Psychological

medicine
Introduction 1273 Mania and hypomania 1294
The psychiatric history 1274 Suicide and attempted suicide 1296
The mental state examination 1274 The anxiety disorders 1297
Classification of psychiatric disorders Obsessive-compulsive disorder 1301
Alcohol misuse and dependence 1302
1278
Drug misuse and dependence 1305
Causes of a psychiatric disorder 1279
Schizophrenia 1307 Organic mental
1279
Psychiatric aspects of physical disease disorders 1309 Eating disorders
Severe behavioural disturbance 1280 The sick
1310 Sexual disorders 1312
role and illness behaviour 1280 Functional or
psychosomatic disorders: medically Personality disorders 1313
unexplained symptoms 1281
Psychiatry and the law 1313
Somatoform disorders 1284 Dissociative
(conversion) disorders 1285 Sleep
difficulties 1287
Mood (affective) disorders
Depressive disorders 1288

1288
INTRODUCTION Box 22.1 The approximate prevalence of
psychiatric disorders in different populations
Psychiatry is concerned with the study and treatment of % (approx.)
disorders of mental function. Psychological medicine, or Community 20%

liaison psychiatry, is the discipline within psychiatry that Neuroses 16%

Psychoses 0.5%
is concerned with psychiatric and psychological disorders
Alcohol misuse 5%
in patients who have physical complaints or conditions.
Drug misuse 2% (an underestimate)
This chapter will primarily concern itself with this parti-
(total in community 20%
cular branch of psychiatry. due to comorbidity)
The long-held belief that diseases are either physical or Primary care 25%
psychological has been broken down by the accumulated General hospital outpatients 30%
evidence that the brain is functionally or anatomically General hospital inpatients 40%
abnormal in most if not all psychiatric disorders. Both
physical and psychological factors, and their interactions
must be considered. This philosophical change of related renal failure), and physical presentations of
approach rejects the Cartesian dualistic approach of the psychiatric disorders (such as weight loss due to anorexia
mind/body medical model and replaces it with the more nervosa). .' . . .
holistic biopsychosotial model.
Culture and ethnicity
Epidemiology (Box 22.1) These can alter either the presentation or the prevalence
The prevalence of psychiatric disorders in the community of psychiatric ill-health. Biological factors in mental ill-
in the UK is about 20%, mainly composed of depressive ness are usually similar across cultural boundaries,
and anxiety disorders and substance misuse (mainly whereas psychological and social factors will vary. For
alcohol). The prevalence is about twice as high in patients example, the prevalence and presentation of schizophrenia

attending the general hospital, with the highest rates in
the accident and emergency department and medical
wards. The higher rates in the general hospital are due to
several factors, such as admission for deliberate self-
harm, a psychiatric disorder or treatment causing
physical harm (e.g. alcohol-induced hepatitis or lithium-
1
vary little between countries, suggesting that biological/
genetic factors are operating independently of cultural
factors. In contrast, conditions in which social factors play
a greater role vary between cultures, so that anorexia
nervosa is found more often in developed cultures. Culture
can also influence the presentation of illnesses, such that

1273
Psychological medicine
physical symptoms are more common presentations of
depressive illness in Asia than in Europe.
THE PSYCHIATRIC HISTORY
The purpose of the history is to help to make a diagnosis,
determine possible aetiology, and estimate prognosis.
Data may be taken from several sources, including
interviewing the patient, a friend or relative (usually with
the patient's permission), or the patient's general
practitioner. The patient interview enables a doctor to
establish a relationship with the patient and is the
primary way to make a psychiatric diagnosis. Box 22.2
gives essential guidance on how to safely conduct such an
interview. It is very unlikely that a patient will physically
harm a healthcare professional. When interviewing a
patient for the first time follow the guidance outlined in
Chapter 1 (see p. 14). The history consists of:
Reason for referral - a brief statement of why and how
the patient came to the attention of the doctor.
Complaints - as reported by the patient.
Present illness a detailed account of the illness from
the earliest time at which a change was noted until the
patient came to the attention of the doctor.
Past psychiatric history previous episodes of psychiatric
illness and their treatments, including responses and
adverse reactions. Always ask after previous episodes
of self-harm.
Past medical history - this should include emotional
reactions to illness and procedures.
Family history - focusing on the way the parents or
carers cared (physically and emotionally) for the
patient, and the occurrence of both mental and
physical illnesses in first-degree relatives.
Personal (biographical) history - a short biography that
covers childhood difficulties including both abuse and
neglect, educational problems (e.g. bullying and
truanting), qualifications (to judge premorbid intelli
gence), job problems, sexual relationships, children,
present housing, financial situation, bereavements and
life stresses. Ways of asking awkward questions might
include:
- 'Do you feel able to tell me what memory most
upsets you/makes you angry?'
- 'Are you able to say what you have done in the past
that you most regret?'
- 'How well do you get on with your partner? Are
you happy in every way? Are there any problems in
your sexual life that you think I should know
about?'
A reproductive history in women should include men-
strual problems, pregnancies, terminations, miscarriages,
contraception and the menopause, if relevant.
Personality - this helps to determine prognosis and
response to treatment. The doctor should find out how
other people would describe the patient. Is the patient
generally a worrier, shy, introverted, dependent on
others, passive, aggressive, irritable, over-emotional,
prone to moodiness, conscientious, or perfectionist?
These are all personality traits that predict a poorer
outcome in both medical and psychiatric disorders.
Drug history - both prescribed and over-the-counter
medication, the use (units per week) and abuse of
alcohol, tobacco, caffeine, and illicit drugs. Forensic
history - you should carefully explain that you need to
ask about this since ill-health can sometimes lead to
problems with the law.
- 'Have you ever had any legal problems or contact
with the police or courts?'
Particularly note any violent or sexual offences. This is
part of a risk assessment and is necessary in order to
assess potential risks to those close to the patient as
well as staff. Ask the patient what is the worst harm
they have ever inflicted on someone else, which will
give an indication of the potential for violence. A
systematic review of physical symptoms is particularly
necessary in patients complaining of physical
symptoms.
THE MENTAL STATE
EXAMINATION (MSE)
 Sox 22.2 The essentials of a safe psychiatric
interview
Beforehand: Ask someone senior who knows the
patient whether it is safe to interview the patient
alone.
Access to others: If in doubt, interview in the view or
hearing of others, or accompanied by another
member of staff.
Setting: If safe; in a quiet room alone for
confidentiality, not by the bed.
Seating: Place yourself between the door and the
patient.
Alarm: If available, find out where the alarm is and
how to use it.
The history will already have assessed several aspects of
the MSE, but the interviewer will need to expand several
areas as well as test specific areas, such as cognition.
Appearance and general behaviour
State and colour of clothes, facial appearance, eye contact,
posture and movement provide information about a
patient's affect. Patients with psychomotor retardation due
to a depressive illness sit with shoulders hunched,
immobile, tearful, with a downcast gaze. Depressed
individuals tend to wear clothes with dark colours.
Agitation (seen with depressive illness) and anxiety cause
an easy startle response, sweating, tremor, restlessness,
fidgeting, visual scanning (for danger) and even pacing
up and down. Patients with mania are often physically
1274
The mental state examination
overactive and disinhibited, wearing colourful clothes.
Someone who is actively hallucinating will seem dis-
tracted and suddenly stop talking or listening and stare
intently at a particular place in the room.
Mood and affect
The patient has an emotion or feeling, tells the doctor their
mood and the doctor observes the patient's affect. In
psychiatric disorders, mood may be altered in three
ways:
A persistent change in mood
Depression is a lowering of mood, such as feeling sad,
tearful, melancholic or low in spirits. Some patients
report anhedonia, which is a lack of positive pleasure or
loss of interest. Depression is the cardinal feature of
depressive illness. Sometimes the word 'depression' is
used as shorthand to describe a depressive illness.
Diurnal variation in mood, feeling worse on waking,
suggests a more severe illness, whereas a reactive mood,
in which the patient can sometimes respond positively,
indicates less severity.
Anxiety is a feeling of constant, inappropriate or
excessive worry, fear, apprehension, tension or inner
restlessness, seen in anxiety and depressive disorders
and drug withdrawal.
Elation is a feeling of high spirits, exuberant happiness,
vitality and even ecstasy, seen in mania and acute drug
intoxication.
Irritability can be either expressed (as in a temper or
impatience) or an internal feeling of exasperation or
anger, seen in both mania and depressive illness,
especially in men.
Blunting of affect is a total absence of emotion, seen
most commonly in chronic schizophrenia.
Fluctuating or labile mood
This occurs when different emotions rapidly follow one
another, so that a patient is crying one moment and
laughing the next. This can occur in mixed affective states
(see p. 1288). Alternatively, the patient is easily and
excessively emotional over banal events or news, but the
emotion is transient. This is seen both in a pseudobulbar
palsy, commonly following a cerebrovascular accident
(see p. 1191), and with mild depressive illnesses.
Inconsistent or incongruous mood
This occurs when emotional expression fails to match
thoughts and actions. For example, a patient may laugh
when describing the death of a close relative. This can
occur in schizophrenia. Such incongruity needs to be
distinguished from the embarrassed laughter that indi -
cates that someone is ill at ease when talking about a
distressing subject.
Speech
Disorders of thinking are usually recognized from the
patient's speech.
Disorders of the stream of thought
These are abnormalities in the amount and speed of the
thoughts experienced.
Pressure of speech occurs in mania and can be recognized
by loudness, rapidity, and difficulty in interrupting speech.
Poverty of speech is the opposite experience, when there
appears to be an absence of any thought and patients
report their minds to be empty. It occurs in depressive
illness.
Thought block occurs in schizophrenia. There is an
abrupt and complete interruption of the stream of
thought, so the mind goes blank. Patients may interpret
the experience in an unusual way (e.g. thought with-
drawal; see below).
Disorders of the form of thought
Flight of ideas. The patient's thoughts rapidly jump from
one topic to another, such that one train of thought is not
completed before another appears. It is often produced by
clang associations (the use of two or more words with a
similar sound: 'sun, son, song'), punning, rhyming, and
responding to distracting cues in the immediate sur-
roundings. Flight of ideas is characteristic of mania and
often accompanies pressure of speech.
Perseveration is the persistent and inappropriate
repetition of the same thoughts or actions. It occurs in
frontal lobe disorders.
Loosening of associations is manifested by a loss of the
normal structure of thinking. The most striking impression
is a lack of clarity so that it is impossible to understand
what is being said. There are several forms. Knight's
move or derailment denotes an illogical transition from
one topic to another, in the absence of flight of ideas.
When this abnormality is extreme and disrupts the
grammatical structure of speech, it is termed 'word
salad'.
Thought broadcast is when the patient experiences their
thoughts as being understood by others without talking,
as though their thoughts are literally being broadcast to
all around them.
Thought insertion occurs when a patient's thought is
perceived as being planted in their mind by someone else.
Thought withdrawal occurs when a patient experiences
their thoughts being taken away from them, without their
control.
The latter three types of thought disorders are all first
rank symptoms, which Schneider suggested were pathog-
nomonic of schizophrenia (see p. 1307).
Thought content
Thought content refers to the worries and preoccupations
manifested by the patient and elicited at interview.
Abnormal beliefs and experiences are, of course, part of
the thought content, but are regarded as sufficient to be
discussed separately (see below).
An obsessional rumination is a recurrent, persistent
thought, impulse, image or musical theme that enters
the mind despite the individual's effort to resist it. The
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Psychological medicine
individual recognizes that the obsessional thought is
their own, but it is usually unpleasant and often 'out of
character', such as the thought that the patient has
accidentally killed someone while driving their car.
Common obsessions concern dirt, contamination and
orderliness.
A compulsion is a repetitive and seemingly purposeful
action performed in a stereotyped way, referred to as a
compulsive ritual. Compulsions are accompanied by a
subjective sense that they must be carried out (or the
patient will be overwhelmed by either anxiety or a
superstitious belief that something bad will occur) and
by an urge to resist. Compulsive rituals are used to
counteract ruminations, so patients repetitively wash
their hands to diminish the fear of contamination with
dirt.
Insight and illness beliefs
Insight is the degree to which a person recognizes that he
or she is unwell, and is minimal in patients with a
psychosis. Illness beliefs are the patient's own expla-
nations of their ill-health, including diagnosis and causes.
These beliefs should be elicited because they can help to
determine prognosis and compliance with treatment,
with any disease.
Abnormal beliefs
The main form of abnormal belief is the delusion (Box
22.3). Delusions can be primary or secondary.
Primary delusions are rare and appear suddenly and
with full conviction but without any preceding mental
events. For example, a patient on being offered a glass
of wine suddenly believes that this indicates that he is
Jesus Christ.
Secondary delusions are derived from a preceding
morbid experience, such as a depressed mood or an
auditory hallucination.
Delusions are also classified according to their content,
and include persecutory delusions, delusions of reference,
guilt, worthlessness, nihilism, religious delusions, and
delusions of grandeur, jealousy or control. These are
further defined when discussed in relation to specific
conditions.
Feelings, thoughts or actions may also be interpreted
by the patient as being under the control of some external
power. Such passivity experiences are first rank symptoms
and are regarded as diagnostic of schizophrenia (see
p. 1307). Patients may develop secondary delusions that
explain this alien control as a result of witchcraft,
hypnosis, radio waves or television - so-called delusions
of passivity.
Delusions should be distinguished from overvalued
ideas - deeply held personal convictions that are under-
standable when the individual's background is known.
Ideas of reference that fall short of delusions are held by
people who are particularly self-conscious. Such indivi-
duals cannot help feeling that people take particular
notice of them in public places, laugh at them or pass
comment about them. Such a feeling is not delusional in
that individuals who experience it realize that it
originates within themselves and that they are no more
noticeable than anyone else, but nevertheless cannot
dismiss the feeling.
Abnormal perceptions
Illusions are misperceptions of external stimuli and are
most likely to occur when the general level of sensory
stimulation is reduced.
Hallucinations are defined in Box 22.4. Healthy people
occasionally experience hallucinations, such as in
normal grief, or during the transition between sleep
ing and waking (hypnagogic and hypnapompic).
Hallucinations can be elementary (e.g. bangs, whistles)
or complex (e.g. faces, voices, music), and may affect
any of the perceptions: auditory, visual, tactile,
gustatory, olfactory or of deep sensation.
Pseudohallucinations are usually auditory, and are
either true externally sited hallucinations, but with
insight into their imaginary nature, or are sited within
internal space (e.g. 'I heard a voice in my head speak
to me'). They can occur in mood disorders and do not
indicate a psychosis.
Depersonalization is a change in self-awareness such
that the person feels unreal or detached from their
body. The individual is aware, however, of the
subjective nature of this alteration.
Derealization is the unpleasant feeling that the external
environment has become unreal and/or remote;
patients may describe themselves as though they are
in a dream-like state. Both this and depersonalization
can occur in healthy people when they are tired, after
sensory deprivation and when using hallucinogenic
drugs. They also occur in anxiety disorders,
schizophrenia and temporal lobe epilepsy.
 Box 22.3 Delusion
Box 22.4 Hallucination
Delusion is defined as an abnormal belief that is:
An hallucination is defined as a perception in the
held with absolute conviction
absence of a stimulus. It is:
not amenable to reason or modifiable by experience
not shared by those of a common cultural or social a false perception and not a distortion
background perceived as inhabiting objective space
experienced as a self-evident truth of great personal perceived as having qualities of normal perception
significance perceived alongside normal perceptions
usually false. independent of the individual's will.
The mental state examination

!
22
Deja vu is a sudden familiarity with a situation or
event as having been encountered before when it is in
fact novel.
Jamais vu is the reverse experience when there is failure
to recognize a situation or event that has been
encountered before. Deja vu experiences occur in
healthy people as well as in extreme anxiety states.
Both types of experience can occur in temporal lobe
epilepsy (see p. 1221).
Increased sensitivity of perceptions, such as photo-
sensitivity and phonosensitivity, occurs in anxiety
disorders (e.g. increased sensitivity to the neon strip-
lights and noise in a supermarket in agoraphobia) as
well as neurological disorders such as migraine.
Observe for verbal perseveration, in which the patient repeats
the same answer as given previously for a different ques-
tion. Abstract thinking is measured by asking the meaning
of common proverbs, a literal meaning suggesting frontal
lobe dysfunction, assuming reasonable premorbid
intelligence.
Mini-mental state examination
Box 22.5 gives the 'mini-mental state' examination of
cognitive function. This is a 5-minute bedside test that is
useful as a screen and in assessing the degree of cognitive
dysfunction in patients with diffuse brain disorders. It
correlates well with more time-consuming Intelligence
Cognitive state
Examination of the cognitive state is necessary to diag-
nose organic brain disorders, such as delirium and
dementia. Poor concentration, confusion and memory
problems are the most common subjective complaints.
Clinical testing is a screening of cognitive functions,
which may suggest the need for more formal psychometry.
A premorbid estimate of intelligence can be made from
asking the patient the final year level of education and the
highest qualifications or skills achieved.
Testing can be divided into tests of diffuse and focal
brain functions.
Diffuse functions - Attention and calculation
Orientation in time, place and person. Consciousness can be
defined as the awareness of the self and the environment.
Clouding of consciousness is more accurately a fluctuating
level of awareness and is commonly seen in delirium.
Attention is tested by saying the months or days
backwards.
Verbal memory. Ask the patient to repeat a name and
address with 10 or so items, noting how many times it
takes to recall it 100% accurately (normal is 1 or 2)
(immediate recall or registration).
Ask the patient to try to remember it and then ask it of
them again after 5 minutes (0 or 1 error is normal)
(short-term memory).
Long-term memory. Ask the patient to recall the news of
that morning or recently. If they are not interested in the
news, find out their interests and ask relevant questions
(about their football team or favourite soap opera).
Amnesia is literally an absence of memory and dysmnesia
indicates a dysfunctioning memory. . ,. ..
Focal functions
Frontal, temporal and parietal function tests are covered
on page 1178. Frontal lobe skills are difficult to test at the
bedside. Note any disinhibited behaviour not explained by
another psychiatric illness, such as mania. Sequential tasks
are tested by asking the patient to alternate making a fist
with one hand at the same time as a flat hand with the
other. Ask the patient to tap a table once if you tap twice
and vice versa. Note any motor perseveration whereby the
patient cannot change the movement once established.
Sox 22.5 The mini-mental state examination
Orientation
Score one point for each correct answer:
What is the: time, date, day, month, year?
Maximum: 5 points
What is the name of: this ward, hospital, 5 points
district, town, country?
Registration
Name three objects only once. Score up to 3 points a
maximum of 3 points for each correct repetition.
Repeat the objects until the patient can repeat
them accurately (in order to test recall later).
Ask the patient to subtract 7 from 100 and 5 points
then 7 from the result four more times.
Score 1 point for each correct subtraction
Recall
Ask the patient to repeat the names of the 3 points
three objects learnt in the registration test.
Language
Score 1 point for each of two simple objects 2 points
named (e.g. pen and a watch) Score 1 point for an
accurate repetition of 1 point
the phrase: 'No ifs, ands or buts' Give a 3-stage
command, scoring 1 point 3 points
for each part correctly carried out; e.g.
'With the index finger of your right hand
touch your nose and then your left ear'
Write 'Close your eyes' on a blank piece 1 point
of paper and ask the patient to follow
the written command. Score 1 point if the
patient closes the eyes.
Ask the patient to write a sentence. 1 point
Score 1 point if the sentence is sensible
and contains a noun and a verb.
Draw a pair of intersecting pentagons 1 point
with each side approximately 1 inch long.
Score 1 point if it is correctly copied
TOTAL MAXIMUM SCORE 30 POINTS
From: Folstein MF, Folstein SE, McHough PR (1975) 'Mini-mental
state': a practical method for grading the cognitive state of patients
for the clinician. Journal of Psychiatric Research 12: 189-198
1277
Psychological medicine
Quotient (IQ) tests, but it will not as easily pick up
cognitive problems caused by focal brain lesions. A score
of 23 or less will pick up about 90% of patients with
cognitive impairments, with about 10% false positives.
Defence mechanisms
Although not strictly part of the mental state examin-
ation, it is useful to be able to identify psychological
defences in ourselves and our patients. Defence mechan-
isms are mental processes that are usually unconscious.
The defence mechanisms described below are among the
most commonly used and are useful in understanding
many aspects of behaviour.
Denial is similar to repression and occurs when
patients behave as though unaware of something that
they might be expected to know. One example would
be a patient who, despite being told that a close
relative has died, continues to behave as though the
relative were still alive.
Displacement involves the transferring of emotion from
a situation or object with which it is properly associ
ated to another that gives less distress.
Identification refers to the unconscious process of
taking on some of the characteristics or behaviours of
another person, often to reduce the pain of separation
or loss.
Projection involves the attribution to another person of
thoughts or feelings that are in fact one's own.
Regression is the adoption of primitive patterns of
behaviour appropriate to an earlier stage of develop
ment. It can be seen in ill people who become child
like and highly dependent.
Repression is the exclusion from awareness of memories,
emotions and/or impulses that would cause anxiety
or distress if allowed to enter consciousness.
Sublimation refers to the unconscious diversion of
unacceptable behaviours into acceptable ones.
The relevant physical examination
This should be guided by the history and mental state
examination. Particular attention should usually be paid
to the neurological and endocrinological examinations
when organic brain syndromes and affective illnesses are
suspected.
CLASSIFICATION OF
PSYCHIATRIC DISORDERS
The classification of psychiatric disorders into categories
is mainly based on symptoms, since there are currently
few diagnostic tests for psychiatric disorders. The fourth
edition text revision (TR) of the Diagnostic and Statistical
Manual of the American Psychiatric Association (DSM-IV-
TR) provides descriptions of diagnostic categories in order
to enable clinicians and investigators to diagnose, com-
municate about, study and treat people with various
mental disorders. This scheme has five axes:
I Psychiatric disorders
II Personality disorders, learning difficulty
III General medical conditions
IV Psychosocial and environmental problems
V Overall level of functioning
Psychiatric classifications have traditionally divided up
disorders into neuroses and psychoses.
Neuroses are illnesses in which symptoms vary only in
severity from normal experiences. Psychoses are illnesses
in which symptoms are qualitatively different from
normal experience, with little insight into their nature.
There are several problems with a neurotic-psychotic
dichotomy. Firstly, neuroses may be as severe in their
effects on the patient and their family as psychoses.
Secondly, neuroses may cause symptoms that fulfil the
definition of psychotic symptoms. For instance, someone
with anorexia nervosa may be convinced that they are fat
when they are thin, and this belief would meet all the
criteria for a delusional belief. Yet we would traditionally
classify the illness as a neurosis.
Another classification system - the International
Classification of Mental and Behavioural Disorders (ICD-10)
-has been published by the World Health Organization.
This system has largely abandoned the traditional divi -
sion between neurosis and psychosis, although the terms
are still used. The disorders are now arranged in groups
according to major common themes (e.g. mood disorders,
schizophrenia and other delusional disorders). A
classification of psychiatric disorders derived from ICD-
10 is shown in Table 22.1, and this is the classification
mainly used in this chapter.
Table 22.1 International classification of psychiatric
disorders (ICD-10)
Summary or formulation
When the full history and mental state have been
assessed, the doctor should make a concise assessment of
the case, which is termed a formulation. In addition to
summarizing the essential features of the history and
examination, the formulation includes a differential diag-
nosis, a discussion of possible causal factors, and an
outline of further investigations or interviews needed. It
concludes with a concise plan of treatment and a
statement of the likely prognosis.
Organic disorders
Mental and behavioural disorders due to psychoactive
substance use
Schizophrenia and delusional disorders
Mood (affective) disorders
Neurotic, stress-related and somatoform disorders
Behavioural syndromes Disorders of adult personality
and behaviour Mental retardation
World Health Organization (1992) The ICD-10 Classification of
Mental and Behavioural Disorders. Geneva: World Health
Organization
1278
Psychiatric aspects of physical disease
22
 FURTHER READING Common psychiatric disorders in the
American Psychiatric Association (2000) Diagnostic and general hospital
Statistical Manual of Mental Disorders - Fourth Edition
Text Revision (DSM-IV-TR). Washington, DC: APA. Delirium is the commonest psychosis seen in the general
World Health Organization (1992) The ICD-10 hospital, with dementia being the commonest chronic
Classification of Mental and Behavioural Disorders: organic brain disorder seen. Mood disorders, particularly
Clinical Descriptions and Diagnostic Guidelines. depressive illness, are common in patients with chronic
Geneva: World Health Organization. painful conditions (severe arthritis), disabling illnesses
(after a stroke), and after being given a life-threatening
diagnosis, such as cancer. Other factors also increase the
risk of a psychiatric disorder in someone with a physical
CAUSES OF A PSYCHIATRIC DISORDER
disease (Table 22.3).
A psychiatric disorder may result from several causes. It
is most helpful to divide causes into the three 'P's: pre-
disposing, precipitating and perpetuating factors.
Table 22.2 Psychiatric conditions sometimes caused by
Predisposing factors often stem from early life and physical diseases
include genetic, pregnancy and delivery, previous Psychiatric disorders/
traumas and personality factors. Physical disease
Precipitating (triggering) factors may be physical, symptom
Depressive illness
psychological or social in nature. Whether they pro
duce a disorder depends on their nature, severity and
the presence of predisposing factors. For instance a
death of a close, rather than distant, family member is
Anxiety disorder
more likely to precipitate a depressive illness or
pathological grief reaction in someone who has not
come to terms with a previous bereavement.
Perpetuating (maintaining) factors prolong the course of
a disorder after it has occurred. Again they may be
Irritability
physical, psychological and/or social, and several are
often active and interacting at the same time. For
example, high levels of criticism at home combined
with taking cannabis, as relief from the criticism, may Memory problem
help to maintain schizophrenia.
Altered behaviour

Hypothyroidism
PSYCHIATRIC ASPECTS OF Cushing's syndrome
PHYSICAL DISEASE Steroid treatment
Brain tumour
Thyrotoxicosis
Hypoglycaemia (transient)
Phaeochromocytoma
Complex partial seizures (transient)
Alcohol withdrawal
Post-concussion syndrome
Frontal lobe syndrome
Hypoglycaemia (transient)
Brain tumour
Hypothyroidism
Acute drug intoxication Post-
ictal state Acute delirium
Dementia Brain tumour
Patients with physical illnesses are more likely to suffer Table 22.3 Factors increasing the risk of psychiatric
from psychiatric disorders than those who are well. The disorders in the general hospital
most common psychiatric disorders in physically ill
patients are mood or adjustment disorders and acute Patient factors Physical conditions
Previous psychiatric history Chronic ill-health Chronic pain
organic brain disorders (delirium). The relationship
Current social or Life-threatening illness
between psychological and physical symptoms may be interpersonal stresses Recent bad prognostic news
understood in one of three ways: Homeless Recent alcohol Disabling condition Brain
Psychological distress and disorders can precipitate misuse disease Recent live birth,
stillbirth or
physical diseases (e.g. anorexia nervosa causing
miscarriage Functional
cardiac arrhythmias, due to hypokalaemia). (psychosomatic)
Physical diseases and their treatments can cause illness
psychological symptoms or ill-health (Table 22.2).
Physical and psychological symptoms and disorders Treatment
may be independently co-morbid, particularly in the Setting Certain drugs (e.g. dopamine
elderly. A&E department agonists)
Neurology, oncology and Second postoperative day
endocrinology wards Surgery affecting body image
Intensive care unit Renal (e.g. emergency
dialysis unit sfomataj
1279
Psychological medicine
Differences in treatment
Although the basic principles are the same as in treating
psychiatric illnesses in the physically healthy, there are
some differences:
Uncertainty regarding the physical diagnosis or prog
nosis, with its attendant tendency to imagine the worst,
is often a triggering or maintaining factor, particularly
in an adjustment or mood disorder. Good two-way
communication between doctor and patient, with time
taken to listen to the patient's concerns, is often the
most effective 'antidepressant' available.
A careful history may reveal the role of a physical disease
or treatment exacerbating the psychiatric condition,
which should then be addressed (see Table 22.2). For
example, the dopamine agonist bromocriptine can
precipitate a psychosis.
When prescribing psychotropic drugs, the dose should
be reduced in disorders affecting pharmacokinetics, e.g.
fluoxetine in renal or hepatic failure.
Drug interactions, e.g. lithium and non-steroidal anti-
inflammatories; lithium and thiazide diuretics.
Drug interactions are most likely to occur when a
patient taking psychotropic is acutely admitted to
hospital and prescribed analgesics.
Sometimes a physical treatment may be planned that
may exacerbate the psychiatric condition. An example
would be high-dose steroids as part of the next cycle of
chemotherapy in a patient with leukaemia and de
pressive illness. Careful thought should be given to the
particular priority for the patient at that moment. It is
often useful to discuss the clinical dilemma with a
psychiatrist.
Always consider the risk of suicide in an inpatient with
a mood disorder and take steps to reduce that risk; for
example, moving the patient to a room on the ground
floor and/or having a registered psychiatric nurse
attend the patient while at risk.
SEVERE BEHAVIOURAL DISTURBANCE
Patients with aggressive or violent behaviour cause
understandable apprehension in all staff, and are most
commonly seen in the accident and emergency depart-
ment. Information from anyone accompanying the
patient, including police or carers, can help considerably.
Box 22.6 gives the main causes of disturbed behaviour.
Management of the severely disturbed
patient
The primary aims of management are control of dangerous
behaviour and establishment of a provisional diagnosis.
Box 22.6 Main causes of disturbed behaviour
Drug intoxication (especially alcohol)
Delirium (acute confusional state)
Acute psychosis Personality
disorder
Three specific strategies may be necessary when dealing
with the violent patient:
reassurance and explanation
physical restraint
medication.
The majority of disturbed patients are themselves
frightened, as well as frightening, and may feel threatened
by those around them, misinterpreting the actions of
others. Staff should always explain the situation and their
intentions. This simple strategy may calm a patient
sufficiently to be interviewed and allow an appropriate
examination.
If the behaviour remains severely disturbed, it may be
necessary to restrain patients from harming themselves
or others. If planned, this should be done with sufficient
numbers of trained staff; at least one person per limb and
another two in charge or delivering medication. Once
brought under physical control, the patient should be
held in the prone position, in order to protect the airway
and allow access for intramuscular medication. Care
must be taken to ensure that neither the airway nor
breathing are impeded, by having someone always
present at the head of the patient.
It is usually necessary to administer medication while
the patient is restrained and they should not be released
until they are visibly calmed. Management depends on
the provisional diagnosis. 'Rapid tranquillization' should
be employed when the patient has a psychosis, so long as
the Mental Health Act has been used (see p. 1314) or the
situation is so dangerous that the doctor is acting under
'common law'. A deep intramuscular injection of
zuclopenthixol acetate in a dose ranging from 50-150 mg
together with 0.5-1 mg. lorazepam is now the treatment
of choice for rapid effect. Used in combination, they have
a synergistic action. Moderate doses of a neuroleptic or
benzodiazepine can also be given at regular, comparatively
short intervals (30-60 minutes) intramuscularly. Another
alternative regimen is intramuscular butyrophenone
(haloperidol 5-10 mg) in patients under 60 years old. This
dose should be reduced in the elderly and those with
known cardiac or hepatic disease. The patient should be
observed for up to 1 hour before a further dose is admin-
istered. Breathing, pulse rate and blood pressure should
be monitored for hypotension, arrhythmias and respiratory
difficulty. In the case of continuing disturbance, it may be
preferable to administer an adjunctive intramuscular
benzodiazepine (lorazepam 2 mg) rather than a further
dose of a neuroleptic. Both neuroleptic drugs and
benzodiazepines may be used as tranquillizers.
THE SICK ROLE AND ILLNESS BEHAVIOUR
The sick role describes behaviour usually adopted by ill
people. Such people are not expected to fulfil their normal
social obligations. They are treated with sympathy by
others and are only obliged to see their doctor and take
medical advice or treatments.
Illness behaviour is the way in which given symptoms
may be differentially perceived, evaluated and acted (or
1280
Psychiatric aspects of physical disease
22
not acted) upon by different kinds of persons. We all have
illness behaviour when we choose what to do about a
symptom. Going to see a doctor is generally more likely
with more severe and more numerous symptoms and
greater distress. It is also more likely in introspective
individuals who focus on their health.
Abnormal illness behaviour occurs when there is a dis-
crepancy between the objective somatic pathology present
and the patient's response to it, in spite of adequate
medical investigation and explanation.
seems that it requires a major stress or a psychiatric dis -
order in order for such sufferers to attend their doctor for
help, which might explain why doctors are so impressed
with the associations with stress and psychiatric dis-
orders. Doctors have historically tended to diagnose
'stress' or 'psychosomatic disorders' in patients with
symptoms that they cannot explain. History is full of such
disorders being reclassified as research clarifies the
pathology. A recent example is writer's cramp (p. 1233)
which most neurologists now agree is a dystonia rather
than a neurosis.
 FUNCTIONAL OR PSYCHOSOMATIC
DISORDERS: MEDICALLY UNEXPLAINED
SYMPTOMS
'Functional' disorders are illnesses in which there is no
obvious pathology or anatomical change in an organ
(thus in contrast to 'organic') and there is a presumed
dysfunction in an organ or system. The word psycho-
somatic has had several meanings, including psychogenic,
'all in the mind', imaginary and malingering. The modern
meaning is that psychosomatic disorders are syndromes
of unknown aetiology in which both physical and
psychological factors are likely to be causative. The
psychiatric classification of these disorders would be
somatoform disorders, but they do not fit easily within
either medical or psychiatric classification systems, since
they occupy the hinterland between them. Medically
unexplained symptoms and syndromes are very common
in both primary care and the general hospital (over half
the outpatients in gastroenterology and neurology clinics
have these syndromes). Because orthodox medicine has
not been particularly effective in treating or under-
standing these disorders, many patients perceive their
doctors as unsympathetic and seek out complementary
treatments of uncertain efficacy. Examples of functional
disorders are shown in Table 22.4.
Because epidemiological studies suggest that having
one of these syndromes significantly increases the risk of
having another, some doctors believe that these syndromes
represent different manifestations in time of 'one functional
syndrome', which is indicative of a somatization process.
Functional disorders also have a significant association
with psychiatric disorders, especially depressive and
panic disorders as well as phobias. Against this view is
the evidence that the majority of primary care patients
with most of these disorders do not have either a
psychiatric disorder or other functional disorders. It also
Table 22.4 Functional or psychosomatic syndromes
(medically unexplained symptoms)
'Tension' headaches Chronic or post-viral fatigue
Atypical facial pain
Atypical chest pain
Fibromyalgia (chronic
widespread pain)
Other chronic pain
syndromes
syndrome
Multiple chemical sensitivity
Premenstrual syndrome
Irritable or functional bowel
syndrome Irritable bladder
syndrome
Chronic fatigue syndrome (CFS)
There has probably been more controversy over the
existence and aetiology of CFS than any other functional
syndrome in recent years. This is reflected in its uncertain
classification as neurasthenia in the psychiatric classifi-
cation and myalgic encephalomyelitis (ME) under neuro-
logical disorders. There is good evidence for this
syndrome, although the diagnosis is made clinically and
by exclusion of other fatiguing disorders. Its prevalence is
0.5% in the UK, although abnormal fatigue as a symptom
occurs in 10-20%. It occurs most commonly in women
between the ages of 20 and 50 years old. The cardinal
symptom is chronic fatigue made worse by minimal
exertion. The fatigue is usually both physical and mental,
with associated poor concentration, impaired registration
of memory, irritability, alteration in sleep pattern (either
insomnia or hypersomnia), and muscular pain. The name
myalgic encephalomyelitis (ME) is decreasingly used
within medicine because it implies a pathology for which
there is no evidence.
Aetiology
Functional disorders often have aetiological factors in
common with each other (see Table 22.5), as well as more
specific aetiologies. For instance, CFS can be triggered by
certain infections, such as infectious mononucleosis and
viral hepatitis. About 10% of patients with infectious
mononucleosis have CFS 6 months after the infectious
onset, yet there is no evidence of persistent infection in
these patients. Those fatigue states which clearly do
follow on a viral infection can be classified as post-viral
fatigue syndromes. Other aetiological factors include
physical inactivity and sleep difficulties. Immune and
endocrine abnormalities noted in CFS may be secondary
to the inactivity or sleep disturbance commonly seen in
patients. Mood disorders are present in a large minority
of patients, and can cause problems in diagnosis because
of the large overlap in symptoms. These mood disorders
may be secondary, independent (co-morbid), or primary
with a misdiagnosis of CFS. The role of stress is uncertain,
with some indication that the influence of stress is
mediated through consequent psychiatric disorders
exacerbating fatigue, rather than any direct effect.
Management
The general principles of the management of functional
disorders are given in Box 22.7. Specific management of
1281
Psychological medicine
 Table 22.5 Aetiological factors commonly seen in
functional disorders
Predisposing
Perfectionist, obsessional and introspective personality
traits
Childhood traumas (physical and sexual abuse)
Similar illnesses in first-degree relatives
Precipitating (triggering)
Infections
Chronic fatigue syndrome (CFS)
Irritable bowel syndrome (IBS)
Psychologically traumatic events (especially accidents)
Physical injuries ('fibromyalgia' and other chronic pain
syndromes) Life events that precipitate changed behaviours
(e.g. going
off sick) Incidents where the patient believes others are
responsible
Perpetuating (maintaining)
Inactivity with consequent physiological adaptation (CFS
and 'fibromyalgia') Avoidant behaviours - multiple
chemical sensitivities
(MCS), CFS Maladaptive illness beliefs (that maintain
maladaptive
behaviours) (CFS)
Excessive dietary restrictions ('food allergies')
Stimulant drugs Sleep disturbance Mood
disorders Somatization disorder Unresolved
anger or guilt Unresolved compensation
Box 22.7 Management of functional disorders
The first principle is the identification and treatment of
maintaining factors (e.g. dysfunctional beliefs and
behaviours, mood and sleep disorders).
Communication
Explanation of ill-health, including diagnosis and
causes Education about management (including self-
help
leaflets) * Stopping drugs (e.g. caffeine causing
insomnia,
analgesics causing dependence)
m Rehabilitative therapies
Cognitive behaviour therapy (to challenge unhelpful
beliefs and change coping strategies)
Supervised and graded exercise therapy for
approximately 3 months (to reduce inactivity and
improve fitness)
Pharmacotherapies
Specific antidepressants for mood disorders,
analgesia and sleep disturbance Symptomatic
medicines (e.g. appropriate analgesia,
taken only when necessary)
CFS should include a mutually agreed and supervised
programme of gradually increasing activity. However,
few patients regard themselves as cured after treatment.
It is sometimes difficult to persuade a patient to accept
what are inappropriately perceived as 'psychological
therapies' for such a physically manifested condition.
Antidepressants do not work in the absence of a mood
disorder or insomnia.
Prognosis
This is poor without treatment, with less than 10% of
hospital attenders recovered after 1 year. Outcomes are
worse with increasing age, co-morbid mood disorders,
and the conviction that the illness is entirely physical.
Fibromyalgia (chronic widespread pain:
CWP)_______________________________
This controversial condition of unknown aetiology over-
laps with chronic fatigue syndrome, with both conditions
causing fatigue and sleep disturbance (see p. 1281).
Diffuse muscle and joint pains are more constant and
severe in CWP, although the 'tender points', previously
considered to be pathognomonic, are now known to be
ubiquitous, associated with psychological distress, and of
no diagnostic importance (p. 547). CWP occurs most
commonly in women aged 40-65 years old, with a
prevalence in the community of between 1 and 11%.
There are associations with depressive and anxiety dis-
orders, other functional disorders, physical deconditioning
and a possibly characteristic sleep disturbance (see
Table 22.5).
Management
Apart from the general principles in Box 22.7, manage-
ment also consists of symptomatic analgesia, reversing
the sleep disturbance, and a physically orientated rehabili-
tation programme. A recent meta-analysis suggests
that tricyclic antidepressants that inhibit reuptake of
both serotonin (5-hydroxytryptamine - 5-HT) and
norepinephrine (noradrenaline) (e.g. amitriptyline,
dosulepin (dothiepin)) have the greatest effect on sleep,
fatigue and pain. The doses used were too low for
antidepressant efficacy and the drugs may work through
their hypnotic and analgesic effects.
Other chronic pain syndromes
A chronic pain syndrome is a condition of chronic
disabling pain for which no medical cause can be found.
The psychiatric classification would be a persistent
somatoform pain disorder, but this is unsatisfactory since
the criteria include the stipulation that emotional factors
must be the main cause, and it is clinically difficult to be
that certain. The main sites of chronic pain syndromes are
the head, face, neck, lower back, abdomen, genitalia and
all over (CWP: fibromyalgia). 'Functional' low back pain
is the commonest 'physical' reason for being off sick long-
term in the UK (p. 540). Quite often a minor abnormality
will be found on investigation (such as mild cervical
spondylosis on the neck X-ray), but this will not be severe
enough to explain the severity of the pain and resultant
disability. These pains are often unremitting and respond
poorly to analgesics. Sleep disturbance is almost universal
1282
Psychiatric aspects of physical disease
and co-morbid psychiatric disorders are found in a large
minority.
Aetiology
The perception of pain involves sensory (nociceptive),
emotional and cognitive processing in the brain. Func-
tional brain scans suggest that the brain may respond
abnormally to pain in these conditions, with increased
activation in response to chronic pain. This could be
related to conditioned behavioural and physiological
responses to the initial acute pain. The brain may then
adapt to the prolonged stimulus of the pain by changing
its central processing. The prefrontal cortex, thalamus
and cingulate gyrus seem to be particularly affected and
some of these areas are involved in the emotional
appreciation of pain in general. Thus it is possible to start
to understand how beliefs, emotions and behaviours
might influence the perception of chronic pain (see
Table 22.5).
Management
Management involves the same principles as used in other
functional syndromes (Box 22.7). Since analgesics are
rarely effective, and can cause long-term harm, patients
should be encouraged to gradually reduce their use. It is
often helpful to involve the patient's immediate family or
partner, to ensure that the partner is also supported and
not unconsciously discouraging progress.
Specific drug treatments are few. Nerve blocks are not
usually effective. Anticonvulsants such as carbamazepine
and gabapentin may be given a therapeutic trial if the
pain is thought to be neuropathic (see p. 1200). The anti-
depressant dosulepin (dothiepin) is an effective treatment in
half of patients with atypical facial pain, and this effect
seems to be independent of dosulepin's effect on mood.
Another tricyclic antidepressant, amitriptyline, is helpful
in tension headaches, which might be related to its inde-
pendent analgesic effect. Amitriptyline has the added
bonus of increasing slow wave sleep, which may be why
it is more effective than NSAIDs in chronic widespread
pain. Tricyclic antidepressants that affect both serotonin
and norepinephrine (noradrenaline) reuptake (e.g.
p. 1292) seem to be more effective than more selective
norepinephrine reuptake inhibitors, e.g. in neuropathic
pain. There is some evidence that tricyclics are generally
superior to SSRIs in chronic pain syndromes.
Irritable bowel syndrome
This is one of the commonest functional syndromes,
affecting some 10-30% of the population in the UK. The
clinical features and management of the syndrome and
the related functional dyspepsia are described in more
detail on page 337. Although the majority of sufferers
with the irritable bowel syndrome (IBS) do not have a
psychiatric disorder, depressive illness should be
excluded in patients with constipation and a poor
appetite. Anxiety disorders should be excluded in
patients with nausea and diarrhoea. Persistent abdominal
pain or a feeling of emptiness may occasionally be the
presenting symptom of a severe depressive illness,
particularly in the elderly, with a nihilistic delusion that the
body is empty or dead inside (see p. 1289).
Management
This is dealt with in more detail on page 339 and in Box
22.7. Seeing a physician who provides specific education
that particularly addresses individual illness beliefs and
concerns can provide lasting benefit. Psychological
therapies that help the more severely affected include
biofeedback, hypnotherapy, cognitive behaviour therapy
and brief interpersonal psychotherapy. If indicated, the
choice of antidepressant should be determined by the
effects of these drugs on bowel transit times, with tricyclic
antidepressants normally slowing and selective serotonin
reuptake inhibitors (SSRIs) (p. 1292) normally speeding
up transit times.
Multiple chemical sensitivity, Candida
hypersensitivity, and food allergies
Some complementary health practitioners, doctors, and
patients themselves make diagnoses of multiple chemical
sensitivities (MCS) (e.g. to foods, smoking, perfumes,
petrol), Candida hypersensitivity, and allergies (to food,
tap-water, and even electricity). Symptoms and syn -
dromes attributed to these putative disorders are numerous
and variable and include all the functional disorders,
mood disorders, and arthritis. Scientific support for the
existence of these disorders has been hard to acquire,
particularly when double-blind methodologies have been
used.
Type 1 hypersensitivities to foods such as nuts
certainly exist, although they are fortunately uncommon
(approximately 3 per 1000) (see p. 220). Direct specific
food intolerances also occur (e.g. chocolate with migraine,
caffeine with IBS).
Candidiasis can occur in the gastrointestinal tract in
immunocompromised individuals, such as those with
AIDS. Vaginal candidiasis can occur after antibiotic treat-
ment in otherwise healthy women. A double-blind and
controlled study of nystatin in women, diagnosed as
having candidiasis hypersensitivity syndrome, showed
that vaginal Candida was the only symptom relieved
more by nystatin than placebo. There is little evidence of
Candida having a systemic role in other symptoms. In
spite of this evidence, the patient is often convinced of the
legitimacy and usefulness of these diagnoses and their
treatments.
Aetiology
Surveys of patients diagnosed with MCS or food allergies
have shown high rates of current and previous psychiatric
disorders (especially mood and anxiety disorders) (see
Table 22.5). Eating disorders (p. 1310) should be excluded
in patients with food intolerances. Some patients, taking
very low carbohydrate diets as putative treatments, may
develop reactive hypoglycaemia after a high carbohydrate
meal, which they then interpret as a food allergy. It has
been shown that classical conditioning can produce
1283
Psychological medicine
intolerances to foods and smells in healthy people and
this may be a causative mechanism in some patients with
intolerance. This study supports the existence of these
intolerance conditions, but suggests they may be con-
ditioned responses with attendant physiological con-
sequences. This might explain why double-blinding
abolishes the reaction to the stimulus.
Management.
The general principles in Box 22.7 apply. If one assumes a
phobic or conditioned response is responsible, graded
exposure (systematic desensitization) to the conditioned
stimulus may be worthwhile. Preliminary studies do
suggest that this approach may successfully treat such
intolerances, in the context of cognitive behaviour
therapy.
Premenstrual syndrome
The premenstrual syndrome (PMS) consists of both
physical and psychological symptoms that regularly
occur during the premenstrual phase and substantially
diminish or disappear soon after the period starts.
Physical symptoms include headache, fatigue, breast
tenderness, abdominal distension and fluid retention.
Psychological symptoms can include irritability, emo-
tional lability or low mood, and tension. The premenstrual
dysphoric disorder (PMDD) is a severe form of PMS with
marked mood swings, irritability, depression and anxiety
accompanying the physical symptoms. Women who
generally suffer from mood disorders may be more prone
to experience this disorder. The prevalence of PMS does
not vary between cultures and is reported by the majority
(75%) of women at some time in their lives. Severely
disabling PMS (PMDD) occurs in about 3-8% of women.
The cause of the premenstrual syndrome remain unclear,
although exacerbating factors include some of those
outlined in Table 22.5. Research suggests that abnor-
malities of reproductive hormone receptors may play a
role.
Management
The general principles in Box 22.7 apply. Treatments with
vitamin B6 (p. 246), diuretics, progesterone, oral contra
ceptives, oil of evening primrose and oestrogen implants
or patches (balanced by cyclical norethisterone) remain
empirical. Psychotherapies aimed at enhancing the
patient's coping skills can reduce disability. Two trials
suggest that graded exercise therapy improves symp
toms. Several studies have demonstrated that SSRIs
(p. 1292) are effective treatments for the premenstrual
dysphoric syndrome. . ;
The menopause______________________
The clinical features and management of the menopause
are described on page 1052. A prospective study has
shown that there is no increased incidence of depressive
disorders at this time. Such a significant bodily change,
sometimes occurring at the same time as children leaving
home, is naturally accompanied by an emotional adjust-
ment that does not normally amount to a pathological
state.
FURTHER READING
Grady-Weliky TA (2003) Premenstrual dysphoric
disorder. New England Journal of Medicine 348:
433^38. Lishman WA (1998) Organic Psychiatry: The
Psychological
Consequences of Cerebral Disorder. Oxford: Blackwell
Science. Royal College of Physicians and Royal
College of
Psychiatrists (2003) The Psychological Care of Medical
Patients: A practical guide, 2nd edn. London: Royal
College of Physicians. White PD, Moorey G (1997)
Psychosomatic illnesses are
not 'all in the mind'. Journal of Psychosomatic
Research 42(4): 329-332. Whiting G et al. (2001)
Interventions for the treatment
and management of chronic fatigue syndrome.
Journal of the American Medical Association 286:
1360-1368.
SOMATOFORM DISORDERS
As explained in the section on functional disorders
(p. 1281), the classification of somatoform disorders is
unsatisfactory because of the uncertain nature and
aetiology of these disorders. However, there are certain
disorders, beyond those described in 'functional disorders',
that present frequently and coherently enough to be use-
fully recognized.
Somatization disorder
One in ten patients presenting with a functional disorder
will fulfil the criteria of a chronic somatization disorder,
sometimes known as Briquet's syndrome. The condition is
composed of multiple, recurrent, medically unexplained
physical symptoms, usually starting early in adult life.
Exhaustion, dizzy spells, headaches, hypersensitivity to
light and noise, paraesthesiae, abdominal, neck and back
pain, nausea, sexual symptoms, and abnormal skin
sensations are among the most common complaints, but
symptoms may be referred to almost any part or bodily
system. The patient, usually female, has often had
multiple medical opinions and repeated negative
investigations. Medical reassurance that the symptoms
do not have a demonstrable physical cause fails to
reassure the patient, who will continue to 'doctor-shop'.
The patient is usually reluctant to accept a psychological
and/or social explanation for the symptoms even when
such a link seems obvious. Abnormal illness behaviour is
evident and patients can be attention-seeking and
dependent on doctors. Yet they can complain about the
medical care and attention they have previously received.
The aetiology is unknown, but both mood and
personality disorders are often also present. It is often
associated with dependence upon or misuse of prescribed
medication, usually sedatives and analgesics. There is
Dissociative (conversion) disorders
22
often a history of significant childhood traumas, or chronic
ill-health in the child or parent, which may play an
aetiological role (see Table 22.5). The condition is
probably the somatic presentation of psychological
distress, although iatrogenic damage (from postoperative
and prescribed-drug-related problems) soon complicates
the clinical picture. The course of the disorder is chronic
and disabling, with long-standing family, marital and/or
occupational problems.
Hypochondriasis
The conspicuous feature is a preoccupation with an
assumed serious disease and its consequences. Patients
commonly believe that they suffer from cancer or AIDS,
or some other serious condition. Characteristically, such
patients repeatedly request laboratory and other
investigations to either prove they are ill or reassure
themselves that they are well. Such reassurance rarely
lasts long before another cycle of worry and requests
begins. The symptom of hypochondriasis may be
secondary to or associated with a variety of psychiatric
disorders, particularly depressive and anxiety disorders.
Occasionally the hypochondriasis is delusional, second-
ary to schizophrenia or a depressive psychosis. Hypo-
chondriasis may coexist with physical disease but the
diagnostic point is that the patient's concern is dis-
proportionate and unjustified.
Management of somatoform disorders
The principles outlined in Box 22.7 also apply to these
disorders. Patients very much appreciate a discussion
and explanation of their symptoms. Further management
consists of ceasing reassurance that no serious disease has
been uncovered, since this simply reinforces dependence
on the doctor. The doctor should sensitively explore
possible psychological and social difficulties, if possible
by demonstrating links between symptoms and stresses.
Useful questions to ask include:
'When were you last completely well and happy?'
Such a patient may have trouble remembering such a
time, which helps to support the diagnosis, and leads to a
discussion as to why they have never been well or happy.
'What can't you do now because you are unwell?' 'What
changes has your ill-health caused in your close
relationships?'
These questions usually give information that can be used
to formulate an agreed plan of management. Repeated
laboratory investigations should be discouraged. It is
vital that all members of staff and close family members
adopt the same approach to the patient's problems. Such
patients often consciously or unconsciously split both
medical staff and family members into 'good' and 'bad'
(or caring and uncaring) people, as a way of projecting
their distress. Since these disorders have a poor
prognosis, the aim is to minimize disability. A contract of
mutually agreed care involving the appropriate pro-
fessionals (general practitioner, and a choice of psycho-
therapist, health psychologist, complementary health
professional, physician or psychiatrist), with agreed
frequency of visits and a review date, can be helpful in
managing the condition.
Cognitive behaviour therapy has been shown to
provide effective rehabilitation in significant numbers of
patients suffering from a somatoform disorder.
FURTHER READING
Boorsky A, Ahern D (2004) Cognitive behaviour
therapy for hypochondriasis. Journal of the American
Medical Association 291:1464-1470. Butler CC
et al. (2004) Medically unexplained
symptoms. Journal of the Royal Society of Medicine 97:
219-222.
DISSOCIATIVE (CONVERSION) DISORDERS
Until recently these disorders were known as 'hysteria';
but because the word hysteria is sometimes used
pejoratively to describe extravagant behaviour, the term
is inappropriate.
A dissociative disorder is a condition in which there is a
profound loss of awareness or cognitive ability without
medical explanation. The term dissociative indicates the
disintegration of different mental activities, and covers
such phenomena as amnesia, fugues, and pseudoseizures
(non-epileptic fits).
The term conversion was introduced by Freud to
explain how an unresolved conflict could be converted
into usually symbolic physical symptoms as a defence
against it. Such symptoms commonly include paralysis,
abnormal movements, sensory loss, aphonia, disorders of
gait, and pseudocyesis (false pregnancy). The lifetime
prevalence has been estimated at 3-6 per 1000 in women,
with a lower prevalence in men. Most cases begin before
the age of 35 years. Dissociation is unusual in the elderly.
Table 22.6 Common dissociative/conversion
symptoms
Dissociative (mental)
Paralysis
Disorders of gait
Tremor
Aphonia
Mutism
Sensory symptoms
Globus hystericus
Hysterical fits
Blindness
Conversion (physical)
Amnesia
Fugue
Pseudodementia
Dissociative identity disorder
Psychosis
Clinical features
The various symptoms are usually divided into dissociative
and conversion categories (Table 22.6). Dissociative
disorders have the following four characteristics that are
necessary in order to make the diagnosis:
They occur in the absence of physical pathology that
would explain the symptoms.
1285
Psychological medicine
 They are produced unconsciously. Aetiology
The illness is always triggered by an unresolved con Preliminary research using functional brain scans where
flict or life event. healthy controls feigning a motor abnormality were
Symptoms are not caused by overactivity of the compared with patients with a similar conversion motor
sympathetic nervous system. symptom suggests that dissociation involves different
Other characteristics include: areas of the brain from stimulation. This supports the
theory of unconscious mechanisms first suggested by
Symptoms and signs often reflect a patient's ideas Charcot (see Fig. 22.1). This research would suggest that
about illness. there is a disinhibition of voluntary will at an unconscious
Patients may take up the symptoms of a relative/ level, so that the patient can no longer will the function to
friend who has been ill. happen.
There is usually abnormal illness behaviour, with The psychoanalytical theory of dissociation is that it is
obvious exaggeration of disability. the result of emotionally charged memories that are
Primary gain is the immediate relief from the emotional repressed into the unconscious at some point in the past.
conflict. Symptoms are explained as the combined effects of
Secondary gain refers to the social advantage gained by repression and the symbolic conversion of this emotional
the patient by being ill and disabled (sympathy of energy into physical symptoms. This hypothesis is
family and friends, being off work, disability pension). difficult to test, although there is some evidence that
There may be a curious lack of concern about the patients with dissociative disorders are more likely to
symptoms or disability ('belle indifference'). have suffered childhood abuse, particularly when the
Physical disease is not uncommonly present (e.g. abuse was both sexual and physical and started early in
pseudoseizures in someone with epilepsy). childhood. Caution should be taken with any such
history obtained by therapies that 'recover' childhood
Dissociative amnesia commences suddenly. Patients are memories that were previously completely unknown to
unable to recall long periods of their lives and may even the patient.
deny any knowledge of their previous life or personal Patients with dissociative disorders, by definition
identity. In a dissociative fugue, patients not only lose adopt both the sick role and abnormal illness behaviour,
their memory but wander away from their usual sur- with consequent secondary gains that help to maintain
roundings, and, when found, deny all memory of their the illness.
whereabouts during this wandering. The differential
diagnosis of a fugue state includes post-ictal automatism,
depressive illness and alcohol abuse.
Dissociative pseudodementia involves memory loss and
behaviour that initially suggest severe and generalized
dementia. A differential diagnosis is depressive pseudo-
dementia (see p. 1289).
Multiple personality disorder is rare, but dramatic, and
may be no more than the consequence of suggestion on
the part of a psychotherapist. There are rapid alterations
between two or more 'personalities' in the same person,
each of which is repressed and dissociated from the other
'personalities'. A differential diagnosis is rapid cycling
manic depressive disorder which would explain sudden
apparent changes in personality.
Epidemic or 'mass hysteria' usually occurs in institutions
for girls or young women, in which the combined effects
of suggestion and shared anxiety produce outbreaks of
sickness or disturbed behaviour, often following sudden
illnesses in leaders of the group at a time of threatened or
actual social change.
Differential diagnosis
Dissociation is usually a stable and reliable diagnosis
over time, although high rates of co-morbid mood and
personality disorders are found in chronic sufferers.
Particular care should be taken to make the diagnosis on
positive grounds, and not simply on the basis of an
absence of a medical diagnosis. Care should also be taken
to exclude or treat co-morbid psychiatric disorders.
Fig. 22.1 Statistical parametric maps superimposed on
an MRI scan of the anterior surface of the brain, orientated
as though looking at a person head on. Red region shows
hypofunction of patients with conversion motor symptoms.
Green region shows hypofunction of healthy controls feigning
the same motor abnormality. Reproduced from Spence SA,
Crimlisk HL, Cope H, Ron MA, Grasby PM (2000) Discrete
neurophysiological correlates in prefrontal cortex during
hysterical and feigned disorders of movement. Lancet
355:1243-1244, The Lancet Ltd. 2000, with permission.
1286
Sleep difficulties
22
Management
The treatment of dissociation is similar to the treatment of
somatoform disorders in general, outlined above and in
Box 22.7. The first task is to engage the patient and their
family with a model of the illness that makes sense to
them, is acceptable, and leads to the appropriate manage-
ment. An invented example of a suitable explanation is
given below:
You told me about the tremendous shock you felt when your
mother suddenly died. This was particularly the case since
you hadn't spoken to her for so long beforehand, after that big
disagreement with her over your wedding to John. You weren't
able to say good-bye before she died. Your brain was
overloaded with grief, guilt and anger all at once. I wonder
whether that is why you aren't able to speak now. I wonder
whether it's difficult to think of anything to say that would
make things right, particularly since you can't speak with your
mother now.
Such an explanation would be modified by mutual dis-
cussion until an agreed understanding was achieved,
which would serve as a working model for the illness.
Provision of a rehabilitation programme that addresses
both the physical and psychological needs and problems
of the patient would then be planned. A graded and
mutually agreed plan of a return to normal function can
usually be led by the appropriate therapist (e.g. speech
therapist for dysphonia, physiotherapist for paralysis). At
the same time, a psychotherapeutic assessment should be
made in order to determine the appropriate form of
psychotherapy. For instance, couple therapy will address
a significant relationship difficulty; individual psycho-
therapy could ease an unresolved conflict from childhood.
Abreaction brought about by hypnosis or by intravenous
injections of small amounts of midazolam may produce a
dramatic, if short-lived, recovery. In the abreactive state,
the patient is encouraged to relive the stressful events that
provoked the disorder and to express the accompanying
emotions; i.e. to abreact. Such an approach has been use-
ful in the treatment of acute dissociative states in wartime,
but appears to be of much less value in civilian life. It
should only be contemplated in the presence of an
anaesthetist with suitable resuscitation equipment to hand.
Hypnotherapy is psychotherapy while the patient is in a
hypnotic trance, the idea being that therapy is more
possible because the patient is relaxed and not using
repression. This may allow the therapist access to the
previously unconscious emotional conflicts or memories.
There are no published trials of this technique in
dissociation, which Freud gave up as unsuccessful in
order to found psychoanalysis, but some hypnotherapists
claim good results. Care should be taken to avoid a catas -
trophic emotional reaction when the patient is suddenly
faced with the previously repressed memories.
Prognosis
Most cases of recent onset recover quickly with treatment,
which is why a positive diagnosis should be made early,
rather than sending the patient on to the next medical
specialist. Those cases that last longer than a year are
likely to persist, with entrenched abnormal illness
behaviour patterns that are hard to shift.
FURTHER READING
Crimlisk HL, Bhatia K, Cope H, David A, Marsden CD,
Ron MA (1998) Slater revisited: 6 year follow up study
of patients with medically unexplained symptoms.
British Medical Journal 316: 582586.
Mersky H (1995) The Analysis of Hysteria, 2nd edn.
London: Gaskell.
SLEEP DIFFICULTIES (p. 1227)
Sleep is divided into rapid eye movement (REM) and non-
REM sleep. As drowsiness begins, the alpha rhythm on an
EEG disappears and is replaced by deepening slow wave
activity (non-REM). After 60-90 minutes, this slow wave
pattern is replaced by low amplitude waves on which are
superimposed rapid eye movements lasting a few
minutes. This cycle is repeated during the duration of
sleep, with the REM periods becoming longer. REM sleep
is accompanied by dreaming and physiological arousal.
Slow wave sleep is associated with release of anabolic
hormones and cytokines, with an increased cellular mitotic
rate. It helps to maintain host defences, metabolism and
repair of cells. For this reason slow wave sleep is increased
in those conditions where growth or conservation is
required (e.g. adolescence, pregnancy, thyrotoxicosis).
Insomnia is difficulty in sleeping; a third of adults
complain of insomnia and in a third of these it can be severe.
Primary sleep disorders include sleep apnoea (p. 1227),
narcolepsy (see p. 1227), the restless legs syndrome (Ekbom's)
(see p. 666) and its related periodic leg movement disorder, in
which the legs (and sometimes the arms) jerk while asleep.
Delayed sleep phase syndrome occurs when the circadian
pattern of sleep is delayed so that the patient sleeps from
the early hours until mid-day or later. Night terrors, sleep-
walking and sleep-talking are non-REM phenomena, most
commonly found in children, which can recur in adults
when under stress or suffering from a mood disorder.
Psychophysiological insomnia commonly occurs with func-
tional, mood and substance misuse disorders, and when
under stress (see Box 22.8). It can often be triggered by one
of these factors, but then become a habit on its own, driven
by anticipation of insomnia and day-time naps. Insomnia
causes day-time sleepiness and fatigue, with consequences
such as road traffic accidents. Assessment should pay parti-
cular attention to mood, life difficulties, and drug intake
(especially alcohol, nicotine and caffeine). Initial insomnia
(trouble getting off to sleep) is common in mania, anxiety,
depressive disorders and substance misuse. Middle
insomnia (waking up in the middle of the night) occurs
with medical conditions, such as sleep apnoea and pro-
statism. Late insomnia (early morning waking) is caused by
depressive illness and malnutrition (anorexia nervosa).
Habitual alcohol consumption should be carefully
estimated since even a small excess can be a potent cause
of insomnia, as well as recent withdrawal. Caffeine is
perhaps the most commonly taken drug in the UK, and its
effects are easily underestimated. Six cups (not mugs) of
1287
Psychological medicine
I
Box 22.8 Common causes of insomnia
Psychiatric disorders
Mood disorders (mania, depressive and anxiety
disorders) Delirium and
dementia
Drug use or misuse
Addictive drug withdrawal (alcohol, benzodiazepines)
Stimulant drugs (caffeine, amfetamines) Prescribed
drugs (steroids, dopamine agonists)
Physical conditions
Pain (classically with carpal tunnel syndrome)
Nocturia (e.g. from prostatism) Malnutrition
Primary sleep disorders
Sleep apnoea Restless
legs syndrome
real coffee a day are likely to cause insomnia in the
average healthy adult. Caffeine is not only found in tea
and coffee, but is also found in chocolate, cola drinks and
some analgesics. Prescription drugs that can either
disturb sleep or cause vivid dreams include most appetite
suppressants, glucocorticoids, dopamine agonists, lipid-
soluble beta-blockers (e.g. propranolol) and certain
psychotropic drugs (especially when first prescribed; e.g.
fluoxetine, reboxetine, risperidone).
Hypersomnia is not uncommon in adolescents with
depressive illness, occurs in narcolepsy, and may tempor-
arily follow infections such as infectious mononucleosis.
Management of insomnia
This is particularly determined by diagnosis. Where none
is immediately apparent, it is worth educating the patient
about sleep hygiene. Simple measures such as decreasing
alcohol intake, having supper earlier, exercising daily,
having a bath prior to going to bed and establishing a
routine of going to bed at the same time should be tried.
Relaxation techniques and cognitive behaviour therapy
have a role in those with intractable insomnia. Short half-
life benzodiazepines can be useful for acute insomnia, but
should not be used for more than 2 weeks continuously to
avoid dependence. Non-benzodiazepine hypnotics
(zaleplon, zopiclone, zolpidem) act at the benzodiazepine
receptors and occasional dependence has been reported.
Certain antihistamines (e.g. promethazine) and anti-
depressants (e.g. amitriptyline, trimipramine, trazodone
mirtazapine) are not addictive and can be used as
hypnotics in low dose, with the added advantage of
improving slow wave sleep. The commonest side-effects
are morning sedation and weight gain. . . - ,
FURTHER READING
Sateia M], Nowell PD (2004) Insomnia. Lancet 364:
1959-1973. Wilson S, Nutt D (2005) Assessment and
management
of insomnia. Clinical Medicine 5: 101-104.
MOOD (AFFECTIVE)
DISORDERS
Classification
The central and common feature of these
disorders is an abnormality of mood. Mood is best
considered in terms of a continuum ranging from
severe depression at one extreme to severe
mania at the other, with the normal, stable mood
at the centre (Fig. 22.2). Mood disorders are
divided into bipolar and unipolar affective
disorders. In bipolar affective disorder (otherwise
known as manic-depressive disorder) patients
suffer bouts of both depression and mania. In
unipolar affective disorder patients suffer from
depressive mood swings alone, although they
are commonly recurrent. Although mania can
rarely occur by itself without depressive mood
swings (thus being classified as unipolar) it is far
more commonly found in association with
depressive swings, even if sometimes it takes
several years for the first depressive illness to
appear. Hypomania is mild mania. Dysthymia is
a chronic low-grade depressive illness.
DEPRESSIVE DISORDERS
Depressive disorders or 'episodes' are primarily
classified
as bipolar or unipolar and secondarily as mild,
moderate
or severe, with or without somatic symptoms.
Severe
depressive episodes are divided according to
the
presence or absence of psychotic symptoms.
About 10%
of patients with depressive illness are eventually
found to
have bipolar illnesses.
. " ' - ,
Clinical features of depressive
disorder
Whereas everyone will at some time or other feel
cheesed off, fed up or down in the dumps, it is
when such symptoms become qualitatively
different, pervasive, or interfere with normal
functioning that a depressive illness has occurred.
Depressive disorder, clinical or 'major' depression
is characterized by disturbances of mood,
speech, energy and ideas (Table 22.7). Patients
often describe their symptoms in physical
terms. Marked fatigue and headache are the two
most common physical symptoms in
depressive illness
and may be the
first
Depressive
psychosis
Mani
Moderate
a depression
Minor depression
Hypo
mani
 l
a ria
H
ft a
Mild
p
p
e
y
u
Fig. 22.2 Continuum of normal and abnormal
p mood.
Gloomy
h Despondent
Sad
o Cheery
Hopefu
1288

^^^^^H Table 22.7 Clinical features of depression
Characteristic Clinical appearance
Mood Depressed, miserable or irritable
Talk Impoverished, slow, monotonous
Energy Reduced, lethargic
Ideas Feelings of futility, guilt, self-reproach,
unworthiness, hypochondriacal
preoccupations, worrying, suicidal
thoughts, delusions of guilt, nihilism
and persecution
Cognition Impaired learning, pseudodementia in
elderly patients
Physical Early waking, poor appetite and weight
loss, constipation, loss of libido,
erectile dysfunction, fatigue, bodily
aches and
pains
Behaviour Retardation or agitation, poverty of
movement and expression
Hallucinations Auditory - often hostile, critical
symptoms to appear. Patients describe the world as look-
ing grey, themselves as lacking a zest for living and
devoid of pleasure and interest in life (anhedonia).
Anxiety and panic attacks are common; secondary
obsessional and phobic symptoms may emerge. Symp-
toms should last for at least 2 weeks and should cause
significant incapacity (e.g. trouble working or relating to
others) to be considered an illness.
In the more severe forms, diurnal variation in mood
can occur, feeling worse in the morning after waking in
the early hours with apprehension. Suicidal ideas are
more frequent, intrusive and prolonged. Delusions of
guilt, persecution and bodily disease are not uncommon,
along with second person auditory hallucinations insult-
ing the patient or suggesting suicide. In severe depressive
illness, particular in the elderly, concentration and
memory can be so badly affected that the patient appears
to have dementia (pseudodementia). Delusions of poverty
and non-existence (nihilism) occur particularly in this age
group. Suicide is a real risk, with the lifetime risk being
approximately 5% in primary care patients, but 15% in
those with depressive illness severe enough to warrant
admission to hospital.
Epidemiology
About a third of the population will feel unhappy at any
one time, but this is not the same as depressive illness.
The point prevalence of depressive illness is 5% in the
community, with a further 3% having dysthymia (see
below). It is more common in women, but there is no
increase with age, and no difference by ethnic group or
socio-economic class (apart from an inverse relationship
only with dysthymia). Married and never married people
have similar prevalence rates, with separated and
divorced people having two to three times the
prevalence. Some studies have suggested that depressive
illness is becoming more common.
Depressive illnesses are more common in the presence
of:
tders
physical diseases, particularly if chronic, stigmatizing
or painful
excessive and chronic alcohol use (probably the most
depressing drug humans use)
social stresses, particularly loss events, such as
separation, redundancy and bereavement
interpersonal difficulties with those close to the
patient, especially when socially humiliated
lack of social support, with no confiding relationship.
Depressed patients with another physical disorder view
themselves as more sick and visit their doctors almost
four times as often as the non-depressed physically ill,
stay in hospital longer, comply less with medical advice
and medication, and undergo more medical and surgical
procedures. Depressive illness may be associated with
increased mortality (excluding suicide) in patients with
physical illness, such as myocardial infarct.
Dysthymia
Dysthymia is a more mild depressive illness that lasts
intermittently for 2 years or more and is characterized by
tiredness and low mood, lack of pleasure, low self-esteem,
and a feeling of discouragement. The mood relapses and
remits, with several weeks of feeling well, soon followed
by longer periods of being unwell. It can be punctuated
by depressive episodes of more severity; so-called
'double depression'.
Seasonal affective disorder
Seasonal affective disorder is characterized by recurrent
episodes of depressive illness occurring during the winter
months in the northern hemisphere. Symptoms are
similar to those found with atypical depressive illness, in
that patients complain of hypersomnia, increased appetite
(with carbohydrate craving) and weight gain, with pro-
found fatigue. Such patients have a higher prevalence of
bipolar affective disorder, and some doctors are uncertain
whether the condition is different from normal depressive
illness, with the accentuation of mood that naturally
occurs by season. However, there is evidence that seasonal
depressive illness can be successfully treated with bright
light therapy given in the early morning, which causes a
phase advance in the circadian rhythm of melatonin. In
contrast, the same treatment given in the early evening,
with consequent phase delay of melatonin secretion, is
less antidepressant. Selective serotonin reuptake inhibitors
(SSRIs) are alternative treatments.
Differential diagnosis
The differential diagnoses of depressive illness are shown
in Table 22.8. Other psychiatric disorders are the most
common misdiagnoses. Ninety per cent of patients
presenting with a depressive illness, while misusing
alcohol, will no longer be depressed 2 weeks after their
last drink.
Pathological (abnormal) and normal grief are described
on page 1300. Pathological grief is closely associated with
depressive illness.
1289
Psychological medicine
 Table 22.8 Common differential diagnoses of
depressive illness
Other psychiatric disorders
Alcohol misuse
Amfetamine (and derivatives) misuse and withdrawal
Borderline personality disorder
Dementia
Delirium
Schizophrenia
Normal and pathological grief
Organic (secondary) affective illness
Physical causes which are both necessary and sufficient as
a cause
Cushing's syndrome Thyroid disease (although sometimes
depression persists
after treatment) Hyperparathyroidism Corticosteroid
treatment Brain tumour (rarely without other neurological
signs)
Investigations
A corroborative history can be valuable in helping to
exclude differential diagnoses such as alcohol misuse and
elucidating maintaining factors such as the relationship
with a partner. Physical investigations should be guided
by the history and examination. They will often include
measurement of free T4 and TSH (particularly in women),
calcium, sodium, potassium, mean corpuscular volume,
y-glutamyl transpeptidase, haemoglobin, white cell
count, ESR or plasma viscosity. Less commonly a chest
X-ray, antinuclear antibody, morning and evening cortisols,
electroencephalogram or a brain scan are indicated.
The aetiology of unipolar depressive
disorders
The aetiology of unipolar depressive disorders is multi-
factorial and a mixture of genetic and environmental
factors.
Genetic
Unipolar depression is probably polygenic, but no linkage
has been firmly identified. The risk of unipolar depression
in a first-degree relative of a patient is approximately three
times the risk of the non-affected. The concordance of
unipolar depression in monozygotic twins is between 30
and 60%, the concordance increasing with more recurrent
illnesses. The issue is complicated by the genetic influence
on sleep habits, 'neurotic' personality, and even life events,
which are all involved in the genesis of depressive illness.
Biochemical
The monoamine theory of depressive illness is supported
by the efficacy of monoamine reuptake inhibitors and the
depressive effect of dietary tryptophan depletion. Neuro-
endocrine tests also suggest that the serotonin neuro-
transmitter system is downregulated. 5-HT la and 5-HT2
receptor subtypes are thought most likely to be involved.
Receptor-labelled functional brain scans suggest that
dopamine underactivity is related to psychomotor
retardation.
Hormonal
Cushing's syndrome is the most potent cause of 'organic'
depressive illness, with 50-80% of patients with Cushing's
suffering from a depressive illness. Corticosteroid treat-
ment causes significant mood disturbance. Nearly half of
patients with 'functional' depressive illness have raised
cortisol levels, and this is associated with adrenal gland
enlargement. Hypercortisolaemia can cause hippocampal
damage, which has been found in chronic severe depress-
ive illness. All these data suggest that cortisol may play a
role in causing depressive illness.
In contrast atypical depressive illness, with prominent
hypersomnia and weight gain, is associated with a down-
regulated hypothalamic-pituitary-adrenal axis, supporting
the heterogeneity of depressive disorders.
Brain imaging
The use of magnetic resonance imaging (MRI) and
positron emission tomography (PET) has revealed a
number of abnormalities in the brains of patients with
major depression. Increased brain ventricle volume,
localized frontal lobe atrophy and reduced blood flow in
specific brain areas have been reported, while more recent
studies suggest that the hippocampus undergoes
selective volume reduction in stress-related neuro-
psychiatric disorders such as recurrent depression. This
may be related to hypercortisolaemia.
Sleep
A reduced time between onset of sleep and REM sleep
(shortened REM latency) and reduced slow wave sleep
both occur in depressive illness. These abnormalities are
persistent in some patients when they are not depressed.
Families with several sufferers of depressive illness can
share these traits, suggesting that sleep patterns may be
inherited and predispose to depression.
Psychological
Poor parenting and physical or sexual abuse in childhood
all predispose adults to depressive illness, but the effect is
non-specific. Both 'neurotic' (emotional) and perfectionist
personality traits are risks for depressive illness, and
these may be determined as much by genetic factors as
early environment.
Social
Thirty per cent of women will develop a depressive ill
ness after a severe life event or difficulty, such as a divorce,
and this is compounded by low self-esteem and a lack of
a confiding relationship. Unemployment is a significant
risk factor in men. ,.-.
An integrated model of aetiology
Stress is more likely to trigger depressive illness in a
person predisposed by lack of social support and/or
certain personality traits. Stress in turn triggers various
brain changes in both stress hormones (such as the release
1290
Mood (affective) disorders
of corticotropin-releasing hormone) and neurotransmitters
(e.g. serotonin) that are both known to be altered in
depressive illness. We can thus start to glimpse the model
of an integrated biopsychosocial model of depressive
illness. This model challenges dualistic ideas that
depressive illnesses are either psychological or physical;
depressive illnesses involve both the mind and the body,
which are themselves indivisible.
Puerperal affective disorders
Affective illnesses and distress are common in women
soon after they have given birth. Such disturbances are
usually divided into maternity blues, postpartum
(puerperal) psychosis and postnatal depressive illness.
'Maternity blues' describe the brief episodes of emotional
lability, irritability and tearfulness that occur in about
50% of women 2-3 days postpartum and resolve
spontaneously in a few days.
Postpartum psychosis occurs once in every 500-1000
births. Over 80% of cases are affective in type and the onset
is usually within the first 2 weeks following delivery. In
addition to the classical features of an affective psychosis,
disorientation and confusion are often noted. Severely
depressed patients may have delusional ideas that the
child is deformed, evil or otherwise affected in some way,
and such false ideas may lead to either attempts to kill the
child or suicide. The response to speedy treatment is
generally good. The recurrence rate for a psychosis in a
subsequent puerperium is 20-30%.
Non-psychotic postnatal depressive disorders occur
during the first postpartum year in 10% of mothers,
especially in the first 3 months. Risk factors are first
pregnancy, poor relationship with the partner, ambi-
valence about the pregnancy, and emotional personality
traits. The Edinburgh Postnatal Depression Scale (EPDS)
is a 10-item questionnaire and can be used as an effective
screening tool. Depressive illness after childbirth is
clinically similar to other depressive illnesses, but lack of
emotional bonding with the baby is common.
Treatment of depressive illness
The patient needs to know the diagnosis to provide
understanding and rationalization of the overwhelming
distress inherent in depressive illness. Knowing that self-
loathing, guilt and suicidal thoughts are caused by the
illness can be 'antidepressant' on its own. The further
treatment of depressive disorders involves physical,
psychological and social interventions (Box 22.9). Patients
who are actively suicidal, severely depressed or with
psychotic symptoms should be admitted (necessary for
perhaps 1 in 1000 patients with clinical depression in
primary care). This provides the patient a break from self-
care, and allows support, listening, observation, preven-
tion of suicide, and close monitoring of treatments. Avoid
the pitfall of not treating a depressive illness just because
it seems an 'understandable' reaction to serious illness
or difficult circumstances. This is particularly likely to
happen if the patient is elderly, severely or even
terminally ill.
Box 22.9 Management of depressive illness
Physical
Stop depressing drugs (alcohol, steroids)
Regular exercise (good for mild to moderate depression)
Antidepressants (choice determined by side-effects, co-
morbid illnesses and interactions)
Adjunctive drugs (e.g. lithium; if no response to two different
antidepressants)
Electroconvulsive therapy (ECT) (if life-threatening or non-
responsive)
Psychological
Education and regular follow-up by same professional
Cognitive behaviour therapy (CBT) (most effective
psychotherapy in clinical depression) Other
indicated psychotherapies (couple, family,
interpersonal therapies)
Social
Financial: eligible benefits, debt counselling
Employment: acquire or change the job or career
Housing: adequate, secure tenancy, safe, social
neighbours Young children: child-
care support
Treatments combined
The most effective treatment is a mixture of CBT and an
antidepressant
Drugs used in the treatment of clinical
depression
Recreational drugs such as alcohol should be stopped.
Prescribed medicines suspected of exacerbating de-
pression, such as corticosteroids, should be gradually
stopped or reduced to a safe minimum.
The first course of antidepressant drugs is effective in
relieving clinical depression in 60-70% of patients, if
given in adequate doses for a sufficient time to the
correctly diagnosed patient. Such treatment is more
successful when accompanied by sufficient patient
education and regular follow-up, particularly in the first
6 weeks of treatment. Dysthymia responds less well to
antidepressants than does a depressive episode.
The commonest two pharmacological types of anti-
depressants are tricyclic antidepressants (TCAs) and
selective serotonin reuptake inhibitors (SSRIs). All anti-
depressants have similar efficacy and speed of onset.
Choice depends on their side-effects, which can be used
to positive effect (sedating drugs given at night to enhance
sleep), and their safety. Patients should be warned about
side-effects and that it will take 2 or more weeks before a
positive benefit is apparent. Drugs should normally be
started at a low dose and increased, depending on side-
effects and efficacy. A course of antidepressants should be
given until 4 months after recovery to prevent relapse.
The two greatest problems with these drugs are persuading
the patient to take them and compliance, since 80% of the
UK public wrongly believe that they are addictive.
Psychotic depression needs either electroconvulsive
therapy or a combination of an antidepressant and an
antipsychotic drug.
1291
Psychological medicine
\ serotonin, by inhibiting their reuptake into nerve

Somatodendritic 5-
HT1A autoreceptors

Selective serotonin reuptake inhibitors (SSRIs)

SSRIs selectively inhibit the reuptake of the monoamine
serotonin (5-HT) within the synapse, and are thus termed
'selective serotonin reuptake inhibitors' or SSRIs.
Citalopram, and its laevo isomer, escitalopram, fluvox-
amine, fluoxetine, paroxetine and sertraline have the
advantage of causing less serious or disabling side-effects
than tricyclics. For instance, SSRIs do not cause signifi -
cant weight gain. Because of their long half-lives they can
also be given just once a day, normally in the morning
after breakfast. For these reasons patients comply more
with treatment and therefore SSRIs are now first-line
treatments for depressive disorders. Normal doses are
between 20 and 60 mg, with sertraline and fluvoxamine
needing higher doses. The most common side-effects
resemble a 'hangover' and include nausea, vomiting,
headache, diarrhoea and dry mouth. Insomnia and
paradoxical agitation can occur when first starting the
drugs. One in five patients also have sexual side-effects,
such as impotence and loss of libido.
A toxic hyperserotonergic state ('serotonin' syndrome)
can be caused by the ingestion of two or more drugs that
increase serotonin levels, e.g. an SSRI combined with a
monoamine oxidase inhibitor (MAOI) or dopaminergic
drugs (e.g. selegiline) or a tricyclic antidepressant. Symp-
toms include agitation, confusion, tremor, diarrhoea,
tachycardia and hypertension; hyperthermia is charac-
teristic. Treatment is supportive.
SSRIs have also been associated with a specific with-
drawal syndrome (discontinuity syndrome). This is charac-
terized by shivering, anxiety, dizziness, headache and
nausea. Patients should be warned not to leave out a dose
and to gradually reduce SSRIs when stopping them.
terminals (Fig. 22.3(c)). Other tricyclics in
common use include nortriptyline, doxepin and
clomipramine. Depending on the particular
drug, normal doses are between 75 and 150
mg. Having been available for more than 40
years, there is more evidence of the effectiveness
of TCAs in depressive illness than for any other
group of anti-depressants. They are the drugs
most commonly used in severe depressive
illness.
TCAs have a number of side-effects (Table
22.9). In long-term treatment or prophylaxis,
weight gain is most troublesome. Because of
their toxicity in overdose, it is wisest NOT to
prescribe them to potentially suicidal outpatients,
without careful monitoring or giving the drugs
to a reliable family member to look after.
SNaRls, NaSSAs and NaRls:
antidepressants
The latest generation of antidepressants block a
number of different neurotransmitter receptors
both at the synapse

Tricyclic antidepressants (TCAs)

Dosulepin (dothiepin), imipramine and amitriptyline are
the three most commonly used in the UK, but many
related compounds have been introduced, some having
fewer autonomic and cardiotoxic effects (e.g. trazodone,
lofepramine). These drugs potentiate the action of the
monoamines, noradrenaline (norepinephrine) and
Fig. 22.3 flow down the axon, reducing 5-HT release. In depression, oxidase inhibitor. From Waller DG, Renwick A, Hillier K
Sites of there is a reduction in amine neurotransmissions which results (eds) (2001) Medical Pharmacology and Therapeutics,
action of in upregulation of postsynaptic and somatodendritic receptors. Edinburgh: Saunders, with permission from Elsevier.
antidepr Using 5-HT, as an example, the depletion of 5-HT results in
essants upregulation of postsynaptic 5-HT2 receptors and presynaptic
with (somatodendritic) 5-HT1A receptors. The many antidepressants Table 22.9 Side-effects of tricyclic
examples now available have different actions on serotonin and antidepressants
. In a noradrenaline (norepinephrine) neuro-transmission. Classical Antimuscarinic effects
normal antidepressants (TCA) have less effects on sedation and Dry mouth
neurone, antimuscarinic and antihistaminergic activities. SSRI, selective Constipation
the serotonin reuptake inhibitors; SNRI, serotonin and noradrenaline
Tremor
stimulatio (norepinephrine) reuptake inhibitors; NRI, noradrenaline
Blurred vision
n of the Convulsant activity Urinary
somatode Lowered seizure threshold retention
ndritic 5-
HT1A Other effects Cardiovascular
autorecep Weight gain QT
tors Sedation Mania prolongation
inhibits (rarely) Arrhythmias
the
Postural
neuronal (norepinephrine) reuptake inhibitor (selective); NE, noradrenaline
impulse (norepinephrine); MAO, monoamine oxidase; MAOI, monoamine hypotension
1292
^Mood (affective) disorders
and elsewhere. Their different receptor profiles cause dif-
ferent side-effects.
Venlafaxine is a potent blocker of both serotonin and
noradrenaline (norepinephrine) reuptake (SNaRI). It has
negligible affinity for other neurotransmitter receptor
sites and so produces less sedation and fewer anti-
muscarinic effects. It can be given in slow-release
form with the advantage of once-daily dosage. Nausea
is the commonest side-effect and high doses can occasion-
ally cause hypertension. It does not cause weight gain.
Mirtazapine is a 5-HT2 and 5-HT3 receptor antagonist
and a potent a2-adrenergic blocker. The consequent effect
is to increase both noradrenaline {norepinephrine) and
selective serotonin transmission: an NaSSA. It can be given
at night to aid sleep and rarely causes sexual side-effects.
Mirtazapine can be sedating in low dose and can
cause weight gain. An uncommon adverse effect is
agranulocytosis.
Reboxetine is a selective noradrenaline (norepinephrine)
reuptake inhibitor (NaRI). It is not sedating and may help
reduced motivation and energy. Weight gain is not
reported. Dry mouth, insomnia, constipation, urinary
hesitancy and tachycardia are reported side-effects.
Monoamine oxidase inhibitors (MAOIs)
These act by irreversibly inhibiting the intracellular
enzymes monoamine oxidase A and B, leading to an
increase of norepinephrine (noradrenaline), dopamine
and 5-hydroxytryptamine in the brain (see Fig. 22.3(b).
Because of their side-effects and restrictions while taking
them, they are rarely used by non-psychiatrists. Psychi-
atrists use them as a second-line treatment of depressive
illnesses, particularly with atypical presentations
(p. 1289). The most widely used is phenelzine, which is
given in doses of 30-60 mg daily. Side-effects include
increased appetite, weight gain, erectile dysfunction and
insomnia. MAOIs also produce a severe and dangerous
hypertensive reaction with foods containing tyramine or
dopamine and therefore a restricted diet is prescribed.
Tyramine is present in cheese, pickled herrings, yeast
extracts, certain red wines, and any food, such as game,
that has undergone partial decomposition. Dopamine is
present in broad beans. MAOIs interact with drugs such as
pethidine and can also occasionally cause liver damage.
MAOIs should not normally be given within 2 weeks of a
serotonin reuptake inhibitor, depending on half-lives.
Reversible inhibitors of monoamine A (RIMAs)
An example is moclobemide; usual dose 300 mg daily.
These drugs appear to have fewer side-effects (insomnia
and headache, but some sexual problems) and constitute
a low risk in overdose. Patients prescribed such anti-
depressants should be told that they can eat a normal
diet, but should be careful to avoid excessive amounts of
food rich in tyramine (see above).
Antidepressant use in general medicine
In patients with cardiac disease, SSRIs, lofepramine and
trazodone are preferred over more quinidine-like com-
pounds. MAOIs and mirtazapine do not affect epileptic
thresholds. SSRIs are metabolized by the cytochrome P450
system, unlike venlafaxine, mirtazapine and reboxetine; the
latter therefore have fewer drug interactions. Care should
be taken not to prescribe antidepressants while a patient
is taking the herbal antidepressant St John's wort, which
interacts with serotonergic drugs in particular. Doses of
antidepressants should initially be halved in the elderly
and in patients with renal or hepatic failure.
Antidepressants should be avoided if possible in preg-
nancy and breast-feeding. If other treatments are in-
effective, the risks of drug therapy should be balanced
against no treatment, which can affect fetal progress and
the future mother-child bonding. Tricyclic antidepressants
are generally believed to be safe in pregnancy, with no
statistical increase in congenital malformations in fetuses
exposed to them. However, occasionally their anti-
muscarinic side-effects produce jitteriness, sucking
problems and hyperexcitability in the new-born. Post-
partum plasma levels of babies breast-fed by treated
mothers are negligible. SSRIs do not seem to be
teratogenic but manufacturers advise against their use in
pregnancy until more data are available. MAOIs should
be avoided during pregnancy because of the possibility of
a hypertensive reaction in the mother.
Electroconvulsive therapy (ECT)
Although the use of ECT is declining in the UK, it is still the
treatment of choice in severe life-threatening depressive
illness, particularly when psychotic symptoms are present.
It is sometimes essential treatment when the patient is
dangerously suicidal or refusing to eat and drink. The
treatment involves the passage of an electric current across
two electrodes applied to the anterior temporal areas of the
scalp, in order to induce an epileptic fit. The fit is the
essential part of the treatment. Before the treatment is given,
the patient is given a general anaesthetic and receives a
muscle relaxant to prevent injury during the fit. Treatments
are normally given twice a week for 3-6 weeks.
ECT is a controversial treatment, yet it is remarkably
safe and free of serious side-effects. Post-ictal confusion
and headache are not uncommon, but transient. Short-
term retrograde amnesia and a temporary defect in new
learning can occur during the weeks of treatment, but
these are short-lived effects.
Uncommonly used treatments
Transcranial magnetic stimulation (TMS) is an experimental
treatment, with promising early results. Psychosurgery is
very occasionally considered in patients with severe
intractable depressive illness, when all other treatments
have failed (see p. 1302). A third improve remarkably,
while a further third improve somewhat. Vagus nerve
stimulation may represent a major advance in the manage-
ment of chronic and treatment-refractory depressive
disorders but definitive clinical trials are awaited.
Psychological treatments
Cognitive behaviour therapy (CBT)
Aaron Beck developed CBT in the 1960s to reverse the
negative cognitive triad with which patients regarded
1293
Psychological medicine
themselves, their situation and their futures. It involves
the identification of the automatic dysfunctional thinking
that maintains the negative perceptions that feed depress-
ion. They commonly include catastrophizing (e.g. making
a 'mountain out of a mole-hill'), overgeneralizing (e.g. 'I
failed an exam; therefore I am a failure as a person.'),
categorical ('black or white') thinking (e.g. 'My work is
either perfect or abysmal.'). CBT then involves identify-
ing the links between these thoughts, consequent
behaviour, and feeling low, and then testing their logic.
This is done by considering the evidence either in the
therapy sessions (e.g. Q: 'Did you pass the other exams
you took?' A: 'Yes; I guess I did.') or by behavioural
'experiments' (e.g. showing the 'abysmal' work to a
colleague and asking their opinion).
There is good evidence that CBT is as effective as
antidepressant drugs for mild and moderate depressive
illness. CBT is also effective in preventing a relapse of
clinical depression. CBT is an effective treatment not only
for depressive illness, but also for anxiety disorders and
functional disorders (see pp. 1297 and 1281). It has even
been shown to help reduce the severity of delusions in
schizophrenia.
Interpersonal psychotherapy
This psychotherapy is probably as effective as anti-
depressants in mild and moderate clinical depression.
The therapist focuses on a patient's interpersonal relation-
ships involved in or affected by their illness (especially
relationship changes or deficiencies), using problem-
solving techniques to help the patient to find solutions.
Other psychotherapies
Couple therapy is particularly effective when a patient with
clinical depression is in a relationship with problems
(practical, emotional or sexual). Both the patient and
partner attend therapy. Family therapy is effective not only
in a family with problems, but also as a way of helping
the family to help the patient get better. It may involve
understanding one family member's 'depression' as a
systemic 'solution' for a wider problem within the family.
Social treatments
Many patients with clinical depression have associated
social problems (see Box 22.9). Assistance with social
problems can make a significant contribution to clinical
recovery. Other social interventions include the provision
of group support, social clubs, occupational therapy and
referral to a social worker. Educational programmes, self-
help groups, and informed and supportive family
members can help improve outcome.
Prognosis
The majority of patients have recovered by 6 months in
primary care and 12 months in secondary care. About a
quarter of patients attending hospital with depressive
illnesses will have a recurrence within a year, and three-
quarters will have a relapse within 10 years. Patients with
recurrent depressive illnesses should be offered preven-
tion. This may involve CBT that concentrates on relapse
prevention, other forms of psychotherapy, or anti-
depressant medication. Full-dose antidepressants are
the most effective prophylaxis in recurrent depressive
disorders.
FURTHER READING
Alexopoulus GS (2005) Depression in the elderly. Lancet
365: 1961-1970. Belmaker RH (2004) Bipolar disorders.
New England
Journal of Medicine 351: 476-486. Brockington I (2004)
Postpartum psychiatric disorders.
Lancet 363: 303-310. Lader M, Cowan P (2001)
Depression. British Medical
Bulletin 57. UK ECT Review Group (2003) Efficacy and
safety of
electroconvulsive therapy in depressive disorders.
Review. Lancet 361: 799-808. Whooley MA, Simon GE
(2000) Managing depression
in medical outpatients. New England Journal of
Medicine 343: 1942-1950.
MANIA AND HYPOMANIA
The clinical features of mania reflect a marked elevation
of mood, characterized by euphoria, overactivity and
disinhibition (Table 22.10). Hypomania is the mild form
of mania. Hypomania lasts a shorter time and is less
severe, with no psychotic features and less disability.
Hypomania can be distinguished from normal happiness
by its persistence, non-reactivity (not provoked by good
news and not affected by bad news) and social disability.
Mania almost always occurs as part of a bipolar affective
disorder. The social disability of mania can be severe,
with disinhibited behaviour leading to significant debts
(from overspending and over-generosity), lost relation-
ships (from promiscuity), social ostracism and lost
employment (from reckless or disinhibited behaviour).
Some patients have a rapid cycling illness, with
frequent swings from one mood state to another. A mixed
affective state occurs when features of mania and
depressive illness are seen in the same episode. Cyclo-
thymia is a personality trait with spontaneous swings in
mood not sufficiently severe or persistent to warrant
another diagnosis.
Table 22.10 Clinical features of mania
Characteristic Clinical appearance
Mood Elevated or irritable
Talk Fast, pressurized, flight of ideas
Energy Excessive
Ideas Grandiose, self-confident, delusions of
wealth, power, influence or of
religious significance, sometimes
persecutory
Cognition Disturbance of registration of memories
Physical Insomnia, mild to moderate weight loss,
increased libido
Behaviour Disinhibition, increased sexual activity,
excessive drinking or spending
Hallucinations Fleeting auditory or, more rarely, visual ^_
1294
Mood (affective) disorders
Differential diagnosis
Acute intoxication with recreational drugs, such as
amfetamines, amfetamine derivatives (MDMA: Ecstasy),
and cocaine can mimic mania. Long-term use of cannabis
can also induce an illness with manic features. In one
study a quarter of patients with Cushing's syndrome had
a secondary manic illness during their illness. Similarly
corticosteroids can induce mania less commonly than
depressive illness. Dopamine agonists (e.g. bromocriptine)
are also known to sometimes induce secondary mania.
The excited phase of catatonic schizophrenia can some-
times be mistaken for mania.
Epidemiology
The lifetime prevalence of bipolar affective disorder is 1%
across the world. Unlike unipolar depressive illness, it is
equally common in men and women, supporting its
different aetiology. There is no variation by socio-
economic class or race. The mean age of onset is 21; earlier
than unipolar depression. The higher prevalence found in
divorced people is probably a consequence of the
condition.
Aetiology
Genetic
There is strong evidence for a genetic aetiology in this
disorder. There is a 60-80% concordance rate in mono-
zygotic twins, compared to 15% in dizygotic twins,
suggesting a high rate of heritability. Adoption studies
show similar rates, so this high rate is probably genetic
and not due to the family environment. Linkage studies
have so far proved disappointing, with several suggestive
chromosome linkages being found, suggesting there is no
single gene with a large effect. Instead it is likely that the
condition will prove to be caused by several genes acting
together. : . .
Biochemical
It is difficult to carry out research on patients with acute
mania, so studies are few. Brain monoamines seem to be
increased in mania. Dexamethasone tends not to suppress
cortisol levels in patients with mania, suggesting a similar
pattern of non-suppression to that seen in severe
depressive illness.
Psychological
The effect of life events is much weaker in bipolar
compared to unipolar illnesses, with most effect apparent
at first onset. Similarly, personality does not seem to be a
major influence, in contrast to unipolar depression,
although there is some evidence of a link with the
creativity and divergent thinking that is an advantage in
the right occupation.
Treatment of mania
Acute mania
Acute mania is treated with lithium and/ or antipsychotic
(neuroleptic) drugs. Lithium is the treatment of choice for
acute mania in the absence of severe hyperactivity. The
advantage of lithium is the lack of motor side-effects seen
with neuroleptics (bipolar patients are particularly prone
to tardive dyskinesia). The main disadvantage is slow
speed of response (normally 2 weeks). The dose of lithium
depends on whether the citrate or carbonate salt is used.
Haloperidol and the more sedating chlorpromazine
are commonly used neuroleptics, given orally or intra-
muscularly. Doses are similar to those used in
schizophrenia. The behavioural excitement and over-
activity are usually reduced within days, but elation,
grandiosity and associated delusions often take longer to
respond. Severe mania is best treated with a combination
of lithium and a neuroleptic, allowing the neuroleptic to
be withdrawn after the first 2 or 3 weeks. First attacks of
mania usually require treatment for up to 3 months. The
anticonvulsants carbamazepine and sodium valproate
are also helpful in hypomania or in rapidly cycling
illnesses (see below). Recent work suggests it can be
sometimes helpful to add to the regimen a benzodiazepine,
such as clonazepam or lorazepam.
Prevention
Since bipolar illnesses tend to be relapsing and remitting,
prevention of relapse is the major therapeutic challenge in
the management of bipolar affective disorder. A patient
who has experienced more than two episodes of affective
disorder within a 5-year period is likely to benefit from
preventative treatments.
Lithium
Lithium (carbonate or citrate) is the main agent used for
prophylaxis in patients with repeated episodes of bipolar
illness. It is rapidly absorbed into the gastrointestinal
tract and more than 95% is excreted by the kidneys; small
amounts are found in the saliva, sweat and breast milk.
Renal clearance of lithium correlates with renal creatinine
clearance. Lithium is a mood-stabilizing drug that
prevents mania more than depression. It reduces the fre-
quency and severity of relapses by half and significantly
reduces the likelihood of suicide. Its mode of action is
unknown, but lithium is known to act on the serotoninergic
system. Poor responses to lithium are associated with a
negative family history, an unstable premorbid personality,
and a rapid cycling illness.
Patients should be screened for thyroid (free T 4, TSH
and thyroid autoantibodies) and renal disease (serum
urea and creatinine, 24-hour urinary volume) before start-
ing on lithium. Lithium interferes with thyroid function
and can produce frank hypothyroidism. The presence of
thyroid autoantibodies increases the risk, so it is worth-
while measuring these before treatment. Long-term treat-
ment with lithium causes two renal problems; nephrogenic
diabetes insipidus (DI) and reduced creatinine clearance
(see p. 609). The therapeutic range for prophylaxis is
0.5-1.0 mmol/L. Lithium levels should be checked every
3 months, along with regular thyroid (free T4 and TSH)
and renal function tests. The best screen for DI is to ask
the patient about polyuria and polydipsia. Tests should
include serum urea and creatinine, and 24-hour urinary
volume if DI is suspected. A creatinine clearance should
be carried out if glomerular disease is suspected. Patients
1295
Psychological medicine
should carry a lithium card with them at all times.
Other side-effects of lithium include:
nausea and diarrhoea
a fine tremor (15%)
polyuria and polydipsia (see above)
weight gain, mainly through increased appetite.
Lithium toxidty begins to occur when the serum concen-
tration exceeds 1.5 mmol/L. Symptoms include drowsi-
ness, nausea, vomiting, blurred vision, a coarse tremor,
ataxia and dysarthria. Toxicity is more likely when
the patient is dehydrated or with a drug interaction
increasing concentrations. Such symptoms progress to
delirium and convulsions, and coma and death can occur.
As a rule, lithium is not advised during pregnancy,
particularly in the first trimester, because of an increased
risk of fetal malformation (Ebstein's anomaly). Between
25-30% of women with a history of bipolar disorder
relapse within 2 weeks of delivery. Restarting lithium
within 24 hours of delivery (if the mother is prepared to
forgo breast-feeding) markedly reduces the risk of relapse.
Anticonvulsant, mood-stabilizing drugs
Carbamazepine and sodium valpwate are used both in
prophylaxis and treatment of manic states. Some patients
who do not respond to lithium may respond to these
anticonvulsants or a combination of both. Patients with
rapid cycling illnesses show a better response to
anticonvulsants than to lithium. For antimanic treatment,
dosage in the initial stage of treatment will be 200 mg
twice daily of carbamazepine, increasing to a normal dose
of 800-1000 mg. Other drugs which appear to exercise a
prophylactic mood-stabilizing effect include sodium
valproate, olanzapine and risperidone. Both carbamazepine
and valproate can be teratogenic (neural tube defects) and
should be avoided in pregnancy. Other side-effects of
these drugs are given on page 1224.
Prognosis
The average duration of a manic episode is 2 months,
with 95% making a full recovery in time. Recurrence is
the rule in bipolar disorders, with up to 90% relapsing
within 10 years.
FURTHER READING
Daly I (1997) Mania. Lancet 349:1157-1160.
admission) will eventually commit suicide, with 6%
doing so in the 10 years after their first admission. Suicide
rates in schizophrenia sufferers are likewise high, being
20-50 times the rate in the general population; 20^0% of
people with schizophrenia make suicide attempts, and
9-13% are successful. A Finnish study suggests that the
suicide rate is higher in women who have sustained a
miscarriage or undergone an induced abortion, whereas
it is significantly reduced in women who are pregnant.
The highest rates of suicide have been reported in rural
southern India (148 per 100 000 in young women
and 58 per 100 000 in young men) and in Hungary
(40 per 100 000), while the lowest are those of Spain
(3.9 per 100 000) and Greece (2.8 per 100 000), but such
variations may reflect differences in reporting, which may
be related to religion, as much as genuine differences.
Factors that increase the risk of suicide are indicated in
Table 22.11.
A distinction must be drawn between those who
attempt suicide - deliberate self-harm (DSH) - and those
who succeed (suicides): .- -. > - -
The majority of cases of DSH occur in people under
35 years of age.
The majority of suicides occur in people aged over 60.
Suicides are more common in men, while DSH is more
common in women.
Suicides are more common in older men, although
rates are falling. Rates in young men are rising fast
throughout the UK and Western Europe.
Suicides in women are slowly falling in the UK.
Approximately 90% of cases of DSH involve self-
poisoning.
A formal psychiatric disorder is common retrospectively
in suicide, but unusual in DSH.
There is, however, an overlap between DSH and suicide.
Between 1-2% of people who attempt suicide will kill
themselves in the year following DSH. The risk of suicide
stays elevated in those with DSH, with 0.5% per annum
committing suicide in the following 20 years. In the UK,
over 100 000 suicide attempts are made each year, and the
overwhelming majority of these are seen and treated
within accident and emergency departments.
Table 22.11 Factors that increase the risk of suicide
 SUICIDE AND ATTEMPTED
SUICIDE (DELIBERATE
SELF-HARM) (see also p. 1002)
Suicide accounts for 2% of male and 1% of female deaths
in England and Wales each year, equivalent to a rate of
8 per 100 000. The rate increases with age, peaking for
women in their sixties and for men in their seventies.
Suicide is the second most common cause of mortality in
15- to 34-year-olds. Approximately 15% of people who
have suffered a severe depressive disorder (requiring
Male sex
Older age
Living alone
Immigrant status
Recent bereavement, separation or divorce
Recent loss of a job or retirement
Living in a socially disorganized area
Family history of affective disorder, suicide or alcohol abuse
Previous history of affective disorder, alcohol or drug abuse
Previous suicide attempt
Addiction to alcohol or drugs
Severe depression or early dementia
Incapacitating painful physical illness
1296
The anxiety disorders
. The guidelines (Box 22.10) for the assessment of such
patients will help ensure that the risk factors relating to THE ANXIETY DISORDERS
suicide are covered. Indications for referral to a psychi- Psychiatric disorder Physical disorder
atrist before discharge from hospital are also given. These are conditions in which anxiety dominates the
In general, it is worth trying to interview a family clinical symptoms. They are classified according to
member or close friend and check these points with them. whether the anxiety is persistent (general anxiety) or
Requests for immediate represcription on discharge episodic, with the episodic conditions classified according
should be denied, except in cases of essential medication to whether the episodes are regularly triggered by the
(e.g. for epilepsy). In such cases, however, only 3 days' same cue (phobia) or not (panic disorder). The differential
supply of medication should be given, and the patient diagnoses of anxiety disorders are given in Table 22.12.
should be requested to report to their general practitioner
or to their psychiatric outpatient clinic for further
General anxiety disorder
supplies. Occasionally involuntary admission under the
Mental Health Act (1983) will be required (p. 1314). This occurs in 4% of the population and is more common
in women. Symptoms are persistent and often chronic.
General anxiety disorder (GAD) and its related panic
FURTHER READING
Kim WJ, Singh T (2004) Trends and dynamics of youth disorder are differential diagnoses for medically un-
suicides in developing countries. Lancet 363: 1090- explained symptoms, owing to the many physical symp-
1091. toms that are caused by these conditions.
Maris RW (2002) Suicide. Lancet 360: 319-326.
Clinical features
The physical and psychological symptoms are outlined in
Box 22.10 Guidelines for the assessment of Table 22.13. The patient looks worried, has a tense
patients who harm themselves posture, restless behaviour, a pale and sweaty skin. The
Questions to ask: be concerned if positive answer
Depressive illness Obsessive Hyperthyroidism
ft Was there a clear precipitant/cause for the attempt?
Was the act premeditated or impulsive? Table 22.12 Anxiety disorders - the differential
m Did the patient leave a suicide note? diagnosis
* Had the patient taken pains not to be discovered?
6 Did the patient make the attempt in strange compulsive disorder Presenile Hypoglycaemia
surroundings (i.e. away from home)? i dementia Alcohol dependence Phaeochromocytoma
Would the patient do it again? Drug dependence
Nervous system
.*sOther relevant factors Benzodiazepine withdrawal
Fatigue Blurred vision
Has the precipitant or crisis resolved? Dizziness Headache
Physical symptoms
K Is there continuing suicidal intent? Sleep disturbance
Castroin testinal
B Does the patient have any psychiatric symptoms? Dry mouth
m What is the patient's social support system? Difficulty in swallowing
* Has the patient inflicted self-harm before? Psychological symptoms
Epigastric discomfort
B Has anyone in the family ever taken their life?
Table 22.13 Physical and psychological symptoms of
B Does the patient have a physical illness?
anxiety
Indications for referral to a psychiatrist
Absolute indications include: Aerophagy Apprehension and fear
Clinical depression 'Diarrhoea' (usually frequency) Irritability
Psychotic illness of any kind - Clearly preplanned Difficulty in concentrating
Respiratory
suicidal attempts which were not Distractability
Feeling of chest constriction
intended to be discovered Persistent suicidal intent Restlessness
Difficulty in inhaling
(the more detailed the plans, Sensitivity to noise
Overbreathing
the more serious the risk) Depersonalization
1
i A violent method used. Cardiovascular Derealization
Palpitations
Other common indications include:
Awareness of missed beats
Alcohol and drug abuse Patients over 45 years,
Feeling of pain over heart
especially if male, and young
adolescents Genitourinary
Those with a family history of suicide in first-degree Increased frequency
relatives Failure of erection
K Those with serious (especially incurable) physical Lack of libido
disease
m. Those living alone or otherwise unsupported t Those in
whom there is a major unresolved crisis ft Persistent
suicide attempts B Any patients who give you cause for
concern.
1297
Psychological medicine
 Box 22.11 The hyperventilation syndrome
Features
Panic attacks - fear, terror and impending doom
-accompanied by some or all of the following:
dyspnoea (trouble getting a good breath in)
palpitations A chest pain or discomfort
* choking sensation
dizziness
paraesthesiae
* sweating
carpopedal spasms.
Cause
Overbreathing leading to a decrease in Paco2 and an increase
in arterial pH.
Diagnosis
i A provocation test - voluntary overbreathing for 2-3
minutes - provokes similar symptoms; rebreathing from
a large paper bag relieves them. Blood gases
Management
f Explanation and reassurance is given.
* The patient is trained in relaxation techniques and
slow breathing.
1
The patient is asked to breathe into a closed paper
bag.
patient takes time to go to sleep, and when asleep wakes
intermittently with worry dreams. Associated conditions
include the hyperventilation syndrome, which is even
more common in panic disorder (Box 22.11). The patient
will sigh deeply, particularly when talking about the
stresses in their life.
Mixed anxiety and depressive disorder
This disorder is probably the commonest mood disorder
in primary care, in which there are equal elements of both
anxiety and depression, showing how closely associated
these two abnormal mood states are.
Panic disorder
Panic disorder is diagnosed when the patient has
repeated sudden attacks of overwhelming anxiety,
accompanied by severe physical symptoms, usually
related to both hyperventilation (Box 22.11) and
sympathetic nervous system activity. The prevalence is
1%. Patients with panic disorder often have catastrophic
illness beliefs during the panic attack, such as convictions
that they are about to die from a stroke or heart attack, or
that they suffer from multiple sclerosis (MS). The fear of a
stroke is related to dizziness and headache. Fear of a heart
attack accompanies chest pain (atypical chest pain), and
the fear of MS follows paraesthesiae.
Aetiology
General anxiety and panic disorder occurs four or more
times as commonly in first-degree relatives of affected
Box 22.12 Phobias
A phobia is an abnormal fear and avoidance of an
everyday object or situation. Phobias are common
(8% prevalence), disabling, and
treatable with behaviour therapy.
patients, suggesting a genetic influence. Sympathetic
nervous system overactivity, increased muscle tension
and hyperventilation are the common pathophysiological
mechanisms. Psychodynamic theory suggests that
anxiety is the emotional response to the threat of a loss,
whereas depression is the response to the loss itself. There
is some evidence that being bullied, with the explicit
threats involved, leads to anxiety disorders in young
people.
Phobic (anxiety) disorders
Phobias are common conditions in which intense fear is
triggered by a single stimulus, or set of stimuli, that are
predictable and normally cause no particular concern to
others (e.g. agoraphobia, claustrophobia, social phobia).
This leads to avoidance of the stimulus (see Box 22.12).
The patient knows that the fear is irrational, but cannot
control it. The prevalence of all phobias is 8%, with many
patients having more than one. Many phobias of
'medical' stimuli exist (e.g. of doctors, dentists, hospitals,
vomit, blood and injections) which affect the patient's
ability to receive adequate healthcare.
Aetiology
Phobias may be caused by classical conditioning, in
which a response (fear and avoidance) becomes con-
ditioned to a previously benign stimulus (a lift) often
after an initiating shock (being stuck in a lift). In children,
phobias can arise through imagined threats (e.g. stories of
ghosts told in the playground). Women have twice the
prevalence of most phobias than men. Phobias aggregate
in families, but genetic factors are probably weak.
Agoraphobia
Translated as 'fear of the market place', this common
phobia (4% prevalence) presents as a fear of being away
from home, with avoidance of travelling, walking down a
road, and shops being common presentations. This can be
a very disabling condition, since the patient can be too
unwell to ever leave home, particularly by themselves. It
is often associated with claustrophobia, a fear of enclosed
spaces. ....... ......
Social phobia
This is the fear and avoidance of social situations: crowds,
strangers, parties and meetings. Public speaking would
be the sufferer's worst nightmare. It is suffered by 2% of
the population.
Simple phobias
The commonest is the phobia of spiders (arachnophobia),
particularly in women. The prevalence of simple phobias
1298
ie anxiety disorders
is 7% in the general population. Other common phobias
include insects, moths, bats, dogs, snakes, heights,
thunderstorms and the dark. Children are particularly
phobic about the dark, ghosts and burglars, but the large
majority grow out of these fears.
Treatment of anxiety disorders
Psychological treatments
For many people with brief episodes of an anxiety dis-
order, a discussion with a doctor concerning the nature of
anxiety is usually sufficient.
Relaxation techniques can be effective in mild/
moderate anxiety. This can be achieved in many ways,
including complementary techniques such as medi
tation and yoga. Conventional relaxation training
involves slow breathing, muscle relaxation, and
mental imagery.
Anxiety management training involves two stages. In the
first stage, verbal cues and mental imagery are used to
arouse anxiety. In the second stage, the patient is
trained to reduce this anxiety by relaxation, distraction
and reassuring self-statements.
Biofeedback is useful for showing patients that they are
not relaxed, even when they fail to recognize it, having
become so used to anxiety. Biofeedback involves
feeding back to the patient a physiological measure
that is abnormal in anxiety. These measures may
include electrical resistance of the skin of the palm,
heart rate, muscle electromyography, or breathing
pattern.
Behaviour therapies are treatments derived from
experimental psychology that are intended to change
behaviour and thus symptoms. The most common and
successful behaviour therapy (with 80% success in
some phobias) is graded exposure, otherwise known as
systematic desensitization. This is the treatment of choice
for a phobia. Firstly, the patient rates the phobia into a
hierarchy or 'ladder' of worsening fears (e.g. in
agoraphobia: walking to the front door with a coat on;
walking out into the garden; walking to the end of the
road). Secondly, the patient practises exposure to the
least fearful stimulus until no fear is felt. The patient
then moves 'up the ladder' of fears until they are
cured.
Cognitive behaviour therapy (CBT) (see p. 1293) is the
treatment of choice for panic disorder and general
anxiety disorder because the therapist and patient
need to identify the mental cues (thoughts and
memories) that may subtly provoke exacerbations of
anxiety or panic attacks. CBT also allows identification
and alteration of the patient's 'schema', or way of
looking at themselves and their situation, that feeds
anxiety.
Drug treatments
Drugs used in the treatment of anxiety can be divided
into two groups: those that act primarily on the centra)
nervous system, and those that block peripheral
autonomic receptors.
Table 22.14 Withdrawal syndrome with
benzodiazepines
Insomnia
Anxiety
Tremulousness
Muscle twitchings
Perceptual distortions
Hypersensitivities (light, sound, touch)
Convulsions
Benzodiazepines are centrally acting anxiolytic drugs.
They bind to specific receptors that stimulate release of
the inhibitory transmitter y-aminobutyric acid (GABA).
Diazepam (5 mg twice daily, up to 10 mg three times
daily in severe cases) and chlordiazepoxide have
relatively long half-lives (20^10 hours) and are used as
anti-anxiety drugs in the short term. Side-effects
include sedation and memory problems, and patients
should be advised not to drive while on treatment.
They can cause dependence and tolerance within
4-6 weeks, particularly in dependent personalities.
The withdrawal syndrome (Table 22.14) can occur
after just 3 weeks of continuous use and is particularly
severe when high doses have been given for a longer
time. Thus, if a benzodiazepine drug is prescribed for
anxiety, it should be given in as low a dose as possible
and for not more than 2 weeks continuously. A with-
drawal programme from chronic use includes changing
the drug to the long-acting diazepam, followed by a
very gradual reduction in dosage.
Buspirone (5-10 mg three times daily) is a 5-HT 1A
partial agonist that is anxiolytic after 2 weeks of treat
ment. It is not yet established as a treatment in the UK.
It does not seem to help panic disorder.
Most SSRIs (e.g. paroxetine, sertraline, citalopram),
venlafaxine, MAOIs (phenelzine) and moclobemide (a
RIMA) are useful symptomatic treatments for general
anxiety and panic disorders, as well as some phobias
(social phobia). Imipramine is an established symp
tomatic treatment for panic disorder, and other
tricyclics such as amitriptyline and clomipramine are
probably equally effective. Treatment response is often
delayed several weeks; a trial of treatment should last
3 months.
Many of the symptoms of anxiety are due to an
increased or sustained release of epinephrine
(adrenaline) and norepinephrine (noradrenaline) from
the adrenal medulla and sympathetic nerves. Thus,
beta-blockers such as propranolol (20-40 mg two or three
times daily) are effective in reducing peripheral
symptoms such as palpitations, tremor and tachycardia,
but do not help central symptoms such as anxiety.
Acute stress reactions and adjustment
disorders
Acute stress reaction
This occurs in individuals without any other psychiatric
disorder, in response to exceptional physical and/ or
1299
Psychological medicine
psychological stress. While severe, such a reaction usually
subsides within hours or days. The stress may be an
overwhelming traumatic experience (e.g. accident, battle,
physical assault, rape) or a sudden change in the social
circumstances of the individual, such as a bereavement.
Individual vulnerability and coping capacity play a role
in the occurrence and severity of an acute stress reaction,
as evidenced by the fact that not all people exposed to
exceptional stress develop symptoms. Symptoms usually
include an initial state of feeling 'dazed' or numb, with
inability to comprehend the situation. This state may be
followed either by further withdrawal from the situation
or by anxiety and overactivity. Autonomic signs of
arousal, including tachycardia, sweating and hyper-
ventilation, are commonly present. The symptoms
usually appear within minutes of the stressor and
disappear within 2-3 days.
Adjustment disorder
This disorder can follow an acute stress reaction and is
common in the general hospital. This is a more prolonged
(up to 6 months) emotional reaction to bad news or a
significant life event, with low mood joining the initial
shock and consequent anxiety, but not of sufficient severity
to fulfil a diagnosis of a mood or anxiety disorder. Sup -
portive counselling is usually a successful treatment,
allowing facilitation of unexpressed feelings, elucidation
of unspoken fears, and education about the likely future.
Pathological (abnormal) grief
This is a particular kind of adjustment disorder. It can be
characterized as excessive and/or prolonged grief, or
even absent grieving with abnormal denial of the
bereavement. Usually the relative will be stuck in grief,
with insomnia and repeated dreams of the dead person,
anger at doctors or even the patient for dying, consequent
guilt in equal measure, and an inability to 'say good-bye'
to the loved person by dealing with their effects. Guided
mourning uses cognitive and behavioural techniques to
allow the relative to stop grieving and move on in life.
Normal grief immediately follows bereavement, is
expressed openly, and allows a person to go through the
social ceremonies and personal processes of bereavement.
The three stages are firstly shock and disbelief, secondly
the emotional phase (anger, guilt and sadness) and
thirdly acceptance and resolution. This normal process of
adjustment may take up to a year, with movement
between all three stages occurring in a sometimes
haphazard fashion. : .'A'~>':-. drop-out from pharmacotherapy is common.
Post-traumatic stress disorder (PTSD)
This arises as a delayed and/ or protracted response to a
stressful event or situation of an exceptionally threaten-
ing nature, likely to cause pervasive distress in almost
anyone. Causes include natural or human disasters, war,
serious accidents, witnessing the violent death of others,
being the victim of sexual abuse, rape, torture, terrorism
or hostage-taking. Predisposing factors such as
personality, previously unresolved traumas, or a history
of psychiatric illness may prolong the course of the
syndrome. These factors are neither necessary nor
sufficient to explain its occurrence, which is most related
to the intensity of the trauma, the proximity of the patient
to the traumatic event, and how prolonged or repeated
it was. Recent functional brain scan research suggests
a possible neurophysiological relationship with OCD
(p. 1301).
Clinical features
The typical symptoms of PTSD include: --
K--
'flashbacks' - repeated vivid reliving of the trauma in
the form of intrusive memories, often triggered by a
reminder of the trauma
insomnia, usually accompanied by nightmares, the
nocturnal equivalent of flashbacks
emotional blunting, emptiness or 'numbness', alternating
with ...
intense anxiety at exposure to events that resemble an
aspect of the traumatic event, including anniversaries
of the trauma
avoidance of activities and situations reminiscent of the
trauma
emotional detachment from other people
hypervigilance with autonomic hyperarousal and an
enhanced startle reaction.
This clinical picture represents the severe end of a
spectrum of emotional reactions to trauma, which might
alternatively take the form of an adjustment or mood
disorder. The course is often fluctuating but recovery can
be expected in two-thirds of cases at the end of the first
year. Complications include depressive illness and alcohol
misuse. In a small proportion of cases the condition may
show a chronic course over many years and a transition
to an enduring personality change.
Treatment and prevention
Compulsory psychological debriefing immediately after a
trauma does not prevent PTSD and may be harmful.
Behaviourally based therapies should be offered for those
with symptoms and CBT is often effective. It can be
normalizing to have therapy in groups with other
patients who have suffered similar trauma. Randomized
controlled trials have now shown that eye movement
desensitization and reprocessing (EMDR) is an effective
treatment for PTSD. SSRIs, venlafaxine and nefazodone
have a place in the management of chronic PTSD, but
The adult consequences of childhood
sexual and physical abuse
Estimates of the prevalence of childhood sexual abuse
(CSA) vary depending on definition but there is reason-
able evidence that 20% of women and 10% of men
suffered significant, coercive and inappropriate sexual
activity in childhood. The abuser is usually a member of
the family or known to the child, and preadolescent girls
are at greatest risk. The likelihood of long-term
consequences is determined by:
1300
The anxiety disorders
 an earlier age of onset
the severity of the abuse
the repeated nature and duration of the period of
abuse
the association with physical abuse.
Consequent adult psychiatric disorders include depress-
ive illness, substance misuse, eating disorders, borderline
personality disorder and deliberate self-harm. Other
negative outcomes include a decline in socio-economic
status, sexual problems, prostitution, and difficulties in
trusting those closest to the patient.
Psychodynamic psychotherapy
Psychodynamic psychotherapy is derived from psycho-
analysis and is based on a number of key analytical
concepts. These include Freud's ideas about psychosexual
development, defence mechanisms, free association as
the method of recall, and the therapeutic techniques of
interpretation, including that of transference, defences
and dreams. Such therapy usually involves once-weekly
50-minute sessions, the length of treatment varying
between 3 months and 2 years. The long-term aim of such
therapy is twofold: symptom relief and personality change.
Psychodynamic psychotherapy is classically indicated in
the treatment of unresolved conflicts in early life, as
might be found in non-psychotic and personality dis-
orders, but to date there is a lack of convincing evidence
concerning its superiority over other forms of treatment.
FURTHER READING
Fricchione G (2004) Generalized anxiety disorders. New
England Journal of Medicine 351: 675-682.
Sher L (2004) Recognising post-traumatic stress
disorder. Quarterly Journal of Medicine 97:1-5.
OBSESSIVE-COMPULSIVE DISORDER
Obsessive-compulsive disorder (OCD) is characterized
by obsessional ruminations and compulsive rituals. It is
particularly associated with and/or secondary to both
depressive illness and Gilles de la Tourette syndrome
(p. 1232). The prevalence is up to 2% in the general
population, although it is probably undiagnosed. There is
an equal distribution by gender, and the mean of onset
ranges from 20-40 years.
Clinical features
The obsessions and compulsions are so persistent and
intrusive that they greatly impede a patient's functioning
and cause considerable distress. There is a constant need
to check that things have been done correctly, and no
amount of reassurance can remove the small amount of
doubt that persists. Some rituals are derived from
superstitions, such as actions repeated a fixed number of
times, with the need to start again if interrupted. When
severe and primary, OCD can last for many years and is
resistant to treatment. However, obsessional symptoms
commonly occur in other disorders, most notably general
anxiety disorder, depressive illness and schizophrenia,
and disappear with the resolution of the primary disorder.
Minor degrees of obsessional symptoms and compul-
sive rituals or superstitions are common in people who
are not ill or in need of treatment, particularly in times of
stress. The mildest grade is that of obsessional personality
traits such as over-conscientiousness, tidiness, punctuality
and other attitudes and behaviours indicating a strong
tendency towards conformity and inflexibility. Such
individuals are perfectionists who are intolerant of
shortcomings in themselves and others, and take pride in
their high standards. When such traits are so marked that
they dominate other aspects of the personality, in the
absence of clear-cut OCD, the diagnosis is obsessional
(anankastic) personality (see p. 1313).
Aetiology
Genetic
OCD is found in 5-7% of the first-degree relatives. Twin
studies showed a 80-90% concordance in monozygotic
twins and about 50% in dizygotic twins.
Basal ganglia dysfunction
OCD is associated with a number of neurological dis-
orders involving dysfunction of the striatum, including
Parkinson's disease, Sydenham's and Huntington's
chorea. OCD can follow head trauma. Neuroimaging
suggests that abnormalities exist in the frontal lobe and
basal ganglia (Fig. 22.4). Hyperactivity of the orbitofrontal
cortex has been a consistent finding in brain imaging
research on OCD patients. The PET images shown here
are from the initial report of this finding by a research
group at the University of California at Los Angeles.
Other work suggests the caudate nucleus is smaller than
in healthy controls.
Serotonin
Serotonin function is probably abnormal in patients with
OCD. Serotonin reuptake inhibitors are effective drugs.
Postsynaptic serotonin receptor hypersensitivity may
follow chronically low levels of synaptic serotonin.
Fig. 22.4 PET images of (left) a normal patient and (right)
an obsessive-compulsive disorder (OCD) patient. The right
image shows the hyperactivity of the orbitofrontal cortex which
is a consistent finding in this condition. Baxter R et al. Archives
of General Psychiatry 44: 211, with permission.
1301
Psychological medicine
Conditioning
This suggests that compulsive rituals are classically
conditioned avoidance responses, which therefore lend
themselves to treatment with graded exposure therapy.
Treatment
Psychological treatments
A behaviour therapy that is particularly effective for
rituals is response prevention. Patients are instructed not to
carry out their rituals. There is an initial rise in distress
but with persistence both the rituals and the distress
diminish. Patients are encouraged to practise response
prevention, while returning to situations that normally
make them worse.
Modelling involves the therapist demonstrating to the
patient what is required and encouraging the patient to
follow this example. In the case of hand-washing rituals,
this might involve holding an allegedly contaminated
object and carrying out other activities without washing,
the patient being encouraged to follow suit.
Thought stopping can reduce obsessional ruminations.
The patient is taught to arrest the obsessional thought by
arranging a sudden intrusion (e.g. snapping an elastic
band, clicking the fingers).
Cognitive behaviour therapy involves exposure to the
provocative stimulus plus cognitive therapy.
Physical treatment
Anxiolytic drugs provide short-term symptomatic relief
for overwhelming anxiety on a short-term basis.
Selective serotonin reuptake inhibitors are the mainstay
of drug treatment. Their efficacy is independent of their
antidepressant action but the doses required are usually
some 50-100% higher than those effective in depression.
Three months' treatment with high doses may be neces -
sary for a positive response. Positive correlations between
reduced severity of OCD and decreased orbitofrontal and
caudate metabolism following behavioural and SSRI
treatments have been demonstrated in a number of
studies. Clomipramine is the tricyclic most commonly
used in the UK.
Psychosurgery
Psychosurgery is very occasionally recommended in cases
of chronic and severe OCD that has not responded to other
treatments. The development of stereotactic techniques has
led to the replacement of the earlier, crude leucotomies with
more precise surgical interventions such as subcaudate
tractotomy and cingulotomy, with small yttrium radio-
active implants, which induce lesions in the cingulate area
or the ventromedial quadrant of the frontal lobe.
Psychosurgery is performed only in a few specialist centres
in the UK, and formal and detailed consent requirements
are laid down in the appropriate mental health act.
Prognosis
Two-thirds of cases improve within a year. The remainder
run a fluctuating or persistent course. The prognosis is
worse when the personality is anankastic and the OCD is
primary and severe. , ..........
FURTHER READING
Jenike MA (2004) Obsessivecompulsive disorder. New
England Journal of Medicine 350: 259-265.
ALCOHOL MISUSE AND
DEPENDENCE
A wide range of physical, social and psychiatric problems
are associated with excessive drinking. Alcohol misuse
occurs when a patient is drinking in a way that regularly
causes problems to the patient or others.
The problem drinker is one who causes or experiences
physical, psychological and/ or social harm as a con
sequence of drinking alcohol. Many problem drinkers,
while heavy drinkers, are not physically addicted to
alcohol.
Heavy drinkers are those who drink significantly more
in terms of quantity and/or frequency than is safe to
do so long term.
Binge drinkers are those who drink excessively in short
bouts, usually 24-48 hours long, separated by often
quite lengthy periods of abstinence. Their overall
monthly or weekly alcohol intake may be relatively
modest.
Alcohol dependence is defined by a physical dependence
on or addiction to alcohol. The term 'alcoholism' is a con
fusing one with off-putting connotations of vagrancy,
'meths' drinking and social disintegration. It has been
replaced by the term 'alcohol dependence syndrome'.
Epidemiology of alcohol misuse
A survey of drinking in England and Wales found that
15% of men admitted drinking more than 35 units per
week and 4% of women drank more than 25 units per
week. In the survey, 4% of men and 2% of women
reported alcohol withdrawal symptoms.
Approximately one in five male admissions to acute
medical wards are directly or indirectly due to alcohol.
Between 33^40% of accident and emergency attenders
have blood alcohol concentrations above the present UK
legal limit for driving. People with serious drinking
problems have a two to three times increased risk of
dying compared to members of the general population of
the same age and sex.
Table 22.15 provides an approximate estimate of what
can be expected in an average individual in the way of
behavioural impairment resulting from a particular blood
alcohol level. The usual drink (1 unit of alcohol: V 2 pint of
ordinary beer (3.5%), a pub measure of wine) contains
about 8 g of absolute alcohol and raises the blood alcohol
concentration by about 15-20 mg/dL, the amount that is
metabolized in 1 hour.
Detection
Alcohol misuse should be suspected in any patient
presenting with one or more physical problems commonly
associated with excessive drinking (see p. 263). Alcohol
1302
Alcohol misuse and dependence
22
 Table 22.15 Approximate correlation between blood
alcohol level and behavioural/motor impairment
Rising blood alcohol Expected effect
(mg/dL)
20-99 Impaired coordination, euphoria
100-199 Ataxia, poor judgement, labile
mood
200-299 Marked ataxia and slurred
speech; poor judgement,
labile mood, nausea and
vomiting
300-399 Stage 1 anaesthesia, memory
lapse, labile mood
400+ Respiratory failure, coma, death
Table 22.16 Common alcohol-related psychological and
social problems
Psychological Social
Depression Anxiety and Marital and sexual difficulties
phobias Memory Family problems Child abuse
disturbances Personality
Employment problems
disturbances Delirium Financial difficulties Accidents
tremens Attempted at home,
suicide Pathological
jealousy
on the roads, at work
Delinquency and crime
Homelessness
withdrawal and compulsive drug-taking behaviour', the
essential element of which is the continued use of the
substance despite significant substance-related problems.
Figure 22.5 outlines the main characteristics of the syndrome
but these do not necessarily present in any particular order.
Symptoms of alcohol dependence in a typical order of
occurrence are shown in Table 22.17. Diagnostic criteria for
alcohol withdrawal syndrome are shown in Table 22.18.
Rapid reinstatement of
syndrome on drinking after
period of abstinence
Relief from or avoidance
of withdrawal symptoms
by further drinking
Withdrawal symptoms, 'bad
nerves', shakiness,
The subjective and blackouts
awareness
through to deliriumto tremens
of a compulsion drink
A narrowing of the
drinking repertoire
Primacy of drinking
over other activities
Increased tolerance to alcohol. Need
for more alcohol to achieve same
results
 Fig. 22.5 Elements of the alcohol-dependence
misuse may also be associated with a number of
syndrome.
psychiatric symptoms/disorders and social problems
(Table 22.16).

Guidelines Unable to keep a drink limit

The patient's frequency of drinking and quantity drunk Difficulty in avoiding
during a typical week should be established. Alcohol con- getting drunk Spending a
sumption can be assessed on the basis of units of alcohol. considerable
time drinking Missing
Drinking up to 21 units of alcohol a week for men and meals Memory lapses,
14 units for women carries no long-term health risk. blackouts Restless without
There is unlikely to be any long-term health damage drink Organizing day around
with 21-35 units (men) and 14-25 units (women), drink
provided the drinking is spread throughout the week. Table 22.17 Symptoms of alcohol dependence
Beyond 36 units a week in men and 24 units a week in Trembling after drinking the
women, damage to health becomes increasingly likely. day before Morning
Drinking above 50 units a week in men (35 units in retching and
women) is a definitive health hazard. .... vomiting Sweating
excessively at
Diagnostic markers of alcohol misuse night
Laboratory parameters indicating alcohol misuse are Withdrawal fits Morning
drinking Increased tolerance
often called markers of recent alcohol misuse. Elevated
Hallucinations, frank
y-glutamyl transpeptidase (y-GT) and mean corpuscular delirium tremens
volume (MCV) may indicate alcohol excess in the last few
weeks. Blood or breath alcohol are useful tests in anyone
suspected of very recent drinking. Table 22.18 Diagnostic criteria for alcohol withdrawal
syndrome
Alcohol dependence syndrome Any three of the following:
__________________________________ Tremor of outstretched hands, tongue or eyelids
Sweating
DSM-IV TR describes dependence as 'a pattern of repeated
Nausea, retching or vomiting
self-administration that usually results in tolerance, Tachycardia or hypertension
Anxiety
Psychomotor agitation
Headache
Insomnia
Malaise or weakness
Transient visual, tactile or auditory hallucinations or illusions
Grand mal convulsions
1303
Psychological medicine
The course of the alcohol dependence
syndrome
About 25% of all cases of alcohol misuse will lead to
chronic alcohol dependence. This most commonly ends in
social incapacity, death or abstinence. Alcohol depen-
dence syndrome usually develops after 10 years of
heavy drinking (3-i years in women). In some indivi-
duals who use alcohol to alter consciousness, obliterate
conscience and defy social canons, dependence and
apparent loss of control may appear in only a few months
or years.
Delirium tremens (DTs)
Delirium tremens is the most serious withdrawal state
and occurs 1-3 days after alcohol cessation, so is com-
monly seen a day or two after admission to hospital.
Patients are disorientated, agitated, and have a marked
tremor and visual hallucinations (e.g. insects or small
animals coming menacingly towards them). Signs
include sweating, tachycardia, tachypnoea and pyrexia.
Complications include dehydration, infection, hepatic
disease or the Wernicke-Korsakoff syndrome (p. 245).
Causes of alcohol dependence
Genetic factors. Sons of alcohol-dependent people who
are adopted by other families are four times more likely to
develop drinking problems than are the adopted sons of
non-alcohol misusers. Genetic markers include dopamine-
2 receptor allele Al, alcohol dehydrogenase subtypes and
monoamine oxidase B activity, but they are not specific.
Environmental factors. A Boston follow-up study
showed that one in ten boys who grew up in a household
where neither parent misused alcohol subsequently
became alcohol dependent, compared with one in four of
those reared by alcohol-misusing fathers and one in three
of those reared by alcohol-misusing mothers.
Biochemical factors. Several factors have been sug-
gested, including abnormalities in alcohol dehydrogenase,
neurotransmitter substances and brain amino acids, such
as GABA. There is no conclusive evidence that these or
other biochemical factors play a causal role.
Psychiatric illness. This is an uncommon cause of
addictive drinking but it is a treatable one. Some
depressed patients drink excessively in the hope of
raising their mood. Patients with anxiety states or
phobias are also at risk.
Excess consumption in society. The prevalence of
alcohol dependence and problems correlates with the
general level (per capita consumption) of alcohol use in a
society. This, in turn, is determined by factors that may
control overall consumption - including price, licensing
laws, the number and nature of sales outlets, and the
customs of society concerning the use and misuse of .
alcohol.
Treatment
Psychological treatment of problem drinking
Successful identification at an early stage can be a helpful
intervention in its own right. It should lead to:
the provision of information concerning safe drinking
levels
a recommendation to cut down where indicated
simple support and advice concerning associated
problems.
Successful alcohol counselling involves motivational
enhancement {motivational therapy), feedback, education
about adverse effects of alcohol, and agreeing drinking
goals. A motivational approach is based on five stages of
change: precontemplation, contemplation, determination,
action and maintenance. The therapist uses motivational
interviewing and reflective listening to allow the patient
to persuade himself along the five stages to change.
This technique, cognitive behaviour therapy and 12-
step facilitation (as used by Alcoholics Anonymous (AA))
have all been shown to reduce harmful drinking. With
addictive drinking, self-help group therapy, which
involves the long-term support by fellow members of the
group (e.g. AA), is helpful in maintaining abstinence.
Family and marital therapy involving both the alcohol
misuser and spouse may also be helpful. . '; -.
Drug treatments of problem drinking
Alcohol withdrawal and DTs
Addicted drinkers often experience considerable diffi-
culty when they attempt to reduce or stop their drinking.
Withdrawal symptoms are a particular problem and
delirium tremens needs urgent treatment (Box 22.13). In
the absence of DTs, alcohol withdrawal can be treated on
an outpatient basis, using one of the fixed schedules in
Box 22.13, so long as the patient attends daily for medi-
cation and monitoring, and has good social support.
Outpatient schedules are sometimes given over 5 days.
Long-term treatment with benzodiazepines should not be
prescribed in those patients who continue to misuse
alcohol. Many alcohol misusers add dependence on
diazepam or clomethiazole to their problems.
Drugs for prevention of alcohol dependence
Naltrexone, the opioid antagonist (50 mg per day), reduces
the risk of relapse into heavy drinking and the frequency
of drinking. Acamprosate (1-2 g per day) acts on several
receptors including those for GABA, norepinephrine
(noradrenaline) and serotonin. There is good evidence
that it reduces drinking frequency. Neither drug seems
particularly helpful in maintaining abstinence. Both drug
effects are enhanced by combining them with
counselling.
Drugs such as disulfiram react with alcohol to cause
unpleasant acetaldehyde intoxication and histamine
release. A daily maintenance dose means that the patient
must wait until the disulfiram is eliminated from the
body before drinking safely. There is mixed evidence of
efficacy. ,
1304
Drug misuse and dependence
22
 Box 22.13 Management of delirium tremens Table 22.19 Commonly used drugs of misuse and
(DTs) dependence
General measures Stimulants Narcotics
Admit the patient to a medical bed. Correct electrolyte Methylphenidate Morphine
abnormalities and dehydration. Treat any co-morbid Phenmetrazine Heroin
disorder (e.g. infection). Give oral thiamine (200 mg daily) Phencyclidine ('angel dust') Codeine
in the absence of Cocaine Pethidine
Wernicke-Korsakoff (W-K) syndrome. Give parenteral Amfetamine derivates Methadone
thiamine in the presence of a W-K Ecstasy (MDMA)
encephalopathy (NB: beware anaphylaxis). Give
Hallucinogens Tranquillizers
prophylactic phenytoin or carbamazepine, if
previous history of withdrawal fits. Cannabis preparations Barbiturates
Solvents Benzodiazepines
Specific drug treatment Lysergic acid diethylamide (LSD)
One of the following orally: Mescaline
Diazepam 10-20 mg
Chlordiazepoxide 30-60 mg
Lorazepam 2-4 mg.
Repeat 1 hour after last dose depending on response.
Causes of drug misuse
Fixed-schedule regimens There is no single cause of drug misuse and/or depen-
Diazepam 10 mg every 6 hours for 4 doses, dence. Three factors appear commonly, in a similar way
then 5 mg 6-hourly for 8 doses OR
to alcohol problems:
Chlordiazepoxide 30 mg every 6 hours for 4 doses,
then 15 mg 6-hourly for 8 doses OR the availability of drugs
Lorazepam 2 mg every 6 hours for 4 doses, then 1 a vulnerable personality
mg 6-hourly for 8 doses. Provide additional social pressures, particularly from peers.
benzodiazepine when symptoms and signs are not
controlled. Once regular drug-taking is established, pharmacological
factors determine dependence.
 One trial has suggested that fluoxetine is helpful in the
treatment of patients who have both a depressive illness
and alcohol dependence.
Outcome
Research suggests that 30-50% of alcohol-dependent
drinkers are abstinent or drinking very much less up to
2 years following traditional intervention. It is too early to
be certain of the long-term outcome of patients treated
with the latest psychological and pharmacotherapies.
FURTHER READING
Fiellin DA, Reid MC, O'Connor PG (2000) New
therapies for alcohol problems: application to
primary care. American Journal of Medicine 108:
227-237.
Kasten TR, O'Connor PG (2003) Management of drug and
alcohol withdrawal. New England Journal of Medicine
348:1786-1795.
Mayo-Smith MF (1997) Pharmacological management of
alcohol withdrawal: a meta-analysis and evidence-
based practice guideline. Journal of the American
Medical Association 278: 144-151.
DRUG MISUSE AND
DEPENDENCE
In addition to alcohol and nicotine, there are a number of
psychotropic substances that are taken for their effects on
mood and other mental functions (Table 22.19).
Solvents
One per cent of adolescents in the UK sniff solvents for
their intoxicating effects. Tolerance develops over weeks
or months. Intoxication is characterized by euphoria,
excitement, a floating sensation, dizziness, slurred speech
and ataxia. Acute intoxication can cause amnesia and
visual hallucinations. About 300 teenagers die in the UK
each year from asphyxiation or acute poisoning.
Amfetamines and related substances
These have temporary stimulant and euphoriant effects
that are followed by fatigue and depression, with the
latter sometimes prolonged for weeks. Psychological
rather than true physical dependence is the rule
with 'Speed'. In addition to a manic-like presentation,
amfetamines can produce a paranoid psychosis indis-
tinguishable from acute paranoid schizophrenia.
Ecstasy
'Ecstasy' (E, white burger, white dove) is the street name
for 3,4-methylenedioxy-methamfetamine (MDMA), a
psychoactive phenylisopropylamine, synthesized as an
amfetamine derivative. It is a psychodelic drug which is
often used as a 'dance' drug'. It has a brief duration of
action (4-6 hours). There is evidence that repeated use of
MDMA can cause permanent neurotransmittei cVianges
in the brain. Deaths have been reported from malignant
hyperpyrexia and dehydration. Acute renal and liver
failure can occur.
1305
Psychological medicine
Cocaine Table 22.20 Opiate withdrawal syndrome
Cocaine is a central nervous system stimulant (with Yawning
similar effects to amfetamines) derived from Erythroxylon Rhinorrhoea
coca trees grown in the Andes. In purified form it may be Lacrimation
Pupillary dilatation 12-16 hours after last dose of opiate
taken by mouth, sniffed or injected. If cocaine hydro-
Sweating
chloride is converted to its base ('crack') it can be smoked. Piloerection
This causes an intense stimulating effect and 'free-basing' Restlessness
is common. Compulsive use and dependence occur more
frequently among users who are free-basing. Dependent Muscular twitches
users take large doses and alternate between the with- Aches and pains
drawal phenomena of depression, tremor and muscle Abdominal cramps
pains, and the hyperarousal produced by increasing doses. Vomiting
Diarrhoea
Prolonged use of high doses produces irritability, restless-
Hypertension 24-72 hours after last dose of opiate
ness, paranoid ideation and occasionally convulsions.
Insomnia
Persistent sniffing of the drug can cause perforation of the Anorexia
nasal septum. Overdoses cause death through myocardial Agitation
infarction, hyperthermia and arrhythmias (p. 1011). Profuse sweating
Weight loss
Hallucinogenic drugs
Hallucinogenic drugs, such as lysergic acid diethylamide
(LSD) and mescaline, produce distortions and intensifi
cations of sensory perceptions, as well as frank halluci
nations in acute intoxication. Psychosis is a long-term
complication.
Cannabis
Cannabis (grass, pot, spliff, reefer) is a drug widely used
in some subcultures. It is derived from the dried leaves
and flowers of the plant Cannabis sativa. It can cause toler-
ance and dependence. Hashish is the dried resin from the
flower tops whilst marijuana refers to any part of the
plant. The drug, when smoked, seems to exaggerate the
pre-existing mood, be it depression, euphoria or anxiety.
It may have specific analgesic properties. An
amotivational syndrome has been reported with chronic
daily use. Cannabis may of itself sometimes cause
psychosis in the right circumstances (see below).
Tranquillizers ________________
Drugs causing dependence include barbiturates and
benzodiazepines. Benzodiazepine dependence is com-
mon and may be iatrogenic, when the drugs are prescribed
and not discontinued. Discontinuing treatment with
benzodiazepines may cause withdrawal symptoms (see
Table 22.14). For this reason, withdrawal should be
supervised and gradual.
Opiates
Physical dependence occurs with morphine, heroin and
codeine as well as with synthetic and semisynthetic opiates
such as methadone and pethidine. These substances
display cross-tolerance - the withdrawal effects of one are
reduced by administration of one of the others. The
psychological effect of such substances is of a calm,
slightly euphoric mood associated with freedom from
physical discomfort and a flattening of emotional
response. This is believed to be due to the attachment of
morphine and its analogues to receptor sites in the CNS
normally occupied by endorphins. Tolerance to this
group of drugs is rapidly developed and marked, but is
rapidly lost following abstinence. The opiate withdrawal
syndrome consists of a constellation of signs and
symptoms (Table 22.20) that reaches peak intensity on the
second or third day after the last dose of the opiate. These
rapidly subside over the next 7 days. Withdrawal is
dangerous in patients with heart disease or other chronic
debilitating conditions.
Opiate addicts have a relatively high mortality rate,
owing to both the ease of accidental overdose and the
blood-borne infections associated with shared needles.
Heart disease (including infective endocarditis), tuber-
culosis and AIDS are common causes of death, while
tetanus, malaria and the complications of hepatitis B and
C are also common.
Treatment of chronic misuse
Blood and urine screening for drugs are required in
circumstances where drug misuse is suspected (Table
22.21). When a patient with an opiate addiction is
admitted to hospital for another health problem, advice
should be sought from a psychiatrist or the patient's drug
Table 22.21 Length of time urine toxicology screens are
likely to remain positive after abstinence
Substance Usual time positive
Amfetamines 48 hours
Barbiturates
Short-acting 24 hours
Long-acting 7+ days
Benzodiazepines 3+ days
Cannabinols 5+ days
Cocaine 3+ days
Codeine 48 hours
Morphine 48 hours
1306
Schizophrenia
clinic regarding management of their addiction while an
inpatient.
The treatment of chronic dependence is directed
towards helping the patient to live without drugs. Patients
need help and advice in order to avoid a withdrawal
syndrome. Alternatively, patients can be helped to
minimize harm to themselves and others. Some patients
with opiate addiction who cannot manage such a regimen
may be maintained on oral methadone. In the UK, only
specially licensed doctors may legally prescribe heroin
and cocaine to an addict for maintenance treatment of
addiction. An overdose should be treated immediately
with the opioid antagonist naloxone.
Drug psychoses
Drug-induced psychoses have been reported with
amfetamine and its derivatives, cocaine, and hallucinogens.
It can occur acutely after drug use, but is more usually
associated with chronic misuse. Psychoses are charac-
terized by vivid hallucinations (usually auditory, but
often in more than one sensory modality), mis-
identifications, delusions and/or ideas of reference (often
of a persecutory nature), psychomotor disturbances
(excitement or stupor) and an abnormal affect. ICD-10
requires that the condition occurs within 2 weeks and
usually within 48 hours of drug use and that it should
persist for more than 48 hours but not more than
6 months.
Cannabis use can result in acute anxiety, depression or
hallucinations. Manic-like psychoses occurring after
long-term cannabis use have been described, but seem
more likely to be related to the toxic effects of heavy
ingestion. However, there are now five prospective
studies which suggest, when taken together, that
cannabis doubles the risk of schizophrenia, and that
perhaps 8% of schizophrenia in the UK would be
prevented if cannabis use ceased. This risk is higher in
people taking cannabis early in their lives and heavily.
FURTHER READING
Arsenault L et al. (2004) Causal association between
cannabis and psychosis: examination of the
evidence. British Journal of Psychiatry 184: 110117.
Cami J, Farre M (2004) Drug addiction. New England
Journal of Medicine 349: 975-986.
SCHIZOPHRENIA
The group of illnesses conventionally referred to as
'schizophrenia' is diverse in nature and covers a broad
range of perceptual, cognitive and behavioural disturb-
ances. The point prevalence of the condition is 0.5%
throughout the world, with equal gender distribution. A
physician primarily needs to know how to recognize
schizophrenia, what problems it might present with in
the general hospital, and how it is treated.
Table 22.22 Genetic risk for schizophrenia
General population 1%
Second-degree relative 2.5%
Parent 4%
Sibling 8%
Child of one affected parent 12%
Child of two affected parents 30-40%
Dizygotic twin 8-19%
Monozygotic twin 40-60%
Causes
No single cause has been identified. Schizophrenia is
likely to be a disease of neural disconnection caused by an
interaction of genetic and multiple environmental factors
that affect brain development. It is likely that cannabis
use is a risk factor. The genetic aetiology is likely to be
polygenic and non-mendelian. Schizophrenia has a
heritability of about 80%. The genetic risk in the general
population and relatives of affected individuals is shown
in Table 22.22. Brain scans and histology often show
ventricular enlargement and disorganized cytoarchitecture
in the hippocampus, supporting the neurodevelopmental
theory of aetiology. Dopamine receptors are upregulated
in the mesolimbic system, but the serotonin system may
also be involved.
Clinical features
The illness can begin at any age but is rare before puberty.
The peak age of onset is in the early twenties. The symp-
toms that have been considered as diagnostic of the
condition have been termed first rank symptoms and were
described by the German psychiatrist Kurt Schneider.
They consist of:
auditory hallucinations in the third person, and/ or
voices commenting on their behaviour
thought withdrawal, insertion and broadcast
primary delusion
delusional perception
somatic passivity and feelings - patients believe that
thoughts, feelings or acts are controlled by others.
The more of these symptoms a patient has the more likely
the diagnosis is schizophrenia. Other symptoms of acute
schizophrenia include behavioural disturbances, other
hallucinations, secondary (usually persecutory) delusions
and blunting of mood. Schizophrenia is sometimes
divided into 'positive' (type 1) and 'negative' (type 2)
types:
Positive schizophrenia is characterized by acute onset,
prominent delusions and hallucinations, normal brain
structure, a biochemical disorder involving dopaminergic
transmission, good response to neuroleptics, and better
outcome.
Negative schizophrenia is characterized by a slow,
insidious onset, a relative absence oi acute symptoms, the
presence of apathy, social withdrawal, lack of motivation,
underlying brain structure abnormalities, and poor
neuroleptic response.
1307
Psychological medicine
Chronic schizophrenia
This is characterized by long duration and 'negative'
symptoms of underactivity, lack of drive, social with-
drawal and emotional emptiness.
Differential diagnosis
Schizophrenia should be distinguished from:
organic mental disorders (e.g. partial complex epilepsy)
mood (affective) disorders (e.g. mania)
drug psychoses (e.g. amfetamine psychosis)
personality disorders (schizotypal).
In older patients, any acute or chronic brain syndrome
can present in a schizophrenia-like manner. A helpful
diagnostic point is that clouding of consciousness and
disturbances of memory do not occur in schizophrenia,
and visual hallucinations are unusual.
A schizoaffective psychosis describes a clinical presen-
tation in which clear-cut affective and schizophrenic
symptoms coexist in the same episode.
Prognosis
The prognosis of schizophrenia is variable. A review of
treatment studies suggests that 15-25% of people with
schizophrenia recover completely, about 70% will have
relapses and may develop mild to moderate negative
symptoms, while about 10% will become seriously
disabled.
Treatment
The best results are obtained by combining drug and
social treatments.
Antipsychotic (neuroleptic) drugs
These act by blocking the D : and D2 groups of dopamine
receptors. Such drugs are most effective against acute,
positive symptoms and are least effective in the manage-
ment of chronic, negative symptoms. Complete control of
positive symptoms can take up to 3 months, and pre-
mature discontinuation of treatment can result in relapse.
As antipsychotic drugs block both D : and D2 dopamine
receptors, they usually produce extrapyramidal side-
effects. This limits their use in maintenance therapy of
many patients. They also block adrenergic and muscarinic
receptors and thereby cause a number of unwanted
effects (Table 22.23).
An infrequent but potentially dangerous unwanted
effect is the neuroleptic malignant syndrome. This occurs in
0.2% of patients on neuroleptic drugs, particularly the
potent dopaminergic antagonists, e.g. haloperidol. Symp
toms occur a few days to a few weeks after starting
therapy and consist of hyperthermia, muscle rigidity,
autonomic instability (tachycardia, labile BP, pallor) and a
fluctuating level of consciousness. Investigations show a
raised creatine phosphokinase, raised white cell count
and abnormal liver biochemistry. Treatment consists of
stopping the drug and general management, e.g. temper
ature reduction. Bromocriptine enhances dopaminergic
activity and dantrolene will reduce muscle tone but no
treatment has proven benefit. . . . .
Common effects
Motor
Acute dystonia
Parkinsonism
Akathisia Tardive
dyskinesia
Autonomic
Hypotension Failure
of ejaculation
Antimuscarinic
Dry mouth Urinary
retention
Constipation Blurred
vision Metabolic
Weight gain
Table 22.23 Unwanted effects of neuroleptic drugs
Rare effects
Hypersensitivity
Cholestatic jaundice
Leucopenia Skin
reactions
Others
Precipitation of glaucoma
Galactorrhoea Amenorrhoea
Cardiac arrhythmias Seizures
Pregnancy. Data on the potential teratogenicity of
antipsychotic (neuroleptic) medications are still limited.
The disadvantages of not treating during pregnancy have
to be balanced against possible developmental risks to the
fetus. The butyrophenones (e.g. haloperidol) are probably
safer than the phenothiazines. Subsequent management
decisions on dosage will depend primarily on the ability
to avoid side-effects, since the antiparkinsonian agents
are still believed to be teratogenic and should be avoided.
Phenothiazines
Phenothiazines are the group of neuroleptics used most
extensively. Chlorpromazine (100-1000 mg daily) is the
drug of choice when a more sedating drug is required.
Trifluoperazine is used when sedation is undesirable.
Fluphenazine decanoate is used as a long-term prophy-
lactic to prevent relapse, as a depot injection (25-100 mg
i.m. every 1-4 weeks).
Butyrophenones
The butyrophenones (e.g. haloperidol 2-30 mg daily) are
also powerful antipsychotics, used in the treatment of
acute schizophrenia and mania. They are highly likely to
cause a dystonia and/or extrapyramidal side-effects, but
are much less sedating than the phenothiazines. A third of
patients with acute schizophrenia will have a good
response to haloperidol and a further third will make a
partial response.
Atypical antipsychotics
These drugs are 'atypical' in that they block D 2 receptors
less than D a and thus cause fewer extrapyramidal side-
effects and less tardive dyskinesia. They are now being
used as first-line drugs for newly diagnosed schizophrenia.
Clozapine. Clozapine is also used in patients with
intractable schizophrenia who have failed to respond to
at least two conventiona] antipsychotic drugs. This drug
is a dibenzodiazepine with a relative high affinity for D :
compared with D 2 dopamine receptors, muscarinic and
oc-adrenergic receptors. It also blocks 5-HT 2 and 5-HTj
1308
Organic mental disorders
receptors. Functional brain scans have shown that
clozapine selectively blocks limbic dopamine receptors
more than striatal ones, which is probably why it causes
considerably fewer extrapyramidal side-effects.
Clozapine has been shown to exercise a dramatic
therapeutic effect on both intractable positive and nega-
tive symptoms. However, clozapine is expensive and
produces severe agranulocytosis in 1-2% of patients.
Therefore it can only be prescribed in the UK to registered
patients by doctors and pharmacists registered with the
Clozaril patient-monitoring service. The starting dose is
25 mg per day with a maintenance dose of 150-300 mg
daily. White cell counts should be monitored weekly for
18 weeks and then 2-weekly for the length of treatment. In
addition to its antipsychotic actions, clozapine may also
help reduce aggressive and hostile behaviour and the risk
of suicide. It can cause considerable weight gain and
sialorrhoea. There is an increased risk of diabetes mellitus.
Risperidone is a benzisoxazole derivative with combined
dopamine D2 receptor and 5-HT2A-receptor blocking
properties. Dosage ranges from 6-10 mg per day. The
drug is not markedly sedative and the overall incidence
and severity of extrapyramidal side-effects is lower than
with more conventional antipsychotics.
Olanzapine has affinity for 5-HT 2, Dj, D2, D4, and
muscarinic receptor sites. Clinical studies indicate it to
have a lower incidence of extrapyramidal side-effects.
The apparent better compliance with the drug may be
related to its lower side-effect profile and its once-daily
dosage of 5-10 mg. Weight gain is a problem with long-
term treatment and there is an increased risk of diabetes
mellitus.
Neither risperidone nor olanzapine seem as specific a
treatment for intractable chronic schizophrenia as
clozapine.
Other atypical antipsychotics include sulpiride, ziprasidone
and quietiapine.
Psychological treatment
This consists of reassurance, support and a good doctor-
patient relationship. Psychotherapy of an intensive or
exploratory kind is contraindicated. In contrast, recent
research shows that cognitive behaviour therapy can help
reduce the intensity of delusions.
Social treatment
Social treatment involves attention being paid to the
patient's environment and social functioning. Family
education can help relatives and partners to provide the
optimum amount of emotional and social stimulation, so
that not too much emotion is expressed (a risk for relapse).
Sheltered employment is usually necessary for the majority
of sufferers if they are to work.
Medical presentations related to treatment
The motor side-effects of neuroleptics are the commonest
reason for a patient with schizophrenia to present to a
physician, followed by deliberate self-harm. Acute dystonia
normally arises in patients newly started on neuroleptics,
causing a torticollis. Extrapyramidal side-effects are
common and present in the same way as Parkinson's
disease. Akathisia is a motor restlessness, most commonly
affecting the legs. It is similar to the restless legs
syndrome (p. 666), but apparent during the day.
Amenorrhoea and galactorrhoea can be caused by
dopamine antagonists. Postural hypotension can affect
the elderly, and neuroleptics can be the cause of delirium
in the elderly, if their antimuscarinic effects are prominent.
FURTHER READING
Freedman R (2003) Schizophrenia. New England Journal
of Medicine 349:1738-1749. Mueser KT, McGurk
SR (2004) Schizophrenia. Lancet
363: 2063-2072.
ORGANIC MENTAL DISORDERS
Organic brain disorders result from structural pathology,
as in dementia (see p. 1254), or from disturbed central
nervous system (CNS) function, as in fever-induced
delirium. They do not include mental and behavioural
disorders due to alcohol and misuse of drugs, which are
classified separately.
Delirium
Delirium, also termed toxic confusional state and acute
organic reaction, is an acute or subacute brain failure in
which impairment of attention is accompanied by abnor-
malities of perception and mood. It is the most common
psychosis seen in the general hospital. Ten to twenty per
cent of older surgical and medical inpatients have delirium
during their admission. Confusion is usually worse at
night, with consequent sleep reversal, so that the patient
is asleep in the day and awake all night. During the acute
phase, thought and speech are incoherent, memory is
impaired and misperceptions occur. Episodic visual
hallucinations (or illusions) and persecutory delusions
occur. As a consequence, the patient may be frightened,
suspicious, restless and uncooperative.
A developing, deteriorating or damaged brain
predisposes a patient to develop delirium (Table 22.24).
A large number of diseases may cause delirium,
particularly in elderly patients. Some causes of delirium
are listed in Table 22.25. Delirium tremens should be
considered in the differential diagnosis (p. 1304) as well
as Lewy body dementia (p. 1255). Diagnostic criteria are
given in Box 22.14.
Management
History should be taken from a witness. Examination
may reveal the cause. Investigation and treatment of the
underlying physical disease should be undertaken (Table
22.25). The patient should be carefully nursed and
rehydrated in a quiet single room with a window that
does not allow exits. If a high fever is present, the
1309
Psychological medicine
Table 22.24 Predisposing factors in delirium Prognosis of delirium
Extremes of age (developing or deteriorating brain) Delirium usually clears within a week or two, but brain
Damaged brain: recovery usually lags behind the recovery of the causative
Any dementia (most common predisposition) physical illness. The prognosis depends not only on the
Previous head injury successful treatment of the causative disease, but also on
Alcoholic brain damage
the underlying state of the brain. Twenty-five per cent of
Previous stroke Dislocation to an unfamiliar
environment (e.g. hospital the elderly with delirium will have an underlying
admission) dementia; 15% of patients do not survive their underlying
Sleep deprivation illness; 40% are in institutional care at 6 months.
Sensory extremes (overload or deprivation)
Immobilization FURTHER READING
Nayeem K, O'Keefe ST (2003) Delirium. Clinical
Medicine 3(5): 412-115.
Table 22.25 Some common causes of delirium
 Sy i olic di I rrhage
EATIN purgin sexual interest
ste t disturba s n Epilepsy g, lanugo hair.
mi h nce e tr
Drug
G exerci
c Hep a a The physical
inf h atic s c
intoxicati DISORD se,
consequences of anorexia
on or
ect i failu e r
Anticonvul
ER appeti
include sensitivity to
ion g re H a cold, constipation,
sants te
h Ren y n Obesity hypotension and
Antimusca
al p ia suppre
rinics bradycardia. In most
f failur o l This is the ssants
Anxiolytic/ cases, amenorrhoea is
e e t c
hypnotics
commonest a
Diso a secondary to the weight
v h Tricyclic eating distort
rder u loss. Vomiting and abuse
e y antidepres disorder (see ion of
s of s of purgatives may lead to
r r sants p. 252), body
elec o e hypo-kalaemia and
troly s
Dopamine which has image
( i agonists alkalosis.
te Tr become so that
e d Digoxin epidemic in
b a the Prevalence
. i
a u Drug/alco some patien
g s Case register data
l m developed t
.
a
m
a
hol suggest an incidence
countries. It regard
n T rate of 19 per 100 000
is usually s
Box 22.14 Delirium - diagnostic criteria (derived females aged between 15
caused by a hersel
from DSM-IV-TR) and 34 years. Surveys
combination f as have suggested a
Disturbance of consciousness: of fat prevalence rate of
4 clarity of awareness of environment constitution when approximately 1%
i ability to focus, sustain or shift attention al and social she is among schoolgirls and
Change in cognition: factors, but a thin university students.
memory deficit, disorientation,
binge eating a However, many more
language disturbance, perceptual disturbance
disorder and morbid young women have
Disturbance develops over a short period (hours or
days) psychologica fear of amenorrhoea
Fluctuation over course of day Disturbance is l fatness
caused by the consequences of a determinant ameno
general medical condition or medication s of 'comfort rrhoea in
An eating' women.
y m c C u should be
withdraw Clinical
a e u m excluded.
patient's temperature should be reduced. All current features
drug therapy should be reviewed and, where possible, include:
stopped. Psychoactive drugs should be avoided if Anorexia onset
possible (because of their own risk of exacerbating nervosa_____________________________
usually in
delirium). In severe delirium, haloperidol is an effective The main adolescen
choice, the daily dose usually ranging between 1.5 mg (in clinical ce
the elderly) to 30 mg per day. If necessary, the first dose criteria for a
can be administered intramuscularly. Olanzapine is an diagnosis previous
effective alternative, especially if given at night for are: history of
insomnia. , ... .,,.,, ... , ,..,,.. ..... chubbine
a
bodyweig ss or
i l H s o fatness
al ht more
n a y h ur the
f r p i A Postoper than 15%
patient
e i o n b below the
ative generally
c a x g s standard
i c states
eats little
t , ' weight,
a e ameno
i s or a body
o s s rrhoea
Vitamin mass
n e s s - an
deficienc index
, p y S early
y (BMI)
p t Thiamin n u sympt
b below om; in
a i (Wernick d
r c r a 17.5 20% it
e-
t a o r (ICD-10) preced
Korsakoff
i e m a weight
syndro es
c m e c loss is
me, weight
u i h self-
beriberi) loss
n
l a Nicotinic induced
oi binge
a ) acid by eating
d
r (pellagra) avoidanc
M h usuall
l Vitamin e of
e a ya
y B12
t e fattening marked
a Endocrin m foods, lack of
w b e o vomiting,
Eating disorders
accompanied by less weight loss than the 15% required
for the diagnosis. The condition is much less common
among men (ratio of 1 : 10). The onset in women is
usually at between 16-17 years of age and it seldom
occurs after the age of 30 years.
Aetiology Biological
factors
Genetic. Six to ten per cent of siblings of affected
women suffer from anorexia nervosa. There is an increased
concordance amongst monozygotic twins, suggesting a
genetic predisposition.
Hormonal. The reductions in sex hormones and the
hypothalamic-pituitary-adrenal axis are secondary to
malnutrition and usually reversed by refeeding.
Psychological factors
Individual. Anorexia nervosa has often been seen as an
escape from the emotional problems of adolescence and a
regression into childhood. Patients will often have had
dietary problems in early life. Perfectionism and low self-
esteem are common antecedents. Studies suggest that
survivors of childhood sexual abuse are at risk of
developing an eating disorder, usually anorexia nervosa,
in adolescence.
Family. Families of such patients are allegedly charac-
terized by overprotection, inflexibility and lack of conflict
resolution. Anorexia is alleged to prevent dissension in
families. However, a case control study suggested that
there is no more evidence of these factors in families of
patients with anorexia nervosa than in control families
with a child with an established physical disease.
Social and cultural factors
There is a higher prevalence in higher social classes, and
a high rate in certain occupational groups (e.g. ballet
dancers and nurses) and in societies where cultural value
is placed on thinness.
Prognosis
The condition runs a fluctuating course, with exacerbations
and partial remissions. Long-term follow-up suggests that
about two-thirds of patients maintain normal weight and
that the remaining one-third are split between those who
are moderately underweight and those who are seriously
underweight. Indicators of a poor outcome include:
a long initial illness ' (d) tetany - from hypokalaemic alkalosis
severe weight loss ; (e) swollen salivary glands - from vomiting
older age at onset
bulimia (see below), vomiting or purging
personality difficulties
difficulties in relationships.
Suicide has been reported in 2-5% of patients with chronic
anorexia nervosa. The mortality rate per year is 0.5% from
all causes. More than one-third have recurrent affective
illness, and various family, genetic and endocrine studies
have found associations between eating disorders and
depression. Fifty per cent of patients make a full recovery,
30% a partial recovery and 20% none.
Treatment
Treatment can be conducted on an outpatient basis unless
the weight loss is severe and accompanied by marked
physical symptoms, dizziness and weakness and/or
electrolyte and vitamin disturbances. Hospital admission
may then be unavoidable and may need to be on a medical
ward initially. Rarely, the patient's weight loss may be so
severe as to be life-threatening. If the patient cannot be
persuaded to enter hospital, compulsory admission may
have to be used. Inpatient treatment goals include:
establishing a good relationship with the patient
restoring the weight to a level between the ideal body-
weight and the patient's ideal weight
the provision of a balanced diet, building up to 12.6 MJ
(3000 calories) in three to four meals per day
the elimination of purgative and/or laxative use and
vomiting.
Outpatient treatment can be conducted on cognitive
behavioural or dynamic psychotherapeutic lines or on a
combination of both. Setting up a therapeutic alliance is
vital. Individual psychotherapy is better than family
therapy if the patient has left home, and vice versa.
Motivational enhancement techniques are being used
with some success.
Drug treatment has met with limited success, except to
symptomatically treat insomnia and depressive illness.
Bulimia nervosa
This refers to episodes of uncontrolled excessive eating,
which are also termed 'binges'. There is a preoccupation
with food and a habitual adoption of certain behaviours
that can be understood as the patient's attempts to avoid
the fattening effects of periodic binges. These behaviours
include:
self-induced vomiting
laxative abuse
misuse of drugs - diuretics, thyroid extract or anorectics.
Additional clinical features include:
physical complications of vomiting:
(a) cardiac arrhythmias
(b) renal impairment - consequences of low K+
(c) muscular paralysis
(f) eroded dental enamel
associated psychiatric disorders:
(a) depressive illness
(b) alcohol misuse
fluctuations in bodyweight within normal limits
menstrual function - periods irregular but amenorrhoea
rare
personality - perfectionism and low self-esteem
present premorbidly. ............._ ........
1311
Psychological medicine
The prevalence of bulimia in community studies is high;
it affects between 5% and 30% of girls attending high
schools, colleges or universities in the USA. Bulimia is
sometimes associated with anorexia nervosa. A pre-
morbid history of dieting is common. The prognosis for
bulimia nervosa is better than for anorexia nervosa.
Treatment
Cognitive behaviour therapy has been shown to be more
effective than both interpersonal psychotherapy and drug
treatments. SSRIs (e.g. fluoxetine) are also an effective
treatment, even in the absence of a depressive illness.
Atypical eating disorders
These include eating disorders that do not conform
clinically to the diagnostic criteria for anorexia nervosa or
bulimia nervosa. Binge eating disorders consist of
bulimia without the vomiting and other weight-reducing
strategies.
FURTHER READING
Fairburn CG, Harrison PJ (2003) Eating disorders.
Lancet 361: 407-117. Mehler PS (2003) Bulimia nervosa.
New England Journal
of Medicine 349: 875-881. Wilson GT, Shafran
R (2005) Eating disorders
guidelines from NICE Lancet 365: 79-81.
refers to a repeatedly unsatisfactory quality of sexual
satisfaction. Problems of sexual dysfunction can usefully
be classified into those affecting sexual desire, arousal
and orgasm. Among men presenting for treatment of
sexual dysfunction, erectile dysfunction is the most fre-
quent complaint. The prevalence of premature ejaculation
is low, while ejaculatory failure is rare.
Sexual drive is affected by constitutional factors,
ignorance of sexual technique, anxiety about sexual
performance, medical and psychiatric conditions and
certain drugs (Tables 22.27 and 22.28).
The treatment of sexual dysfunction involves careful
assessment, the participation (where appropriate) of the
patient's partner, and specific therapeutic techniques,
including relaxation, behavioural therapy (Masters and
Johnson) and psychotherapy. The introduction of
phosphodiesterase type 5 inhibitors (e.g. sildenafil) has
introduced an effective therapy for the treatment of
erectile dysfunction (see p. 1055).
Sexual deviation
Sexual deviations are regarded as unusual forms of
behaviour rather than as an illness. Doctors are only
likely to be involved when the behaviour involves break-
Table 22.27 Medical conditions affecting sexual
performance
 SEXUAL DISORDERS Endocrine
Diabetes mellitus
Neurological
Neuropathy Spinal
Hyperthyroidism cord lesions
Sexual disorders can be divided into sexual dysfunctions, Hypothyroidism
deviations, and gender role disorders (Table 22.26). Musculoskeletal
Cardiovascular Arthritis
Angina pectoris
Respiratory
Sexual dysfunction Previous myocardial infarction Asthma
Disorders of peripheral circulation
Sexual dysfunction in men refers to repeated inability to COPD
achieve normal sexual intercourse, whereas in women it Hepatic Psychiatric
Cirrhosis, particularly alcohol-related Depressive illness
Renal Substance misuse
Renal failure
1312 laoie &..4O oiassiu canon OT sexual disorders
Sexual Sexual Disorders of the
dysfunction deviations gender role 1 Table 22.8 Drugs affecting sexual arousal
Affecting sexual Variations of the Transsexualism Male arousal Female arousal

desire sexual 'object'

Low libido Fetishism Alcohol Alcohol
Transvestism
11 IA1 I**J V w t*J LI wl 1 1
Benzodiazepines CNS depressants
Impaired sexual Paedophilia Neuroleptics Antidepressants (SSRIs)
arousal Bestiality Cimetidine Oral combined contraceptives
Erectile dysfunction Necrophilia Opiate analgesics Methyldopa
Failure of arousal Methyldopa Clonidine
in women Clonidine
Variations of the Spironolactone
Affecting orgasm sexual act Antihistamines
Premature ejaculation Exhibitionism Metoclopramide
Retarded ejaculation Voyeurism Diuretics
Orgasmic dysfunction Sadism Beta-blockers
in women Masochism Cannabis
Frotteurism Alcohol increases the desire but diminishes the performance
Psychiatry and the law
22
ing the law (e.g. paedophilia or bestiality) and when there
is a question of an associated mental or physical disorder.
Homosexuality was formerly classified as an illness but it
is now an accepted alternative sexual lifestyle. Men are
more likely than women to have sexual deviations.
Gender role disorders
Transsexualism involves a disturbance in gender identity
in which the patient is convinced that their body is the
wrong gender. A person's gender identity refers to the
individual's sense of masculinity or femininity as distinct
from sex. It is thought to arise from a biological
component (prenatal endocrine influences), psychological
imprinting and social conditioning. Disturbances in these
three areas have variously been blamed for the cause of
transsexualism.
For males, treatment includes oestrogen administration
and, if surgery is to be recommended, a period of living
as a woman as a trial beforehand. In the case of female
transsexuals, treatment involves surgery and the use of
methyltestosterone.
FURTHER READING
Halaris A (ed.) (1997) Sexual dysfunction. In: Bailliere's
Clinical Psychiatry: International Practice and Research,
Vol 3. London: Bailliere Tindall.
Tomlinson J (1997) ABC of sexual health. London: British
Medical Books.
PERSONALITY DISORDER
These disorders comprise deeply ingrained and enduring
patterns of behaviour which manifest themselves as
inflexible responses to a broad range of personal and
social situations. Personality disorders are developmental
conditions that appear in childhood or adolescence and
continue into adult life. They are not secondary to another
psychiatric disorder or brain disease, although they may
precede or coexist with other disorders. In contrast,
personality change is acquired, usually in adult life, fol-
lowing severe or prolonged stress, extreme environmental
deprivation, serious psychiatric disorder or brain injury
or disease.
Personality disorders are usually subdivided accord-
ing to clusters of traits that correspond to the most
frequent or obvious behavioural manifestations. The
main categories of personality disorder are described
below.
Borderline (emotionally unstable). Such people act
impulsively and develop intense, but short-lived,
emotional attachments to others. They describe chronic
internal emptiness with frequent self-harm, self-abuse
(eating disorders, substance misuse) and they may
develop transient psychotic features of uncertain signifi-
cance. There is often a strong family history of mood
disorders.
Paranoid. A paranoid personality is characterized by
extreme sensitiveness, suspiciousness, litigiousness, a
tendency to excessive self-importance, and a preoccupation
with unsubstantiated conspiratorial explanations of
events.
Schizoid. A schizoid personality is characterized by
emotional coldness and detachment, a limited capacity to
express emotions, indifference to praise or criticism, an
almost invariable preference for solitary activities, lack of
close friendships, and a marked insensitivity to prevailing
social norms and conventions.
Antisocial. An antisocial personality is characterized
by a callous unconcern for the feelings of others, an
incapacity to maintain enduring relationships, a very low
tolerance of frustration, an incapacity to experience guilt
and to profit from experience, and a marked proneness to
rationalize and blame others.
Histrionic. A histrionic personality is characterized by
self-dramatization, theatricality, suggestibility, shallow
and labile emotions, a continual seeking for excitement
and appreciation by others, and an inappropriate
seductiveness in appearance or behaviour.
Anankastic (obsessive-compulsive). Such a personality
is characterized by feelings of excessive doubt and
caution, preoccupation with details, rules, lists, order,
perfectionism, excessive conscientiousness, scrupulousness,
excessive pedantry, rigidity and stubbornness, and
intrusion of unwelcome thoughts or impulses.
Dependent. People with dependent personality
encourage others to make their personal decisions, sub-
ordinate their needs to others on whom they are dependent,
are unwilling to make demands on others, feel unable to
care for themselves, are preoccupied with fears of being
abandoned. Such patients have a limited capacity to
make everyday decisions without an excessive amount of
advice and reassurance from others.
Many individuals with disturbed personalities do not fit
neatly into such categories, but manifest a mixture of
features.
PSYCHIATRY AND THE LAW
The law in most developed countries provides for the
compulsory admission and/or treatment of mentally
disordered persons for their own protection and/or the
protection of others and for mitigation in the case of
mentally disordered individuals who commit a criminal
offence (see also p. 6). In England and Wales the Act of
Parliament that is crucially involved is the Mental Health
Act 1983, although a new Act is about to go through
parliament. The Mental Health (Scotland) Act 1984 and
the Mental Health (Northern Ireland) Order 1986 contain
clauses broadly similar to those in England and Wales.
1313
Psychological medicin
 Apart from one provision of the National Assistance
Act 1948, the Mental Health Act 1983 is the only method
whereby individuals can legally be deprived of their
liberty without having committed a crime or being
suspected of committing a crime. It is, therefore, neces -
sary that doctors understand the seriousness of their
responsibility and the details of the legislation.
There are three conditions that need to be met before
an appropriate compulsory section form is signed. The
patient must be: . ; .
suffering from a defined mental disorder
at ri sk to h i s/ h er and /o r oth er p e opl e ' s h e a lt h or
safety
unwilling to accept hospitalization voluntarily.
The reasons why there is no alternative approach to the
treatment suggested for the patient should be outlined.
Sexual deviance or alcohol/drug dependence are not
defined mental disorders, but otherwise the definition of
mental disorder is broad. Any registered medical practi-
tioner may sign a medical recommendation under the
Act, but the added signature of a specialist psychiatrist is
needed for c ompulsory orders lasting for more tha n
72 hours. Unless the patient is already in hospital, the
nearest relative or an approved mental health social
worker is also required to sign the application form.
Relevant sections of the Act are detailed in Table 22.29.
Physicians are likely to be involved in sections 5(2)
and 2. It should be remembered that a section does not
give a doctor the right to treat a physical disease,
although it could be argued that a section would apply if
the physical disease was causing the mental disorder (e.g.
delirium). This has never been legally tested.
Although much of the process of detention against one's
will is formalized, there is no liability for a doctor who acts
in good faith with a patient's best interests at heart. Clearly
written medical notes, accepted forms of treatment and
common sense remain the basis of good practice.
Table 22.29 Commonly used sections of the Mental Health Act 1983
Section Duration Purpose
Signatures required
23 28 days 6
Assessment and treatment
4 5(2) months Two doctors (one approved) plus nearest
relative or social worker Two doctors (one approved) plus
5(4) 72 hours Emergency admission
72 hours Emergency detention of a patient already
136 in hospital Emergency detention
6 hours of a patient
already in hospital Psychiatric
72 hours assessment of those in
public places thought by police to be
mentally ill and in need of a place of
safety
nearest relative or Treatment
social worker
One doctor plus relative or social worker
Doctor in charge of patient's care

Nurse (RMN)

Police officer
FURTHER READING
Duggan C (ed.) (1997) Assessing risk in the mentally disordered. British Journal of Psychiatry 170 (Suppl 32).
CHAPTER BIBLIOGRAPHY
Davies T, Craig TKT (1998) ABC of Mental Health.
London: BMJ Books. Gelder M, Lopez-Ibor JI,
Andreasen N (2000) New Oxford
Textbook of Psychiatry, 3rd edn. Oxford: Oxford
University Press. Goldberg D (ed.) (1997) Maudsley
Handbook of Practical
Psychiatry, 3rd edn. Oxford: Oxford University Press.
Johnstone EC, Freeman CPL, Zealley AK (1998)
Companion to Psychiatric Studies, 6th edn. Edinburgh:
Churchill Livingstone. Shorter E (1998) A History of
Psychiatry. Chichester: John
Wiley. Stahl SM (2000) Essential Psychopharmacology,
2nd edn.
Cambridge: Cambridge University Press
SIGNIFICANT WEBSITES
http://www.rcpsych.ac.uk
UK Royal College of Psychiatrists
http://www.connects.org.uk
Website for mental health in general
http://www.cebmh.com
Centre for Evidence-Based Mental Health
http://www.mentalhealth.org.uk
Mental Health Foundation - charity
http://www.sleepfoundation.org
National Sleep Foundation
http://www.edauk.com
Eating Disorders Association
http://psych.org
American Psychiatric Association
1314