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Psychopathology
Psychopathology is the branch of psychology concerned with abnormal behaviour that puts
forward theories on the origins, development and symptoms of mental and behavioural
disorders. Psychopathology uses both biological and psychological approaches, on which
many varied therapies for the treatment of abnormal conditions have been developed.
For this section (Section A) of your Unit 4 exam, you are required to study one mental
disorder from 4 choices: Schizophrenia, depression, phobic disorders and obsessive
compulsive disorder. The disorder that we are going to study, and about which you’ll be
tested in your Unit 4 exam is Schizophrenia.
The sections of psychopathology studies are:
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Clinical characteristics
Issues and Classification and Diagnosis, including reliability and validity.
Biological explanations, for example genetics, biochemistry.
Psychological explanations, for example psychodynamic, cognitive, socio cultural.
Biological therapies, including their evaluation in terms of appropriateness and
effectiveness.
 Psychological therapies, for example behaviour, psychodynamic and cognitivebehavioural including their evaluation in terms of appropriateness and effectiveness.
Put ‘schizophrenia’ into Google images and reflect on why I have selected the above image,
rather than the more common pictures representing this disorder.
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Schizophrenia
Clinical characteristics
‘Schizophrenia is a generic name for a group of disorders, characterised by a progressive
disintegration of emotional stability, judgement, contact with and appreciation of reality,
producing considerable secondary impairment of relationships and intellectual functioning.’
(Stafford-Clarke, 1964).
Schizophrenia is a serious mental disorder affecting thought processes and the
ability to determine reality. Degree of severity varies between sufferers: some only encounter
one episode, some have persistent episodes, but live relatively normal lives through taking
medication, while others have persistent episodes, are non-responsive to medication and remain
severely disturbed.
Some would say that schizophrenia may be a group of disorders, with different causes and
explanations.
To be diagnosed with schizophrenia, two or more symptoms must be apparent for more than 1
month, as well as reduced social functioning.
 Positive symptoms are additional to everyday experience, e.g. distortion of
perception such as hallucinations, disordered speech and delusions.
 Negative symptoms consist of a reduction or loss of normal functioning, e.g.
avolition (lack of motivation to pursue goals in life), alogia (lack of communication),
affective flattening (lack of emotion).
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Other differentiations are chronic onset schizophrenia, where sufferers become increasingly
disturbed through gradual withdrawal and motivational loss over a prolonged period; and acute
onset schizophrenia, where symptoms appear suddenly, after a stressful incident.
Schizophrenia commonly occurs between 15 and 45 years of age, with an equal incidence rate
between males and females, though males generally show onset at an earlier age.
Since 1994, the two main classification systems in use worldwide are DSM-IV and the ICD-10.
DSM-V diagnostic criteria for schizophrenia.
Characteristic symptoms: two (or more) of the following, each present for a significant portion of time
during a 1-month period (or less if successfully treated):
1. Delusions
2. Hallucinations
3. Disorganised speech (e.g. frequent derailment or incoherence)
4. Grossly disorganised or catatonic behaviour
5. Negative symptoms affective flattening (lack of emotion), alogia (lack of communication) or
avolition (lack of motivation or desire to pursue goals).
Only one criterion A symptom is required if delusions are bizarre or hallucinations consist of a
voice keeping up a running commentary on the person’s behaviour or thoughts, or two or more
voices conversing with each other.
Duration: continuous signs of the disturbance persist for at least 6 months.
 The above symptoms must not be due to the physiological effects of a drug of abuse or
medication.
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Extension task: There is no such thing as a ‘normal’ schizophrenia person exhibiting ‘usual’
symptoms. Therefore several subtypes have been proposed. The ICD-10 classification system
lists seven subtypes, while the DSM-V has five. Examples include ‘Paranoid’ and ‘Catatonic’
schizophrenia.
 Look up all 7 subtypes of schizophrenia, and see if you can identify the key differences.
 Ask yourself what are the benefits and what are the problems of categorising all these
subtypes are.
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SCHIZOPHRENIA: Issues of Classification and Diagnosis
As with physical conditions, mental disorders first have to be diagnosed; in order to
do this, clinicians use classification systems. These are based on the idea that
certain groups of symptoms can be classed together as a syndrome, which has an
underlying cause and is separate from other syndromes. In this way, mental
disorders are perceived in a similar way to physical disorders, as mental illnesses,
which can be identified (diagnosed), treated and cured.
ICD – Is the diagnostic classification system produced by the World Health
Organisation.
DSM: The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSMV) is the official classification system of the American Psychiatric Association, but is
used worldwide.
DSM-V does acknowledge that ‘there is now assumption that each category of
mental disorder is a completely distinct unit with absolute boundaries dividing it
from other mental disorders or from no mental disorder.’
IMPORTANT: The key focus of this section is on the reliability and
validity. In plain language:
 Is Schizophrenia diagnosed consistently between psychiatrists and over
time? (Reliability)
 Is Schizophrenia a real disorder? (Validity)
Reliability of diagnosis
Reliability refers to the consistency of symptom measurement and affects classification and
diagnosis in two ways:
 Test-retest reliability – occurs when a practitioner makes the same consistent diagnosis
on separate occasions from the same information.
 Inter-rater reliability – occurs when several practitioners make identical, independent
diagnoses of the same patient.
Making reliable diagnoses of mental illness is problematic, as practitioners have no physical signs,
but only symptoms (mostly which the patient reports) to base decisions on.
Practitioners have to make subjective decisions due to the wording of DSM-IV – for example,
comparing patients to ‘average people’.
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Research: reliability
Beck et al. (1962) reported a 54 per cent concordance rate between experienced practitioners’
diagnoses when assessing 153 patients, while Söderberg et al (2005) reported a concordance
rate of 81 per cent using DSM-IV-TR, the most up-to-date form of the DSM classification system.
This suggests that classifications systems have become more reliable over time.
Read et al. (2004) reported a test-retest reliability of schizophrenia diagnosis to have only a 37
per cent concordance rate, and noted a 1970 study where 194 British and 134 US psychiatrists
provided a diagnosis on the basis of a case description; 69 per cent of the Americans diagnosed
schizophrenia, but only 2 per cent of the British. This suggests that the diagnosis of schizophrenia
has never been reliable.
However, Jackobsen et al. (2005) tested the reliability of the ICD-10 classification system in
diagnosing schizophrenia. A hundred Danish patients with a history of psychosis were assessed
using operational criteria, finding a concordance rate of 98 per cent, demonstrating the high
reliability of clinical diagnosis of schizophrenia using up-to-date classifications.
Reliability: general evaluation.
 There are several diagnostic tools in addition to the DSM and ICD that have been
created specifically to help clinician diagnose schizophrenia (e.g. Schneider
Criteria). The use of these criteria can actually improve the reliability of diagnosis.
For example, Farmer et al. (1988) found high levels of reliability using the standard
interviewing technique known as PSE (Present State Examination).
 However, the fact that different criteria have been used to diagnose schizophrenia
makes it difficult to research studies. For example, in outcome research
(investigating the outcome of treatment) it is hard to compare data based on
individuals who have been diagnosed with schizophrenia using different criteria.
Conclusion: Even if reliability of diagnosis based on classifications systems is not
perfect, they do provide practitioners with a common language, permitting
communication of research ideas and findings, which may ultimately lead to a better
understanding of the disorder and the development of effective treatments
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Validity of diagnosis
Validity concerns how accurate, meaningful and useful diagnosis is. There are several ways in
which validity can be assessed:
 Predictive validity: if diagnosis leads to successful treatment, the diagnosis is seen as
valid.
 Descriptive validity: to be valid, patients diagnosed with different disorders should differ
from each other. Descriptive validity is reduced by comorbidity, where patients have two
or more disorders simultaneously, suggesting that such disorders are not actually separate.
Research: validity
Heather (1976) argued that few causes of mental disorders are known [consider this claim in the
next section on explanations of schizophrenia] and there is only a 50 per cent chance of predicting
what treatment patients will receive based on diagnosis, suggesting that diagnosis of schizophrenia
is not valid.
Hollis (2000) studied 93 cases of early onset schizophrenia, applying DSM classification
diagnoses to patient case notes. The findings indicated that the diagnosis of schizophrenia had
high level of stability, suggesting that diagnoses are to a large extent valid.
Cochrane (1977) reported the incidence of schizophrenia in the West Indies and Britain to be
similar, at around 1 per cent, but that people of Afro-Caribbean origin are seven times more likely
to be diagnosed with schizophrenia when living in Britain. This suggests that Afro-Caribbean
people living in Britain either have more stressors leading to schizophrenia, or that invalid
diagnoses are being made due to cultural bias.
Whaley (2004) believed the main reason for the incidence of schizophrenia among black
Americans being greater than among white Americans is cultural bias, where ethnic differences in
symptom expression are overlooked or misinterpreted by practitioners. This suggests a lack of
validity in diagnosis.
Conclusion: Kendell and Jablensky (2007) responded to the claim that schizophrenia should be
abolished as a concept for being scientifically meaningless. They stated that diagnostic categories
are justifiable concepts, as they provide a useful framework for organising and explaining the
complexity of clinical experience, allowing clinicians to derive inferences about outcomes and to
guide decisions about treatment.
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Extension reading: Additional issues of classification and
diagnosis
The effects of labelling: Critics of diagnosis have suggested that it is
stigmatising to attach a ‘label’ of schizophrenia to an individual. Scheff
(1966) believed that people labelled with a diagnosis will conform to the
label and it therefore becomes a self-fulfilling prophecy. While this is
clearly and inadequate explanation for a serious mental disorder like
schizophrenia, it is nonetheless true that mental illness labels stick, and
they can be used to describe the person rather than the disorder.
Anti-psychiatry perspective (The question of whether schizophrenia is
a mental disorder at all. Mental illness as dehumanising and a form of
political control). There are those, such as Thomas Szasz, who have
questioned the whole concept of mental illness and has suggested that the
process of diagnosis is just a form of political control. He argues that
physical illness is different from mental illness.
Szasz’s main objection to the concept of mental illnesses, such as
schizophrenia, is that it dehumanises people. To say that someone is ill is to
remove responsibility from them for their problems. Szasz mounted a
strong and direct challenge to the medical model of mental disorders. His
work may have helped to give rise to the ‘patient power’ movement in the
early 1960s.
For more on Tomas Szasz, read the article in the back of this booklet:
‘Anti-psychiatry and the mental illness debate’.
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Classic research
Rosenhan (1973)
On being sane in insane places.
It would be expected that psychiatrists make valid diagnoses – that is, correctly
identify the mental disorders people suffer from. However, this famous study casts
doubts on this expectation.
Aims
To test the validity of schizophrenia diagnosis using the DSM-II classification system.
Procedure
Eight volunteers presented themselves to different mental hospitals, claiming to hear
voices. All were admitted and acted normally. Time taken to be released and reactions
to them were recorded.
Findings
The eight volunteers took between 7 and 52 days to be released, diagnosed as
schizophrenics in remission. Normal behaviours were interpreted as signs of
schizophrenia. However, 35 out of 118 actual patients suspected they were sane.
Conclusions
The diagnosis of schizophrenia lacks validity, as psychiatrists cannot distinguish
between real and pseudo-patients.
Being diagnosed as schizophrenic is a stigmatic, ‘sticky label’ – difficult to remove, with
serious consequences (think about what these consequences may be, then read the
section on the problem of labelling.
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Biological explanations of Schizophrenia
Biological explanations have focused on several areas, including genetics and biochemistry.
Although causes of schizophrenia are not fully understood, and indications are that that several
contributory factors combine to cause the onset of the disorder, evidence does suggest that
biological factors play a major contributory role.
Genetics
Research traditionally uses twin, family and adoption studies to assess what role genetics plays in
the causation of schizophrenia, by examining concordance rates of schizophrenia between people
with different degrees of genetic relationship. Research has indicated a genetic component, though
separating out environmental influences is problematic.
More recently gene mapping studies have compared genetic material from families with high
incidence and low incidence of schizophrenia. Results indicate that several genes are involved and
that genes make some individuals more vulnerable than others in developing the disorder.
Research: genetics
Gottesman (1991) reported on several twin studies carried out since 1966, and found that the
risk of a particular individual developing schizophrenia is proportional to the amount of genes they
share. For example, for monozygotic twins (who share 100% of their genes), the risk is
48%, whereas for dizygotic twins (who share about 50% of their genes), the risk is 17%.
This suggests that genetics are a significant part of the picture when looking at the causes of
schizophrenia, though they are not the only factor, otherwise concordance rates for MZ twins
would be 100%.
Gottesman and Shields (1976) reviewed five twin studies and reported a concordance rate of
between 75 and 91 per cent for MZ twins with severe forms of schizophrenia, suggesting
that genetics plays a larger role with chronic forms of the disorder.
Kety and Ingraham (1992) found that prevalence rates of schizophrenia were ten times higher
among genetic than adoptive relatives of adopted schizophrenics, suggesting that genetics plays a
greater role than environmental factors.
Gurling et al. (2006) used evidence from family studies indicating that schizophrenia was
associated with chromosome 8p21-22, to identify a high-risk sample. Using gene mapping, the
PCM1 gene was implicated in susceptibility to schizophrenia, providing more evidence for
genetics.
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Genetics: Evaluation
 If genes caused schizophrenia on their own, concordance rates between MZ twins would
be 100 per cent which they are not. Twin studies also produce conflicting evidence, with
heritability estimates ranging from 58 per cent down to as low as 11 per cent for MZ
twins.
 Leo (2006) argued that Kety’s adoption study evidence is not as convincing as it first
appears. Sample sizes were very small, making generalisations difficult, and many of the
biological relatives found to have schizophrenia were quite distant relatives, such as halfsiblings, with low biological similarity.
 Gene mapping studies offer the possibility of developing tests to identify high-risk
individuals, though this raises socially sensitive ethical concerns.
 Findings from genetic studies provide evidence for the diathesis-stress model (see
end of this section.
Think about it:
 Gene mapping research is potentially
socially sensitive. Why do you think this is
the case?
 Can you think of a way of remembering the
findings of Kety and Ingrahams’ study, and
Leo’s criticisms?
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Biochemical explanation
The biochemical explanation centres on the idea that the neurotransmitters dopamine is
connected to the onset of the disorder. Neurotransmitters are chemicals acting on the biology of
the body associated with the transmission of signals along the nervous system, especially signals
sent across gaps between neurons across synapses.
IMPORTANT: it is important to understand that genetic and biochemical explanations should
not be seen as completely separate. Genes influence all aspects of our biology, and this might
include biochemical activity. The key debate is to what extent do they determine our biochemistry,
and to what extent is biochemical activity linked to environmental and psychological influences?
Snyder (1976) proposed that too much dopamine released across synapses, leads to the onset of
schizophrenia, with sufferers showing high levels of D-2 receptors on receiving neurons, which
creates increased dopamine binding and more neurons firing.
The theory developed after it was discovered that Phenothiazines, antipsychotic drugs that
lessen the symptoms of schizophrenia, inhibit dopamine activity. Also, the dopamine-releasing
drug L-dopa (which can be used to treat motor neuron diseases, such as Parkinsons disease) can
create schizophrenic-like behaviour in non-psychotic people. Other drugs influencing the
dopaminergic system, like LSD, a hallucinogenic, also create schizophrenic-like behaviour in nonpsychotics and aggravate symptoms in those susceptible to the disorder. It is possible that genetic
factors may also be involved in creating faulty dopaminergic systems in those with schizophrenia.
Davis et al. (1991) updated the original theory, because high levels of dopamine are not found in
all individuals with schizophrenia, and the modern anti-schizophrenic drug clozapine, with very
little dopamine-blocking activity, works effectively against the disorder. Davis suggested that high
levels of dopamine in the mesolimbic dopamine system are associated with positive
symptoms, while high levels in the mesocortical dopamine system are associated with
negative symptoms.
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Research: biochemical explanations
Iversen (1979) reported that post-mortems on the people who had had schizophrenia found
excess dopamine in the limbic system, suggesting that the neurotransmitter is involved in the
disorder.
Kessler et al. (2003) used PET and MRI scans to compare people with schizophrenia with nonsufferers, finding that the former had elevated dopamine receptors levels in the basal forebrain,
suggesting that dopamine is important in the onset of schizophrenia.
Evaluation: biochemical explanations
 Overall, the evidence is inconclusive. There is no consistent difference in dopamine
levels between drug-free schizophrenics and non-sufferers.
 The dopamine hypothesis could also be criticized for being reductionist. It reduces a
complex and varied disorder to the action of one chemical operating in specific areas of
the brain.
 One issue with the dopamine hypothesis is that Phenothiazines do not work for everyone
diagnosed with schizophrenia. Additionally, they also tend to only treat the positive
symptoms and not the negative symptoms. This leads some such as Crow (1985) to the
conclusion that different types of schizophrenia have different causes.
 Several neurotransmitters may be involved in the development of schizophrenia. Along
with dopamine and glutamine, newer anti-psychotic drugs implicate serotonin’s
involvement too.
 Lloyd et al. (1984) believed that even if dopamine is a causative factor, it may be
indirect, because abnormal family circumstances may lead to high levels of dopamine that
in turn trigger the symptoms.
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Biochemical explanations: ACTIVITY
In the table below, see how many arguments/studies you can list that support or
question the biochemical explanation of schizophrenia.
For
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Against
Extension Reading:
Summary of research into neuroanatomical factors (brain structures)
AO1 Several researchers have argued that brain abnormalities may be involved in
schizophrenia. There are several sophisticated techniques for studying the brain, some of which
have been used to study brain structure in schizophrenia.
For example, the frontal lobes, which are known to have an important role in intellectual
functioning and clear communication, are smaller than in controls. Also ventricles, which are
fluid-filled cavities in the brain, have been shown by numerous studies to be larger in people
with schizophrenia.
AO2/3 Buchsbaum (1990) used sophisticated PET scans to reveal reduced cerebral blood
flow in the frontal lobes of people with schizophrenia. Andreasen et al. (1990) conducted a
well-controlled CT scan study and found significant enlargement of the ventricles in
schizophrenic patients compared to controls.
Though these studies have provided scientific/empirical evidence to support the role of brain
structure in the development of schizophrenia, there have been contradictory findings. Also, as
the participants in these studies have been suffering from schizophrenia for many years, and
most likely taking medication, it is difficult to establish whether these brain abnormalities are
the cause or effect of schizophrenia.
Biological explanations of schizophrenia: CONCLUSION
It is hard to pinpoint a single cause for such a complex and varying
disorder such as schizophrenia.. Zubin and Spring (1977) put forward the idea that
stressful life events could trigger psychotic symptoms in individuals with an
underlying predisposition/vulnerability to schizophrenia. Genetic factors and
prenatal insults (trauma to the unborn child), could lead to a biological vulnerability, and
this can take the form of biochemical abnormalities. This could in turn lead to cognitive
deficits, which could become delusions and hallucination when exposed to environmental
stress. This diathesis-stress model attempts to integrate different potential causes, to
give a more complete explanation of schizophrenia. [THIS CAN ALSO BE USED TO
CONCLUDE A DISCUSSION OF PSYCHOLOGICAL EXPLANATIONS]
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Activity: Tips for exam answer on
biological explanation of schizophrenia. Using an
appropriate Mark Scheme and Examiner’s report, identify at least 5 top
tips for answering a question on biological explanations:
1.
2.
3.
4.
5.
6.
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PSYCHOLOGICAL EXPLANATIONS OF
SCHIZOPHRENIA
If you are asked to outline ‘psychological explanations’ in a 24 marker, then you have the choice on
which theories to apply. You would be advised to focus on more than one; this way it’ll give you
better scope for your AO2/3 discussion.
Below is a discussion of 3 of the main psychological explanations for schizophrenia:



The traditional psychodynamic approach
Family Systems Theory (a development of the traditional psychodynamic approach)
Cognitive explanations
You could also receive credit for discussing socio-cultural factors. You can ask for further
reading on this approach if you wish.
The psychodynamic approach (including family systems theory)
Traditional psychodynamic approach
AO1 According to traditional psychodynamic explanations, schizophrenia is caused by a problem
with an ego defence mechanism called regression. Freud believed that if a child is raised by
cold and uncaring parents, their Ego will attempt to protect them from the trauma
this causes. To do this it employs the defence mechanism of regression, which is when a person
psychologically reverts back to a past stage in their development. The person in a cold and
uncaring environment will have a weak Ego, and so, in dealing with the huge demands placed on t
by employing its defence mechanisms, the Ego shatters, leaving the Id in charge of the sufferer’s
personality. The person becomes totally focused on themselves, to such an extent that they lose
all touch with reality. This is the cause of the visual and auditory hallucinations of
schizophrenia.
AO2/3
The androcentric nature of Freud’s theories, heaping much of the blame on the mothers of
schizophrenics, has attracted considerable criticism. A great deal of research has found that the
parents of the vast majority of schizophrenic sufferers are not cold and uncaring as Freud
described them, but sensitive and caring individuals, scared and devastated by their child’s illness.
Another criticism that has been applied to the psychodynamic theory of schizophrenia relates to
the therapies that have been established to try and cure individuals. If Psychodynamic theory can
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explain why schizophrenia has occurred, it can propose a way to cure it. So far, there have been no
real breakthroughs with sufferers of schizophrenia who have undergone psychodynamic therapy.
Family systems theory
AO1 In another psychodynamic explanation, Fromm-Reichman (1948) proposed that
schizophrenia was caused by ‘schizophrenogenic families’ and in particular a schizophrenogenic
mother (a mother who causes schizophrenia). The mothers, she suggested, seem to convey
conflicting messages to the child. They are cold and distant but dominating and severe. They were
often rejecting of the child, but still demanded that the child show emotional expression and were
dependent on the mother at all times.
Repeated exposure to such contradictory messages causes the child to resort to self-deception and
to develop a false concept of reality and an inability to communicate effectively. For FrommReichman, there also seemed to be a link between schizophrenogenic families and those with high
emotional tension, many secrets and plots. They had very high levels of conflict and lacked the
abilities to arrive at resolutions.
AO2/3
Brown et al (1966 and 1972) focused on one aspect of the theory proposed by FrommReichman, and that was the emotion expressed (e.g. criticism, hostility and over concern) within
the family of a schizophrenic sufferer. They conducted a nine-month follow-up study of
schizophrenic patients who had returned to their family homes after being discharged from
hospitals. In the nine months following their return home, 10% of the patients returning to low EE
(expressed emotion) homes had relapsed. In the high EE group of families, 58% had relapsed.
However, the concept of expressed emotion is more of a predictor of relapse, than an explanation
of the initial development of schizophrenia.
A problem with family systems theory is that we cannot infer a cause and effect relationship
between the behaviour of the family and the presence of a schizophrenic child. The data gathered
from research into this will almost always be retrospective [recording past events, usually by selfreport] and therefore it is difficult to draw conclusions relating to the accuracy and reliability of the
information.
It may also be the case that the disturbed behaviour in the family is not the cause of a child
developing schizophrenia, but rather that the disturbed behaviour in the family is the result of the
family having a schizophrenic in their midst.
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Cognitive explanation
AO1 Whilst a number of different cognitive explanations have been put forward, they all have in
common the idea that schizophrenia is caused by disorganised thinking.
One of the most important general cognitive theories of schizophrenia is the attention deficit
theory. According to Frith (1979), schizophrenia is the result of a faulty attention system.
Preconscious thought (i.e. thought that occurs without awareness contains huge quantities of
information from our senses that would normally be filtered, leaving only a small amount to enter
into conscious thought.
Schizophrenia may be the result of a breakdown of the filtering process, resulting in overload. It is
this that gives rise to cognitive abnormality. For example, thoughts that would usually be filtered
out as irrelevant or unimportant are now interpreted in conscious awareness as more significant
than they really are.
Because there is a problem with attention, schizophrenics have difficulty focussing on anything for
any period of time, giving the impression of disordered thought. For Frith, this accounts for the
positive symptoms of schizophrenia, such as delusions, auditory hallucinations and disorganised
speech.
AO2/3 If schizophrenics have an attentional problem then they would have difficulty doing tasks
that require focused attention. However, schizophrenics do not seem to be any easier to distract
than normal, when engaged on cognitive tasks (Mckenna, 1994). McKay et al (1996) point out
that a lack of experimental support has resulted in the attention deficit theory being abandoned by
most researchers. Most cognitive research now focuses on explaining specific symptoms of
schizophrenia rather than the disorder as a whole.
AO2/3 Schizophrenics clearly have disordered thoughts, but it is debatable whether this is a cause
of the disorder or a symptom of it. This means that it is not clear whether cognitive deficits cause
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schizophrenia (and the associated biological changes), or whether the cognitive deficits are an
effect of other causes, such as neurochemical changes.
AO2/3 Whilst cognitive theories appear to explain many of the positive symptoms of
schizophrenia satisfactorily, they don’t adequately explain negative symptoms.
Psychological explanations: general conclusion
Garety et al. (2001) believed that schizophrenia is best understood by linking together different
explanations, both biological and psychological, with cognitive explanations being the vital link in
the chain.
You can conclude by applying the diathesis stress model (Zubin and Spring), to give a complete
explanation of schizophrenia, integrating both nature and nurture.
•
Genetic factors or prenatal insults can lead to a biological vulnerability
•
This can lead to cognitive distortions
•
If the individual is exposed to stressful life events
•
…or a family environment high in Expressed Emotion
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•
Could lead to schizophrenic symptoms such as delusions and hallucinations
Biological Treatments for Schizophrenia
ASSUMES THAT THE CAUSE OF THE
DISORDER IS BIOLOGICAL (WITHIN THE
BODY) SO ATTEMPTS TO TREAT THE
DISORDER BY CHANGING FUNCTIONING
WITHIN THE BODY.
DRUG TREATMENT
Keys Terms
Agonists: Drugs that increase Neurotransmitter availability, e.g. stimulants.
Antagonist: Drugs that reduce Neurotransmitter availability, e.g. Blockers.
Anti-psychotics: Drugs used to treat Schizophrenia. They reduce psychotic symptoms.
Neuroleptics: Another name for Antipsychotics. There are subtle differences between
Neuroleptics and Antipsychotics, e.g. on which Dopamine receptors they work on: D1, D2, D3 etc.
Typical Antipsychotic drugs: Conventional Antipsychotics (1950’s) that reduce Dopamine
only. Also they usually only reduce positive symptoms. They are very likely to cause the side effect
of Tardive Dyskinesia in 20-30 % of users.
Atypical Antipsychotic drugs: Newer Antipsychotics (1990’s) that reduce Dopamine and
Serotonin. Also they reduce positive and negative symptoms. They are much less likely to cause the
side effect of Tardive Dyskinesia. Although more likely to cause Agranulocytosis.
Tardive Dyskinesia: is a difficult-to-treat form of Dyskinesia (disorder resulting in involuntary,
repetitive body movements) that can be Tardive (having a slow or belated onset). It frequently
appears after long-term or high-dose use of Typical antipsychotic drugs. Tardive Dyskinesia is
characterized by repetitive, involuntary, purposeless movements, such as grimacing, tongue
protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid
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movements of the extremities may also occur. Impaired movements of the fingers may also appear.
For comparison, patients with Parkinson's disease have difficulty moving, while patients with
Tardive Dyskinesia have difficulty not moving.
Agranulocytosis: A lowered number of white blood cells (these are vital for fighting infection).
Agranulocytosis may be asymptomatic or it may clinically present with sudden fever, rigors and
sore throat. Infection of any organ may be rapidly progressive (e.g. pneumonia, urinary tract
infection). Septicaemia may also progress rapidly. Neutrogena and Agranulocytosis is associated
with gum diseases, such as gingival bleeding, saliva increase, halitosis, osteoporosis, and
destruction of periodontal ligament Causes: A large number of drugs have been associated with
Agranulocytosis, including some antipsychotics (the Atypical antipsychotic clozapine. Clozapine
users in the US must be nationally registered for monitoring of low white blood cell counts.
DRUG TREATMENT: AO1
Also known as chemotherapy (chemical therapy), drug treatments have revolutionised the
treatment of Schizophrenia. These are known as anti-psychotic drugs or neuroleptics.
In 1952, French psychiatrists Delay and Deniker discovered that Chlorpromazine (from a
type of drugs known as phenothiazines) had a therapeutic effect on Schizophrenic patients and
alleviated symptoms of hallucinations and delusions.
These drugs work by binding to Dopamine receptors in the
brain and prevent activation of the neuron by Dopamine. They
are Dopamine Antagonists.
ACTION WITHOUT THE DRUG PRESENT
-
The neuron releases dopamine into the synaptic gap
Dopamine binds to the receptor sites on the next neuron
The neuron is activated
ACTION WITH THE DRUG PRESENT
-
The neuron releases dopamine into the synaptic gap
The drugs bind to the receptor sites
Dopamine cannot bind to the receptor sites
The neuron is not activated
Antipsychotic drugs seem to reduce the positive symptoms of Schizophrenia (hallucinations and
delusions) and improve cognitive and behavioural effects as well.
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First and Second Generation Drug Treatment
Chlorpromazine is known as a typical or 1st generation drug therapy. In the 1990’s atypical or
2nd generation antipsychotic drug treatment was introduced. One well known example of these
is Clozapine. These work on Serotonin production as well as Dopamine. These appear to be
affective on negative symptoms of Schizophrenia as well as positive symptoms.
When acting on Dopamine, they temporarily act on the Dopamine receptor by occupying it
temporarily, but rapidly dissociate to allow normal Dopamine transmission.
Evidence for Drug Treatment
In order to determine effectiveness (or efficacy) of medication, experiments have been conducted
examining reductions in symptoms of typical and atypical anti-psychotic medications.
Often these experiments compare the reduction in symptoms between patients treated with
medication and patients treated with a placebo.
 Why is it important that there is a comparison between an experimental group and a control
group?
Davis et al (1989) performed a meta-analysis of over 100 studies comparing anti-psychotic
medications with placebos. This showed that drugs were more effective. Over 70% of sufferers
showed an improvement when treated with anti-psychotic drugs after 6 weeks, compared to 25%
of patients treated with placebo.
Lieberman et al (2005) compared the use of typical and atypical antipsychotic medications in
treating patients with Schizophrenia. Examining 1423 individuals, it was found that 74% of
individuals with chronic Schizophrenia discontinued treatment within 18 months due to
intolerable side effects. Whilst the discontinuation was similar for both types of anti-psychotic, the
reasons given were different. The side effects causing discontinuation for typical anti-psychotics
was issues such as muscular disorders, whereas the side effects causing discontinuation for
atypical anti-psychotics was for issues such as weight gain and metabolic effects.
Schooler et al (2005) compared 1st and 2nd generation anti-psychotics and found 75% of patients
experienced at least a 20% reduction in symptoms.
Kahn et al (2008) examined the effectiveness of treating 1st instance Schizophrenia with 1st and 2nd
generation medications. They found anti-psychotics are effective for at least a year but that 2nd
generation medications were not necessarily any more effective than 1st generation ones.
Evaluation of Drug Treatment
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 Typical antipsychotic medications only treat positive symptoms and do not seem to tackle the
negative symptoms such as apathy, social withdrawal and impaired personal hygiene.
 BUT, atypical anti-psychotic medications have been reputed to tackle negative symptoms
as well as positive symptoms.
------------------------- Drug treatments reduce the symptoms of Schizophrenia, but symptoms may re-appear if
medication is stopped. This can cause what is known as a revolving door phenomenon.
Where patients cease treatment, relapse, return to hospital, are re-treated and leave, discontinue
medication and relapse again. The relapse rate for Schizophrenia is high (40% in first year and
15% in subsequent years) and this is generally due to medication being stopped due to the side
effects.
 BUT this can be overcome by using injections of medications which are long-lasting and
don’t rely on the patient having to remember/choose to take their medication
 BUT, BUT, this can lead to questions regarding the ethics of this as it is taking away the
patients choice. Is it right to force treatment onto individuals in this manner? Are we assuming
control for them to help the patient or to make the treatment easier for practitioners?
------------------------- A weakness of drug treatment is that medications can had side-effects, which can be severe.
This means that patients may stop taking medication (see point above) and thus relapse. Sideeffects can include drowsiness, visual disturbances, changes in weight and depression. More
severe side effects include tardive dyskinesia, which is an irreversible change in muscle control
and leads to patients having uncontrollable muscle spasms such as lip and tongue movements and
facial tics. Research shows that approximately 24% of patients treated with typical anti-psychotics
for 7 years will develop this.
 Would you take a medication knowing such a severe side –effect could occur?
 Is the side-effect less that the symptoms of the disorder? (cost-benefit analysis)
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 Are patients treated with antipsychotics even in a position to give their informed consent
to these treatments?
 BUT, newer medications (atypical anti-psychotic medications) avoids the problems of the
older typical medications as they do not have the same side-effects such as tardive dyskinesia.
 BUT, BUT, these medications have their own side-effects. For example, they can cause a
condition that damages the immune system and affects white blood cells.
 BUT, BUT, BUT, this condition can be managed with regular monitoring of blood and
other medications
 BUT, BUT, BUT, BUT, this means that treatment is not only more complex, but more
expensive.
 Which piece of research can be quoted when examining the issue of side-effects?
------------------------- Medication doesn’t work for everyone diagnosed with Schizophrenia. About 30% of patients
treated with typical antipsychotic medication do not respond to treatment or are intolerant to
them.
 BUT, about half of these treatment resistant patients can be treated effectively with
atypical antipsychotic medication such as Clozapine (Wahlbeck, et al, 1999)
 BUT, BUT, this still means that there are some patients who are treatment resistant and
cannot be treated with medication. What happens to these patients? How can these be helped?
------------------------- Another problem with the use of drug treatments for Schizophrenia is the maintenance of
treatment following an acute phase of the disorder. Some patients require maintenance doses of
medication to prevent relapse occurring and others do not. The dose required is varied individually
also, meaning gauging the dose level for each patient is problematic. Too little, and the risk of
relapse occurs which can put the patient in danger but too much, and the risks of side-effects are
increased.
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 A strength of drug treatment is that it is relatively cheap and cost-effective. Providing regular
medication is a cheaper alternative to providing a safe and secure hospital environment for the
patient. This is a particular issue in the UK where treatments are funded by the state (National
Health Service) and therefore funding is tight and resources need to be used effectively
------------------------- Biological treatments are passive. They assume the patient has something wrong with them,
and medication is taken to correct the wrong. This may mean the patient lacks the motivation to
examine the other causes, such as life stressors, and attempt to manage these.
------------------------- Drug treatments can be examined for their ethical issues. They can be seen as a chemical
straitjacket, to control and pacify patients. Patients may not be able to fully consent to
treatments that could potentially permanently harm them.
------------------------- One of the biggest strengths of drug treatments is the improvement in an individual’s quality of
life. They are effective at controlling positive symptoms and preventing relapse. Prior to the
introduction of drug treatments, patients lived in institutions which were often overcrowded,
unstimulating and primitive. Patients may have been restrained using straitjackets to protect both
the patient and staff in the institution. Less than 3% of individuals diagnosed with Schizophrenia
live permanently in institutions nowadays.
------------------------- SUMMARISE THE STRENGTHS AND WEAKNESSES OF DRUG TREATMENTS IN THE
TABLE BELOW


. Side –effects
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 Activity: Using issues such as cost, side effects, overall effectiveness and effectiveness
at treating different types of symptoms, analyse which type of anti-psychotic is best and
why. Write a paragraph explaining your choice and the reasons for this.
OTHER BIOLOGICAL TREATMENTS
Electroconvulsive therapy (ECT) was first used by Cerletti (1938). It involves inducing an
epileptic fit in a patient. An electric shock is applied across the brain for a fraction of a second
which produces a seizure similar to an epileptic fit. Patients receive 2 or 3 treatments a week for a
total of up to 12 treatments.
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Tharyan and Adams (2005) reviewed 26 studies on the effectiveness of ECT and found it to be
fairly effective in the short-term (better than no treatment) but was not as effective as antipsychotic medications.
 Despite what people might expect, the treatment is no more effective than minor surgery, with a
death rate of 1 in 10,000.
 It has a bad image and seems brutal. Patients may view it as a punishment for their condition.
ECT is no longer recommended in the management of Schizophrenia by NICE (National Institute
for Health and Clinical Excellent).
Another treatment used prior to drug treatment was the use of a Pre-frontal Lobotomy. This
involved surgically disconnecting the frontal lobe from the rest of the brain. Moniz (1936) claimed
this treatment had a high success rate but later research has found limited evidence of its success.
This treatment was not only controversial but is also unlikely to be effective, and causes severe
cognitive and emotional impairment. Therefore, this treatment is not used anymore.
Psychological Treatments for Schizophrenia
Patients with Schizophrenia often find medication effective at reducing Schizophrenia, but often
this is first administered in a protective hospital environment. However, when discharged from
hospital and back in a potentially stressful family or social environment, medication isn’t sufficient
to prevent the continuing cycle of re-admission to hospital.
PSYCHOLOGICAL INTERVENTIONS ARE USED
TO COMPLEMENT MEDICATION, NOT AS AN
ALTERNATIVE
COGNITIVE BEHAVIOURAL THERAPY
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The basic aspect of a cognitive behavioural approach to treatment is that the interpretation of the
event is more important that the actual event. This means that it is how the individual thinks
about and views what is happening to them, rather than what is actually happening to them.
Therefore, Cognitive Behavioural Therapies seek to modify or change the way an individual thinks
and responds to an event.
When applying this to Schizophrenia, CBT seeks to collaborate with the client in order to analyse
the clients thinking and reactions to symptoms experienced, and help to teach them techniques to
improve their self-management of symptoms.
Key parts to CBT  identify and correct
Tarrier (1987) used detailed interviews and found people with Schizophrenia often identify their
own triggers and precursors to an onset of their Schizophrenic symptoms. They often start to find
their own way of coping with the distress caused by hallucinations and delusions. They used
techniques such as distracting themselves, concentrating on a specific task or positive self-talk.
They also used relaxation techniques, breathing exercises or ways of drowning out the voices by
shouting or turning the volume of the TV up. 73% of patients interviewed reported that these
strategies were successful in managing their symptoms.
This research has led to a form of Cognitive Behavioural therapy known as Coping Strategy
Enhancement (CSE). This therapy aims to help patients identify their own signs of an
occurrence of their symptoms, and start to develop their own strategies and techniques to reduce
the intensity and frequency of their psychotic symptoms.
CSE works by a thorough analysis of coping strategies the individual may already employ and
assessment of this, i.e. how well the strategies already used work. The therapy includes
interviewing patients to investigate the frequency, duration triggers and consequences of
symptoms experienced. Patients may be asked to keep a diary to monitor their onset of symptoms
to increase their awareness of triggers. The patient is then systematically trained in the use of
appropriate coping strategies in response to each of their symptoms experienced. The therapy may
then involve practicing the coping strategy in the session, to help the client use it, and the client
may then be given homework tasks to practice using the strategy when the symptom is
experienced. The success of the strategy may be assessed in follow up therapy sessions.
Components to CSE therapy includes:
1) Building rapport between client and therapist and educating the client regarding what the
therapy involves. They may examine coping strategies already used.
2) Specific symptom targeting, where a specific symptom is selected and a specific coping strategy
developed.
The therapy aims to ensure that at least 2 strategies are adopted to be used for each distressing
symptom.
Strategies used may involve statements that individuals can repeat to themselves. They may also
include ways the client can reality test the content of the hallucination or delusion.
Is the treatment effective?
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 How can the effectiveness of a treatment be reliably and validly measured?
Tarrier et al (1993) found significant alleviation of positive symptoms experienced in a group of
individuals diagnosed with Schizophrenia treated with Coping Strategy Enhancement compared to
a group of individuals diagnosed with Schizophrenia who were placed on a waiting list.
 What does this study suggest about the effectiveness of CSE?
 In the sample used by Tarrier, 45% of participants refused to co-operate in the study or
dropped out.
 Why might this be a problem for the conclusiveness of this study?
CSE doesn’t cure Schizophrenia but can help with the day to day management of the condition.
 What does this suggest about the effectiveness of the therapy?
CBT in isolation does not tent to be offered to patients with Schizophrenia. It is almost always
offered alongside anti-psychotic medication.
 Why is this then a problem when it comes to measuring the effectiveness of CBT?
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Gould et al (2001) conducted a meta-analysis of 7 studies investigating the effectiveness of
CBT. He reported a statistically significant decrease in the positive symptoms of schizophrenia
after treatment.
 What does this suggest about the effectiveness of CBT?
 Why does conducting a meta-analysis improve the generalisability of the research?
Bradshaw (1999) undertook a case study on a girl hospitalised 12 times in the 7 years prior to CBT.
The girl received CBT sessions over a 3 year period and showed significant progress in her
physiological functioning. Her symptoms reduced dramatically and there were no hospital
readmissions
 What does this suggest about the effectiveness of CBT?
 Why does this study lack external validity?
Is the treatment appropriate?
Part of the treatment involves the client being able to articulate and express the symptoms
experienced.
 Why might this be a problem? Why might this not be appropriate for all sufferers of
Schizophrenia?
The treatment involves the client being sufficiently motivated to practice and apply learnt
techniques.
 Why might this be a problem?
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 Which specific schizophrenic symptoms experienced might interfere with this?
Kingdon and Kirschen (2006) in a study of 142 schizophrenic patients in Hampshire, found many
patients were not deemed suitable for CBT because patients did not believe that they could fully
engage in the therapy.
 What does this suggest about the appropriateness of the therapy?
In general, it was less effective on older folk than younger ones.
 What does this suggest about the appropriateness of the therapy?
A strength of CBT is that it can be used alongside drug therapy.
 Why is this a strength for the appropriateness of the therapy?
A weakness of CBT is that it requires specially trained therapists and can be an expensive
treatment.
 Why is this a weakness for the appropriateness of the therapy?
Another weakness of CBT is that it can be time consuming and require repeated appointments.
 Why is this a weakness for the appropriateness of the therapy?
 Summarise the evaluation of CBT into the table below.
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EFFECTIVENESS
Strengths
Weaknesses
APPROPRIATENESS
Strengths
Weaknesses
FAMILY INTERVENTION
Research into Expressed Emotion (EE) as a possible factor into the development and relapse of
Schizophrenic symptoms, has shown that the interaction patterns and nature of family
relationships among the family caregivers and patients can have an effect.
This has led to the development of family intervention programmes to improve family
relationships and provide an environment that can support and protect the sufferer.
Central to family intervention programmes is an emphasis on inclusion within the family and a
sharing of information.
Family therapy usually takes place within the people’s homes and typically two family therapists
will work with the relatives and patient. It lasts between 3-12 months with sessions every 2-4
weeks. A minimum of 10 sessions are recommended by NICE.
The sessions aim to start by developing a co-operative and trusting relationship within the family
group and developing an ethos that contributions of all family members are valued.
The therapists work with the family and the patient to develop strategies to cope
better with the mental disorder and its symptoms. This hopefully leads to a more
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supportive and warm atmosphere which helps the patient make better progress and the relatives to
feel more positive about, and more effective in, their supporting roles.
The therapist provides information about the cause, course and symptoms of Schizophrenia.
Family members, including the individual with Schizophrenia, bring their own experiences of the
disorder and living with it, to the group. The therapist encourages the relatives to ask questions
and learn more about the disorder so they can properly understand the difficulties the patient
faces.
The goal of the sessions is to provide the family with practical coping strategies that enable them to
manage the everyday difficulties arising as a consequence of having Schizophrenia in the family.
Family members learn more constructive ways of interaction and communication and are
encouraged to focus on positive experiences rather than negative experiences.
It is accepted that the family may feel angry and impatient some times and ways are discussed that
these feelings can be expressed without resorting to high Expressed Emotion patterns of
behaviour.
The family and individual are also trained to identify early signs of relapse so that they can
respond rapidly and reduce the severity of the relapse.
In the therapy, the focus is on: 1) improving communication; 2) lowering expressed emotion; 3)
adjusting expectations within the family; and 4) expanding the individual’s social networks.
The goal of the sessions is to provide the whole family with practical coping skills that
enable them to manage the everyday difficulties arising as a consequence of having
schizophrenia in the family.
EFFECTIVENESS
Evidence: National Collaborating Centre for Mental Health (NCCMH, 2009)
Sample: A meta-analysis involving 32 studies and nearly 2500 participants.
Method: Compared those having family intervention therapy to those receiving
standard (drug) therapy.
Findings: The relapse rate in the family intervention condition was 26% and in the control
(standard care) condition it was 50%. There was also a reduction in hospital admissions during
treatment and in the severity of symptoms both during and up to 24 months following
intervention. There was also a reduction in hospital admissions during treatment and in the
severity of symptoms both during and up to 24 months following intervention.
 THIS SHOWS THAT……
Evidence: Hogarty et al (1991).
Sample: 103 Schizophrenic patients who lived in a high EE household.
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Method: Compared relapse rate of those receiving family intervention compared to
medication.
Findings: At a 2-year follow-up 25% of those who received family intervention therapy relapsed
compared to 62% of those receiving medication only.
 THIS SHOWS THAT……
Tarrier et al (1994) found relapse rates 8 years following family intervention was 67%
compared to 88% of those having standard medication in a sample of 83 Schizophrenic patients
 THIS SHOWS THAT……
BUT: Most patients undergoing family intervention to treat Schizophrenic, are usually doing so in
addition to taking medication.
Therefore it makes it very hard to accurately assess the effectiveness of family therapy alone as we
cannot be sure that the decrease in relapse rates is solely due to the effectiveness of family therapy.
It could also be due to effective use of antipsychotics
 A likely explanation of why family intervention reduces relapse is that the support of the family
can increase the compliance of the patient in taking their medication.
 However, if a patient has no family or social support or is estranged from their family, the
potential for an effective treatment is lost. This is also the case if the family are unwilling to
engage in the therapy.
APPROPRIATENESS
 Family intervention requires specially trained therapists and can be costly
 But reviews have demonstrated that family intervention is associated with significant cost
savings when offered to people with Schizophrenia in addition to standard care. The extra cost of
family intervention is offset by a reduction in costs of hospitalisation because of the lower relapse
rates associated with family intervention.
TAKING IT FURTHER……
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There are a range of other psychological therapies.
These include:
1)
2)
3)
4)
Social skills training
Psychodynamic therapies
Token Economies
Milieu Therapy
Choose one of these therapies and using a textbook,
make some notes about the therapy and the
appropriateness and effectiveness of it
EXAM QUESTIONS
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