joint diseases:
• Dental and orofacial pain, extravasation, myasthenia gravis, osteoarthritis and soft-tissue
disorders and rheumatoid arthritis and other inflammatory disorders.
Endocrine system:
• Adrenal suppression during illness, trauma or surgery, serious infections in patients taking
corticosteroids, osteoporosis and breast pain (mastalgia).
Central Nervous System:
• Psychosis and related disorders, depression, attention deficit hyperactivity disorder, obesity,
nausea and vertigo, pain, epilepsy, Parkinson’s and related neuro-degenerative diseases,
substance dependence, dementia.
Psychiatric disorders:
• Anxiety disorders, dissociative disorders, drug use and dependence, eating disorders, mood
disorders, personality disorders, schizophrenia and related disorders, sexuality and
factitious disorders and suicidal behaviour.
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Paediatrics:
• Various childhood diseases
Respiratory:
• Acute severe asthma, anaphylaxis, angiodema, chronic asthma, croup.
294
Appendix 10: The
management
British
295
guidelines
for
asthma
Appendix 11: ESS normative scores
Normative scores for participants who have been scored on the ESS. Scores in mild,
moderate and severe Obstructive sleep apnoea syndrome.
Diagnoses
Total number of Pp
ESS scores
Range
(mean ± SD)
Mild OSAS
22
9.5 ± 3.3
4-16
Moderate OSAS
20
11.5 ± 4.2
5-20
Severe OSAS
13
16.0 ± 4.4
8-23
Source: Johns, M.W (1991) A New Method for Measuring Daytime Sleepiness: The Epworth Sleepiness Scale.
Sleep, (14(6): 540-545.
296
Appendix 12: SF-36 normative scores and z-scores
To achieve the final two scales transformed physical (PCS) and transformed mental
(MCS) a series of calculations were performed. First, each SF-36 scale was
standardized using z-score transformation and SF-36 scale means and standard
deviations from the general UK population. A z-score for each scale is computed by
subtracting the general population mean from SF-36 scale score and dividing the
difference by the corresponding scale standard deviation from the general population.
After a z-score has been computed for each SF-36 scale, the second step involves
computation of aggregate scores for the physical and mental components using the
physical and mental coefficients from the general population.
The final step involves transforming each component score to the norm-based
scoring. The PCS and MCS are constructed to reduce the SF-36 from a nine-scale
profile to two summary measures.
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298
299
Appendix 13: GHQ-12 normative scores
What are the thresholds for GHQ?
Thresholds are only relevant for screening use of the GHQ, i.e. for identifying
‘caseness’. For this use, the GHQ scoring is advocated by the test author. For GHQ30 and GHQ-60, the user will need to determine their required threshold value – we
have no data on which to base a default threshold for such scoring.
In general, it is best if the user specifies their required threshold value, based on past
clinical use or research evidence relevant to their assessment circumstances. The
following gives some threshold values that can be entered as default options. These
have been derived from information in the original GHQ Manual, the User’s Guide
and the following paper: Goldberg, D.P. et al (1997).
The validity of two versions of the GHQ in the WHO study of mental illness in
general health care. Psychological Medicine, 27, 191-197.
N.B. For people who are physically ill, a higher threshold than the default one
will probably be needed for optimal discrimination between cases and noncases.
Suggested Default Thresholds
Suggested default threshold using:
GHQ
GHQ Scoring
Likert
GHQ12
1/2 (max score 12)
11/12 (max score 36)
GHQ28
4/5* (max score 28)
23/24 (max score 84)
GHQ30
4/5 (max score 30)
--- (max score 90)
GHQ60
11/12 (max score 60)
--- (max score 180)
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Appendix 14: BDI normative scores
Means and standard deviations of the BDI-II scores by sample and diagnostic groups
Sample (N)
Mean
Std Dev
Sample
22.45
12.75
12.56
9.93
26.57
12.15
28.05
11.75
29.45
11.74
Dysthymia (49)
24.02
11.86
Bipolar (34)
20.59
12.71
Depression NOS (16)
22.81
10.05
Anxiety Disorders (88)
19.38
11.46
Adjustment disorders (80)
17.29
12.33
Other disorders (68)
16.50
11.61
Outpatients (500)
Sample
College students (120)
Diagnostic groups
Mood disorders (264)
Single episode,
Major depression (62)
Recurrent episode
Major depression (103)
Beck, A.T, Steer, R.A., & Brown, G.K. (1996) Beck Depression Inventory-Second edition. The Psychological
Corporation, Harcourt Brace & Company.
301
Appendix 15: Phase 1 raw data
302