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NEHRU ARTS AND SCIENCE COLLEGE
PG DEPARTMENT OF SOCIAL WORK
E-LEARNING
CLASS
SUBJECT
: II MSW
: FOUNDATIONS OF PSYCHIATRY-1
UNIT I
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Anatomy & physiology of brain, nervous system, endocrinal system and its functioning.
Mental health: definition, factors affecting mental health. Definition of psychiatry,
Historical development of psychiatry.
--------------------------------------------------------------------------------------------------------------------PART A
1. What is Mental Health?
Soundness of mind is called Mental Health.
2. Nerve cells are known as…neurons…
3. Expand GABA?
Gama amino beutric acid
PART B
1. ExplainAnatomy & physiology of brain, nervous system, endocrinal system and
its functioning
The human nervous system consists of the central nervous system (CNS) and peripheral
nervous system (PNS). The former consists of the brain and spinal cord, while the latter
composes the nerves extending to and from the brain and spinal cord. The primary functions of
the nervous system are to monitor, integrate (process) and respond to information inside and
outside the body. The brain consists of soft, delicate, non-replaceable neural tissue. It is
supported and protected by the surrounding skin, skull, meninges and cerebrospinal fluid.
Skull
Depending on their shape, bones are classified as long, short, flat or irregular. Bones of different
types contain different proportions of the two types of osseous tissue: compact and spongy bone.
While the former has a smooth structure, the latter is composed of small needle-like or flat pieces
of bone called trabeculae, which form a network filled with red or yellow bone marrow. Most
skull bones are flat and consist of two parallel compact bone surfaces, with a layer of spongy
bone sandwiched between. The spongy bone layer of flat bones (the diploë) predominantly
contains red bone marrow and hence has a high concentration of blood.
The skull is a highly complex structure consisting of 22 bones altogether. These can be divided
into two sets, the cranial bones (or cranium) and the facial bones. While the latter form the
framework of the face, the cranial bones form the cranial cavity that encloses and protects the
brain. All bones of the adult skull are firmly connected by sutures. The frontal bone forms the
forehead and contains the frontal sinuses, which are air filled cells within the bone. Most
superior and lateral aspects of the skull are formed by the parietal bones while the occipital bone
forms the posterior aspects. The base of the occipital bone contains the foramen magnum, which
is a large hole allowing the inferior part of the brain to connect to the spinal cord. The remaining
bones of the cranium are the temporal, sphenoid and ethmoid bones.
Meninges
The meninges are three connective tissue membranes enclosing the brain and the spinal cord.
Their functions are to protect the CNS and blood vessels, enclose the venous sinuses, retain the
cerebrospinal fluid, and form partitions within the skull. The outermost meninx is the dura
mater, which encloses the arachnoid mater and the innermost pia mater.
Cerebrospinal fluid
Cerebrospinal fluid (CSF) is a watery liquid similar in composition to blood plasma. It is formed
in the choroid plexuses and circulates through the ventricles into the subarachnoid space, where
it is returned to the dural venous sinuses by the arachnoid villi. The prime purpose of the CSF is
to support and cushion the brain and help nourish it..
Major regions of the brain and their functions
Cerebral hemispheres
The cerebral hemispheres , located on the most superior part of the brain, are separated by the
longitudinal fissure. They make up approximately 83% of total brain mass, and are collectively
referred to as the cerebrum. The cerebral cortex constitutes a 2-4 mm thick grey matter surface
layer and, because of its many convolutions, accounts for about 40% of total brain mass. It is
responsible for conscious behaviour and contains three different functional areas: the motor
areas, sensory areas and association areas. Located internally are the white matter, responsible
for communication between cerebral areas and
between the cerebral cortex and lower regions of the CNS, as well as the basal nuclei (or basal
ganglia), involved in controlling muscular movement.
Diencephalon
The diencephalon is located centrally within the forebrain. It consists of the thalamus,
hypothalamus and epithalamus, which together enclose the third ventricle. The thalamus acts as
a grouping and relay station for sensory inputs ascending to the sensory cortex and association
areas. It also mediates motor activities, cortical arousal and memories. The hypothalamus, by
controlling the autonomic (involuntary) nervous system, is responsible for maintaining the
body’s homeostatic balance. Moreover it forms a part of the limbic system, the ‘emotional’ brain.
The epithalamus consists of the pineal gland and the CSF producing
choroid plexus.
Brain stem
The brain stem is similarly structured as the spinal cord: it consists of grey matter surrounded by
white matter fibre tracts. Its major regions are the midbrain, pons and medulla oblongata. The
midbrain, which surrounds the cerebral aqueduct, provides fibre pathways between higher and
lower brain centres, contains visual and auditory reflex and subcortical motor centres. The pons
is mainly a conduction region, but its nuclei also contribute to the regulation of respiration and
cranial nerves. The medulla oblongata takes an important role as an autonomic reflex centre
involved in maintaining body homeostasis. In particular, nuclei in the medulla regulate
respiratory rhythm, heart rate, blood pressure and several cranial nerves. Moreover, it provides
conduction pathways between the inferior spinal cord and higher brain centres.
Cerebellum
The cerebellum, which is located dorsal to the pons and medulla, accounts for about 11% of total
brain mass. Like the cerebrum, it has a thin outer cortex of grey matter, internal white matter,
and small, deeply situated, paired masses (nuclei) of grey matter. The cerebellum processes
impulses received from the cerebral motor cortex, various brain stem nuclei and sensory
receptors in order to appropriately control skeletal muscle contraction, thus giving smooth,
coordinated movements.
The cerebral circulatory system
Blood is transported through the body via a continuous system of blood vessels. Arteries carry
oxygenated blood away from the heart into capillaries supplying tissue cells. Veins collect the
blood from the capillary bed and carry it back to the heart. The main purpose of blood flow
through body tissues is to deliver oxygen and nutrients to and waste from the cells, exchange gas
in the lungs, absorb nutrients from the digestive tract, and help forming urine in the kidneys. All
the circulation besides the heart and the pulmonary circulation is called the systemic circulation.
Blood supply to the brain
The major arteries are the vertebral and internal carotid arteries. The two posterior and single
anterior
communicating arteries form the circle of Willis, which equalises blood pressures in the brain’s
anterior and posterior regions, and protects the brain from damage should one of the arteries
become occluded. However, there is little communication between smaller arteries on the brain’s
surface. Hence occlusion of these arteries usually results in localised tissue damage.
Endocrine system
The endocrine system is under the direct supervision of the nervous system, using the negative
feedback principal of homeostasis, to create hormones which act as chemical instant messengers.
The hypothalamus connects directly to the pituitary gland, both through the circulatory system
and by direct connection of neurons. Also, within the cranium, the pineal gland, which attaches
to the thalamus, controls the body's 24 hour rhythms circadian rhythm through the release of
melatonin. Endocrine indicates that the secretion is used within the body. Endocrine glands are
termed as ductless and release their secretions directly into the blood.
The pituitary gland
It is also called hypophysis, or master gland. It secretes hormones that directly impact the body
as well as hormones that indirectly control body functions because they activate other endocrine
glands, such as the adrenal cortex (ACTH) and the thyroid gland (TSH). These two glands when
stimulated by pituitary hormones then release their own hormones. The pituitary gland has two
lobes, the anterior lobe and the posterior lobe. The anterior lobe secretes: growth hormone (GH),
Luteinizing hormone (LH), Follicle stimulating hormone (FSH), Adrenocorticotropic hormone
(ACTH), Thyroid-stimulating hormone (TSH), Prolactin (PRL), and the posterior lobe secretes:
Antidieuretic hormone (ADH), and Oxytocin (OT). There is an intermediate lobe, in adult
humans it is just a thin layer of cells between the anterior and posterior pituitary, nearly
indistinguishable from the anterior lobe. The intermediate lobe produces melanocyte-stimulating
hormone (MSH).
Intermediate lobe
There is also an intermediate lobe in many animals. For instance, in fish, it is believed to control
physiological color change. In adult humans, it is just a thin layer of cells between the anterior
and posterior pituitary. The intermediate lobe produces melanocyte-stimulating hormone (MSH),
although this function is often (imprecisely) attributed to the anterior pituitary.
Functions
The pituitary hormones help control some of the following body processes:
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Growth
Blood pressure
Some aspects of pregnancy and childbirth including stimulation of uterine contractions
during childbirth
Breast milk production
Sex organ functions in both men and women
Thyroid gland function
The conversion of food into energy (metabolism)
Water and osmolarity regulation in the body
Secretes ADH (antidiuretic hormone) to control the absorption of water into the kidneys
Temperature regulation
Thyroid
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In vertebrate anatomy, the thyroid is one of the largest endocrine glands in the body.
This gland is found in the neck, inferior to (below) the thyroid cartilage (also known as
the Adam's apple) and at approximately the same level as the cricoid cartilage. The
thyroid controls how quickly the body uses energy, makes proteins, and controls how
sensitive the body should be to other hormones.
The thyroid participates in these processes by producing thyroid hormones, principally
thyroxine (T4) and triiodothyronine (T3). These hormones regulate the rate of metabolism
and affect the growth and rate of function of many other systems in the body. Iodine and
tyrosine are used to form both T3 and T4. The thyroid also produces the hormone
calcitonin, which plays a role in calcium homeostasis.
The thyroid is controlled by the hypothalamus and pituitary. The gland gets its name
from the Greek word for "shield", after the shape of the related thyroid cartilage.
Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the
most common problems of the thyroid gland
PART C
1.Explain the Factors affecting mental health
Studies of the significant causes and processes involved in the development of mental illness
have found that there are physical, social, environmental and psychological causes for mental
illness.
Physical causes are those which are biological in nature. They can include our individual
genetic make-up and the way that this might put us at more or less risk than others. It has also
been found that those who have suffered (usually more severe) head injuries can also experience
changes to their personality, and in some cases may begin to experience schizophrenia and
psychotic type symptoms.
The misuse of substances or illness of mothers during pregnancy, (such as through picking up
viruses like the flu) can also lead to changes in their baby's development which may ultimately
effect their mental health. Recent reports have also suggested that vitamin and mineral
deficiencies such as Vitamin D, zinc and certain fatty acids may also be related to our mental
health and the development of neurological symptoms.
Social and environmental causes are those factors around us such as where we live, whether
we have strong support networks, (close family and friends who make us feel safe and who we
can rely on) our place of work and how and where we can relax. Physical environments such as
the neighborhood where you live can be very stressful, particularly when there are problems with
neightbours, or where there are high crime rates and other such issues. Whether you enjoy your
work, or feel you are under too much pressure, are unable to find employment or hold down a
job, can all put pressure on your mental well-being.
These kinds of problems will increase the amount of stress people are under, and can cause
depression and anxiety, especially in situations where individuals are unable to make changes to
alleviate the stressors. When we face difficult times our support networks become very important
– those who do not have close friends or families, or those who do not live near the people who
support them may find it increasingly difficult to cope alone.
Psychologicalfactors
your psychological state and influence your mental and emotional state, particularly if you are
are coping with traumatic and abusive past or current experiences, significant life events like
bereavement or divorce,or if you have self-destructive thought patterns and perceptions - our
psychological state can and will influence and our mental health.
For example, post-traumatic stress disorder (PTSD), anxiety and in more extreme cases
Dissociative Identity Disorder (DID – in the past referred to a multiple personality disorder) are
all mental health conditions that are commonly found in people who have been abused.
2.Evolution of Psychiatry?
Introduction: The history of western psychiatry may be viewed from many directions: the train
of scientific advancements that have brought it to its present level of technology; the flow of
underlying philosophical assumptions and tenets, especially the relation of mental and physical
phenomenon, across time; the influence of social and religious institutions on mental illness and
the field of psychiatry; the development of the different modern schools of psychiatric and
psychological practice; and the actual place and treatment of the mentally ill in society.
Pre-Classical and Classical Influences: Most non-western and probably early western cultures
distinguish between natural and supernatural causes of illness and hardship, not isolating what
would be presently considered mental illness. Methods are culturally designated for the
understanding and response to these events. All societies recognize episodes of extremely
aberrant behavior, which we would consider madness or insanity. The evidence for very early
aspects of mental illness in western society is little and limited. Nonetheless, some indications
can be addressed.
Egyptian and ancient Middle Eastern influences can be seen, often as they were incorporated into
Greek culture.
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The increasing emphasis on natural knowledge and an equal de-emphasis of the role of the gods
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occurs in the 5 and 6 centuries B.C.
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These continue into the theories of Hippocrates in the 4 century B.C. who believed that illness
was the result of an imbalance between the four bodily humors: blood, black bile, yellow bile,
and phlegm, which correspond to the four basic qualities of matter: heat, cold, moisture, and
dryness. A predominance of one element also determined basic character types.
He further argued that certain illnesses, especially epilepsy were not divine, but nervous
illnesses. Madness was often seen as a disturbance of black bile (melaina chole) or later
melancholia.
Hysteria was attributed to the movement of the uterus. As a consequence of these beliefs,
treatment was aimed at restoring hormonal balance through the use of purgative, vapors, baths,
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and special diets. These ideas formed the center of much of medicine until the 17 century.
The philosophy underlying these beliefs saw people as endowed with characteristics at birth that
needed education and training to be fulfilled. There was an increasing acceptance of natural laws.
Passion and immorality were increasingly seen as derived from the interaction of natural laws
(physis) and the influence of irrational customs (nomos). For instance Plato (428-348 B.C.) saw
the psyche or soul as active and immortal. The psyche had three parts: appetite, reason, and
temper. Irrational behavior was seen as an inevitable part of human life, to be overcome by
reason. Illness came from a loss of balance between the psyche and the body or soma, or through
self-deception. Reason and rational thought are the highest of virtues. Whereas the body was
temporary and of secondary importance.
Aristotle (384-322 B.C.) the student of Plato, accepted the humoral theory of Hippocrates, taking
it further seeing that bile mediated between the mind and the body. Whereas Platonic ideas
emphasized a division between mind/soul and body, Aristotelian ideas recognized more of an
interaction between these entities. He also taught knowledge was the direct consequence of the
senses, rather than innate or divinely given. This exemplifies the interaction between mind and
body. He emphasized experience and empirical knowledge. In a parallel manner, he emphasized
the role of ritual in treatment, providing by catharsis.
During the Hellenistic period, with the spread of Greek culture through the Middle East and the
eastern Mediterranean region, there was a growth of both rationalistic religion and mystery cults.
Both focused on individual salvation. Eastern ideas entered the western tradition from India and
the Middle East. Important centers for learning and experimentation developed, especially at
Alexandria. Here a school of anatomy developed that argued for different functional areas in the
brain.
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. Asclepiades (1 century BC) building on the atomic hypothesis of Democritus, rather than the
humors, distinguished phrenitis (metal excitement with fever) from mania (mental excitement
without fever) and advocated treatments consisting of the use of light, diet, music, intellectual
stimulation, and physiotherapy. Stoic philosophers and other healers emphasized the control of
rational thought over emotions and passions.
Middle Ages: With the ascendancy of Christianity to predominance in the Roman Empire and
the later collapse of the Roman Empire, Christian dogma became the basis of philosophical
inquiry in the west. Platonic ideas were combined with Christian teachings, creating a worldview
that dominated in the west for several centuries. St. Augustine (354-430 A.D.) championed
Platonic conceptions of the mind, including the essential dichotomy between body and
mind/soul. The mind was seen as having three parts: reason, memory, and will, while memory, in
turn, had three parts: the unconscious, the preconscious, and the associative. Posidonius, in the
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century, postulated three divisions of the brain with imagination in the forebrain,
understanding in the midbrain, and memory in the hindbrain..
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During the High Middle Ages, from the 11 century on, there was a gradual change in the
worldview. Through contact in Spain and in the Holy Lands via the Crusades, Islamic culture
had a strong impact on western culture.
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In the Islamic world of the 7 century and beyond, classical Greek and other Hellenistic ideas
were elaborated. The teachings of Hippocrates, Galen, and the philosophy of Aristotle were
combined to create an advanced level of science and medicine.
Through the Koran’s teachings that the mentally ill are precious to God, asylums were
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established in Baghdad in the 8 century,
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Damascus in the 9 century, and several in Egypt, that were renowned for their humane
treatment of the mentally ill.
There was a focus on providing a calm and relaxed environment, with fountains, gardens, and the
use of soothing baths, perfumes, music and special diets.
Under this influence, Constatinus Africanus (1020–1087) founded a medical school in Salerno.
The introduction of Aristotle to the west resulted in a shift away from Plato and a growing
emphasis on empiricism. St. Thomas Aquinas (1225-1274) reintroduced Aristotelian ideas of the
mind into western thought. A growing separation of mind and soul developed. The mind was
equated with the Greek psyche and the Latin animus, while the soul was equated with the Greek
pneuma and the Latin anima.
This proposition has been seen as a precursor of the later organic school of psychiatry that
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developed principally in 19 century Germany. The growing emphasis on reason over faith laid
the groundwork for later Renaissance and Enlightenment philosophies.
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Early Modern (Renaissance Period): From the 15 and 16 centuries there was an increasing
secularism of society and a decreasing power of the Church. There is an important demographic
Nonetheless, humoral concepts of illness developed in the 4th century B.C. by Hippocrates and
expanded by Galen (130-200 A.D.), persisted until the 17th and 18th centuries.
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Modern Period (17 and 18 Centuries): During this period there was increasing urbanism and
commerce. States became all powerful and world exploration and domination increased.
Industrialization increased and large segments of the population were displaced.
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During the 17 and 18 centuries there was an increasing number of mentally ill. Whether this
was an actual increase in the number or the loss of traditional supports for the mentally ill
through the loss of extended families with industrialization and urbanization, resulting in their
being cast out on society more, is unclear. However, the growing number of socially recognized
mentally ill, combined with the growing number of people displaced into poverty. Prisons,
almshouses, and other institutions expanded greatly to meet the threat that these people were
perceived as demonstrating toward the orderly movements of the state. Protestant ethics places a
person’s value on their ability to work and be productive. Increasing wealth was seen as a sign of
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Modern Period (19 and 20 Century):
During this period clear national trends can be identified. Early on Germany remained
preoccupied by the metaphysics of mental processes, developing the idea of Vitalism in which
there is a transformation of the concepts of soul/spirit into a vital force in all organisms. Rational
control over emotions was stressed, but little difference in the practical treatment of those with
mental illness is recorded.
In England, the early 1700s brought legal efforts to end witchcraft accusations and to separate
the insane from other inmates in almshouses and other institutions. The first facilities for pauper
insane were opened. Battie (1704–1776) worked to provide treatment to the poor insane and not
to just house them. He hypothesized that madness was the result of either the over excitement of
the sensibilities or insensibility. He separated internal and external causes. He advocated
treatment that included separation from the family, decreased stimuli, routine activity and
occupation, what later came to be known as the Moral Treatment. Cullen (1710–1790) also saw
mental illness as the over excitement or the atony of the nervous system, with mania being an
example of over excitement. He advocated the use of opium as a sedative. He too urged
moderation over the passions and appetites. The influence of Protestant ideas can be seen in
these therapies.
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Consequently, by the 19th century two schools of etiological beliefs existed, the somatic and
psychic. The somatic school saw mental illness as having physical causes such as brain lesions or
disturbed nerves, whereas, the psychic school understood mental illness as due to emotional
stress. Yet these two schools shared a common model of the mind. In the 19th century, through
the work of Kraepelin, Bleuler, and Janet, Associationist concepts became important in theories
of psychopathology. Mental illness was seen as the result of breakdown in the associative
functioning of the mind. Inherited vulnerability to associative breakdown (dissociation) was
stressed. It is at this point that the modern schools of psychology and psychiatry with their own
models of the mind emerge. These are the Functional-Descriptive, Behaviorist (CognitiveBehaviorist), Psychoanalytic, Interpersonal, and Gestalt/Existentialist/Humanists schools.
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The development of the various shock treatments in the first half of the 20 century and the
later use of medications, including the discovery of the antimanic effects of lithium in 1949,
further contributed to this position.
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It was debated at the turn of the 20 century whether or not the cellular theory applied to the
brain or if the brain was the result of a large syncytium or reticular net. Cajal was able to
demonstrate the integrity of neurons in the 1890s.
evolutionary in nature.
Precursors to Psychoanalysis
Freud read Darwin and was very influenced by his ideas, including the presence of unconscious
mental processes and conflicts, the significance of dreams, the symbolic nature of bizarre
behavior, and the importance of sexual excitement. Darwin (via Romanes, to whom Darwin had
given his notes on social behavior) wrote on the mental evolution of man, especially in the
relation of childhood behavior to adult behavior and in the appearance in childhood of sexual
drive. Darwin wrote that people are driven by biological forces (love and hunger).
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Hedonism of the 18 and 19 centuries, which stated that people are motivated to gain pleasure
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and avoid pain, also influenced Freud. In 19 century Europe, especially Vienna, there was a
popular and academic focus on sexuality, prior to Freudian theorizing, especially on sexual
dysfunctions and childhood sexuality.
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UNIT II
Mental illness – symptoms – disorders of perception, cognition, speech, motor and
emotional disorders.
Mental disorders, classification of mental disorders, mental status examination, psychiatric
interview.
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1. What is Euphoria?
Feeling of intense happiness and grandeur.
2. What is echopraxia?
Prsons repeats the movements performed by other persons.
3. What is Pica?
Mud eating habit.
Part B
1.Point out the major symptoms and signs of Mental illness?
Abnormalities of behaviour and movements.
Abnormalities of mood and emotion.
Abnormalities of speech.
Abnormalities of thinking.
Abnormalities of perception.
Abnormalities of awareness of self and others.
Abnormalities of consciousness.
Abnormalities of attention and concentration.
Abnormalities of memory.
Abnormality of judgment.
Abnormality of insight.
Abnormality of sleep, eating and sex
2. Explain the motor disorders ?
Psychomotor Retardation:
Slowed mental and motor activities.
Stupor:
A state in which a person does not react to the surroundings:
(mute, immobile and unresponsive).
Catatonic Stupor:
Stupor with rigid posturing
Psychomotor Agitation:
Restlessness with psychological tension.
(Patient is not fully aware of restlessness.)
Catatonic Excitement:
Marked agitation, impulsivity and aggression without external
provocation.
Aggression:
Verbal or physical hostile behaviour, with rage and anger.
Akathisia:
Inability to keep sitting still, due to a compelling subjective
feeling of restlessness.
(Patient is fully aware of restlessness).
Dyskinesia:
Restless movement of group of muscles (face, neck, hands).
Dystonia:
Painful severe muscle spasm.
Torticollis:
Contraction of neck muscles.
Tics:
Sudden repeated involuntary muscle twisting.
e.g. repeated blinking, grimacing.
Compulsions:
Compelling repeated irrational actions associated with
obsessions.
e.g. repeated hand washing.
Echopraxia:
Imitative repetition of movement of somebody.
Waxy Flexibility:
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Patient‟s limbs may be moved like wax, holding position for long
period of time before returning to previous position.
Stereotypies:
Purposeless repetitive involuntary movements.
e.g. foot tapping, thigh rocking.
Mannerism:
Odd goal-directed movements.
e.g. repeated hand movement resembling a military salute.
3. Explain the abnormalities of mood / emotion?
Anxiety: feeling of apprehension accompanied by autonomic
symptoms (such as muscles tension, perspiration and
tachycardia), caused by anticipation of danger.
Free-floating anxiety: diffuse, unfocused anxiety,
not attached to a specific danger.
Fear: anxiety caused by realistic consciously recognized danger.
Panic: acute, self-limiting, episodic intense attack of anxiety
associated with overwhelming dread and autonomic symptoms.
Phobia: irrational exaggerated fear and avoidance of a specific
object, situation or activity.
Agitation: severe feeling of inner tension associated with motor
restlessness.
Irritable mood: easily annoyed and provoked to anger.
Dysphoria: mixture feelings of sadness and apprehension.
Depressed mood: feeling of sadness, pessimism and a sense of
loneliness.
Anhedonia: lack of pleasure in acts which are normally
pleasurable.
Grief: sadness appropriate to a real loss (e.g. death of a relative)
Guilt: unpleasant emotion secondary to doing what is perceived
as wrong.
Shame: unpleasant emotion secondary to failure to live up to
self-expectations.
Perplexity: anxious mood with bewilderment.
Ambivalent Mood: coexistence of two opposing emotional tones
towards the same object in the same person at the same time.
Alexithymia: inability to, or difficulty in, expressing one‟s own
emotions.
Elevated Mood: a mood more cheerful than usual.
Elation: feeling of elevated mood with optimism and selfsatisfaction.
Euphoria: intense elation with feeling of grandeur.
Ecstasy: very intense elation beyond reason and control.
Expansive Mood: expression of euphoria with an overestimation
of self-importance.
Grandiosity: feeling and thinking of great importance (in
identity or ability).
Constricted Affect: significant reduction in the normal
emotional responses.
Flat Affect: absence of emotional expression.
Apathy: lack of emotion, interest or concern, associated with
detachment.
Labile Affect: rapid, abrupt changes in emotions in the same
setting, unrelated to external stimuli.
La Belle Indifference: inappropriate denial of expected affect
and lack of concern about physical disability (seen in conversion
disorders).
Inappropriate Affect: disharmony between emotions and the
idea, thought, or speech, accompanying it.
4. Explain the abnormalities of speech?
Echolalia: imitation of words or phrases made by others.
Pressure of Speech: rapid, uninterrupted speech that is increased
in amount.
Mutism: inability to speak.
Elective Mutism: refusal to speak in certain circumstances.
Poverty of Speech: restricted amount of speech.
Stuttering (Stammering): frequent repetition or prolongation of
a sound or syllable, leading to markedly impaired speech fluency.
Cluttering: dysrhythmic rapid and jerky speech.
Clang Associations (Rhyming): association of word similar in
sound but not in meaning (e.g. deep, keep, sleep)
Punning: playing upon words, by using a word of more than one
meaning (e.g. ant, aunt)
Word Salad: incoherent mixture of words and phrases.
Dysarthria: difficulty in articulation and speech production.
Sensory Aphasia: nonsensical fluent speech due to lesion
affecting Wernick‟s (receptive) area.
Motor Aphasia: impairment in the ability to formulate fluent
speech due to lesion affecting Broca‟s (motor) area.
Dysphoria: difficulty in voicing speech clearly, due to
dysfunction of vocal cords or soft palate.
Circumstanciality: overinclusion of details delaying reaching
the desired goal.
5. Explain the abnormalities in thinking/ cognition?
Poverty of Thoughts
A- Abnormal Thought Stream Pressure of Thoughts
Thought Block
Loosening of Association
B- Abnormal Thought Link Flight of Ideas
Thought Perseveration
Overvalued Ideas
C- Abnormal Thought Content Obsessions
Delusions
A. Abnormal Thought Stream
Poverty of Thoughts:
Few, slow, unvaried thoughts associated with poverty of speech.
Pressure of Thoughts:
Rapid abundant varying thoughts associated with pressure of speech
and flight of ideas.
Thought Block:
Sudden cessation of thought flow with complete emptying of the
mind, not caused by an external influence.
B. Abnormal Thought Link
Also called „formal thought disorders‟.
Loosening of Associations:
Lack of logic connection between thoughts.
Flight of Ideas:
Successive rapidly shifting incomplete ideas but with an
understandable link.
Thought Perseveration:
Repeating the same sequence of thoughts persistently and
inappropriately.
Abnormal Thought Content
Overvalued Ideas:
Strongly held false ideas but shakable (e.g. personal conviction that
vitiligo is a contagious disease)
Obsessions:
Repetitive ideas, images, feelings or urges insistently entering
person‟s mind despite resistance. They are unwanted, distressful and
recognized as senseless and irrational. Obsessions are frequently
followed by compelling actions (compulsions)
Common Obsessional Contents:
dirt/contamination/cleaning
orderliness/symmetry
doubts/checking/counting
aggressive impulses/inappropriate acts
religion (blasphemous thoughts)
ruminations: obsessional thoughts.
rituals: certain repeated compulsions.
Delusions:
Unshakable false beliefs out of keeping with the person‟s cultural
background, not arrived at through logic thinking and not
amenable to reasoning.
Common Delusional Contents:
1. Persecutory (paranoid) delusion:
Delusion of being persecuted (cheated, mistreated, harassed, etc.)
2. Grandiose delusion:
Delusion of exaggerated self-importance, power or identity.
3. Delusion of reference:
Delusion that some events and others‟ behaviour refer to oneself.
4. Delusion of jealousy:
Delusion that a loved person (wife/husband) is unfaithful
(infidelity delusion).
5. Erotomanic delusion:
Delusion that someone, (usually inaccessible, high social class
person) is deeply in love with the patient.
6. Nihilistic delusion:
Delusion of nonexistence of self, part of the body, belongings,
others or the world.
7. Delusion of self - accusation:
Delusion that a patient has done something sinful, with excessive
feeling of remorse and guilt.
8. Delusion of influence:
Delusion that person‟s thoughts, actions, or feelings are
controlled by outside forces. Passivity phenomena : person
reports being made feel, made think or made act.
6. Explain the abnormalities of perception?
Illusions:
Misperceptions or misinterpretations of real external sensory
stimuli:
e.g. Shadows may be misperceived as frightening figures.
Hallucinations:
Perception in the absence of real external stimuli; experienced
as true perception coming from the external word (not within
the mind).
e.g. hearing a voice of someone when actually nobody is
speaking within the hearing distance.
Auditory hallucinations (voice, sound, noise).
Second-person hallucinations: voice speaking to the
person addressing him as “you”.
Third-person hallucinations: voice talking about the
person as “he” or “she”:
Thought echo: hearing one‟s own thoughts spoken aloud.
Visual hallucinations (images/sights)
Olfactory hallucinations (smell/odour)
Gustatory hallucinations (taste)
Tactile hallucinations (touch/surface sensations)
Somatic hallucinations (visceral and other internal
sensations).
Hypnagogic hallucinations: hallucinations when falling
asleep.
Hypnopompic hallucinations: hallucinations when waking
from sleep.
7. Explain the classification of Mental Disorders?
Purposes of diagnosis and classification: 1. To identify groups of patients who are
similar in their clinical features, response to treatment and outcome, and to distinguish one
diagnosis from another. 2. To bring order to the great diversity of phenomena met in clinical
practice. 3. To enable clinicians to communicate with one another about their patients’
symptoms, treatment and prognosis. For many years it was not clear that psychiatrists were
speaking to each other in the same language, as one doctor’s mania was another doctor’s
Schizophrenia. 4. To ensure that psychiatric research can be conducted with comparable groups
of patients stress-related.
The International Classification of Diseases (ICD)
This system was developed by the World Health Organization (WHO).
Mental disorders were first included in it’s 6th edition (ICD-6)in 1948.
The latest version is ICD - 10, introduced in 1992. The section on
mental and behavioural disorders (chapter V of ICD -10) is used in
most countries of the world for clinical purposes. It has been translated
into all the widely spoken languages of the world.
.
ICD-10 –
Organic, including symptomatic, mental disorders.
Mental and behaviour disorders due to psychoactive
substance use.
Schizophrenia, schizoaffective and delusional
disorders.
Mood (affective) disorders.
Neurotic, stress-related, and somatoform disorders.
Behavioural syndromes associated with physiological
disturbances and physical factors.
Disorders of adult personality and behaviour.
Mental retardation.
Disorders of psychological development.
Behavioural and emotional disorders with onset
usually occurring in childhood or adolescence.
Dementia Delirium Alcohol use disorders
Drug use disorders Tobacco use disorders
Phobic disorders Panic disorders
Generalized anxiety Mixed anxiety and depression
Adjustment disorders Dissociative (conversion) disorder
Unexplained somatic complaint
Eating disorders Sleep disorders
The Diagnostic and Statistical Manual (DSM)
This system was developed by the American Psychiatric Association
(APA). The first edition (DSM – 1) was published in 1952 as an
alternative to ICD – 6 which had been widely criticized. It is now in it’s
fourth edition DSM-IV which was introduced in 1994, and reviewed
(DSM IV Text Revision) in 2000. Although designed for use in the United
states, it is used in other countries, especially for research purposes.
Categories of Disorders in DSM – IV
Disorders usually first diagnosed in infancy,
childhood, or adolescence.
Delirium, dementia and amnestic, and other cognitive
disorders.
Mental disorders due to a general medical condition.
Substance – related disorders.
Schizophrenia and other Psychotic disorders.
Mood disorders.
Anxiety disorders.
Somatoform disorders.
Factitious disorders.
Dissociative disorders.
Sexual and gender identity disorders.
Eating disorders.
Impulse – control disorders.
Adjustment disorders.
Other conditions that may be a focus of clinical
attention.
DSM –IV classification was developed for use in clinical – educational,
and research settings.
.
Multiaxial Classification:
DSM –IV is a multiaxial system that evaluates patients along several
variables and contains five axes:
Axis I: it consists of clinical disorders and other conditions that
may be a focus of clinical attention.
Axis II: it consists of personality disorders and / or mental
retardation ( none may be present )
Axis III: it lists any physical disease relevant to mental disorder.
Axis IV: it is used to code the psychosocial and environmental
problems that significantly contribute to the development or
exacerbation of the current disorder.
Axis V: it is a global assessment of functioning scale.
Only the first three axes are used commonly in everyday clinical
practice, and can be recorded without assigning them to separate
axes
Part C
1. Write down the psychiatric interview and its importance?
PSYCHIATRIC ASSESSMENT :A thorough assessment of a psychiatric patient consists of a
psychiatric history, mental status examination, physical examination, and certain relevant
laboratory and psychological tests. The psychiatric history and mental status examination are
usually obtained during the initial interview. There are many goals for psychiatric interview:
1. To establish a relationship with the patient.
2. To obtain information.
3. To assess psychopathology (nature, severity …), of the illness.
4. To provide feedback and formulate a treatment plan.
PSYCHIATRIC HISTORY :The psychiatric history is the chronological story of the patient’s
life from birth to present. It includes information about who the patient is, his problem and its
possible causes and available support. It should be emphasized that:
1. much more attention needs to be paid to psychological and social aspects.
2. patient’s feelings, thoughts, perception and behaviour during the interview are considered part
of the mental status examination (not the psychiatric history). The history should be compiled
from information elicited both from the patient and from one or more informants (the
informant’s relationship to the patient should be noted together with the interviewer’s impression
of the informant’s reliability). The following outline is a usual format for writing the psychiatric
history.
Psychiatric History Identification data Referral Source Chief Complaint History of
present illness Family history Medical history Past Psychiatric history Personality traits
Medical History:
All major illnesses should be listed (nature, extent, dates,
treatment, outcome, and patient’s reaction and attitude). Women
should be asked about menstrual (and, if appropriate, about
menopausal) difficulties.
Past Psychiatric History:
Any previous psychiatric illness (nature, extent, dates, treatment,
outcome and patient’s reaction and attitude).
Personality Traits:
:
Attitude to self (self-appraisal, performance, satisfaction, past
achievements and failures, future..)
Moral and religious attitudes and standards.
Prevailing mood and emotions.
Reaction to stress (ability to tolerate frustration and
disappointments, pattern of coping strategies).
Personal interests, habits, hobbies and leisure activities.
Interpersonal relationships.
MENTAL STATE EXAMINATION
The mental status examination (MSE) is a cross-sectional, systemic
documentation of the quality of mental functioning at the time of interview.
It serves as a baseline for future comparison and to follow the progress of
the patient.
The Mental State Examination
1. Appearance
2. Behaviour
3. Attitude
4. Speech
5. Affect
6. Perception
7. Awareness of self and others
8. Thoughts
9. Cognitive functions and consciousness
consciousness
attention
concentration
orientation(time, place, person)
memory
10. Abstract thinking
11. Visuospatial ability
12. Language and reading.
13. Judgment
14. Insight
---------------------------------------------------------------------------------------------------------------------
UNIT III
Neurosis – symptoms of Neurosis – etiology and clinical manifestations and differential
diagnosis of anxiety, phobia, panic disorder, OCD, post traumatic order, conversion &
disassociative disorders, psychosomatic disorders.
--------------------------------------------------------------------------------------------------------------------PART A
1. Expand PTSD?
Post traumatic stress disorder
2. What is hydro phobia ?
Fear of water.
3. Expand OCD?
Obsessive compulsive disorder.
PART B
1. Explain the symptoms of Panic disorder?
It is characterized by recurrent unexpected panic attacks about which there
is persistent concern or anticipatory anxiety for at least one month.
Panic Attack:
A discrete period of sudden onset of intense fear or discomfort that builds
up to a peak rapidly (usually in 5-15 minutes) and is often accompanied by a
sense of imminent danger or impending doom and an urge to escape.
There are some somatic and cognitive symptoms that accompany fear.
These include:
Palpitation ● Sensations of shortness of breath
Feeling o choking ● Chest pain
Shaking ● Tremor ● Chills or hot flushes ● Sweating
Paraesthesia
Feeling dizzy, unsteady or faint
Fear of going mad, dying or losing control.
Derealization (feelings of unreality) or depersonalization (being
detached from one self)
Panic attacks (as attacks, not as a disorder) can occur in a variety of
psychiatric disorders other than panic disorder:
Generalized anxiety disorder
Phobias
Stress disorders (acute & post traumatic)
Substance abuse
Depressive disorders
Obsessive Compulsive Disorder (OCD)
In determining the differential diagnostic significance of a panic attack, it is
important to consider the context in which the panic attack occurs. There
are three characteristic types of panic attacks with different relationships
between the onset of the attack and the presence or absence of situational
triggers.
1. Unexpected panic attacks:
not associated with a situational trigger (spontaneous)
essential for the diagnosis of panic disorder
2. Situationally bound panic attacks:
occur immediately on exposure to, or in anticipation of, the
situational cue ( trigger ).
associated with specific phobia (e.g. seeing a snake).
associated with panic attacks.
3. Situationally predisposed panic attacks:
more likely to occur on exposure to (but are not invariably
associated with) the situational trigger. (e.g. Attacks are more
likely to occur while driving.)
Epidemiology:
Women > men
Lifetime prevalence is 1 – 3 % (throughout the world).
One-year prevalence rates 1 – 2 %.
Age at onset: bimodal distribution, with one peak in late
adolescence and a second smaller peak in the
mid 30s
Aetiology:
Genetic basis (panic disorder occurs more often among relatives).
The biochemical hypothesis (panic attacks can be induced by
chemical agents like sodium lactate, and can be reduced by drugs
like imipramine).
Panic disorder develops in a person with poorly regulated
autonomic responses to stressors when he becomes afraid of the
consequences of symptoms of autonomic arousal.
The neurotransmitters involved are noradrenaline and serotonin.
Locus coeruleus is essential for anxiety expression (alarm system
in the body).
Course and Prognosis:
The usual course is chronic but waxing and waning.
Some patients recover within weeks.
Others have a prolonged course (those symptoms persist for 6
months or more).
Prognosis is excellent with therapy.
Treatment:
Attention to any precipitating or aggravating personal or social
problems.
Support and reassurance.
Cognitive therapy: eliciting and correcting the patient’s wrong
assumptions and beliefs about the origin, meaning, and
consequence of symptoms.

Drugs:
Tricyclic antidepressants
imipramine: start with small dose (e.g. 25 mg) then
increase gradually , guided by the symptom control.
Patient may require 150 mg. or more.
clomipramine has been found to be at least as
effective as imipramine (in small doses).
Selective Serotonin reuptake inhibitors
fluvoxamine (50 - 150 mg / day)
citalopram (20 – 40 mg / day)
Benzodiazepines
alprazolam (2 – 6 mg / day), but there is a high risk
of dependence.
2. Explain about symptoms and management of Phobias?
Phobic disorders are characterized by:
intense dread of certain objects or situations, beyond voluntary
control.
being out of proportion to the demands of the situation and cannot
be reasoned away.
avoidance or endurance with distress.
significant distress and/or functional impairment (social,
occupational …).
a disturbance not due to a general condition, substance abuse or a
mental disorder.
AGORAPHOBIA
Literally it means fear of open spaces (misleading term). Although fear of
open spaces is common, agoraphobic patients have anxiety about being in
places from which escape seems difficult or help may not be available in
case of sudden incapacitation (places cannot be left suddenly without
attracting attention e.g. a place in the middle of a row in mosque).
Common feared and avoided situations:
Overcrowding: a social situation (mass of people), shops and
markets.
Distance from home: travelling away.
Confinement: closed spaces, e.g. elevators (claustrophobia)
bridges, public transport.
Features:
Anxiety about fainting and / or loss of control when patient is
away from home, in crowds, or in situations that they cannot
leave easily.
Anxiety symptoms identical to those of any other anxiety state
(see physical and psychological features of anxiety).
Anticipatory anxiety (hours before the individual enters the feared
situation).
Other symptoms that can accompany agoraphobia :
depersonalization and derealization.
obsessional thoughts related to the feared situation.
Depressive symptoms may arise (> 30 % of cases) as a consequence of
the limitations to normal life caused by phobia.
As the condition progresses, patients with agoraphobia may become
increasingly dependent on some of their relatives or spouse for help
with activities that provoke anxiety (such as shopping).
Epidemiology:
Women – men : 2 : 1
Onset: most cases begin in the early or middle twenties, though
there is a further period of high onset in the middle thirties.
Both of these ages are later than the average onset of specific
phobia (childhood) and social phobias (late teenagers or early
twenties).
Prevalence : ● one year prevalence:
Men : about 2 %.
Women : about 4 %.
● Life time prevalence: 6 – 10 %.
Aetiology:
Personality: anxious, dependent (overprotected in childhood,
separation anxiety…)
Biological predisposition to respond with anxiety (possibly
because defective normal inhibitory mechanisms).
Conditioning: avoidance learning.
Often precipitated by major life events.
Psychodynamic factors: repression, displacement and
symbolization.
Treatment:
Cognitive-Behaviour Therapy:
detailed inquiry about the situations that provoke anxiety and how
much they are avoided.
hierarchy is drown up (from the least – to the most anxiety
provoking).
the patient is then taught to relax (relaxation training).
exposure : the patient is persuaded to enter the feared situation
(to confront situations that he generally avoids).
the patient should cope with anxiety experienced during exposure
and try to stay in the situation until anxiety has declined.
when one stage is accomplished the patient moves to the next
stage.
negative cognitive assumptions are challenged.
the patient is trained to overcome avoidance (escape during
exposure will reinforce the phobic behaviour).
Drugs:
Antidepressants: imipramine – clomipramine – MAOI, (e.g.
moclobemide) – SSRI
Anxiolytics: e.g. alprazolam (there is a risk of dependence).
Prognosis:
If not treated early, agoraphobia can be chronic disabling disorder
complicated by depressive symptoms.
House-bound housewife syndrome may develop a severe stage of
agoraphobia when the patient cannot leave the house at all.
Panic disorders (moderate – severe).
SOCIAL PHOBIA
The essential problem here is a marked persistent inappropriate fear and
anxiety (with physical and psychological features) when a person is exposed
to unfamiliar people or to a possible scrutiny by others in social or
performance situations in which embarrassment may occur. The person has
anticipatory anxiety. Such situations are avoided (wholly or in part) or else
endured with distress. The problem leads to significant interference with
functioning (social, occupational, academic…).
The most common feared situations
Gatherings (e.g. meetings, parties).
Speaking to authority figures or in public (e.g. leading prayers,
lecturing).
Performing under scrutiny (e.g. serving coffee or tea to guests).
The symptoms are the same as those of generalized anxiety
disorder.
Common complaints: palpitation, trembling, sweating, and
blushing.
The response may take a form of panic attack (situationally
bound or situationally predisposed).
Negative thoughts about performance (others will judge them
to be anxious, weak, stupid, inarticulate…).
Avoidance of the situation or endurance with distress.
Associated Features:
Hypersensitivity to criticism and negative evaluation or
rejection (avoidant personality traits).
Other phobias.
Complications:
Secondary depression.
Alcohol or stimulant abuse to relieve anxiety and enhance
performance.
Deterioration in functioning (underachievement in school, at
work, and in social life).
Epidemiology:
Age: - late teenage or early twenties.
- may occur in children.
Lifetime prevalence : 3 – 13 %
In the general population, most individuals fear public
speaking and less than half fear speaking to strangers or
meeting new people.
Only 8 – 10 % are seen by psychiatrists.
Reports from Saudi Arabia suggested that social phobia is a
notably common disorder among Saudis, and social phobic
compose 80 % of phobic disorders.
Social and cultural differences have some effect on social
phobia in terms of age at treatment, duration of illness and
some social situations.
Aetiology:
Genetic factors: some twins studies found genetic basis for
social phobia.
Social factors: excessive demands for social conformity and
concerns about impression a person is making on others,
(high cultural superego increases shame feeling), some Arab
cultures are judgmental and impressionistic.
Behavioural factors: sudden episode of anxiety in a social
situation followed by avoidance.
Cognitive factors: exaggerated fear of negative evaluation and
feelings that other people will be critical.
Differential Diagnosis:
Other phobias, however, multiple phobias can occur together.
Generalized anxiety disorder.
Panic disorder.
Depressive disorder primary or secondary to social phobia.
Patients with persecutory delusions avoid certain social
situations.
Avoidant personality disorder may coexist with social phobia
(axis II diagnosis).
Treatment:
A. Psychological:
1. Cognitive-Behaviour Therapy:
Exposure to feared situations is combined with
anxiety management (relaxation training with
cognitive techniques designed to reduce the effects of
anxiety-provoking thoughts).
It is the treatment of choice for social phobia.
2. Social Skill Training: how to initiate, maintain and end
conversation.
3. Assertiveness Training: how to express feelings and thoughts
directly and appropriately.
B. Drugs:
1. Beta-adrenergic antagonists help to control palpitation and
tremor.
2. Benzodiazepines (e.g. alprazolam): small divided doses for
short time (to avoid the risk of dependence).
3. Antidepressants:
Specific serotonin reuptake inhibitors (e.g. fluoxetine)
or
Monoamine oxidase inhibitors (e.g. moclobemide).
Prognosis:
If not treated, social phobia often lasts for several years and the episodes
gradually become more severe with increasing avoidance. When treated
properly the prognosis is usually good.
SPECIFIC PHOBIA
Also called: Simple Phobia.
The central problem is irrational and persistent fear of a specific object or
situation (other than those of agoraphobia and social phobia ) accompanied
by strong desire to avoid the object or the situation, with absence of other
psychiatric problems.
Common feared objects and Situations
Animals (including spiders).
Storms and thunder.
Heights (acrophobia), flying.
Closed spaces (claustrophobia).
Injury, blood, hospitals.
Illness, death.
Epidemiology;
It is common in the general population though not necessarily among those
seeking treatment (less than 20 % of patients are seen by psychiatrists).
Animal phobia: common in children and women.
Most specific phobias occur equally in both sexes.
Most specific phobias of adult life are a continuation of childhood
phobias. A minority begins in adult life (usually in relation to a
highly stressful experience).
Aetiology:
It tends to run in families (? genetic or environmental).
Modelling: (observing the reaction in another person, usually a
parent).
Pairing of a specific object or situations with the emotions of fear
and panic.
Differential Diagnosis:
Obsessive compulsive disorder (some patients have fear and
avoidance of specific objects e.g. dirt, knives). Both can be
diagnosed if criteria are met.
Depressive disorder: some patients with specific phobia seek help
for long standing problem when a depressive disorder makes them
less able to tolerate their phobic symptoms.
Social phobia and agoraphobia.
Treatment:
Behaviour therapy (exposure technique).
Drugs (e.g. benzodiazepines, beta adrenergic antagonists) before
exposure sessions.
Prognosis:
If started in adult life after stressful events the prognosis is usually
good.
If started in childhood, it usually disappears in adolescence but
may continue for many years.
3.Explain about symptoms and management ofObsessive Compulsive disorders?
OBSESSIVE COMPULSIVE DISORDER OBSESSIONS: Recurrent, persistent ideas,
images or impulses which enter the mind despite patient’s resistance. The patient regards them a
silly product of his own mind (coming within the self). Attempts to resist or dispel the
unwelcome thoughts or urges lead to severe inner struggle, with intense anxiety.
COMPULSIONS: Repeated compelling acts done in response to obsessions. Healthy people
experience occasional intrusive thoughts. It is the persistence, intensity and frequency that make
a disorder.
OBSESSIVE COMPULSIVE DISORDER (OCD): A psychiatric disorder characterized by:
recurrent obsessions or compulsions that are severe enough to be time consuming (> 1 hour a
day) or causes marked distress or significant impairment. the person recognizes that the
obsessions or compulsive are excessive and unreasonable. the disturbance is not due to the
direct effect of a medical condition, substance or another mental disorder. at least two weeks’
duration (ICD-10 criterion). Anxiety is an important component of OCD; that is why these
conditions are classified as anxiety disorders in DSM IV. (However, some European researches
consider OCD as a separate category!
THE MAIN THEMES OF OCD
Contamination and washing (e.g. contaminated by one’s own excreta, shaking hands with
others, etc.)
Repeated doubts concerning actions that may not have been completed adequately (e.g.
ablutions, prayers, gas checking).
Insistence on symmetry: needs to have things in a particular order.
Aggressive or horrific impulses (e.g. fear of harming a child).
Sexual imagery (e.g. violent abnormal sexual practices).
Blasphemous thoughts: obsessions about religious matters.
Obsessional ruminations: internal debates in which arguments for and against even the simplest
everyday actions are reviewed endlessly.
Obsessional phobias: obsessional thoughts with fearful content such as thoughts a harmful use
of knives. Associated features:
Avoidance of situations that involve the content of the obsessions, such as dirt or
contamination.
Anxiety is an important component of OCD. Some rituals (compulsions) are followed by a
diminution of anxiety, which reinforces OCD.
Depressive features either secondary or independent to OCD.
Guilt due to a pathological sense of responsibility to such absurd thoughts (especially in
blasphemous, aggressive and sexual obsessions).
Hypochondrical concerns are common.
A proportion of obsessional patients report depersonalization

Epidemiology:
Obsessive Compulsive Disorder, until recently, was considered to be a rare
disorder (0.5 %), but new data have revealed that it is in fact a common illness.
Lifetime prevalence: 2 – 3 % of the population.
Sex distribution is equal.
Mean age at onset = 20 – 25 years.
Mean age of seeking psychiatric help = 27 years. In many Arabic countries, OCD may not be
recognized as a mental disorder and religious leaders are usually consulted first for its diagnosis
and treatment.
Aetiology:
1. Genetic Factors:
OCD have been found in about 7 % of the parents of patients with these disorders.
Few twin studies, monozygotic 50 – 80 % for concordance rate compared to only 25 % in
dizygotic twins.
2. Neurobiology: (Neurobiological hypothesis) There is evidence that specific serotonin
reuptake inhibitors (SSRIs) are partially effective treatment for OCD. However, there is no
evidence of baseline serotonergic dysfunction in OCD patients. Multiple neurotransmitter system
is suggested. MRI and PET have indicated abnormalities in the frontal lobes, cingulum and
basal ganglia of OCD patients. More gray matter and less white matter, suggesting a
developmental abnormality
3. Psychodynamic Theories: There are unconscious impulses of an aggression or sexual nature.
These impulses could potentially cause extreme anxiety, but anxiety is reduced by the action of
the
mechanisms of repression, isolation, undoing, and reaction
formation.
4. Learning Theory:
Some obsessions are results of abnormalities in mechanisms of
learning (avoidance responses).

Differential
Diagnosis:
OCD should be differentiated from other mental disorders in which
some obsessional symptoms occur, like:
Depressive disorders
Anxiety, panic and phobia disorders
Hypochondriasis
Schizophrenia: some schizophrenic patients have obsessional
thoughts, these are usually odd with peculiar content (e.g.
sexual or blasphemous). The degree of resistance is doubtful.
Organic disorders: some organic mental disorders are
associated with obsessions e.g. encephalitis, head injury,
epilepsy, dementia.



Course
and Prognosis:
In most cases onset is gradual (but acute cases have been noted).
The majority have a chronic waxing and waning course with
exacerbations related to stressful events.
Severe cases may become persistent and drug resistant.
Prognosis is worse when the personality is obsessional, (Obsessive
Compulsive Personality disorder).
Patient’s age, sex, age of onset and duration of OCD showed no
significant correlation with outcome.
Good lasting outcome was found to be related to compliance with
treatment (exposure and drugs), presence of mood component and
family support.
Treatment:
Search for a depressive disorder and treat it, as effective treatment
of a depressive disorder often leads to improvement in the
obsessional symptoms.
Reassure the patient that these symptoms are not early signs of
madness.
Explain the nature of the illness and clarify to the patient the
intrusive nature of the obsessions (against his will). This helps the
patient to reduce the guilt that results from the sense of
responsibility.
Frequent supportive interviews providing continuing hope.
The most effective treatment is pharmacobehavioural approach.
Drugs.
1. Antiobsessional drugs
a. Clomipramine: required doses may reach 200 mg / day.
b. Selective serotonin-reuptake inhibitors (e.g.
Fluvoxamine)
2. Anxiolytics can give some short-term symptomatic relief.
Most Saudi OCD patients are treated with drugs only.
Behaviour therapy (combined with drugs):
It is more effective with prominent compulsions (less effective
for obsessional thoughts).
About 60 % may improve greatly (though not completely).
Techniques used are:
Exposure to any environmental cue that increase obsessions
along with response prevention.
Thought stopping
Mass practice and habituation.
Behaviour therapy may be done at out – patient clinics, day center or as in –
Psychosurgery: for severe and resistant incapacitating cases.
3. Briefly explain PTSD?
1. The onset is usually after a latency period which ranges from (a
week to months).
2. symptoms last more than one month :
if less than three months acute.
If three months or more chronic.

Differential
Diagnosis (for both acute and post-traumatic stress
disorders).
1. Head injury sequence (if the traumatic event has included injury to the
head, e.g. from a road accident). Neurological examination should be
carried out to exclude a subdural haematoma or other forms of cerebral
injury.
2. Substance abuse (intoxication or withdrawal).
3. Adjustment disorders.
4. Anxiety disorders (Generalized / panic).

Treatment:
The major approach is psychological:
Support – reassurance – explanation – education.
Encourage discussing stressful events and overcome patient’s
denial.
Environmental support: family, friends, etc.
Relaxation
Cognitive-behaviour therapy
Group therapy (for group of people who were involved in a
disaster).
Pharmacological:
Symptomatic treatment (sedatives, anxiolytics, antidepressants, etc).

Prognosis:
good if
(1) the person has healthy premorbid function
(2) the trauma was not severe
(3) early intervention and social support exist.
PART C
1. Somatoform disorders and its management?
There are five main recognized somatoform disorders:
1. Somatization Disorder.
2. Hypochondriasis.
3. psychogenic Pain Disorder.
4. Body Dysmorphic Disorder.
5. Conversion Disorder.
1. SOMATIZATION DISORDER (previously called Briquet’s Syndrome)
Multiple somatic symptoms (affecting multiple organ system) that cannot be explained
adequately on the basis of physical examination and laboratory investigations.
The symptoms are not intentionally produced.
The disorder is chronic ( several years ) beginning before age 30 ( DMS-IV criteria, not in ICD
- 10 )
It is a associated with excessive medical help-seeking behaviour.
It leads to significant distress and functional impairment (social, occupational…).
DSM requires at least 4 pain symptoms – 2 GI symptoms – 1 neurological symptom and 1
reproductive or sexual symptom.
Epidemiology: Women > men 5 - 10 : 1
The lifetime prevalence in the general population is about 2 %.
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More common in patients with obsessional and avoidant personalities.
Aetiology: Genetic factors: About 15 % of the first-degree female relatives have the
disorder. Monozygotic twins concordance rate 29 % (compared with dizygotic 10 %).
However, as yet there is no enough evidence of true genetic transmission.
Neuroscience: Faulty perception and assessment of somatosensory inputs due to characteristic
attention impairment. Psychological: Displacement of unpleasant emotions into a physical
symptom. Alleviation of guilt through suffering. To obtain attention or sympathy.
Differential Diagnosis: 1. Medical diseases (e.g. SLE, endocrinopathies, chronic infections).
Vigilance is required to ensure that such developments are not overlooked. It is important to keep
in mind that patients with somatozation have the same chance of developing genuine physical
diseases as any other individual at that age; they may also suffer from iatrogenic diseases.
2. Depression (multiple somatic complaints are associated with low mood and / or loss of
interest).
3. Anxiety (many physical manifestations of anxiety e.g. headache, low back pain are
accompanied with apprehension).!
4. Hypochondriasis (the emphasis is on overconcern with a serious disease). 5. Psychogenic pain
disorder (limited to one or two pain symptoms).
Course and Prognosis: Chronic disorder. Fluctuating course (exacerbation of symptoms is
associated with stressful events). Risk of multiple unnecessary operations and possible
complications.
Treatment: The number of medical staff involved is better limited (a single identified
physician as the primary care taker) because opportunity of the patient to express somatic
complaints increases when more than one physician is involved. Arrange brief regularly
scheduled appointments, e.g. every month. Repeat physical examination. Avoid additional
diagnosis procedures. Shift the patient’s awareness to psychological factors, and support him.
Minimize the use of psychotropic drugs (patients tend to use drugs unrealiably and erratically).
Encourage graded return to normal activities. Antidepressants are useful in secondary
depression.
2. Explain Disassociative disorder?
A normal person has a unitary sense of self as a single human being with integrative functions of
identity, consciousness, memory and motor behaviour. In dissociative disorder that unitary state
is partially lost through mental cleavages which arise as defense mechanisms against certain
psychological stresses.
There are four Dissociative Disorders (according to DSM-IV)
1. Dissociative amnesia.
2. Dissociative fugue.
3. Dissociative personality disorder (previously called multiple personality disorder).
4. Depersonalization syndrome.
DISSOCIATIVE AMNESIA A sudden inability to recall important information already stored in
the patient’s memory. The forgotten information is usually about a stressful or traumatic event in
the person’s life (painful memory). It cannot be explained by ordinary forgetfulness and there is
no evidence of an underlying brain disorder. The capacity to learn new information is retained.
Termination of amnesia is typically abrupt with complete recovery. It is the most common of
the dissociative disorders. Women > men. Young adults > old. It is more common during
natural disasters and in wartime. Stressful events include: rape, abandonment by a spouse,
discovery of extramarital affair by a spouse, threat of physical injury or death..
Management: Support with compassionate approach. Establish a sense of safety. Promote
appreciation of the person encouraging positive expectancy. Abreaction (sodium amytal or
diazepam aided interview). Most of the cases recover spontaneously.
DISSOCIATIVE FUGUE Sudden unexpected purposeful wandering away from the usual
surrounding (unexpected travel from home or work) associated with confusion about one’s
identity. It is rare (in wartime, after natural disaster or as result of intense personal crisis).
etiology:
Primitive denial: a desire to withdraw from emotionally painful experiences (“not me” defense
Predisposing factors include certain personality disorders (e.g. borderline, historic) and mood
disorders. The fugue is usually brief (days) followed by spontaneous rapid recovery. If fugue
continued for several weeks, with assumption of new identity, malingering should be suspected.
Treatment: similar to that of dissociative amnesia.
DISSOCIATIVE IDENTITY DISORDER Sudden alternations between the patient’s normal
state and another complex pattern of behaviour (a second personality). Each is forgotten by the
patient when the other is present. It is extremely rare chronic, and the most serious of the
dissociative disorders. It occurs in females more than males.
Aetiology: It is still ambiguous.
The following factors have been mentioned to have some role in the development of
dissociative identity disorder:
biological tendency and capacity to dissociate.
shattered security, self-esteem and future orientation.
subjective dyscontrol and passively endured assaults.
buried psychological trauma (e.g. sexual abuse) and sequestered affect.
broken psychological boundaries.
a traumatic life event mobilizing the dissociative defences.
the absence of support from significant others (parents, relatives, teachers…).
In so many cultures most of these cases are claimed to be possessed by devils (jinn), usually
resistant to faith healing sessions. Patients may continue suffering for years in spite of repeated
exorcisms.
DEPERSONALIZATION DISORDER
Depersonalization as a symptom is the feeling that one’s body or one’s
personal self is unreal and strange. Patient may feel detached from his
body, in a dream, or feel as if he were mechanical.
Depersonalization disorder is the occurrence of one or more episodes
of depersonalization that cause social or occupational impairment. The
individual maintains grossly intact reality and does not accept these
unpleasant feelings (ego dystonic).
.
Epidemiology:
Transient depersonalization symptoms may occur in as much as 70 % of
a given population with no significant difference between men and
women.
Depersonalization disorder: two-thirds of patients are women.
Age: adolescence or early adult life ( rarely after 40 ).
Aetiology:
The causes of primary depersonalization disorder are not yet
known.
Psychological, neurological and systemic diseases have been
considered.
Anxiety and depressed mood are known precipitating factors.
Possible association with schizoid personality disorder.
Differential Diagnosis:
1. Neurological diseases: temporal lobe epilepsy, brain tumour, head
trauma, etc.
2. Substance abuse.
3. Endocrine diseases.
4. Schizophrenia.
5. Other dissociative disorders.
Treatment:
Search of a primary cause and treat it.
Anxiolytic drugs may give relief (short-term treatment).
Anti depressants and anticonvulsants may be helpful in some
patients.
Supportive therapy.
Counselling: enable the patient to live as normal life as possible.
Prognosis: Primary cases tend to be long lasting conditions.
--------------------------------------------------------------UNIT IV
Psychosis – symptoms of Psychosis – Types-functional and organic Psychosis – their
differences, etiology, clinical manifestations and differential diagnosis of functional
Psychosis- Schizophrenia and Affective
disorder.

PART A
1. Lithium is used for ……….. Mania
2. Expand ICD?
International classification diseases
3. Write one of the organic psychosis?
Delirium
PART B
1. Explain schizophrenia and its types?
SCHIZOPHRENIA Schizophrenia is a term coined by the Swiss psychiatrist Eugen
Bleuler in 1911 in his classic text “ Dementia Praecox or the Group of Schizophrenia”, which
means mind splitting. Bleuler distinguished certain symptoms of schizophrenia that he regarded
as primary or essential
1. Association loosening in the logical thoughts.
2. Affective blunting or incongruity.
3. Ambivalence: the co- existence of strongly conflicting feelings, attitudes and ideas leading to
inconsistent behaviour and vacillitation.
4. Autism (withdrawal in thinking and behaviour).
. The Acute Syndrome The Chronic Syndrome
Presence of positive (productive) features which include :
Delusions ( prominent )
Hallucinations ( prominent )
Disorganized thinking and speech
Disturbed behaviour
Mood incongruity Presence of negative (deficit features which include:
Poor self care and hygiene.
Lack of initiative and ambition.
Social withdrawal.
Poverty of thought and speech.
Delusions and hallucinations. become less prominent.
Restricted flat or apathetic affect.
Some cognitive impairment. PDF-XChange Viewer
The most widely used and accepted criteria of schizophrenia are DSM – IV
criteria which :
Six months duration of disturbance (including the prodromal and
residual phases).
At least one month period of psychotic features (two out of five).
1. delusions
2. hallucinations
3. disorganized speech (e.g. incoherence)
4. catatonic features or disorganized behaviour.
5. negative features (e.g. flat affect).
Significant functional impairment (social, occupational,
academic...etc.)
Exclusion of other psychotic disorders (see the differential
diagnosis).
VARIOUS SUBTYPES OF SCHIZOPHRENIA :
1. Paranoid Schizophrenia:
Prominent paranoid delusion with frequent auditory hallucinations
related to the delusion.
Patient is usually potentially aggressive, angry or fearful,
uncooperative and difficult to deal with. No prominent
disorganized behaviour or mood.
The onset is usually late (compared to other subtypes of
schizophrenia).
The prognosis is better than the other subtypes and deterioration in
functioning is usually much less.
2. Catatonic Schizophrenia:
Presence of one or more of the catatonic features: stupor, mutism,
rigidity, negativism, posturing, echopraxia, echolalia, waxy
flexibility or purposeless exicitement.
3. Disorganized Schizophrenia:
Disorganized behaviour.
Marked incoherence and loosening of association.
Inappropriate affect.
Grimacing and bizarre mannerism are common.
4. Undifferenriated Schizophrenia :
Prominent delusions and hallucinations.
Prominent disorganization behaviour.
Incoherence.
5. Residual Schizophrenia :
Schizophrenia in remission from active psychosis: absence of
prominent delusions, hallucinations, disorganized speech or
behaviour.
Presence of negative features or attenuated form of positive
features (e.g. odd belief).
In ICD-10
Hebephrenic Schizophrenia subtype is used (almost equivalent
to disorganized type in DSM-IV). It affects adolescents and young adults.
Features include:
Childish unpredictable behaviour ( e.g. silly smiles and giggles )
Prominent affective changes ( e.g. inappropriate, shallow affect )
Delusions are common and not highly organized.
Hallucinations also are common, and are not elaborate.
In the traditional sub-grouping of schizophrenia another subgroup is
mentioned,
Simple Schizophrenia, which is characterized by insidious
onset of:
Social withdrawal.
Loss of drive and ambition.
Deterioration of functioning.
Odd behaviour.
Simple Schizophrenia is difficult to identify reliably because of absence of
clear psychotic features (delusions, hallucinations…). It has the worst
prognosis of all subtypes.

EPIDEMIOLOGY:
Prevalence - Worldwide life - time prevalence is about I %.
Incidence
- Worldwide, 2 million new cases appear each year.
Incidence is about 20 per 100,000 per year.
The lifetime risk of developing schizophrenia is
about 1%.
Age
- Most common between 15 - 35 years.
Paranoid type: later onset than other types.
Sex
- Sex ratio is 1 : 1
Males have earlier onset (median age at onset is =
32 years).
AETIOLOGY:
No single aetiological factor is considered causative. The model is
most often used:
The person who develops schizophrenia has a specific biological
vulnerability (or diathesis) that is triggered by stress and leads to
emergence of schizophrenic symptoms.
1. Genetic:
Single gene (serotonin receptor on chromosomes 5, D4 dopamine
receptor gene on chromosome11).
Polygenic theory appears to be more consistent with heterogeneity
of the presentation of schizophrenia.
Consanguinity:
- Incidence in families is higher than in general population.
- Monozygotic twin concordance rate is greater than dizygotic
concordance rate (50 % , 15 % respectively)
Adoptive Studies:
- Test for genetic versus environmental influence by examining rates
of schizophrenia in adopted away offspring and of normal parents.
(10 % from schizophrenic parents versus 0 % from normal
parents).
Family Studies:
Morbid Risk Relationship to Schizophrenic
5%
10 %
14 %
46 %
Prevalence:
10 - 12 %
5-6%
Parents
Siblings
Child of one schizophrenic parent
Child of two schizophrenic parents
First degree relative
Second degree relative
2. Neurobiological:
A. Dopamine hypothesis (very influential theory): schizophrenic
symptoms are in part a result of hypersensitive dopamine receptors or
increased dopamine activity in mesolimbic pathways.
Evidences include:
1. Amphetamine increases central dopamine release and induces
schizophrenia-like psychosis.
2. Antipsychotics block dopamine postsynaptic receptors to the extent
that correlates with clinical potency.
B. Seratonin hypothesis:
Abnormal serotonin metabolism in some patients.
Evidence include:
1. LSD (serotonin agonist) induces psychosis.
2. Serotonin antagonist, such as clozapine, improves psychosis.
C. Disturbed balance between dopamine and serontonin as supported by
the new generation of antipsychotics (dopamine-serotonin antagonists).
3. Neuropathology and Neuroimaging :
CT scan studies:
- Cortical atrophy in 10 - 35 %
- Enlargement of the lateral and third ventricles in 10 - 50 %.
- Findings correlate more with negative features and with
cognitive impairments.
MRI and PET (Positron Emission Tomography):
- Abnormal frontal, parietal and temporal lobe structure and
metabolism.
4. Psychosocial and Environmental:
Slow virus infection: increased frequency of perinatal
complications and seasonality of birth data suggests an infectious
hypothesis.
5. Psychosocial and Environmental:
A. Life Events:
Life stressors, particularly in the three months before onset, can
induce schizophrenia in those who are vulnerable.
B. Family Psychodynamic (obsolete theories).
Precipitation of schizophrenia can be due to :
1. Schizophrenogenic mother.
2. Marital skew (submissive father and dominant mother)
3. Marital schism (contradicting parental messages).
4. Double – bind communication (a parent conveys two conflicting
incompatible messages at the time, one is overt and the other is
covert).
C. High Expressed Emotions (EE) of the family which include critical
comments and emotional over-involvement.
Patients whose families have high expressed emotions have higher relapse
rate than those whose families have low expressed emotions.

.
MANAGEMENT:
Multidisciplinary: Bio, Psycho, Social
approach.
Hospitalization is usually indicated in the acute phase in order to:
Clarify diagnosis (rule out possible organic causes).
Control the disturbed behaviour.
Protect the patient and / or others (risk of dangerousness or
suicide)
Give electroconvulsive theraphy (ECT) for Catatonic type,
those with concomittent depression and in resistant cases.
Psychosocial :
- Family therapy education and explanation can significantly
reduce relapse rate and high-EE family interaction can be
diminished. Compliance may also be enhanced.
- Supportive therapy and counselling.
- Rehabilitation (Community - based process):
Social skill training (e.g. self-care).
Illness-management skills (e.g. when to take
medication).
Vocational rehabilitation (for more stable cases).
- Token economy:
Useful for institutionalized chronic schizophrenics.
Positive and negative reinforcement are used to alter
patient’s unacceptable behaviour.
It should be part of a behaviuoral programme.


Prognostic
Factors:
Good Prognostic Factors Bad Prognostic Factors
Late onset
Acute onset
Obvious precipitating
factors
Good premorbid personality
Presence of mood
symptoms
(especially depression)
Presence of positive
symptoms
Good support (married,
stable family)
Young age at onset
Insidious onset
No precipitating factors
Poor premorbid Personality
Low IQ
Many relapses
Poor compliance
Negative symptoms
Poor support system
Family history of
Schizophrenia
MISCONCEPTIONS:
- Schizophrenia means personality splitting.
- The cause is abnormal parenting.
!
2. Explain about mood disorders?
MOOD (AFFECTIVE) DISORDERS
The mood disorders are so called because one of their essential features is abnormality of mood;
abnormal feelings of depression or euphoria, with associated psychotic features in some severe
cases. In mood disorders the sense of mood control is lost, and patient experiences considerable
distress. Mood disorders are usually accompanied by disturbances in thinking, perception and /
or behaviour. Although anxiety is a variant of normal mood, anxiety disorders are not considered
as part of mood disorders in the modern classification. Illnesses in which the prevailing mood is
depression are much commoner than those presenting with elevation of mood, and people who
suffer from episodes of mood elevation almost invariably suffer from depression as well, at some
stage of their illness Major depressive disorder: characterized by one or more major
depressive episodes (at least 2 weeks of depressed mood or loss of interest accompanied by at
least four additional symptoms of depression, see later). Dysthymic disorder: characterized by
at least 2 years of depressed mood for more days than not, accompanied by additional depressive
symptoms that do not meet criteria for major depressive episode. Bipolar I disorder:
characterized by one or more manic or mixed episodes, usually accompanied by major
depressive episodes. Bipolar II disorder: characterized by one or more major depressive
episodes accompanied by at least one hypomanic episode

Psychomotor retardation (sometimes agitation).
- lack of motivation and irritation.
- slow movements.
- slow interactions.
Social isolation and withdrawal.
Delay of tasks and decisions.
Loss of interest in work and pleasure activities.
C. Biological Features (Neurovegetative Signs):
Change in appetite (usually reduced but in some patients
increased).
Change in sleep (usually reduced but in some patients
increased).
Early morning (terminal) insomnia; waking 2 - 3 hours
before the usual time, this is usually associated with severe
depression.
Change in weight (usually reduce but may be increased).
Fatigability, low energy level, (simple task is an effort)
Low libido and /or impotence.
Change in bowel habit (usually constipation).
Change in menstrual cycle (amenorrhoea).
Diurnal variation of mood (usually worse in the morning).
D. Cognitive Functions & Thinking:
Poor attention and concentration.
Poor memory (subjective).
Pessimistic thoughts; depressive cognitions as suggested by Beck:
Present: patient sees the unhappy side of every event (discounts any
success in life, no longer feels confident, sees himself as failure).
Past: unjustifiable guilt feeling and self-blame.
Future: gloomy preoccupations; hopelessness, helplessness, death
wishes ( may progress to suicidal ideation and attempt ).
A. Delusions (mood-congruent)
1. Delusion of guilt (patient believes he deserves severe punishment).
2. Nihilistic delusion (patient believes that some part of his body
ceased to exist or function, e.g. bowel, brain…).
3. Delusion of poverty and impoverishment.
4. Persecutory delusion (patient accepts the supposed
persecution as something he deserves, in contrast to
schizophrenic patient).
B. Hallucinations (mood-congruent)
1. Usually second person auditory hallucinations (addressing
derogatory repetitive phrases).
2. Visual hallucinations (scenes of death and destruction) may be
experienced by a few patients.

Epidemiology of Major Depression
It is more prevalent than bipolar mood disorder (more in women).
Lifetime risk is in the range of 10 - 15 %.
Lifetime prevalence is in the range of 15 - 25 %.
The mean age of onset is about 40 years (25 - 50 years).
It may occur in childhood or in the elderly.
In adolescents may be precipitated by substance abuse.
More common in those who lack confiding relationship (e.g.
divorced, separated, single…).
No correlation has been found between socio - economic status and
major depressive disorder.
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
Aetiology of Major Depression:
The causative factors are multifactorial (interacting together)
as supported by family and twin
studies.
Reduced levels of:
Noradrenaline
Serotonin
Dopamine

Differential Dianosis of Major Depression :
Depression secondary to medical diseases:
- Thyroid dysfunction.
- Diabetes mellitus.
- Cushing’s disease.
- Parkinson’s disease.
- Stroke.
- Carcinoma (especially of the pancreas and
lung).
- Multiple sclerosis.
Depression secondary to medications:
- Antihypertensives (resepine, beta-blockers).
- Corticosteroids.
GENETIC FACTORS
BIOLOGICAL FACTORS PSYCHOLOGICAL FACTORS
Stressful events
Premorbid personality factors
Cognitive faults (distortions)
- Antineoplastic drugs (e.g. trimethoprim).
- Bromocriptine.
- Indomethacin.
- L - dopa.
Psychiatric disorders:
Dysthymic disorder (less severe, and chronic).
Adjustment disorder with depressed mood.
Substance - induced mood disorder.
Schizophrenia, schizoaffective disorder.
Somatization disorder

Management of Major Depression:
Hospitalization is indicated for:
Suicidal or homicidal patient.
Patient with severe psychomotor retardation who is not
eating or
drinking (for ECT).
Diagnostic purpose (observation, investigation…).
Drug resistant cases (possible ECT).
Severe depression with psychotic features (possible ECT).
Medications have proven to be very useful in the
treatment of severe depression. They shorten the
duration in most cases.
prolonged for at least a year after clinical recovery to reduce the risk of
relapse.
- Lithium Carbonate can be used as prophylaxis.
Electroconvulsive therapy ( ECT ):
. The effect of ECT is best in severe depression especially with
marked biological (neurovegetative) and psychotic features.
. It is mainly the speed of action that distinguishes ECT from
antidepressant drug treatment.
Psychosocial:
- Supportive therapy.
- Family therapy.
- Cognitive-behaviour therapy (for less severe cases or after
improvement with medication). See chapter 23.
Prognosis of Unipolar Depressive Disorders
- About 25 % of patients have a recurrence within a year.
- Ten percent will eventually develop a manic episode.
- A group of patients have chronic course with residual
symptoms and significant social handicap.
At least two years history of chronic low mood.
No remission periods more than two months.
During low mood there should be at least 2 out of the following:
1. low energy or fatigue.
2. low selfesteem.
3. feeling of hopelessness.
4. insomnia (or hypersomnia).
5. poor appetite (or overeating).
6. poor concentration or difficulty in making
decisions.
Not better accounted for by any other psychiatric or medical
diseases (e.g. major depression, hypothyroidism).
It leads to impairment in functioning or significant distress.

Differential Diagnosis:
This is essentially identical to that of major depression. However, two
disorders require consideration:
1. Chronic Fatigue Syndrome / Neurasthenia
Disabling chronic fatigue of uncertain aetiology associated with
variable extent of somatic and / or psychological symptoms.
2. Recurrent Brief Depressive Disorder:
Brief less than two-week periods during which
depressive features are present with greater severity than
that of dysthymic disorder. The course is episodic and
recurrent.
The most effective treatment is the combination of
pharmacotherapy and either cognitive or behaviour therapy.
A. Pharmacological:
Serotonin-specific reuptake inhibitors (SSRI).
Or Monoamino oxidase inhibitors (MAOI). Avoid
combining with SSRI or tricyclic antidepressants.
- These groups may be more beneficial than tricyclic
drugs in the treatment of dysthymic disorders.
B. Psychological:
Supportive therapy.
Cognitive therapy (to replace faulty negative self image, negative
attitudes about the world and the future).
Behaviour therapy (to enable the patient to meet life challenges
with a positive sense by altering personal behaviour through
implementing positive reinforcement).

Course and Prognosis:
The onset is usually insidious before age 25; the course is chronic.
Some patients may consider early onset dysthymic disorder as
part of life. Patients often suffer for years before seeking
psychiatric help.
About 25 percent never attain a complete recovery.
PART C
1.WRITE ABOUT BIPOLAR MOOD DISORDERS?
Bipolar I Disorders:
Patient has met the criteria for a full manic or mixed episode,
usually sufficiently severe to require hospitalization. Depressive
episodes may / may not be present.
Bipolar II Disorders :
Mania Mania
Depression
Patient has at least one major depressive episode and at least one
hypomanic episode, but NO manic episode.

MANIA (manic episode)
Features (with varying degrees of severity)
At least one week period of elevated (or irritable) mood.
- elevated: cheerful, euphoric unduely
optimistic.
- irritable: tense, easily provoked into anger.
Overactivity with excessive energy.
Overtalkativeness with flight of ideas.
Expansive ideas (inflated selfesteem or grandiosity).
Distractibility (reduced concentration).
Excessive involvement in pleasurable acts (e.g. buying).
Decreased need for sleep.
Increased libido (may lead to sexual indiscretions).
Delusions occur in severe cases (mood - congruent grandiose
delusions).
At times, delusions of persecutions, delusions of reference, passivity feeling
and first rank symptoms may occur.
The delusions often change in content over days.
Hallucinations (mood-congruent) occur in severe cases. Voices talking
to the patient about his special powers or, occasionally hallucinations of
vision with religious content (e.g. seeing Angels).

Epidemiology:
- Prevalence: 1 %.
- Incidence: 1.5 %.
Hypomania
Depression
- Lifetime expectancy: 1 %.
- Age: 30 years is the mean age (onset is most often in mid- 20s).
- Sex: no gender differences.

Aetiology:
1. Genetic:
One parent with bipolar I 25 % chance of mood
disorder in child.
Two parents with bipolar I more than 50 % chance of
mood disorder in child.
Some studies found some defects in chromosomes 5,11 and
X.
2. Neurochemical:
Increased biogenic amines (noradrenaline, dopamine and
serotonin).

Differential Diagnosis :
1. Substance-induced mood disorder e.g. amphetamine
intoxication.
2. Organic brain diseases involving the frontal lobes.
3. Schizophrenia (in acute phase, elevated mood and grandiosity
may occur along with delusions and hallucinations but
usually these not mood-congruent).
4. Schizoaffective disorder (see later)
HYPOMANIA:
- It is delineated from mania on grounds of severity which includes
both symptomatic features and social incapacity.
- The episode is not severe enough to cause marked impairment in
social or occupational functioning or to necessitate hospitalization.
- There are no psychotic features.
- Otherwise the features are basically those of mania; elevated mood,
grandiosity, overactivity … etc.

MIXED & ALTERNATING AFFECTIVE STATES
In mixed affective state: manic and depressive symptoms occur
simultaneously (e.g. overactive overtalkative patient may have
profound depressive thoughts including suicidal ideas).
In alternating affective states: manic and depressive features follow
one another in a sequence of rapid changes in a short time (e.g. a
manic patient may be intensely depressed for few hours and then
quickly becomes manic).
RAPID-CYCLING BIPOLAR DISORDER
Alternating episodes (4 or more) of depression, mania or
hypomania in the previous 12 months, separated by intervals of
48 - 72 hours.
Usually more chronic than non-rapid cycling disorders.
Around 80 % are lithium-treatment failures.
Carbamazepine or sodium valporate are usual agents of choice.

SEASONAL AFFECTIVE DISORDER
Recurrent major depressive episodes that come with shortened day
light in winter and disappear during summer (may be followed by
hypomania).
Absence of clear-cut seasonally changing psychosocial variables.
Characterized by atypical features of depression: hypersomnia,
hyperphagia (carbohydrate craving), weight gain, increased fatigue.
Related to abnormal melatonin metabolism.
Treated with exposure to light (artificial light for 2 – 6 hours a
day).
It may occur as part of bipolar I or II disorders.
CYCLOTHYMIC DISORDER
Less severe bipolar mood disorder with continuous mood swings;
alternating periods of hypomania and moderate depression. It is
non-psychotic chronic disorder.
It starts in late adolescence or early adulthood.
The treatment is similar to that of bipolar mood disorder.
****

Treatment of Bipolar Mood Disorder
Acute mania or mixed episode:
Manic behaviour can be damaging for the patient and others (e.g. loss
of career, financial disaster, and sexual insult). Hospitalization can
provide a secure, protective environment. The initial task is to quieten
the agitation that commonly occurs. This is usually accomplished with
antipsychotic medication. Chlorpromazine and halperidol are widely
used to treat mania.
They reduce psychotic symptoms and over-activity. Thus they bring the
acute symptoms of mania under control. Haloperidol is a potent
antipsychotic, less sedative and causes less postural hypotention
compared with chlorpromazine which is sometimes the drug of choice
for its sedative property.
Recently serotonin-dopamine antagonists (e.g. clozapine, risperidone,
olanzapine) have been found effective in mania.
When the manic patient settles (within weeks) he can be treated as an
outpatient with close observation and frequent assessment.
Antipsychotics can be then reduced gradually and carefully.
Long-Term Treatment :
Mood disorders often recur and have relapsing course, thus preventive
(prophylactic) treatment is required. Lithium has been found to be
effective in preventing recurrence of manic depressive episodes.
Carbamazepine appears to be as effective as lithium in the prophylaxis of
bipolar mood disorder, and can be considered in patients who are
intolerant of lithium or who respond poorly to lithium (e.g. rapidcycling
mood disorders).
Sodium valproate has been found effective in patients with refractory
bipolar illness, even when there has been a poor response to lithium and
carbamazepine.
Combination of lithium with carbamazepine can be used, particularly in
rapid-cycling disorders, and combination of lithium with sodium
valproate has been shown to be effective in the treatment of resistant
patients.
Electroconvulsive therapy (ECT):
ECT is used when antipsychotics are ineffective. It has a therapeutic
effect in both mania and depression.
Psychosocial treatment:
Education of the patient and the family about:
- the nature of the illness and its course.
- how to recognize early features of recurrence.
* Increase support and reduce stresses.
* Counselling (for occupational, marital, financial or academic
difficulties).
Course and Prognosis
If left untreated, most manic episodes will resolve within 8 - 12
weeks (rarely last longer than 24 weeks). The risk of
recurrence is particularly high (50 %). About 80 % of manic
patients eventually experience a full depressive episode. About 50
% will have multiple relapses with good interepisodic functioning.
UNIT V
Organic Disorders- etiology, clinical manifestations and differential diagnosis of Dementia,
Delirium, organic amensitic Syndrome.
PART A
1. What is dementia?
False belief
2. Name one organic psychosis disorder?
Dementia
3. Expand DSM?
Diagnostic statistical manual
PART B
1.Explain delirium and its symptoms?
DELIRIUM
Definition: acute reversible global cognitive impairment with fluctuating disturbed
consciousness.
Features: The clinical presentation differs considerably from patient to patient; however, there
are several characteristic features that help make the diagnosis:
1. Disturbed consciousness.
2. Attention deficit.
3. Memory impairment (typically a recent memory deficit).
4. Disorientation to time, place and lastly person.
5. Perpetual disturbances: illusions & hallucinations (mainly visual).
6. Disturbed thoughts and speech.
7. Affective changes: mood liability, perplexity, irritability…etc.
8. Behaviour disturbances: shouting, hostility, agitation, restlessness. (Some patients may be
excessively somnolent, and some may fluctuate from one state to the other, usually restless at
night and sleepy during the day.) . The patient may be dangerous to himself of others. . It is one
of the serious medical emergencies.
Epidemiology: . Among hospitalized patients about 10 % . Postburn patients 20% . Intensive
care unit 30% - More common among very young and elderly patients.
Aetiology: The presence of delirium indicates a serious physical problem affecting the brain and
requires a search for causes.
Common causes include:
Metabolic disturbances:
- Endocrinopathies (e.g. hypoglycemia)
- Organ failure: uremia, hypoxia…
- Electrolyte imbalance.
Infectious:
- Systemic: septicaemia
- Specific: encephalitis
Medications ( multiple drugs with multiple interactions )
Substance abuse:
- Alcohol withdrawal ( delirium tremens )
- Intoxication
Neurological diseases:
- Seizure
- Head truma
Differential Diagnosis
1. Other organic psychiatric disorders:
• dementia • amnestic syndrome
2. Acute functional psychosis (no disturbed consciousness)
Course and Prognosis:
The course is usually short (7-10 days). Delirium if not treated
may progress rapidly into death or dementia, or spontaneously clear.
When treated, it usually resolves rapidly. However, some
residual deficit may persist.
Patients may have another episode later in their life.
Treatment: (Should be in a medical ward)
1. Search for the cause and treat it properly. A referring physician
should do this job.
2. Correct any metabolic abnormality:
ensure nutrition, hydration, electrolyte balances.
3. Low doses of a high potency antipsychotic for agitation
(e.g. haloperidol or droperidol 2 mg oral or IM three
times a day).
Although benzodiazepines may be appropriate for
promoting sleep at night, they should generally be
avoided in the daytime because their effects may
increase disorientation, drowsiness and ataxia with
possible falls, head trauma and fractures.
4. Keep the patient in a quiet, well lit-room; avoid over
and under stimulation.
5. Frequently re-orient, reassure and explain clearly to the patient.
2.Explain dementia and its symptoms?
Definition: Chronic global impairment of cognitive functions
without disturbed consciousness.
. Reversible = 60% Controllable = 25% Irreversible = 15%
Features: The essential feature is a loss of intellectual abilities
of sufficient severity to interfere with social or
occupational functioning or both.
In early stages features include :
- subtle changes in personality.
- a decrease in the range of interest and enthusiasm.
- shallowness and lability of affect, and agitation.
- multiple somatic complaints and vague psychiatric
symptoms.
- a gradual loss of social and intellectual skills (first noticed in
work setting where high performance is required).
Early dementia may present primarily with emotional (depressive or
anxiety) rather than cognitive disturbance.
In late stages cognitive disturbances emerge:
- increasing memory impairment (recent memory first).
- attention impairment (patient becomes less sharp).
- impaired judgment.
- Disorientation: particularly to time, and when severe to place
and person.
- significant change in mood and personality: often
exaggeration of previous personality.
- behaviour: shrinkage of social interaction.
- language: vague and imprecise speech with persevaration.
- psychotic features: hallucinations and delusions.
.
Aetiology:
Causes of dementia are better classified into:
A. Treatable
B. Non-treatable
A. Treatable Causes:
1. Vascular (multi-infarct) dementia:
Stepwrise deterioration of intellectual functioning due to
multiple infarcts of varying sizes caused by thromboelism
from extracnial arteries or arteriosclerosis in main vessels,
usually in patients with hypertension or diabetes.
2. Normal pressure hydrocephalus:
Progressive memory impairment, slowness and marked unsteady gait (urine incontinence in late
stages). 3. Metabolic causes: Vitamin deficiency (e.g. B12), endocrinopathy ...etc. 4. Chronic
infections affecting the brain, e.g. T.B. 5. Alcoholic dementia:
B. Non-treatable: 1. Alzheimer’s disease: continuous degenerative process affecting the whole
cortex, especially cholinergic neurons. 2. Pick’s disease (dementia of frontal lobe type). 3.
Huntington’s chorea: global intellectual impairment with extra pyramidal features. 4. AIDS
dementia. 5. Creutz Feldt–Jakob’s disease.
Course and Prognosis: The course depends on the cause. Dementias with non-treatable causes
(especially Alzheimer’s) show progressive slow deterioration. The patient may become
incontinent of urine and / or stool.
Treatment:
1. Supportive measures:
a. provide good physical care (meals, hygiene, …).
b. encourage the family’s involvement.
c. support the care giver.
d. keep in familiar settings if possible to avoid
accidents, wandering away,…etc.
2. Specific measures:
a. identify and correct any treatable condition.
b. Symptomatic treatment:
depression: small doses of antidepressants (serotonin reuptake
inhibitors or tricyclics).
agitation, aggression: small doses of antipsychotics
(e.g. haloperido;l mg p.o. t.i.d.).
insomnia: a sedative antidepressant or antipsychotic in small doses.
(e.g. thioridazine 25 mg. p.o. nocte).
No specific drug treatment for dementia has been found to be
consistently useful although many are being investigated.
3.Explain amnestic syndrome and its symptoms?
Definition:
Impaired memory (recent memory mainly) due to a specific organic cause,
in the absence of generalized intellectual impairment. It leads to social and
occupational dysfunctioning. It is often known as Wernicke – Korsakoff’s
syndrome, which starts as an acute syndrome (Wernicke’s encephaopathy)
characterized by impairment of memory, ataxia, opthalmoplegia and
impaired consciousness. Then followed by Korsakoff’s psychosis (chronic
memory defect, peripheral neuropathy and irritably). The immediate
memory (frontal lobe function) is usually intact: i.e. digit span test is
normal.
Aetiology:
The condition usually results from lesions in the posterior hypothalamus and
nearby mid-line structures, occasionally due to bilateral hippocampal
lesions. The most common cause is thiamin, vitamin B1, deficiency
associated with alcohol abuse. Thiamin is essential for the enzyme
transketolase which is essential for glucose metabolism. Other causes of
thiamine deficiency include gastric carcinoma and persistent vomiting (e.g.
typhoid fever).
Treatment:
Identity and reverse the cause if possible.
Thiamine supply (if due to thiamine deficiency).
Supportive medical measures (no specific treatment).
Prognosis:
If it is due to thiamine deficiency and thiamine is provided promptly,
prognosis is good. Otherwise, the course is usually chronic and may be
progressive. Psychiatric symptoms occur with increased frequency in
patients with seizures as a result of underlying brain tissue injury, side
effects from anticonvulsant medications, or seizure-specific psychiatric
disturbances.