Professional Documents
Culture Documents
Psychiatry
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Examination Notes in
Psychiatry
4th edition
DEL PREWETTE MD
Child and Adolescent Psychiatry Fellow, Palmetto
Health/University of South Carolina School of
Medicine, Columbia, South Carolina, USA
Hodder Arnold
A MEMBER OF THE HODDER HEADLINE GROUP
LONDON
First published in Great Britain in 2005 by
Hodder Education, a member of the Hodder Headline Group,
338 Euston Road, London NW1 3BH
www.hoddereducation.co.uk
© 2005 Peter Buckley, Del Prewette, Jonathan Bird and Glynn Harrison
Whilst the advice and information in this book are believed to be true and
accurate at the date of going to press, neither the author[s] nor the publisher
can accept any legal responsibility or liability for any errors or omissions
that may be made. In particular, (but without limiting the generality of the
preceding disclaimer) every effort has been made to check drug dosages;
however it is still possible that errors have been missed. Furthermore,
dosage schedules are constantly being revised and new side-effects
recognized. For these reasons the reader is strongly urged to consult the
drug companies’ printed instructions before administering any of the
drugs recommended in this book.
1 2 3 4 5 6 7 8 9 10
What do you think about this book? Or any other Arnold title? Please
visit our website at www.hoddereducation.co.uk
Contents
Preface vii
1 Research methodology and statistics 1
2 Descriptive psychopathology 13
3 Schizophrenia 24
4 Affective disorders 43
5 Neurotic disorders 60
6 Personality: development and disorders 77
7 Eating disorders 86
8 Human sexuality 96
9 Alcohol dependence 109
10 Drug dependence and gambling 123
11 Suicide and non-fatal deliberate self-harm 134
12 Uncommon psychiatric syndromes 144
13 Organic psychiatry 150
14 Psychiatric aspects of epilepsy and sleep disorders 175
15 EEG and brain imaging in psychiatry 185
16 Psychophysiological, somatoform, dissociative and related disorders 195
17 Psychogeriatrics 205
18 Forensic psychiatry 215
19 Child psychiatry 233
20 Mental retardation 253
21 Drug therapy 266
22 Physical treatments 289
23 Psychotherapy 297
24 Community-orientated psychiatry 312
25 Specific psychiatric problems of women 318
26 Transcultural psychiatry 328
27 Psychiatry and the Internet 333
Index 337
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Preface
As with any subject worthy of human study and endeavour, pshychiatry develops,
understandings change, new facts emerge or old ones are seen in a new light. Since the
first edition of this book some 20 years ago there have been tremendous advances in
neuroscience and, as a result, major new insights into the functioning of the brain
have emerged. Yet, at the same time, major changes are also taking place in the organ-
ization and delivery of mental health services throughout the world.
We hope that the fourth edition of this widely read text will prove even more useful
to mental health trainees of various disciplines (psychiatrists, psychologists, nurses and
other professionals), to interested medical students, and to mental health clinicians
wishing to prepare lectures or brush up on the main essentials of psychiatry. This edi-
tion has been almost totally revised and, inevitably, expanded. Almost every subject
has been revisited in the light of the most current knowledge and theories. ‘New’
conditions (e.g. Internet addiction) and new investigations (e.g. functional MRI) sit
beside all the old favourites.
References are included where these are considered to be ‘key’ papers or reviews
which could be quoted and which readers should look up for themselves. There are
also suggestions for further reading.
Finally, we would reiterate what we have written in previous prefaces, that this book
is not intended as a substitute for wider reading or experience, but as a detailed and
comprehensive aide-mémoire. In order to gain fluency in the subject, readers might
carry it with them, rehearse its content, follow up its references, debate its currently
received wisdom and enjoy the fruits of their labours by achieving the success that
their endeavours deserve.
Peter Buckley
Del Prewette
Jonathan Bird
Glynn Harrison
Acknowledgements
Material in Tables 3.1, 3.3, 4.1, 5.1, 6.1, 7.3, 7.4, 8.1, 16.1, 18.1 and 19.1 is reproduced,
with permission from: The ICD-10 classification of Mental and Behavioural Disorders:
Diagnostic Criteria for Research. Geneva, World Health Organization, 1993.
Material in Tables 3.2, 3.8, 7.3, 7.4 and 18.1 is reproduced, with permission from:
The Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American
Psychiatric Association.
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Research methodology and 1
statistics
PHILOSOPHY OF SCIENCE
Science is only one approach to understanding the world. According to Popper, it involves:
• Hypothesis formulation.
• Observation based on the hypothesis.
• Attempts to falsify the hypothesis.
• Control of variables.
• Predictions based on the hypothesis.
• Replication of results.
HOW TO DO RESEARCH
PLANNING RESEARCH
Write a protocol:
• Title
• Introduction – survey of background information and reasons for doing the research
2 RESEARCH METHODOLOGY AND STATISTICS
BASIC DEFINITIONS
VARIABLES
Variables are any constructs or events which research studies.
• Independent variable – the antecedent condition manipulated by the experimenter
(e.g. drug levels).
• Dependent variable – the variable used to measure the effect of the independent
variable (e.g. recovery rates).
• Confounding variable – any extraneous variable whose potential influence on the
dependent variable has not been controlled for; a source of error (e.g. age or sex
imbalances).
• Controlled variable – a variable whose influence is kept constant by the experi-
menter (e.g. other medications).
• Uncontrolled variable – a variable which is not manipulated or held constant,
though it may be measured (e.g. life events).
RESEARCH DESIGN
Simple designs may be:
• Cross-sectional in time
• Longitudinal in time.
They may also be:
• Between-group
• Within-group
• Within-individual.
BASIC DEFINITIONS 3
RELIABILITY
Reliability is the extent to which there is repeatability of an individual’s score or other
test result.
• Test–retest reliability – high correlation between scores on the same test given on
two occasions.
• Alternate-form reliability – high correlation between two forms of the same test.
• Split-half reliability – high correlation between two halves of the same test.
• Inter-rater reliability – high correlation between results of two or more raters of the
same test.
Inter- or intra-reliability is measured using intraclass correlation coefficient (ICC – range
0–1; ICC of ⭓0.7 is acceptable).
VALIDITY
Validity is the extent to which a test measures what it is designed to measure.
• Predictive validity – ability of the test to predict outcome.
• Content validity – whether the test selects a representative sample of the total tests
for that variable.
• Construct validity – how well the experiment tests the hypothesis underlying it.
The ‘reliability paradox’ is that a very reliable test may have low validity precisely
because its results do not change; i.e. it does not measure true changes.
4 RESEARCH METHODOLOGY AND STATISTICS
SOURCES OF ERROR
• Response set – subject always tends either to agree or to disagree with questions.
• Bias towards centre – subject tends to choose the middle response and shun extremes.
MEASUREMENT IN PSYCHIATRIC RESEARCH 5
General health General Health Questionnaire Commonly used screening, used in primary care
(GHQ) and general population studies.
Global Clinical Global Impressions (CGI) Global observation of severity of psychiatric
assessment/screening illness, 7-point scale.
Nurses Observation Scale for Very commonly used observational scale, mostly
Inpatient Evaluation (NOSIE) used for inpatients with psychosis.
Global Assessment Scale (GAS) Evaluates social functioning and severity of
symptoms.
Hopkins Symptom Checklist 90-item checklist of 9 symptom dimensions,
(SCL-90) with 3 global indices of distress.
Structured interview NIMH Diagnostic Interview (DIS) Generates Research Diagnostic Criteria
schedules diagnosis.
Schedule for Affective Disorders Generates RDC or DSM-III-R diagnosis of
and Schizophrenia (SADS) psychotic disorders.
Schedule for Clinical Assessment Incorporates Present Status Examination 10
in Neuropsychiatry (SCAN) with an updated CATEGO program.
Evaluates different time periods – primary and
secondary and lifetime.
Generates both ICD-10 and DSM – IV diagnoses.
Structured Clinical Interview for Generates DSM-III-R diagnosis.
DSM-III-R (SCID)
Schizophrenia Brief Psychiatric Rating Scale Widely used measure of psychotic symptoms
(BPRS) (not just schizophrenia) and psychopathology,
18 items.
Comprehensive Assessment of Evaluates major psychoses re: symptoms, past
Symptoms and History (CASH) history, premorbid function and cognitive status.
Schedule for the Assessment of Details hallucinations, delusions, bizarre
Positive Symptoms (SAPS) behaviour, formal thought disorder.
Schedule for the Assessment of Details alogia, affective blunting, avolition,
Negative Symptoms (SANS) asociality, attentional impairment.
Positive and Negative Symptoms Developed from BPRS, more detailed, more
Scale (PANSS) structured, includes general psychopathology
section.
Depression Beck Depression Inventory (BDI) Self-rating, 21 items.
Hamilton Depression Scale (HamD) Observer rating, 17 items and severity
dimension, widely used in depression research.
Zung Depression Scale Self-rating, 20 items.
Mania Young Mania Scale 11-item observer scale.
Anxiety Hamilton Anxiety Rating Scale 14-item observer scale covering psychic and
(HARS) somatic dimensions.
Zung Anxiety Scale Combined observer and brief report formats,
20 items.
Obsessive–compulsive Maudsley Obsessional– Self-report, 30 items.
disorder Compulsive Inventory (MOCI)
Yale-Brown Obsessive– Observer scale, 19 items.
Compulsive Scale (YBOCS)
Psychosomatic/eating Eating Attitudes Test (EAT) Self-report on eating behaviour.
disorders McGill Pain Questionnaire Detailed self-report.
Psychosocial Adjustment to Self-report and interview – based on adjustment
Illness Scale (PAIS) to (chronic) illness.
Personality Eysenck Personality 90-item questionnaire yielding sub-scales of
Questionnaire (EPQ) neuroticism, extroversion, psychoticism, lie
score.
(Continued)
6 RESEARCH METHODOLOGY AND STATISTICS
• Social acceptability – subject chooses the acceptable answer rather than the
true one.
• Halo effect – answers are chosen to ‘fit’ with previously chosen answers; responses
become what is expected by the observer.
• Hawthorne effect – researchers alter the situation by their presence.
PSYCHOMETRIC TESTING
• Personality, e.g.:
– Minnesota Multiphasic Personality Inventory
– Eysenck Personality Inventory
– Projective tests – which analyse fantasy material (e.g. Rorschach Ink Blot Test,
Thematic Apperception Test).
• Neuropsychological status:
– Usually aimed at assessing whether diffuse or focal brain change is present,
whether localization of pathology is possible, and what rehabilitation measures
might help.
– Screening tests used include Bender Gestalt, Benton Visual Retention Test, Trail
Making Task, Memory for Designs, WAIS, Wechsler Memory Scale.
– Batteries of tests are often used – e.g. the Halstead–Reitan and Luria–Nebraska
batteries.
Also assess interests, aptitudes and attitudes.
PSYCHOPHYSIOLOGICAL TECHNIQUES
STATISTICS
DESCRIPTIVE STATISTICS
MEASURES OF DISPERSION
• Range – from largest to smallest score.
• Variance – a measure of the dispersion of data about the mean; the average squared
deviation from mean.
• Standard deviation – 64% of scores in a normal distribution fall within one stand-
ard deviation either side of the mean; square-root of the variance.
• Standard error – an estimate of the discrepancy between sample mean and
true population mean; standard deviation divided by square-root of number of
cases.
• Z score – number of standard deviations on each side of the mean.
• Skewness – measures deviation from the normal distribution curve.
• Kurtosis – measures peakedness or flatness of curve.
INFERENTIAL STATISTICS
Student’s t-test can use paired or non-paired relationships between variables, so that either within-subject or between-subject
comparisons can be studied.
ANOVA may be one- or two-way ANOVA (takes multiple relationships into account).
ANCOVA ‘partials out’ an observed effect that may contribute to group difference (e.g. gender, educational status).
• Factor analysis – segregates data into the minimum number of dimensions that
define a group (e.g. principal component analysis, principal factor analysis,
eigenvalue determination, verimax factor rotation). It is used, e.g., to generate posi-
tive, negative and disorganization syndromes in schizophrenia (see Liddle, 1987).
• Cluster analysis – segregates data into groups, but with some overlap; e.g. Pakel’s
classification of depression (see Chapter 4).
• Meta-analysis – statistical technique in which related data from numerous studies
on a topic are pooled to determine the size and strength of a proposed association;
e.g. treatment response in schizophrenia and dose of atypical antipsychotics (see
Leucht et al., 2003).
DESIGNING A TRIAL
Patient selection
Specify inclusion and exclusion criteria, source of recruitment, diagnostic criteria
(operationally defined).
Treatment
Prepare active drug in a form identical to the placebo or to a comparison drug. Ensure
that new drug and standard drug have similar bio-availability. Compliance should be
assessed in outpatients at least by a tablet count. Plasma drug level may also be monitored.
Control group
Important variables influencing response must be spread across the treatment and
control groups (i.e. age, sex, duration of symptoms). Randomization must be ensured.
Crossover designs, where patients receive two or more treatments one after the other,
should ensure ‘order effect’. Ensure adequate ‘washout’ to avoid overlapping of patients,
and exclude rapid placebo responders.
Evaluation
Each outcome variable should be precisely defined, objective and reliably detected.
Use standardized rating scales with training of observers for inter-rater reliability.
Ensure ‘blindness’ as far as possible.
Trial size
The number of subjects needed should be calculated from the proportion of patients
expected to respond, and the smallest difference between treatments considered worth
measuring. Power analysis should be part of the initial protocol.
• Methods – ideally, readers should be able to perform study on the basis of the depth
of description. Sample should be appropriate in selection and size; also, well-
matched with controls.
• Results – clearly stated, no excess of analyses (Bonferroni correction, if needed).
Tables and figures enhance clarity and interpretation of results.
• Discussion – major findings should be explicitly stated; should not be overinter-
preted. Methodological constraints should be acknowledged.
• References – should be scholarly. Other relevant work of the authors cited; not
under/over-referenced. Readers need to know some background of topic to judge
merit of the study, its importance – breaking new ground or replication?
• EBM is the integration of the best research evidence with the expertise of the clin-
ician in delivering care to individual patients (Sacket et al., 2000).
• Swift access to the latest published scientific data is available from numerous com-
mercial, as well as free, Internet sites (see Chapter 26).
• EBM allows guidelines to be formulated that aid the clinician in making an accur-
ate diagnosis and prescribing the most effective treatment.
• The central limitation of EBM involves the reliability of the scientific evidence.
In psychiatry, EBM is further encumbered by the relative lack of neuropathology
with many psychiatric illnesses and the complexity of psychosocial aspects of
individuals.
Bech P, Malt UF, Dencker SJ et al. (1993) Scales for assessment of diagnosis and severity of men-
tal disorders. Acta Psychiatr. Scand. 372(87).
Brandon TH, Irvin JE, Hendricks PS et al. (2002) The increasing power of placebos in trials of
antidepressants. JAMA 288, 44.
Cooper B (2003) Evidence-based mental health policy: a critical appraisal. Br. J. Psychiatry 183, 10.
Croudace T, Evans J, Harrison G et al. (2003) Impact of the ICD-10 Primary Health Care (PHC)
diagnostic and management guidelines for mental disorders on detection and outcome in
primary care: cluster randomized controlled trial. Br. J. Psychiatry 182, 20.
Daley LE, Bourke GJ, McGilvray J (1991) Interpretation and Uses of Medical Statistics. Blackwell
Scientific, Oxford.
Edwards E, Kornacki MJ, Silversin J (2002) Unhappy doctors: what are the causes and what can
be done? BMJ 324, 83.
Everitt BS, Dunn G (1992) Applied Multivariate Data Analysis. Edward Arnold, Oxford.
Freeman C, Tyrer P (1992) Research Methods in Psychiatry: a Beginner’s Guide, 2nd edn. Gaskell,
London.
Gilbody SM, Whitty P (2002) Improving the delivery and organization of mental health services:
beyond the conventional randomized controlled trial. Br. J. Psychiatry 180, 1.
Gilbody SM, House AO, Sheldon TA (2002) Outcomes research in mental health: a systematic
review. Br. J. Psychiatry 181, 170.
Higgit A, Fonagy P (2002) Reading about clinical effectiveness. Br. J. Psychiatry 181, 170.
12 RESEARCH METHODOLOGY AND STATISTICS
Hrobjartssom A, Gotzsche PC (2001) Is the placebo powerless? An analysis of clinical trails com-
paring placebo with no treatment. New Engl. J. Med. 344, 159.
Kotzin S (2002) MEDLINE and PubMed will be able to synthesise clinical data. BMJ 324, 79.
Lancet (1993) Facts, figures and fallacies [series on statistics]. Lancet 342, 15.
Leucht S, Wahlbeck K, Hamann J, Kissling W (2003) New generation antipsychotics versus
low-potency conventional antipsychotics: a systematic review and meta-analysis. Lancet 361,
1581.
Leuchter AF, Cook IA, Witte EA et al. (2002) Changes in brain function of depressed subjects
during treatment with placebo. Am. J. Psychiatry 159, 12.
Liddle PF (1987) The symptoms of chronic schizophrenia: a reexamination of the positive–
negative dichotomy. Br. J. Psychiatry 151, 14.
Rose D (2003) Collaborative research between users and professionals: peaks and pitfalls.
Psychiatr. Bull. 27, 40.
Sackett DL, Straus SE, Richardson WS et al. (2000) Evidence Based Medicine: How to Practice and
Teach EBM. Churchill Livingston, New York.
Safer DJ (2002) Design and reporting modifications in industry-sponsored comparative psy-
chopharmacology trials. J. Nerv. Ment. Dis. 190, 58.
Snaith P (1993) What do depression rating scales measure? Br. J. Psychiatry 163, 29.
Stolk P, Berg MJ, Hemels ME, Einarson TR (2003) Meta-analysis of placebo rates in major
depressive disorder trails. Ann. Pharmacother. 37, 189.
Swales J (2000) The troublesome search for evidence: three cultures in need of integration.
J. R. Soc. Med. 93, 40.
Tansella M (2002) The scientific evaluation of mental health treatments: an historical perspec-
tive. Evidence Based Mental Health 5, 4.
Thompson C (1989) The Instruments of Psychiatric Research. John Wiley, Chichester.
Trivedi P, Wykes T (2002) From passive subjects to equal partners: qualitative review of user
involvement in research. Br. J. Psychiatry 181, 46.
Tryer P, King M, Fluxman J (2003) Treatment of common mental disorders in general practice:
are current guidelines useless? Br. J. Psychiatry 183, 7.
Williams DD, Garner J (2002) The case against ‘the evidence’: a different perspective on evidence-
based medicine. Br. J. Psychiatry 180, 8.
Descriptive psychopathology 2
The degree and quality of activity are important. There may be increased restless
motor activity in agitation or in hypomania, but the quality will differ.
14 DESCRIPTIVE PSYCHOPATHOLOGY
NON-ADAPTIVE MOVEMENTS
Spontaneous movements – habitual, not goal-directed
• Tics are sudden involuntary twitchings of groups of muscles, particularly facial
(seen in extreme form in Gilles de la Tourette syndrome).
• Static tremor of hands, head or upper trunk indicates anxiety, hyperthyroidism,
hysteria or ‘essential’ tremor, lithium toxicity, parkinsonism.
• Spasmodic torticollis involves spasm of neck muscles with twisting of head, which
may become permanent.
• Chorea is abrupt, random jerky movements resembling fragments of goal-directed
behaviour.
• Athetosis is slow, semi-rotary writhing movements.
• Orofacial dyskinesia is restless movements of tongue, mouth and facial muscles
(seen in the elderly and following chronic neuroleptic ingestion).
• Stereotypies are regular, repetitive non-goal-directed movements; e.g. repetitive
foot tapping, body rocking. Stereotyped utterances can occur. Stereotypies are seen
in chronic schizophrenia, mental handicap and infantile autism.
Induced movements
• Automatic obedience – the subject does whatever is asked of him or her.
• Echopraxia – the subject imitates the movements of the interviewer.
• Echolalia – words or phrases are imitated.
• Perseveration – the senseless repetition of a previously requested movement; i.e.
the repetition of a response after withdrawal of the stimulus. Special variants of
this are palilalia (the perseverated word is repeated with increasing frequency) and
logoclonia (perseveration of the last syllable of the last word). These are seen in
organic disorders and occasionally in catatonia.
• Forced grasping – the offered hand is repeatedly grasped and shaken, despite
requests not to do so. Seen in frontal lobe lesions.
• Mitmachen – the body can be put into any posture, despite instructions to resist.
• Mitgehen – an extreme form of mitmachen in which very slight pressure leads to
movement in any direction.
• Negativism – apparently motiveless resistance to suggestion or attempts at
movement.
DISORDERS OF PERCEPTION 15
Disorders of posture
• Postural mannerisms – strange and abnormal postures adopted habitually.
• Perseveration of posture – may be seen in schizophrenia and lesions of the mid-
brain. If the subject’s body is placed in an awkward posture and left, the posture is
held for a period before slowly relaxing, despite asking the patient to relax. If a
plastic resistance is felt to initial movement, this is termed ‘waxy flexibility’ (or
flexibilitas cerea).
DISORDERS OF PERCEPTION
SENSORY DISTORTIONS
Sensory distortions are changes in the quality, intensity or spatial form of a percep-
tion. Examples are:
• Hyperacusis – in mania, hyperthyroidism.
• Hypoacusis – in some acute organic states.
• Xanthopsia, micropsia – produced by psychedelics and temporal lobe lesions.
SENSORY DECEPTIONS
Hallucinations
Hallucinations are perceptions which arise in the absence of any external stimulus
(Esquirol, 1833). They are actual sense deceptions, not distortions of real perceptions.
Hallucinations are perceived as being located in the external world. They are per-
ceived as having the same qualities as normal perceptions – i.e. vivid, solid.
Hallucinations are not subject to conscious manipulation, in the same sense that
normal perceptions cannot be produced or dismissed at will.
Illusions
Illusions are distortions of perceptions of real objects; e.g. flowery wallpaper is per-
ceived as swarming snakes. Illusions are perceived as having the same qualities as
normal perceptions, but often are more fleeting than hallucinations.
Pseudohallucinations
Pseudohallucinations are not perceived by the actual sense organs, but experienced as
emanating from within the mind. They are a form of imagery. Although vivid they
lack the substantiality of normal perceptions.
Pseudohallucinations are located in subjective rather than objective space. They are
not subject to conscious control or manipulations.
DISORDERS OF THOUGHT
DISORDERED CONTENT
DELUSIONS
A delusion is a fixed false idea held in the face of evidence to the contrary, and out of
keeping with the patient’s social milieu.
• Held unshakeably.
• Not modified by experience or reason.
• Content often bizarre.
• Not dependent on disintegration of general intellectual functioning or reasoning
abilities.
• Often infused with a sense of great personal significance.
Types
• Autochthonous or primary delusions have no discernible connection with any pre-
vious interactions or experiences. They arise fully formed as sudden intuitions, like
sudden ‘brainwaves’. They are often preceded by a period of ‘delusional mood’ (or
‘delusional atmosphere’) in which the subject is aware of something strange hap-
pening; he/she then suddenly realizes the personal significance of this feeling with
a complete delusional understanding. This period of delusional perception is seen
as having two stages: first, the real perception of some object or event and, second,
the delusional misinterpretation of that event.
• Secondary delusions emerge understandably from other psychic experiences or current
preoccupations; e.g. prevailing affect, fears, personal stress, habitual attitudes of mind.
• Overvalued ideas are intense preoccupations with marked associated emotional
investment. The patient holds tenaciously to the idea, demonstrably false, with vir-
tual certainty but not unshakeable conviction.
PASSIVITY PHENOMENA
Passivity phenomena are a variety of phenomena which have in common the apparent
disintegration of boundaries between the self and the surrounding world. The individual
DISORDERS OF THOUGHT 17
experiences outside control of, or interference with, his/her thinking, feeling, perception
or behaviour.
• Thought insertion and withdrawal – the experience of thoughts being put into or
taken out of the mind by some external agency or force.
• Thought broadcast – the experience that others can read or hear the individual’s
thoughts as they are ‘broadcast’ from him or her.
• ‘Made actions’ – either simple motor actions or more complex patterns of behav-
iour are experienced as being caused by an outside agency.
ACCELERATED TEMPO
This produces increased rate of delivery of speech (‘pressure of speech’) and ‘flight of
ideas’. There is loss of coherent goal-directed thinking with increasingly obscure asso-
ciations between ideas. Vague connections may be prompted by rhyme, sounds of words
(‘clang associations’) and associations only acceptable in other contexts. Punning is
a common feature.
It is characteristic of hypomania, mania and may occur in delirium, and in rare
organic states, e.g. hypothalamic lesions.
• Desultory thinking – ideas are expressed correctly in terms of syntax and grammatical
construction, but juxtaposed inappropriately. The ideas would be comprehensible if
expressed in another context or in isolation.
DISORDERS OF EMOTION
• Mood – the emotional ‘tone’ prevailing at any given time. A ‘mood state’ will last
over a longer period.
• Affect – synonymous with ‘emotion’ and also meaning a short-lived feeling state.
Related to cognitive attitudes and understandings, and to physiological sensations.
When examining for disorders of emotion, look for:
1 The quality of the emotion: anxiety, sadness, cheerfulness, suspiciousness, irritabil-
ity, apathy
2 The appropriateness of the emotion to what is being said and to behaviour
3 The constancy of the emotion at interview and what factors appear to influence it.
DISORDERS OF SELF-AWARENESS
CONSCIOUSNESS
Consciousness is the state of awareness of the self and its environment. Reduced levels
of consciousness are seen in:
• Clouding of consciousness – disorientation in time, place, person, disturbances of
perception and attention and subsequent amnesia.
• Drowsiness – further reduction in level of consciousness, with unconsciousness if
unstimulated, but can be stimulated to a wakeful state.
• Stupor – further loss of responsiveness, which can be only aroused by considerable
stimulation. Awareness of environment is often maintained in depressive or catatonic
stupor, but not in organic stupor (cf. neurological and psychiatric definitions).
• Coma – profound reduction of conscious level with very little or no response to
stimulation.
The intensity and extent of attention may be abnormal, as may the ability to sustain
attention (i.e. to concentrate). Attention may be intensified in a restricted area in those
with preoccupations (depressive, hypochondriacal, etc.). Attention may be reduced or
absent in certain restricted areas in those with hysterical denial.
Attention may be easily distracted in hypomania or organic psychoses. In the latter,
the ability to concentrate may be very variable.
Tests of attention
1 Reverse order of months of year.
2 Subtraction of serial 7s from 100.
3 A series of digits repeated forwards and backwards.
Record time and accuracy for these tests.
MEMORY
Memory involves the registration of data, the retention in the mind and recall at will –
both immediately and at a later time. Thus anything interfering with registration (e.g.
alcohol, organic psychosis, head injury), retention (e.g. Korsakoff ’s psychosis) or
recall (organic or hysterical amnesia) will lead to defect of memory.
INSIGHT 21
Tests of memory
1 Recall of past personal life events which can be corroborated.
2 Recall of recent personal life events. Note any specific periods of amnesia (e.g. retro-
grade or anterograde amnesia) or any particular topics which are forgotten (e.g.
hysterical amnesia).
3 Short-term memory can be tested using recall of a simple name and address after
5 minutes, repeating a sentence (e.g. Babcock sentence) and digit span.
4 General knowledge tests (e.g. names of royal family, prime minister, recent events
in the newspapers, dates of first and second world wars).
Note any confabulation to fill in the memory gaps with false information.
Visuospatial functioning is tested by observation and by direct testing. Test the ability
to copy an asymmetrical object, to draw a clock face, to construct a star from match-
sticks (constructional dyspraxia). Test right–left orientation and ability to name fin-
gers (finger agnosia). Observe any difficulty in dressing and in finding his/her way
about (dressing apraxia, topographical disorientation).
INSIGHT
Amador XF, David AS (2004) Insight and Psychosis, 2nd edn. Oxford University Press, London.
Amador XF, Strauss DH, Yale SA, Flaum MM et al. (1993) Assessment of insight in psychosis.
Am. J. Psychiatry 150, 873.
American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders,
4th edn: DSM-IV-TR. American Psychiatric Association, Washington, DC.
Boyce WT, Essex MJ, Woodward HR et al. (2002) The confluence of mental, physical, social, and
academic difficulties in middle childhood. I: Exploring the ‘head waters’ of early life mor-
bidities. J. Am. Acad. Child Adolesc. Psychiatry 41, 580.
Chessick RD (2002) Psychoanalytic peregrinations. IV: What is phenomenology? J. Am. Acad.
Psychoanal. 30, 673.
Fabrega H (2001) Culture and history in psychiatric diagnosis and practice. Psychiatr. Clin. North
Am. 24, 391.
Flashman LA (2002) Disorder of awareness in neuropsychiatric syndromes: an update. Curr.
Psychiatry Rep. 4, 246.
Flashman LA, McAllister TW (2002) Lack of awareness and its impact in traumatic brain injury.
NeuroRehabilitation 17, 285.
Hamilton M (ed.) (1974) Fish’s Clinical Psychopathology. Wright, Bristol.
Harrison PJ (1991) Are mental states a useful concept? Neurophilosophical influences on phe-
nomenology and psychopathology. J. Nerv. Ment. Dis. 179, 309.
Jaspers K (1959) General Psychopathology, 7th edn, trans. Hoenig J and Hamilton M. Manchester
University Press, Manchester.
Leff JP, Isaacs AD (eds) (1981) Psychiatric Examination in Clinical Practice, 2nd edn. Blackwell
Scientific, Oxford.
Lewis A (1934) The psychopathology of insight. Br. J. Med. Psychol. 14, 332.
Manschreck TC (1992) Delusional disorders. Psych. Ann. 22(5).
Markova IS, Berios GE (1992) The meaning of insight in clinical psychiatry. Br. J. Psychiatry
160, 850.
Maser JD, Patterson T (2002) Spectrum and nosology: implications for DSM-V. Psychiatr. Clin.
North Am. 25, 855.
McDougall GM, Reade B (1993) Teaching biopsychosocial integration and formulation. Can.
J. Psychiatry 38(5), 359.
McGuire MD, Marks I, Neese RM et al. (1992) Evolutionary biology: a basic science for psychi-
atry? Acta Psychiatr. Scand. 86, 89.
REFERENCES AND FURTHER READING 23
Miller LJ, O’Connor E, DiPasquale T (1993) Patients’ attitudes toward hallucinations. Am. J.
Psychiatry 150(4), 584.
Mortimer AM (1992) Phenomenology: its place in schizophrenia research. Br. J. Psychiatry
161, 293.
Schneider K (1959) Clinical Psychopathology, trans. Hamilton M. Grune & Stratton, New York.
Sims A (ed.) (1988) Symptoms of the Mind: an Introduction to Descriptive Psychopathology.
Ballière Tindall, London.
Spitzer M (1992) The phenomenology of delusions: the need for a detailed description of symp-
toms. Psych. Ann. 22(5), 252.
World Health Organization (1992) The ICD-10 Classification of Mental and Behavioural
Disorders: Clinical Descriptions and Diagnostic Guidelines. WHO, Geneva.
Schizophrenia 3
CONCEPTS
OTHER CONCEPTS/CLASSIFICATIONS
• Langfeldt (1939): process schizophrenia (insidious onset, chronic course) versus
schizophreniform (acute onset, affective symptoms, good outcome).
• Leonhard (1957): systemic schizophrenia (catatonia, hebephrenia, paraphrenia)
versus non-systemic (affect-laden paraphrenia, schizophasia and periodic
catatonia).
• Strömgen (1968): brief reactive psychosis (‘psychogenic psychosis’).
• Schneider (1959): strict phenomenological approach, devoid of aetioloical theory.
SYMPTOM RANKING
• ICD-10 (International Classification of Diseases, 10th edn; WHO, 1992; see Table 3.1).
This groups together schizophrenia, schizotypal states and delusional disorder. It has
greater congruence with the DSM system (see below), but differs because there is
more reliance on FRS. Only one month’s illness duration is necessary. The category of
post-schizophrenic depression is included.
• DSM-IV (APA, 1994; see Table 3.2). This was developed from DSM-III-Revised.
There is greater emphasis on negative symptoms. Delusional disorder is not classi-
fied separately. There is no mention of prodromal symptoms. Schizoaffective dis-
order is not classified under Mood.
Table 3.3 compares ICD-10 and DSM-IV.
A minimum of 1 very clear symptom (and usually ⭓2 if less clear-cut) from groups (a)–(d) below, or symptoms
from ⭓2 of the groups (e)–(h), which have been present for most of the time during a period of 1 month
or more:
VIEW 1
Schizophrenia is a single aetiopathological process leading to diverse manifestations
(e.g. neurosyphilis).
VIEW 2
There are multiple disease entities of different aetiopathological processes leading to
schizophrenia (e.g. mental retardation, epilepsy).
A. Characteristic symptoms: ⭓2 of the following, present for a significant time period during 1 month (or less if
successfully treated):
(1) delusions
(2) hallucinations
(3) disorganized speech (e.g. frequent derailment or incoherence)
(4) grossly disorganized or catatonic behaviour
(5) negative symptoms (e.g. affective flattening, alogia, avolition)
[NB: Only one ‘A’ symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a
running commentary on the person’s behaviour or thoughts, or two or more voices conversing.]
B. Social/occupational dysfunction: For a significant time-period since the illness onset, ⭓1 major area of
functioning such as work, interpersonal relations or self-care is markedly below the level achieved prior to the
onset (or of onset in childhood/adolescence – failure to achieve expected level of interpersonal, academic, or
occupational achievement).
C. Duration: Continuous signs of illness for ⭓6 months; period must include at least one month of symptoms
that meet criterion ‘A; (i.e. active-phase symptoms), and may include periods of prodromal or residual
symptoms. During prodromal or residual periods, illness may manifest by only negative symptoms or
⭓2 symptoms listed in criterion ‘A’ present in attenuated form (e.g. odd beliefs, unusual perceptual
experiences).
D. Schizoaffective and mood disorder exclusion: Schizoaffective disorder and mood disorder with psychotic
features have been ruled out since: (1) no major depressive or manic episodes occurred concurrently with
active-phase symptoms; or (2) if mood episodes occurred during active-phase symptoms, their total duration
was brief relative to the duration of active and residual periods.
E. Substance/general medical condition exclusion: Not due to the direct effects of a substance (e.g. drugs of
abuse, medication) or a general medical condition.
Subtypes:
• Paranoid – prominent delusions and/or auditory hallucinations.
• Catatonic – dominated by stupor, negativism, posturing.
• Disorganized – prominent disorganization of speech and behaviour, inappropriate/flat affect.
• Undifferentiated – prominent delusions, hallucinations, disorganization; but not meeting criteria of other
types.
• Residual – meets ‘A’ criteria but criteria for other subtypes no longer met; yet some continuing disturbance
(i.e. negative symptoms).
Schizophreniform disorder: Meets ‘A’, ‘D’ and ‘E’ criteria but episode greater than 1 month, less than 6 months.
28 SCHIZOPHRENIA
Table 3.3 ICD-10 and DSM-IV classifications of schizophrenia and schizophrenia-like disorders
ICD-10 DSM-IV
Schizophrenia Schizophrenia
– paranoid – paranoid
– hebephrenia – disorganized
– catatonic – catatonic
– undifferentiated – undifferentiated
– residual – residual
Post-schizophrenic depression
Simple schizophrenia
Other schizophrenia
Unspecified schizophrenia
Schizoaffective disorder Schizoaffective disorder
Schizotypal disorder
Persistent delusional disorder Delusional disorder
Acute and transient psychotic disorder Brief psychotic disorder
Induced psychotic disorder Schizophreniform disorder
Shared psychotic disorder
Psychotic disorder
Other non-organic psychotic disorder caused by Psychotic disorder
a medical condition
Unspecified non-organic psychosis Substance-induced psychosis
Psychotic disorder not otherwise specified
VIEW 3
There are specific symptom clusters within schizophrenia reflecting different disease
processes that combine differently in patients.
• Neurodevelopment (Lewis and Levitt, 2002; Keshavan and Murray, 2004) – static
lesion from CNS disruption in utero; typical symptoms emerge later. Evidence
includes:
– Post-mortem and neuroimaging findings.
– Excess of obstetric complications, minor physical anomalies, abnormal
dermatoglyphics.
– Season of birth phenomenon.
– Epidemiological association with prenatal exposure to influenza infection.
• Neurodegenerative – progressive degeneration (Kraepelin). Evidence includes:
– Deteriorative course of illness.
– Gliosis seen in earlier post-mortem (PM) studies, but not found in recent PM
studies.
This view holds that there is a single psychosis, with schizophrenia most severe, affective
disorders least severe, schizoaffective disorders occupying an intermediate position.
EPIDEMIOLOGY
INCIDENCE
• 15–20 per 100 000 per year.
• 6–8 fold increased incidence among Britains of Afro-Caribbean family descent
(Harrison et al., 1988).
• Lifetime risk: 0.9 per cent.
• Median age at onset: males ⫽ 28 years, females ⫽ 32 years.
30 SCHIZOPHRENIA
PREVALENCE
• 0.5–1 per cent; higher in Sweden, Croatia, Southern India; lower among US
Hutterites.
• Increased prevalence among lower social classes – the breeder hypothesis (poor social
conditions inducing schizophrenia) versus the social drift hypothesis (patients drift
down the social scale while paternal occupations show normal class distribution).
• Increased prevalence in urban versus rural settings, especially for males.
MORTALITY
Between 4 and 10 per cent die by suicide (see Chapter 11). There are also increased
cardiovascular and respiratory deaths, and deaths by homicide.
AETIOLOGICAL FACTORS
GENETICS
Family studies
See Table 3.4. There is a 0.5 per cent morbid risk in relatives of normal subjects.
Twin studies
Twin studies address the nature/nurture issue. Monozygotic:dizygotic (MZ:DZ)
rate ⫽ 48%:4%, suggesting a strong genetic component (especially for paranoid sub-
type). However, MZ twins discordant for schizophrenia show more brain abnormali-
ties than the normal co-twin (Suddath et al., 1990).
Parent 5
Sibling 10
Child of schizophrenic 14
Child of two schizophrenics 46
AETIOLOGICAL FACTORS 31
Adoptive studies
Adoptive studies test for genetic versus environmental influences by examining rates
of schizophrenia in adopted-away offspring of schizophrenic and of normal parents.
Results: 10 per cent and 13 per cent, versus 0 per cent from normal parents.
Schizophrenia spectrum
‘Good genetics requires good phenotypes’ (Kendler and Diehl, 1993) – unclear whether
genetic liability is restricted (to schizophrenia only) or broad (many disorders)? Studies
(Kendler and Diehl, 1993) suggest a moderate inheritance risk which includes
schizophrenia-like personality disorders and schizophrenia-like non-affective psychoses.
See Table 3.5.
Molecular genetics
This is a major focus of research (Waterwort et al., 2002). How many genes are
involved? Where are they? How common are they? What is their functional impact:
• Effect on cellular processes (functional genomics)?
• Effect on protein development and expression (proteomics)?
Genome-wide scans provide evidence (but confusing and inconsistent) of suscepti-
bility genes on chromosome 5, 6, 8, 10, 13, 15, 22; research is complicated by differing
thresholds Lod score values for linkage analysis, diagnostic variability, phenocopy
selection.
Recent focus has been on candidate genes; e.g. chromosome 15 abnormal alleles at
the locus of the alpha-7 nicotinic acetylcholine receptor subunit gene, and abnormal
alleles on chromosome 6 region related to dysbindin (a developmental protein) gene.
Polymorphisms of COMT (catechol O-methyltransferase) gene are associated with
poorer prefrontal cortex functioning in schizophrenia (Weinberger et al., 2001).
There is intense interest in examining genes regulating neurodevelopment (e.g. SNAP
23 – synaptosomal-associated protein 23, neuroregulin) to determine whether these are
differentially expressed (under/over-expressed, different alleles) in schizophrenia.
The genetics of treatment response (pharmacogenetics) is now also a major focus
(Malhotra, 2001).
Vulnerability markers
• Evoked potential (P 300) abnormalities in ‘unaffected’ first-degree relatives.
• Smooth-pursuit eyetracking abnormalities in 34 per cent of parents of schizo-
phrenics (Holzman et al., 1974) and in schizotypal patients (Siever et al., 1993).
High-risk studies
Repeated, longitudinal evaluations (cognitive, neurological, psychiatric) of children of
schizophrenic parents suggest early, subtle manifestations of schizophrenic genotype
(CNS soft signs, attentional deficits, social deficits – ‘pandysmaturation’; Fish et al.,
1992). The general pattern of CNS maldevelopment permits evaluation of relative
genetic and environmental contributions to illness (Cannon et al., 1993).
Prodromal studies
There is intense interest in early detection of psychosis in the prodrome stage
(McGorry et al. 2003; McGlashan, 2003). Educational programmes may help bring
patients into treatment earlier – shorten the duration of untreated psychosis (DUP)
which may be ‘biologically toxic’. Early use of antipsychotics may delay onset of
psychosis (McGorry et al., 2002). These approaches are contentious and of ethical
concern (McGlashan, 2001).
NEUROCHEMISTRY
Dopamine hypothesis
This view postulates dopamine (DA) overactivity in mesolimbic pathways. It is a very
influential theory, largely based on:
Serotonin (5-HT)
• LSD (5-HT agonist) induces psychosis; m-chlorophenyl-piperazine (MCPP; a
5-HT agonist) worsens psychosis.
• Ritanserin (5-HT2/5-HT1c antagonist) improves psychosis; clozapine (5-HT2
antagonist) is an effective treatment for psychosis.
Noradrenaline
• There is evidence for over- and underactivity; clozapine induces potent noradren-
ergic blockage.
NEUROPATHOLOGY
NEUROIMAGING
LIFE EVENTS
FAMILY DYNAMICS
MANAGEMENT
clozapine (Meltzer et al., 2003) and a possible antiaggressive effect (Buckley et al.,
2003).
However, medication and treatment compliance is a major challenge (Lacro et al., 2002).
PSYCHOTHERAPY
Psychotherapy is supportive, practical problem-oriented, and encourages compliance.
Cognitive–behavioral therapy (CBT) is now advocated for persistent delusions
Family intervention 10 33
Routine treatment 48 71
36 SCHIZOPHRENIA
PROGNOSIS
SCHIZOAFFECTIVE DISORDER
Kasanin (1933) described patients with illness of both affective and schizophrenic
symptoms, with sudden onset after a stressor, and good premorbid adjustment.
Subsequent definitions and application of different diagnostic criteria led to confusion
and poor reliability of schizoaffective (SA) disorder – ⫽ 0.19 for concordance among
seven diagnostic criteria (Brockington and Leff, 1979). See Table 3.8.
A. Uninterrupted period of illness during which, at some instances, either a major depressive or manic episode is
concurrent with symptoms satisfying criterion ‘A’ for schizophrenia.
B. Delusions or hallucinations present for 2 weeks during the same period of illness in the absence of
prominent mood symptoms.
C. Mood symptoms present for significant extent of total duration of active and residual phases of the illness.
D. Exclusion of substance/general medical condition.
Subtypes: bipolar, depressive.
DELUSIONAL DISORDER 37
SA is unlikely to be either:
• Co-occurrence of schizophrenia and affective disorder in a patient.
• A separate disease entity.
SA is more likely to be either:
• A subtype of schizophrenia.
• A subtype of affective disorder.
• A heterogeneous disorder, intermediate between schizophrenia and affective dis-
order (i.e. continuum model).
Available data from family and twin studies suggest a continuum.
A schizodepressive subtype is more related to schizophrenia; a schizomanic subtype is
more related to affective disorder.
DELUSIONAL DISORDER
Subtypes:
• Persecutory.
• Jealous (corresponds to description of ‘morbid jealously’ – Shepperd, 1961).
• Erotomanic (corresponds to description of ‘de Clerambaut’s Syndrome, see Chapter 15).
• Somatic (corresponds to description of ‘monosymptomatic hypochondrical psychosis – Munro, 1992).
• Grandiose.
• Mixed and unspecified.
Genetic and outcome studies support the present classification under the rubric of
schizophrenia/related psychotic disorders. See Tables 3.10 and 3.11.
Adams CE, Fenton KP, Quraishi S, David AS (2001) Systematic meta-review of depot antipsy-
chotic drugs for people with schizophrenia. Br. J. Psychiatry 179, 290.
Adler CM, Strakowski SM (2003) Boundaries of schizophrenia. Psychiatr. Clin. North Am. 26, 1.
Aleman A, Khan RS (2001) Effects of the atypical antipsychotic risperidone on hostility and aggres-
sion in schizophrenia: a meta-analysis of controlled trails. Eur. Neuropsychopharmacol. 11, 289.
REFERENCES AND FURTHER READING 39
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders,
4th edn. APA, Washington, DC.
Andreasen NC, Flam M, Swayze VW et al. (1990) Positive and negative symptoms of schizophre-
nia. Arch. Gen. Psychiatry 47, 615.
Arseneault L, Cannon M, Murray R et al. (2003) Chidlhood origins of violent behaviour in adults
with schizophreniform disorder. Br. J. Psychiatry 183, 520.
Basile VS, Masillis M, Potkin SG, Kennedy JL (2002) Pharmacogenomics in schizophrenia: the
quest for individual therapy. Hum. Mol. Genet. 11, 2517.
Buckley PF, Noffsinger SG, Smith DA et al. (2003) Treatment of the psychotic patient who is vio-
lent. Psychiatr. Clin. North Am. 236, 231.
Braff DL (1993) Information processing and attention dysfunctions in schizophrenia. Schiz. Bull.
19, 233.
Brockington IF, Leff JP (1979) Schizoaffective psychoses: definitions and incidence. Psychol. Med.
8, 91.
Callicott JH, Egan MF, Mattay VS et al. (2003) Abnormal fMRI response of the dorsolateral
prefrontal cortex in cognitively intact siblings of patients with schizophrenia. Am. J.
Psychiatry 160, 709.
Cannon TD, Mednick SA, Parnas J et al. (1993) Developmental brain abnormalities in the off-
spring of schizophrenic mothers. I: Contributions of genetic and perinatal factors. Arch. Gen.
Psychiatry 50, 551.
Cannon TD, Huttunen MO, Dahlstrom M et al. (2002) Antipsychotic drug treatment in the pro-
dromal phase of schizophrenia. Am. J. Psychiatry 159, 1230.
Carlsson A (1995) Dopamaine hypothesis of schizophrenia. In: Hirsch SR, Weinberger DR (eds),
Schizophrenia, Blackwell Scientific, London.
Carpenter WT, Strauss J (1991) The prediction of outcome in schizophrenia. IV: Eleven-year
follow up of the Washington IPSS cohort. J. Nerv. Ment. Dis. 179, 517.
Carpenter WT, Wagman AH, Kirkpatrick BK (1988) The deficit syndrome: concept and charac-
teristics. Am. J. Psychiatry 145, 168.
Chakos M, Lieberman J, Hoffman E et al. (2002) Effectiveness of second-generation antipsy-
chotics in patients with treatment resistant schizophrenia: a review and meta-analysis of ran-
domized trials. Am. J. Psychiatry 158, 518.
Cotter D, Pariante CM (2002) Stress and the progression of the developmental hypothesis of
schizophrenia. Br. J. Psychiatry 181, 363.
Crow TJ (1980) Schizophrenia: more than one molecular process. BMJ 280, 66.
Crow TJ (1990) Nature of the genetic contribution to psychotic illness: a continuum viewpoint.
Acta Psychiatr. Scand. 81, 401.
Crow TJ, Done DJ (1992) Prenatal exposure to influenza does not cause schizophrenia. Br. J.
Psychiatry 161, 390.
Daniel DG, Potkin SG, Reeves KR et al. (2001) Intramuscular (IM) ziprasidone 20 mg is effective
in reducing acute agitation associated with psychosis: a double-blind randomized trail.
Psychopharmacology 155, 128.
Duke PJ, Pantelis C, McPhillips MA, Banes TRE (2001) Comorbid non-alcohol substance misuse
among people with schizophrenia. Br. J. Psychiatry 179, 509.
Egan MF, Golberg TE, Kolachana BS et al. (2001) Effect of COMT Val108/159 Mer genotype on
frontal lobe function and risk for schizophrenia. Proc. Natl. Acad. Sci. USA 98, 6917.
Farde L, Wiesel F-A, Hall H et al. (1987) No D2 receptor increase in PET study of schizophrenia.
Arch. Gen. Psychiatry 44, 671.
Fayek M, Flowers C, Signorelli D, Simpson G (2003) Psychopharmacology: underuse of
evidence-based treatments in psychiatry. Psychiatr. Serv. 54, 1453.
Fish B, Marcus J, Hans SL et al. (1992) Infants at risk for schizophrenia: sequelae of a genetic neu-
rointegrative defect. Arch. Gen. Psychiatry 49, 221.
40 SCHIZOPHRENIA
Freedman R, Leonard S, Gault JM et al. (2001a) Linkage disequilibrium for schizophrenia at the
chromosome 15 q13-14 locus of the alpha7-nicotinic acetylcholine receptor subunit gene
(CHRNA7). Am. J. Med. Genet. 105, 20.
Freedman R, Leonard S, Olincy A et al. (2001b) Evidence for the multigenic inheritance of schiz-
ophrenia. Am. J. Med. Genet. 105, 794.
Freidman JI, Adler DN, Temporini HD et al. (2001) Guanfacine treatment of cognitive impair-
ment in schizophrenia. Neuropsychopharmacology 25, 402.
Fuller R, Nopoulos P, Arndt S et al. (2002) Longitudinal assessment of premorbid cognitive func-
tioning in patients with schizophrenia through examination of standardized scholastic test
performance. Am. J. Psychiatry 159, 1183.
Glatt SJ, Faraone SV, Tsuang MT (2003) Meta-analysis identifies an association between the
dopamine D2 receptor gene and schizophrenia. Mol. Psychiatry 8, 911.
Grace AA (1992) The depolarization block hypothesis of neuroleptic action; implications for the
etiology of schizophrenia. J. Neur. Trans. 536, 91.
Harrison G, Mace P (1993) Falling incidence and better outcome? Br. J. Psychiatry 163, 535.
Harrison G, Owens D, Holton T et al. (1988) A prospective study of severe mental disorder in
Afro-Caribbean patients. Psychol. Med. 18, 643.
Harrison G, Hopper K, Craig T et al. (2001) Recovery from psychotic illness: a 15- and 25-year
follow-up study. Br. J. Psychiatry 178, 506.
Hirsch SR, Weinberger DR (2003) Schizophrenia. Blackwell Scientific, London.
Holzman PS, Proctor LR, Levy DL et al. (1974) Eye-tracking dysfunction in schizophrenics and
their relatives. Arch. Gen. Psychiatry 31, 143.
Jablensky A, Sartorius N, Ernberg G et al. (1992) Schizophrenia: manifestations, incidence and
course in different cultures. A World Health Organization Ten-Country Study. Psychol. Med.
(Monograph Suppl. 20).
Jones HM, Pilowsky LS (2002) Dopamine and antipsychotic drug action revisited. Br. J.
Psychiatry 181, 271.
Jones PL, Buckley P (2003) Rapid Reference to Schizophrenia. Mosby, Philadelphia.
Joubert AF (2003) Providing quality care to patients with schizophrenia. Psychiatr. Clin. North
Am. 26, 213.
Kahn RS, Davidson M (1993) On the value of measuring dopamine, norepinephrine and their
metabolites in schizophrenia. Neuro-psychopharmacology 8, 93.
Kane J, Honigfeld G, Singer J et al. (1988) Clozapine for the treatment of resistant schizophrenia:
a double-blind comparison with chlorpromazine. Arch. Gen. Psychiatry 45, 789.
Kapur S (2002) Psychosis as a state of aberrant salience: a framework linking biology, phenom-
enology, and pharmacology in schizophrenia. Am. J. Psychiatry 160, 3.
Kavanaugh DJ, McGrath J, Saunders JB et al. (2002) Substance misuse in patients with schizo-
phrenia. Drugs 62, 743.
Kendler KS, Diehl SR (1993) The genetics of schizophrenia. Schiz. Bull. 19, 261.
Keshavan M, Murray M (2004) Neurodevelopment and Adult Psychopathology. Oxford University
Press, London.
Kubicki M, Westin CG, Maier S et al. (2002) Uncinate fasciculus findings in schizophrenia: a
magnetic resonance diffusion tensor imaging study. Am. J. Psychiatry 159, 813.
Lacro JP, Dunn LB, Leckband SG, Jeste DV (2002) Prevalence of and risk factors for medication
nonadherence in patients with schizophrenia: a comprehensive review of recent literature.
J. Clin. Psychiatry 63, 892.
Larsen TK, McGlashan TH, Johannessen JO et al. (2001) Shortened duration of untreated first
episode of psychosis: changes in patient characteristics at treatment. Am. J. Psychiatry 158, 1917.
Lauriello J, Lenroot R, Bustillo JR (2003) Maximizing the synergy between pharmacotherapy and
psychosocial therapies for schizophrenia. Psychiatr. Clin. North Am. 26, 191.
Lawrie SM, Whalley HC, Abukmel SS et al. (2002) Temporal lobe changes in people at high risk
of schizophrenia with psychotic symptoms. Br. J. Psychiatry 181, 138.
REFERENCES AND FURTHER READING 41
Levey DL, Holzman PS, Matthysse S (1993) Eye-tracking dysfunction and schizophrenia: a crit-
ical perspective. Schiz. Bull. 19, 461.
Lewis DA (2002) Atypical antipsychotic medications and the treatment of schizophrenia. Am. J.
Psychiatry 159, 177.
Lewis DA, Levitt P (2002) Schizophrenia as a disorder of neurodevelopment [review]. Annu. Rev.
Neuroscience 25, 409.
Lewis S, Tarrier N, Haddock G et al. (2002) Randomised controlled trial of cognitive–behavioural
therapy in early schizophrenia: acute-phase outcomes. Br. J. Psychiatry 181 (Suppl. 43), s91.
Liu H, Heath SC, Sobin C et al. (2002) Genetic variation at the 22 q11 PRODH2/DGCR6 locus
presents an unusual pattern and increases susceptibility to schizophrenia. Proc. Natl. Acad.
Sci. USA 99, 2717.
Malhotra AK (2001) Pharmacogenomics and schizophrenia: clinical implications. Pharmacogenomics
1, 109.
Mathalon DH, Sullivan EV, Lim KO, Pfefferbaum A (2001) Progressive brain volume changes
and the clinical course of schizophrenia in men: a longitudinal magnetic resonance imaging
study. Arch. Gen. Psychiatry 58, 148.
Maynard TM, Sikich L, Lieberman JA, LaMantia AS (2001) Neural development, cell–cell signal-
ing, and the two-hit hypothesis of schizophrenia. Schizophr. Bull. 273, 457.
McGlashan TH (2001) Psychosis treatment prior to psychosis onset: ethical issues. Schizophr. Res.
51, 47.
McGlashan TH (2003) Commentary: progress, issues and implications of prodromal research:
an inside view. Schizophrenia Bull. 29, 851.
McGorry PD, Yung AR, Phillips LJ et al. (2002) A randomized controlled trial of interventions
designed to reduce the risk of progression to first episode psychosis in a clinical sample with
subthreshold symptoms. Arch. Gen. Psychiatry 59, 921.
McGorry PD, Yung AR, Philips LJ (2003) The “close-in” as ultra high-risk model: a safe and
effective strategy for research and clinical intervention in prepsychotic mental disorder.
Schizophrenia Bull. 29, 771.
Medalia A, Revheim N, Casey M (2002) Remediation of problem-solving skills in schizophrenia:
evidence of a persistent effect. Schizophr. Res. 57, 165.
Meltzer HY, Alphs L, Green AI et al. (2003) Clozapine treatment for suicidality in schizophrenia:
International Suicide Prevention Trail (InterSePT). Arch. Gen. Psychiatry 60, 82.
Munro A (1992) Delusional disorders: clinical concepts and diagnostic strategies. Psych. Ann. 22, 241.
Newcomer JW, Haupt DW, Fucetola R et al. (2002) Abnormalities in glucose regulation during
antipsychotic treatment of schizophrenia. Arch. Gen. Psychiatry 59, 337.
Nose M, Barbui C, Gray R, Tansella M (2003) Clinical interventions for treatment non-adherence
in psychosis: meta-analysis. Br. J. Psychiatry 183, 197.
Os JV, McGuffin P (2003) Can the social environment cause schizophrenia? Br. J. Psychiatry 182, 291.
Rasanen S, Hakko H, Viilo K et al. (2003) Excess mortality among long-stay psychiatric patients
in Northern Finland. Soc. Psychiatry Psychiatr. Epidemiol. 38, 297.
Reichenberg A, Weiser M, Rabinowitz J (2002) A population-based cohort study of premorbid
intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaf-
fective disorder, and nonpsychotic bipolar disorder. Am. J. Psychiatry 159, 2027.
Reynolds GP, Zhang ZJ, Zhang XB (2002) Association of antipsychotic drug-induced weight gain
with a 5-HT2C receptor gene polymorphism. Lancet 259, 2086.
Rosh A, Sampson BA, Hirsch CS (2003) Schizophrenia as a cause of death. J. Forensic. Sci. 48, 164.
Roth, Sir Martin (1991) Regarding the causation of paranoid disorders and the relationship to
other psychiatric illnesses. In: Weller MPI (ed.), International Perspectives on Schizophrenia.
John Libby, Oxford.
Seidman LJ, Faraone SV, Goldstein JM et al. (2002) Left hippocampal volume as a vulnerability
indicator for schizophrenia: a magnetic resonance imaging morphometric study of nonpsy-
chotic first-degree relatives. Arch. Gen. Psychiatry 59, 839.
42 SCHIZOPHRENIA
Sernyak MJ, Leslie DL, Alarcon RD et al. (2002) Association of diabetes mellitus with use of atyp-
ical neuroleptics in the treatment of schizophrenia. Am. J. Psychiatry 159, 561.
Sharma T, Antonova L (2003) Cognitive function in schizophrenia: deficits, functional conse-
quences, and future treatment. Psychiatr. Clin. North Am. 26, 25.
Shenton ME, Dickey CC, Frumin M, McCarley RW (2001) A review of MRI findings in schizo-
phrenia. Schizophr. Res. 49, 1.
Siever LJ, Kalus OF, Keefe RSE (1993) The boundaries of schizophrenia. In: Powchic P, Schulz SC
(eds), The Psychiatric Clinics of North America. WB Saunders, Philadelphia.
Siris SG (2001) Suicide and schizophrenia [review]. J. Psychopharmacol. 15, 127.
Smith TE, Hull JW, Huppert JD, Silverstein SM (2002) Recovery from psychosis in schizophrenia
and schizoaffective disorder: symptoms and neurocognitive rate-limiters for the develop-
ment of social behavior skills. Schizophr. Res. 55, 229.
Suddath RL, Christison GW, Torrey EF et al. (1990) Anatomical abnormalities in the brains of
monozygotic twins discordant for schizophrenia. New Engl. J. Med. 322, 789.
Tait L, Birchwood M, Trower P (2003) Predicting engagement with services for psychosis: insight,
symptoms and recovery style. Br. J. Psychiatry 182, 123.
Thompson PM, Vidal C, Giedd JN et al. (2001) Mapping adolescent brain change reveals dynamic
wave of accelerated gray matter loss in very early-onset schizophrenia. Proc. Natl. Acad. Sci.
USA 98: 11650.
Tienari P, Wynne LC, Sorri A et al. (2004) Genotype–environmental interaction in
schizophrenia–spectrum disorder: long-term follow-up of Finnish adoptees. Br. J. Psychiatry
184, 216.
Turnington D, Kingdon D, Turner T (2002) Effectiveness of a brief cognitive–behavioral therapy
intervention in the treatment of schizophrenia. Br. J. Psychiatry 180, 523.
Vaughn C, Leff JP (1976) The influence of family and social factors on the course of schizo-
phrenic illness. Br. J. Psychiatry 129, 125.
Walsh E, Buchanan A, Fahy T (2002) Violence and schizophrenia: examining the evidence. Br. J.
Psychiatry 180, 490.
Walsh E, Moran P, Scott C et al. (2003) Prevalence of violent victimisation in severe mental ill-
ness. Br. J. Psychiatry 183, 233.
Waterwort DM, Bassett AS, Brzustowicz LM (2002) Recent advances in the genetics of schizo-
phrenia. Cell. Mol. Life Sci. 59, 331.
Weinberger DR, Egan MF, Bertolino A et al. (2001) Prefrontal neurons and the genetics of schizo-
phrenia. Biol. Psychiatry 50, 825.
Weinberger DR, McClure RK (2002) Neurotoxicity, neuroplasticity, and magnetic resonance
imaging morphometry: what is happening in the schizophrenic brain? Arch. Gen. Psychiatry
59, 553.
Wong DF, Wagner HN, Tune LE et al. (1986) Positron emission tomography reveals elevated D2
dopamine receptors in drug-naive shizophrenics. Science 234, 1558.
World Health Organization (1992) The ICD-10 Classification of Mental and Behavioural
Disorders: Clinical Descriptions and Diagnostic Guidelines. WHO, Geneva.
Wykes T, Brammer M, Mellers J et al. (2002) Effects on the brain of a psychological treatment.
Cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia.
Br. J. Psychiatry 181, 144.
Zygmunt A, Olfson M, Boyer CA et al. (2002) Interventions to improve medication adherence in
schizophrenia. Am. J. Psychiatry 159, 1653.
Affective disorders 4
CLASSIFICATIONS
CLINICAL FEATURES
Mood
• Persistent depression of mood.
• Qualitatively different from normal unhappiness.
• Loss of reactivity to circumstances (‘autonomous’).
• Diurnal rhythm.
• Pervasive.
Speech and cognition
• Decreased tempo and reduction in quantity of speech.
• Guilt, self-blame, worthlessness and hypochondriasis.
• Impaired concentration or slowed thinking, indecisiveness, not associated with
incoherence or loosening of associations.
• Suicidal, morbid and paranoid ideation.
Somatic/biological/behavioural features
• Poor appetite, weight loss or, less commonly, increased appetite or significant
weight gain.
• Insomnia or hypersomnia – characteristic early morning wakening but also onset
of insomnia.
• Psychomotor retardation, agitation – loss of energy and fatigue, decreased libido
and loss of interest in pleasure and work activities.
Mood
• Persistent elevation of mood.
• Irritability a common feature.
• May be intermingled with transient depression of mood (‘manic’/‘hypomanic’
may be used to indicate degree of severity, or presence or absence of delusions and
hallucinations).
Somatic/biological/behavioural features
• Increased drive and activity: physical, social, work, libido.
• Excessive activity in risk-taking pursuits, indiscretion socially.
• Insomnia often earliest sign, but no fatigue (EEG shows reduction in delta sleep)
• Appetite good; weight loss is due to overactivity.
EPIDEMIOLOGY
Other observations
• There is concern over increased depression and bipolar illness in young people.
• Onset:
– Bipolar disorder most often in mid-20s.
– Unipolar disorder in late 20s.
– Women have peak onset in 30s, males in 40s.
• There is a higher prevalence of depression in lower social group females (Brown
and Harris, 1978).
• Prevalence is higher in urban areas and among the divorced.
• Ethnic differences in the USA appear more related to social class differences.
Depression may be becoming more common. From 1910 to 1950 the risk of depres-
sion rose in each generation with associated earlier age at onset – the ‘birth cohort effect’.
Unipolar depression was the biggest cause of lifetime disability in the WHO Global
Burden of Disease study.
AETIOLOGICAL FACTORS
GENETICS
Family studies
High rates of mood disorders have been found in first-degree relatives of bipolar
patients – about 20 per cent. The rate of mood disorder in first-degree relatives of
unipolar patients is about 10 per cent.
AETIOLOGICAL FACTORS 47
Bipolar adoptees 28 12
Bipolar non-adoptees 26 –
Normal controls 5 9
Unipolar forms tend to ‘breed true’, but bipolar forms are associated with elevated
risk of both unipolar and bipolar disorder in relatives.
Twin studies
• Unipolar – MZ:DZ ⫽ 54%:24%.
• Bipolar – MZ:DZ ⫽ 79%:19%.
Adoptive studies
Mendlewicz and Rainer (1977) studied relatives of adult bipolar probands who
had been adopted early in life and compared them with those of normal adoptees,
biological parents of patients with poliomyelitis and bipolar non-adoptees (see
Table 4.2).
Molecular genetics
This is a major area of research. For bipolar disorder, genome-wide search reveals
evidence of susceptibility genes on chromosomes 4, 12, 13, 18, 21 and 22 (Berrettini,
2001; Liang et al., 2002; Sklar, 2002; Shaw et al., 2003). Chromosomes 13 and 22 are
also associated with schizophrenia (see Chapter 3).
For unipolar depression, studies suggest that genetic factors may account for 40–70
per cent of the risk. Genome-wide search reveals susceptibility genes on chromosomes
1, 2, 5, 8, 10, 11, 15, 18, 19 (Zubenko et al., 2003).
NEUROCHEMISTRY
NEUROTRANSMITTER ABNORMALITIES
Serotonin
Evidence includes:
• Decreased:
– Plasma tryptophan
– CSF 5-hydroxyindoleacetic acid (5-HIAA) (especially in suicides)
– Platelet 5-HT uptake
– 3H-imipramine binding in platelet, in frontal cortex, and in hippocampus
– Prolactin response to neuroendocrine challenge tests (intravenous tryptophan,
oral fenfluramine) – responses are then normalized with antidepressant therapy.
• Increased:
– 5-HT2 receptor binding in platelets, in cortex of suicides.
48 AFFECTIVE DISORDERS
Noradrenaline
Evidence includes:
• Decreased:
– Growth hormone response to neuroendocrine challenge tests (amphetamine,
clonidine, desipramine)
– Platelet CAMP turnover with stimulation by clonidine.
• Increased:
– Platelet ␣2-adrenergic-receptor binding
– Beta-adrenergic receptors in suicides.
• Normal:
– CSF, plasma, urinary measures of noradrenaline and MHPG.
Acetylcholine
There is little evidence of abnormality, apart from the cholinergic basis for sleep dis-
turbances in affective disorder (see Chapter 14), findings which are consistent with
postsynaptic muscarinic supersensitivity.
Dopamine
There have been mixed results in studies of neuroendocrine responses to either apo-
morphine or amphetamine.
NEUROENDOCRINE ABNORMALITIES
• There is blunted growth hormone in response to insulin challenge, and blunted
thyroid-stimulating hormone in response to TRH.
• Hypercortisolaemia and loss of normal circadian rhythm of cortisol.
• Failure of cortisol suppression in a dexamethasone suppression test (DST) is seen
in 50–60 per cent of depressed patients. Initial optimism that this would be a ‘trait’
marker rather than a ‘state’ marker has not held up, and DST non-suppression is
seen also in alcoholism, anorexia nervosa, schizophrenia, etc.
Neurochemical and neuroendocrine studies are difficult to assimilate and to detect
a consistent pattern for various reasons:
• There is uncertainty about the origin of metabolites; i.e. does plasma MHPG
reflect central noradrenaline metabolism?
• Effects of diet and menstrual status need to be accounted for. Some of these
(e.g. appetite) are behavioural features of depression.
• There are varying methodologies, assay techniques, etc.
• There are variable criteria for affective illness and patient selection between studies
(e.g. unipolar vs. bipolar).
Collectively, the results suggest the overall possibility of:
• Subsensitivity of noradrenaline postsynaptic receptors
• Presynaptic 5-HT dysfunction.
It is most likely that there is an interaction between two or more neurotransmitter
systems, perhaps modulated by neuropeptides.
AETIOLOGICAL FACTORS 49
NEUROPEPTIDES
The exact role of neuropeptides on mood is unknown. Elevated corticotropin releas-
ing factor (CRF) is associated with depression, and CRF neural pathways interact
extensively with serotonergic and noradrenergic systems. Administration of CRF in
animal studies produces depressive behavior. Research into the effect of CRF receptor
antagonists on depression is ongoing.
Antagonists to human substance P (neurokinin 1) receptors were originally developed
as a treatment for pain but did not meet with success. However, their efficacy for
improving depressive symptoms has been demonstrated in a placebo-controlled trial
(Kramer et al., 1998) and further research is under way (Stout et al., 2001).
PSYCHOIMMUNOLOGY
• There are decreased numbers of natural killer cells, and T-cell replication.
• There is decreased interleukin-2.
• There is increased monocyte activity.
Immune deficits are thought to be related to the end-products of sympathetic ner-
vous system and hypothalamic–pituitary–adrenal axis activation (i.e. glucocorticoids
and catecholamines), which modulate the immune system.
Animal models support the involvement of catecholamine and glucocorticoid lympho-
cyte receptors in the immune alterations related to depression (Silberman et al., 2004).
MRI studies suggest a reduction of hippocampus and caudate nucleus size in depres-
sion. PET studies indicate reduced metabolic activity and perfusion in cingulate
gyrus, dorsolateral prefrontal cortex and left angular cortex (pronounced in depres-
sive ‘pseudodementia’ patients).
In stroke victims, dysphoria is associated with lesions in the anterior left hemi-
sphere, whereas euphoria is associated with right hemispheric strokes.
ORGANIC CAUSES
Endocrine disorders
• Hypothyroidism • Cushing’s syndrome
• Hyperparathyroidism • Addison’s disease
Infective causes
• Post-influenza • Infectious mononucleosis
• Brucellosis • Hepatitis
Metabolic causes
• Iron-deficient anaemia • Hypercalcaemia
• B12/folate-deficient anaemia • Hypomagnesia
Neurological causes
• Post CVA • Intracranial tumours
• Multiple sclerosis • Epilepsy
• Parkinson’s disease
Depression, particularly epilepsy – associated with non-dominant (right-sided)
temporal lesions, although later refuted in several studies.
Drugs
• Reserpine • Steroids
• Alpha-methyldopa • Barbiturates
• L-dopa • Prolonged use of amphetamines
The oral contraceptive pill is no longer considered to be ‘depressogenic’.
PSYCHOLOGICAL THEORIES
Psychodynamics
• Loss of love object.
• Regression to primitive emotional level where lost object is ‘incorporated into self ’
and bitterly attacked by superego.
• Depressive position characterized by guilt, helplessness, and fear of the loss
of love.
Cognitive/behavioural theories
• Wolpe – depression is conditioned by repeated losses in the past.
• Seligman – ‘learned helplessness’ is a consequence of repeated exposure to uncon-
trollable traumas.
• Beck – there is a ‘negative cognitive trait’ of self-defeating thoughts.
Premorbid personality
Early research suggested that depressed patients were premorbidly more introverted,
shy and obsessional, while manic patients had vivacious, cyclothymic personalities.
However, depression compounds ‘retrospective’ assessment, and in more recent research
premorbid characteristics show only a minor association.
SOCIOLOGICAL THEORIES
Brown and Harris (1978) described high rates of depression among inner-city
London lower social group females. This suggested vulnerability factors which predis-
pose to depression only in the presence of provoking agents.
Vulnerability factors
• Excess of threatening life events or major difficulties prior to onset of depression.
• Unemployed status.
• Unsupportive relationship with spouse or partner.
• Three or more children under age of 15 living at home.
• Loss of mother before age 11.
Subsequent studies (Brown et al., 1986) only partly replicated Brown and Harris’
hypothesis, and further suggest that low self-esteem is a major vulnerability factor.
These are dependent on concepts and definitions of affective disorder used in studies and
clinical policies. The original Kraepelinian view of good outcome of ‘manic–depressive
insanity’ (relative to the chronicity of schizophrenia) is now questioned.
Short-term prognosis
Approximately 67 per cent of patients respond to treatment within 8 weeks. Even
when treated, the risk of recurrence of major depression is substantial:
• 50 per cent after one episode
• 70 per cent after two episodes
• 90 per cent after three episodes.
Thirty per cent of patients will become chronically depressed.
Long-term prognosis
Inter-episode intervals of depression and mania tend to lengthen over time, although
this pattern is reversed in elderly people, where affective episodes also last longer and
are more likely to leave residual symptoms.
In a 25-year follow-up (Angst and Preisig, 1995), 13 per cent of patients failed to
recover and had continued symptoms and disability, resembling dysthymia rather
than major depression; severity of initial psychopathology was predictive of outcome.
Thirteen per cent died of suicide.
In an 18-year follow-up (Lee and Murray, 1988), 25 per cent had poor outcome
(death, continued disability); only 11 per cent recovered and showed no further
psychiatric morbidity. Severity of the initial psychopathology was predictive.
TREATMENT
PHYSICAL APPROACHES
COMBINATION THERAPIES
Combination therapies are reserved primarily for treatment-resistant depression (see
later). The addition of low-dose lithium to an antidepressant regimen may augment
the effect. Atypical antipsychotics given in combination with SSRIs have shown clinical
efficacy.
Lithium
• Treatment of mania (3–4 days for therapeutic effect) – 75 per cent response rate.
• Prophylaxis for bipolar disorder usually commenced when there are two or more
affective disturbances within 2 years.
• 50 per cent of patients relapse within 3 years, with poor compliance with medica-
tion being the key factor.
Valproate
Valproate is another first-line agent in mania. Patients with mixed affective disorder
may respond better than those with ‘pure’ mania (McElroy et al., 1992).
Carbamazepine
The overall response rate in mania is 65 per cent; i.e. less than with lithium. It is gen-
erally used as a second-line drug, for treatment resistance or lithium intolerance.
There is no evidence yet to support its use in unipolar disorder.
Atypical antipsychotics
Atypical antipsychotics are effective for the management of acute mania.
54 AFFECTIVE DISORDERS
ELECTROCONVULSIVE THERAPY
See Chapter 22.
Sleep deprivation
Total sleep deprivation is reported to induce rapid clinical improvement in about
30 per cent of patients. REM deprivation (causing ‘REM pressure’) results in improve-
ment in 30–60 per cent. The mechanism is unclear – it may restore circadian rhythm
through an improved sensitivity of neurotransmitter/melatonin.
1 Review the diagnosis, physical investigations and social/family factors. Pay particular
attention to interpersonal and family dynamics that may inhibit resolution of symp-
toms. Continue with periodic review/update of diagnosis, management, etc.
2 Enhance present physical treatments:
– Maximize dose of antidepressant.
– Switch to a different class of antidepressant if failure follows an adequate trial.
3 Add in:
– Atypical antipsychotic
– Lithium.
4 Physical treatment measures (see Chapter 22):
– Electroconvulsive therapy
– Vagal nerve stimulation (VNS)
– Transcutaneous magnetic stimulation (TMS).
OTHER SYNDROMES
States were usually transitional, but sometimes persistent. Some studies suggest
up to 30 per cent of bipolar patients present with mixed symptoms in their first
episode.
OTHER SYNDROMES 55
BEREAVEMENT REACTIONS
Uncomplicated bereavement or typical grief
1 ‘Stunned’ phase – emotions blunted – lasts few hours to 2 weeks.
2 Mourning phase – intense yearning and distress – autonomic features – unhappi-
ness, futility, anorexia, restlessness, irritability, preoccupation with deceased –
transient hallucinatory episodes and guilt-denial.
3 Acceptance and readjustment – several weeks after onset of mourning.
The duration of typical grief varies with culture – on average 6–12 months.
Atypical grief
• Chronic grief – typical depressive illness may emerge with morbid preoccupation
with worthlessness, prolonged functional impairment, marked psychomotor
retardation. Other features include: excessive guilt, denial, identification, antisocial
behaviour.
• Inhibited grief or delayed grief.
• Non-specific and mixed reactions – psychosis, neurosis, etc.
ATYPICAL OR ‘MASKED’ DEPRESSION
This is illness presenting as either (1) physical conditions or (2) non-affective psychi-
atric disorders:
• Chronic pain, hypochondriasis, somatoform disorders, conversion disorders –
usually show absence of significant organic pathology, poor response to medical
treatment and some depressive features.
• Pseudodementia, anxiety states, behavioural change (e.g. shoplifting in middle-
aged women).
Pathophysiology
Pathophysiology is unknown. The dysregulation of melatonin postulate is:
• Melatonin deficit.
• ‘Phase shift’ in normal circadian output of melatonin.
• Dopamine-mediated abnormality in melatonin secretion.
56 AFFECTIVE DISORDERS
Treatment
Ultraviolet light therapy (bright, but not dim) suppresses blood melatonin – unclear
whether morning therapy is best time of day.
Abas M, Hotopf M, Prince M (2002) Depression and mortality in a high-risk population: 11-year
follow-up of the Medical Research Council Elderly Hypertension Trial. Br. J. Psychiatry
181, 123.
American Psychiatric Association (2002) Work Group on Bipolar Disorder: Practice Guideline
for the Treatment of Patients with Bipolar Disorder Revised. Am J Psychiatry 159, 1.
Andrews G, Szabo M, Burns J (2002) Preventing Major Depression in Young People.
Br. J. Psychiatry 181, 460.
Angst J, Preisig M (1995) Course of a clinical cohort of unipolar, bipolar and schizoaffective
patients. Results of a prospective study from 1959 to 1985. Schweiz. Arch. Neurol. Psychiatr.
146, 5–16.
Arnold LM (2003) Gender differences in bipolar disorder. Psychiatr. Clin. North Am. 36, 595.
Austin MP, Mitchell P, Goodwin GM (2001) Cognitive deficits in depression: possible implica-
tions for functional neuropathology. Br. J. Psychiatry 178, 200.
Bearden CE, Hoffman KM, Cannon TD (2001) The neuropsychology and neuroanatomy of
bipolar affective disorder: a critical review. Bipolar Disorders 3, 106.
Berrittini W (2001) Molecular genetic studies of bipolar disorder. Bipolar Disorders 3, 276.
Breslau N, Kilbev MM, Andreski P (1993) Nicotine dependence and major depression. New
evidence from a prospective investigation. Arch. Gen. Psychiatry 50, 31.
Brown GW, Harris T (1978) Social Origins of Depression. Tavistock, London.
Brown GW, Andrews B, Harris T et al. (1986) Social support, self esteem and depression.
Psycholog. Med. 16, 813.
Casacalenda N, Perry JC, Looper K (2002) Remission in major depressive disorder: a comparison
of pharmacotherapy, psychotherapy, and control conditions. Am. J. Psychiatry 159, 1354.
Coryell W, Solomon D, Turvey C et al. (2003) The long-term course of rapid-cycling bipolar
disorder. Arch. Gen. Psychiatry 60, 914.
Eagles JM, Howie FL et al. (2002) Use of health care services in seasonal affective disorder.
Br. J. Psychiatry 180, 449.
Ferrier IN, Thompson JM (2002) Cognitive impairment in bipolar affective disorder: implica-
tions for the bipolar diathesis. Br. J. Psychiatry 180, 293.
Harmer C, Hill SA, Taylor MJ et al. (2003) Towards a neuropsychological theory of antidepres-
sant drug action: potentiation of norepinephrine activity increases positive emotional bias.
Am. J. Psychiatry 160, 990.
Harrison PJ (2002) The neuropathology of primary mood disorder. Brain 125, 1428.
Heim C, Nemeroff CB (2001) The role of childhood trauma in the neurobiology of mood and
anxiety disorders: pre-clinical and clinical studies. Biol. Psychiatry 49, 1023.
REFERENCES AND FURTHER READING 57
Hill J, Pickles A, Burnside E et al. (2002) Child sexual abuse, poor parental care and adult depres-
sion: evidence for the different mechanisms. Br. J. Psychiatry 179, 104.
Hokfelt T, Bartfai T, Bloom F (2003) Neuropeptides: opportunities for drug discovery. Lancet
Neurology 2, 463.
Hume W (2001) Exercise was more effective in the long term than sertraline or exercise plus ser-
traline for major depression in older adults. Evidence-Based Ment. Health 4, 105.
Irwin M (2002) Psychoneuroimmunology of depression: clinical implications. Brain Behav
Immun. 16, 1.
Jaffee SR, Moffitt TE, Caspi A et al. (2002) Differences in early childhood risk factors for juvenile-
onset and adult depression. Arch. Gen. Psychiatry 59, 215.
Jane-Llopis E, Hosman C, Jenkins R, Anderson P (2003) Predictors of efficacy in depression pre-
vention programmes: meta-analysis. Br. J. Psychiatry 183, 384.
Kasper S, Wehr TA, Bartko JJ et al. (1989) Epidemiological findings of seasonal changes in mood
and behaviour. Arch. Gen. Psychiatry 46, 823.
Kendler KS, Kessler RC, Neale MC et al. (1993) The prediction of major depression in women:
toward an integrated etiological model. Am. J. Psychiatry 150, 1139.
Kendler KS, Gardner CO, Prescott CA (2002) Toward a comprehensive developmental model for
major depression in women. Am. J. Psychiatry 159, 1133.
Klerman GL (1988) The current age of youthful melancholia. Br. J. Psychiatry 152, 4.
Knapp M (2003) Hidden costs of mental illness. Br. J. Psychiatry 183, 477.
Koike AK, Unutzer J, Wells KB (2002) Improving the care for depression in patients with comor-
bid medical illness. Am. J. Psychiatry 159, 1738.
Kramer MS, Cutler N, Feighner J (1998) Distinct mechanism for antidepressant activity by
blockade of central substance P receptors. Science 281, 1640.
Kupfer DJ (1992) Maintenance treatment in recurrent depression: current and future directions.
Br. J. Psychiatry 161, 309.
Kupfer DJ, Frank E, Perel JM et al. (1992) Five-year outcome for maintenance therapies in recur-
rent depression. Arch. Gen. Psychiatry 49, 769.
Lecrubier Y, Clerc G et al. (2002) Efficacy of St John’s Wort Extract WS 5570 in major depression:
a double-blind, placebo-controlled trial. Am. J. Psychiatry 159, 1361.
Lee AS, Murray RM (1988) The long-term outcome of Maudsley depressives. Br. J. Psychiatry
153, 741.
Levinson DF, Zubenko GS, Crowe RR et al. (2003) Genetics of recurrent early-onset depression
(GenRED): design and preliminary clinical characteristics of a repository sample for genetic
linkage studies. Am. J. Med. Genet. 119B, 118.
Liang SG, Sadovnick AD, Remick RA et al. (2002) A linkage disequilibrium study of bipolar
disorder and microsatellite markers on 22q13. Psychiatr. Genet. 12, 231.
Liotti M, Mayberg HS, McGinnis S, Brannan SL et al. (2002) Unmasking disease-specific cerebral
blood flow abnormalities: mood challenge in patients with remitted unipolar depression.
Am. J. Psychiatry 159, 1830.
Marangell LB, Rush AJ, George MS et al. (2002) Vagus nerve stimulation (VNS) for major
depressive episodes: one year outcomes. Biol. Psychiatry 51, 280.
Marks IM (2002) The maturing of therapy: some brief psychotherapies help anxiety/depressive
disorders but mechanisms of action are unclear. Br. J. Psychiatry 180, 200.
Martin JLR, Barbanoj MJ, Schlaepfer TE et al. (2003) Repetitive transcranial magnetic stimulation
for the treatment of depression: systematic review and meta-analysis. Br. J. Psychiatry 182, 480.
Matthews K, Eljamel MS (2003) Vagus nerve stimulation and refractory depression: please can
you switch me on doctor? Br. J. Psychiatry 183, 181.
McElroy SL, Keck PE, Pope HG (1992) Valproate in the treatment of bipolar disorder: literature
review and clinical guidelines. J. Clin. Psychopharmacol. 12(Suppl.), s42.
McLoughlin DM (2003) Repetitive transcranial magnetic stimulation is of unknown effective-
ness in people with depression [review]. Evidence-Based Ment. Health 6, 118.
58 AFFECTIVE DISORDERS
Ustun TB, Kessler TC (2002) Global burden of depressive disorders: the issue of duration.
Br. J. Psychiatry 181, 181.
Volkmar FR (2002) Changing perspectives on mood disorders in children. Am. J. Psychiatry 159,
893.
Whitfield G, Williams C (2003) The evidence base for cognitive–behavioural therapy in depres-
sion: delivery in busy clinical settings. Adv. Psychiatr. Treat. 9, 21.
Zubenko GS, Maher B, Hughes HG et al. (2003) Genome-wide survey for genetic loci that influ-
ences the development of depressive disorders in families with recurrent, early-onset, major
depression. Am. J. Med. Genet. 123B, 1.
Neurotic disorders 5
ANXIETY DISORDERS
Reaction to severe stress and adjustment Reaction to severe stress and adjustment
Acute stress reaction Acute stress disorder
Post-traumatic stress disorder Post-traumatic stress disorder
Adjustment disorders
ANXIETY DISORDERS 61
PANIC DISORDER
Clinical symptoms
• There is sudden onset of intense apprehension, anxiety, fear, often with feeling of
impending doom or even death. Feelings of unreality may occur.
• Somatic effects can include dyspnoea, palpitations, chest pain, choking or smother-
ing sensations, paraesthesias, flushes, sweating, faintness, etc.
• There may develop ‘anticipatory fear’ of loss of control, so the individual becomes
afraid of being left alone in public places. Anticipatory fear may itself precipitate
an attack.
There is a generalized persistent anxiety without the specific symptoms that characterize
phobic anxiety disorder or panic disorder.
Clinical symptoms
• There is subjective apprehension, fear, worries (see above).
• Motor tension.
• Autonomic hyperactivity.
• Vigilance and scanning – the person complains of feeling ‘on edge’, has difficulty
sleeping, has interrupted sleep or fatigue on waking.
An anxiety disorder often begins in early adult life, but may occur for the first time in
middle age. Women are more affected than men.
There is a 4–7 per cent prevalence in the normal population. It accounts for 27 per
cent of psychiatric consultations in general practice, and 8 per cent of psychiatric
outpatients.
62 NEUROTIC DISORDERS
GENETICS
• There is a problem of small samples and diagnosis.
• MZ:DZ ⫽ 65%:13% (Slater and Shields).
• There is some evidence of genetic influence on neurotic ‘traits’ measured by per-
sonality tests and reflected in autonomic reactivity (e.g. GSR habituation).
EARLY CHILDHOOD
• Separation experiences.
• Childhood trauma.
• Undue emphasis on achievement.
• Demands for excessive conformity.
OTHER
• Current situational stress, uncertainty, conflict.
• Biological factors (see p. 66)
There is a variable course and prognosis – the more chronic and established the condi-
tion, the worse the prognosis.
Males are (?) more likely to improve than females. Premorbid stability has an
important influence. Agoraphobia may develop, or secondary depression.
Alcohol abuse and abuse of anxiolytics are not uncommon.
PSYCHOTHERAPY
• Cognitive–behavioural: more effective in panic disorder. Identify and ‘label’ mor-
bid anticipatory thoughts and replace with realistic cognitions.
• Insight-orientated: explore covert conflicts.
• ‘Anxiety management’ training:
– Distraction techniques.
– Cognitive control.
– Breathing/relaxation exercises – reduce chronic hyperventilation.
– Education – somatic effects of anxiety and overbreathing.
DRUG THERAPY
• Serotonin reuptake inhibitors are a first-line treatment. They are more effective
than benzodiazepines in reducing anxiety, anger, and hostility in the long term.
PHOBIC DISORDERS 63
PSYCHOSURGERY
Surgery is reserved only for cases of chronic, intractable, incapacitating anxiety that is
unresponsive to other measures.
PHOBIC DISORDERS
AGORAPHOBIA
Agoraphobia is strictly a fear of open spaces, but the term is often used for fear of
shopping, crowds, etc.
Agoraphobia accounts for 60 per cent of phobic patients seen by psychiatrists;
66 per cent are female. Most develop symptoms between the ages 15 and 35.
Other non-phobic symptoms are common, including generalized anxiety, panic
attacks, depression and depersonalization.
SOCIAL PHOBIA
Social phobia accounts for 8 per cent of phobic patients seen by psychiatrists; 60 per
cent are women. It usually develops after puberty and peaks in late years.
It is a persistent, irrational fear of, and compelling desire to avoid, situations in
which the individual may be exposed to the scrutiny of others. There is also fear that
the individual may behave in a manner (e.g. blushing, shaking, vomiting) that will be
humiliating or embarrassing.
Social phobia is probably not a homogeneous clinical entity but may represent
the prominent symptomatic manifestation of a wide variety of psychological
disorders.
ILLNESS PHOBIA
Illness phobia accounts for 15 per cent of phobic patients consulting psychiatrists. It
occurs equally in both sexes.
Illness phobia is a persistent, intense fear of illness, focused on specific disorders
such as cancer, heart disease or veneral illness, or an intense fear of death and dying.
There are chronic ruminations but no apparent attempts at resistance. A previous ill-
ness in a relative or individual may act as the precipitant.
The patient may have other mental illness (e.g. depression), and illness phobia fades
as this is treated.
BEHAVIOUR THERAPY
Systematic desensitization
There is gradual exposure to the phobic stimulus with increasing intensity until the
patient habituates and the avoidance response is extinguished. This is combined with
relaxation training, then practice in fantasy before situational exposure.
Good response is associated with:
Flooding (implosion)
This can be in fantasy or in real life. There is supervised maximum exposure to the
feared stimulus until anxiety reduction/exhaustion. This is effective (especially expos-
ure in vivo) for phobias where free-floating anxiety is prominent.
Modelling
The patient observes the therapist (the model) engaging in non-avoidance behaviour
with the feared stimulus.
There is some evidence that a combination of flooding, associated modelling and
moderate doses of diazepam given 4 hours before sessions is particularly effective in
treating agoraphobia.
DRUG THERAPY
• SSRIs are the drug treatment of choice and are well tolerated with no abuse
potential.
• Benzodiazepines are effective but only for short-term management of fear-associated
anxiety until other measures are successful.
• Beta-blockers are effective for short-term management of performance fears.
• MAOIs and TCAs are less effective and have a greater side-effect burden.
PSYCHOTHERAPY
Behavior therapy is effective using either systematic desensitization or flooding.
Cognitive–behavioural therapy is effective at modifying dysfunctional thoughts
involving fear.
66 NEUROTIC DISORDERS
Cardiac function
• Higher basal rate.
• Less deceleration after stress.
• More beat-to-beat fluctuation.
• Increased awareness of heart function.
Electrodermal response
• Increased skin conductance.
• Decreased habituation.
• More spontaneous fluctuation.
Neurotransmitter abnormalities
Findings conflict, probably owing to differences in diagnostic groups studied.
• Circulating adrenaline – increased.
• Circulating noradrenaline – ? increased.
• Platelet MAO – increased.
• Central noradrenaline and 5-HT – increased activity.
Both MVP and panic may form part of a general syndrome of primary autonomic
dysfunction.
or
MVP may act as an autonomic precipitant interacting with a predisposition (genetic)
to panic disorder.
Hyperventilation syndrome
Physiological effects of reduced PCO2:
• Vasoconstriction of cerebral arteries.
• Reduced availability of O2 in oxyhaemoglobin.
• Increased irritability of autonomic sensory and motor nervous system.
• Bronchoconstriction and tachycardia.
• Exaggerated sinus rhythm.
Symptoms produced:
• Light-headedness or faintness.
• Breathlessness and palpitations.
• Sweating, fatigue and stiffness.
• Dry mouth with aerophagy and globus.
• Chronic malaise.
Some researchers think that hyperventilation causes panic attacks, others that it is
merely a consequence (see diagram below).
Anticipatory
cognitions
Symptoms
Familiar terms are ‘combat neurosis’, ‘shell-shock syndrome’ and ‘traumatic neurosis’ in
the UK – stemming from experiences in war, but PTSD is also now seen as a response
to natural disasters (e.g. Hillsborough deaths Pugh and Trimble, 1993; Australian bush
fire-fighters McFarlane et al., 1990; Coconut Grove fire), to rape, to traffic accidents, to
trauma, etc.
68 NEUROTIC DISORDERS
Rates of PTSD are related to specific types of traumatic events (Kessler et al., 1995):
• rape – 65 per cent
• combat – 38.8 per cent
• natural disaster – 3.7 per cent
• criminal assault – 1.8 per cent.
The lifetime prevalence in the community is 1–9 per cent. Chronic PTSD is seen in
1.3 per cent of males and in 4.7 per cent of females (Breslau et al., 1995).
There are high rates of co-morbidity (Kessler et al., 1995):
• alcohol abuse/dependency – 52 per cent
• depression – 48 per cent
• substance dependency – 34 per cent
• social phobia – 28 per cent
• generalized anxiety disorder – 17 per cent
• panic disorder – 7 per cent.
1 There has been exposure to a traumatic event, lying outside normal human experi-
ence and which would clearly cause suffering in almost everyone. The person’s
response involves intense fear, helplessness.
2 There is persistent re-experiencing – recurrent nightmares, flashbacks, reliving of
episode, psychological distress and/or physiological reactivity on exposure to cues
which resemble/symbolize the trauma.
3 There is persistent avoidance of stimuli related to the trauma.
4 Symptoms of hyperarousal are present – hypervigilance, startle reflexes, sleep dis-
turbance, decreased habituation to auditory stimuli.
5 There is psychosocial impairment: ICD-10 criteria emphasize onset within 6 months
of the traumatic event.
AETIOLOGY OF PTSD
There has been much debate about the extent of individual determinants of PTSD.
Not everyone experiencing major trauma develops PTSD, and the neurobiological
basis is not clear.
• PTSD may be due to a complex neurobiological response mechanism that engen-
ders maximal and sustained response to stress.
• There is evidence of increased hypothalamic–pituitary–adrenal axis reactivity.
• Lower basal cortisol levels and more glucocorticoid receptors are seen in individ-
uals with PTSD.
• Elevated catecholamine levels may account for some PTSD symptoms.
• Smaller hippocampal volumes are seen in those with PTSD.
• A previous traumatic event and/or prior history of psychiatric illness are predis-
posing factors for PTSD.
OBSESSIONAL/COMPULSIVE STATES 69
MANAGEMENT OF PTSD
OBSESSIONAL/COMPULSIVE STATES
Obsessions are recurrent, persistent ideas, thoughts, images or impulses that the patient
regards as alien and absurd, while recognizing them as products of his/her own mind.
Attempts are made to ignore and suppress them.
70 NEUROTIC DISORDERS
Compulsions are voluntary motor actions which are reluctantly performed despite
being regarded as alien or absurd. The act is performed with a subjective sense of com-
pulsion coupled with a desire to resist it (at least initially). When the individual does
attempt to resist, there is a mounting sense of tension which can only be relieved by
yielding.
The phenomenology of obsessional–compulsive states is shown in Table 5.2.
Symptoms may complicate:
• Depressive illness (found in 30 per cent) – low rate of suicide in depressed patients
with obsessive–compulsive disorder (OCD).
• Schizophrenic disorder.
• Early dementia and other organic brain syndromes.
• Anorexia nervosa.
• Generalized anxiety state.
Fears of harming a baby may occur as part of puerperal illness.
EPIDEMIOLOGY OF OCD
The sex distribution is equal. The most common age at onset is early adulthood:
• 65 per cent of patients onset ⬍25 years.
• 15 per cent after age 35 years.
• Mean age at onset ⫽ 20 years.
• Mean age of presenting to psychiatric services ⫽ 27.5 years (Rasmussen and Tsuang,
1986).
Prevalence
• 0.5 per cent of general population, but recorded lifetime rates of 2–3 per cent in
ECA study (overestimated).
• 1 per cent of psychiatric outpatient and inpatient population.
• 4 per cent of the ‘neurotic’ group.
AETIOLOGY OF OCD
GENETICS
Up to 20 per cent of first-degree relatives have subclinical OCD symptoms. There have
been few twin studies: MZ ⫽ 50–80 per cent; DZ ⫽ 25 per cent. The condition is
strongly linked to Tourette’s disorder.
OBSESSIONAL/COMPULSIVE STATES 71
NON-GENETIC FACTORS
Neurochemistry and neuroanatomy
Glutamatergic-serotonin modulation in the caudate nucleus is thought to be involved.
The primary pathology may be in the caudate nucleus. The frontal lobe also is impli-
cated. PET studies show glucose hypermetabolism in fronto-orbital gyrus and caudate
nuclei (Baxter et al., 1992); these abnormalities are normalized with effective pharma-
cotherapy (Swedo et al., 1992, Rosenberg et al., 2000).
PANDAs
Paediatric autoimmune neuropsychiatric disorders are associated with streptococcal
infection. They are characterized by the abrupt onset of OCD or tics and are thought
to be the result of an autoimmune response to group A -haemolytic streptococcal
infection.
Premorbid personality
The meticulous (‘anankastic’) type personality is associated in 15–35 per cent. Concern
is with orderliness, cleanliness, checking, rigidity.
Psychoanalytic theory
Freud’s views were expounded in his lecture ‘Notes upon a Case of Obsessional Neurosis’
(the Rat Man):
• Defensive regression to pregenital anal-erotic stage of development.
• Defensive mechanism against aggressive and cruel impulses.
• Key defences: reaction formation, undoing, isolation (see p. 298).
Psychological theory
One view is that OCD is a defect of the arousal system (Beech). Major defensive reac-
tions are precipitated by minor alterations to incoming stimuli, perceived as danger-
ous and threatening. The defensive response is thus seen as preventive or placatory
activity aimed at controlling unpleasant internal states.
Learning theory cannot account fully for obsessional phenomena, which are not a
motor response to an anxious thought, but simply the repetitive intrusion into con-
sciousness of an anxious thought or impulse alone.
TREATMENT OF OCD
Psychotherapy
Cognitive–behavioural therapy has been shown to decrease symptomology (Benazon
et al., 2002). Ruminations are more difficult to treat. ‘Thought stopping’ may be helpful.
Loop-type techniques also are helpful.
With treatment, the majority of individuals diagnosed with OCD experience a chronic,
fluctuating course. About half of those with OCD will experience partial remission;
and of those, half will experience relapse. Only 12 per cent achieve full remission.
Monitor treatment with Yale–Brown Obsessive Compulsive Scale (YBOCS).
Poor prognostic factors are:
• Co-morbid psychiatric disorder.
• Earlier onset, longer duration of illness.
• Poor insight into the illness.
• More severe, bizarre symptoms – symmetry, ordering, hoarding obsessions.
Ackerman DL, Greenland S (2002) Multivariate meta-analysis of controlled drug studies for
obsessive–compulsive disorder. J. Clin. Psychopharmacol. 22, 309.
Allgulander C, Hirschfeld RM, Nutt DJ (2002) Long-term treatment strategies in anxiety disorders.
Psychopharmacol. Bull. 36 (Suppl. 2), 79.
American Psychiatric Association (1998) Practice guideline for the treatment of patients with
panic disorder. Am. J. Psychiatry 155 (Suppl. May), 1.
Andersch S, Hetta J (2002) A naturalistic fifteen-year follow-up study of panic disorder patients.
Eur. Psychiatry 17 (Suppl. 1), 166.
Andrews G, Slade T (2002) Agoraphobia without a history of panic disorder may be part of the
panic disorder syndrome. J. Nerv. Ment. Dis. 190, 624.
Arnold PD, Richter MA (2001) Is obsessive–compulsive disorder an autoimmune disease? CMAJ
165, 1353.
Baldwin D, Evans D, Hirschfeld RSK (2002) Can we distinguish anxiety from depression?
Psychopharmacol. Bull. 36, 158.
Ballenger J (2001) Overview of different pharmacotherapies for attaining remission in general-
ized anxiety disorder. J. Clin. Psychiatry 62 (Suppl.), 11.
Ballenger J, Davidson J, Lecrubier Y et al. (2000) Consensus statement on posttraumatic stress
disorder from the International Consensus Group on Depression and Anxiety. J. Clin.
Psychiatry 61, 60.
Barzega G, Maina G, Venturello S, Bogetto F (2001) Gender-related distribution of personality
disorders in a sample of patients with panic disorder. Eur. Psychiatry 16, 173.
Baxter LR, Schwartz JM, Bergman KS et al. (1992) Caudate glucose metabolic rate changes with both
drug and behavior therapy for obsessive–compulsive disorder. Arch. Gen. Psychiatry 49, 681.
REFERENCES AND FURTHER READING 73
Benazon NR, Ager J, Rosenberg DR (2002) Cognitive behavior therapy in treatment-naive children
and adolescents with obsessive–compulsive disorder: an open trail. Behav. Res. Ther. 40, 529.
Benazon NR, Moore GJ, Rosenberg DR (2003) Neurochemical analyses in pediatric obsessive–
compulsive disorder in patients treated with cognitive–behavioral therapy. J. Am. Child Adolesc.
Psychiatry 42, 1279.
Borkovec TD, Newman MG, Castonguay LG (2003) Cognitive–behavioral therapy for general-
ized anxiety disorder with integrations from interpersonal and experiential therapies. CNS
Spectr. 8, 382.
Brawman-Mintzer O (2002) Pharmacologic treatment of generalized anxiety disorder. Psychiatr.
Clin. North Am. 24, 119.
Breslau N (2002a) Post-traumatic stress disorder. New Engl. J. Med. 346, 1495.
Breslau N (2002b) Gender differences in trauma and posttraumatic stress disorder. J. Gend.
Specif. Med. 5, 34.
Breslau N, Davis GC, Andreski P (1995) Risk factors for PTSD-related traumatic events: a prospect-
ive analysis. Am. J. Psychiatry 152, 529
Breslau N, Chilcoat H, Kessler R, Davis G (1999) Previous exposure to trauma and PTSD effects of
subsequent trauma: results from the Detroit Area Survey of Trauma.. Am. J. Psychiatry 156, 902.
Brunello N, Davidson J, Deahl M et al. (2001) Posttraumatic stress disorder: diagnosis and
epidemiology, comorbidity and social consequences, biology and treatment. Neuropsychobiology
43, 150.
Carlbring P, Gustafsson H, Ekselius L, Andersson G (2002) 12-month prevalence of panic dis-
order with or without agoraphobia in the Swedish general population. Soc. Psychiatry Psychiatr.
Epidemiol. 37, 207.
Craske MG, Roy-Byrne P, Stein MB et al. (2002) Treating panic disorder in primary care: a col-
laborative care intervention. Gen. Hosp. Psychiatry 24, 148.
Davidson JRT (2002) Surviving disaster: what comes after the trauma? Br. J. Psychiatry 181, 366.
Dougherty DD, Baer L et al. (2002) Prospective long-term follow-up of 44 patients who received
cingulotomy for treatment-refractory obsessive–compulsive disorder. Am. J. Psychiatry
159, 269.
Dugas MJ, Ladouceur R, Leger E et al. (2003) Group cognitive–behavioral therapy for generalized
anxiety disorder: treatment outcome and long-term follow-up. J. Consult. Clin. Psychol. 71, 821.
Falsetti SA, Davis J (2001) The nonpharmacologic treatment of generalized anxiety disorder.
Psychiatr. Clin. North Am. 24, 99.
Fava GA, Rafanelli C, Grandi S et al. (2001) Long-term outcome of panic disorder with agora-
phobia treated by exposure. Psychol. Med. 31, 891.
Foa EB, Davidson JRT (eds) (1999) The Expert Consensus Guideline Series. Treatment of
Posttraumatic Stress Disorder. J. Clin. Psychiatry 60 (Suppl. 16), 3–76.
Friedman MJ (2002) Future pharmacotherapy for post-traumatic stress disorder: prevention and
treatment. Psychiatr. Clin. North Am. 25, 427.
Gershuny B, Baer L, Jenike M et al. (2002) Comorbid PTSD; impact on treatment outcome for
OCD. Am. J. Psychiatry 159, 852.
Gillette GM, Skinner RD, Rasco LM et al. (1997) Combat veterans with posttraumatic stress disorder
exhibit decreased habituation of the P1 midlatency auditory evoked potential. Life Sci. 61, 1431.
Golier J, Yehuda R (2002) Neuropsychological processes in post-traumatic stress disorder.
Psychiatr. Clin. North Am. 25, 295.
Golier J, Yehuda R, Bierer LM et al. (2003) The relationship of borderline personality disorder to
posttraumatic stress disorder and traumatic events. Am. J. Psycyhiatry 160, 2018.
Golier J (2002) Neuropsychological processes in post-traumatic stress disorder. Psychiatr. Clin.
North Am. 25, 295.
Gorman JM (2003) Treating generalized anxiety disorder. J. Clin. Psychiatry 64 (Suppl. 2), 24.
Grossman R, Buchsbaum MS, Yehuda R (2002) Neuroimaging studies in post-traumatic stress
disorder. Psychiatr. Clin. North Am. 25, 317.
74 NEUROTIC DISORDERS
Grossman R, Yehuda R, New A et al. (2003) Dexamethasone suppression test findings in subjects
with personality disorders: associations with posttraumatic stress disorder and major depres-
sion. Am. J. Psychiatry 160, 1291.
Hanna GL, Veenstra-VanderWeele J, Coz NJ et al. (2002) Genome-wide linkage analysis of families
with obsessive–compulsive disorder ascertained through pediatric probands. Am. J. Med. Genet.
114, 541.
Hansen ES, Hasselbalch S, Law I et al. (2002) The caudate nucleus in obsessive–compulsive
disorder. Reduced metabolism following treatment with paroxetine: a PET study. Int.
J. Neuropsychopharmacol. 5, 1.
Hemmings S, Kinnear C, Niehaus D et al. (2003) Investigating the role of dopaminergic and
serotonergic candidate genes in OCD. Eur. Neuropsychopharmacol. 13, 93.
Hendin H, Haas AP (1991) Suicide and guilt as manifestations of PTSD in Vietnam combat vet-
erans. Am. J. Psychiatry 148, 586.
Hollander E, Kaplan A, Allen A, Cartwright C (2000) Pharmacotherapy for obsessive–compulsive
disorder. Psychiatr. Clin. North Am. 23, 643.
Hull AM (2002) Neuroimaging finding in post-traumatic stress disorder: a systematic review.
Br. J. Psychiatry 181, 102.
Kessler RC (2000) Posttraumatic stress disorder: the burden to the individual and to society.
J. Clin. Psychiatry 61 (Suppl. 5), 4.
Kessler RC, Sonnega A, Bromet E et al. (1995) Posttraumatic stress disorder in the National
Comorbidity Survey. Arch. Gen. Psychiatry 52, 1048.
Kessler RC, Keller MB, Wittchen HU (2001) The epidemiology of generalized anxiety disorder.
Psychiatr. Clin. North Am. 24(1), 19.
Kessler RC, Andrade L, Bijl R et al. (2002) The effects of co-morbidity on the onset and persistence
of generalized anxiety disorder in the ICPE surveys. International Consortium in Psychiatric
Epidemiology. Psychol. Med. 32, 1213.
Lepine J (2002) The epidemiology of anxiety disorder: prevalence and societal costs. J. Clin.
Psychiatry 63 (Suppl.), 4.
Liebowitz MR, Turner SM, Piacentini J et al. (2002) Fluoxetine in children and adolescents with
OCD: a placebo-controlled trail. J. Am. Acad. Child Adolesc. Psychiatry 41, 1431.
Lipstiz JD, Marshall RD (2001) Alternative psychotherapy approaches for social anxiety disorder.
Psychiatr. Clin. North Am. 24, 817.
Marshall RD, Garakani A (2002) Psychobiology of the acute stress response and its relationship
to the psychobiology of post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 385.
Mataix Cols D, Rauch SL, Baer L et al. (2002) Symptom stability in adult obsessive–compulsive
disorder: data from a naturalistic two-year follow-up study. Am. J. Psychiatry 159, 263.
Matthews K, Eljamel MS (2003) Status of neurosurgery for mental disorder in Scotland: selective
literature review and overview of current clinical activity. Br. J. Psychiatry 182, 404.
McDonough M, Kennedy N (2002) Pharmacological management of obsessive-compulsive dis-
order: a review for clinicians. Harvard Rev. Psychiatry 10, 127.
McFarlane A (1990) An Australian disaster: the 1983 bushfires. Int. J. Mental Health 19(2), 36.
McFarlane AC, Yehuda R, Clark CR (2002) Biologic models of traumatic memories and post-
traumatic stress disorder. Psychiatr. Clin. North Am. 25, 253.
Mellman TA, David D, Bustamante V et al. (2001) Predictors of post-traumatic stress disorder
following severe injury. Depress. Anxiety 14, 226.
Millet B, Chabane N, Delorme R et al. (2003) Association between the dopamine receptor D4
gene and OCD. Am. J. Med. Genet. 116, 55.
Moreau C, Zisook S (2002) Rationale for a posttraumatic stress spectrum disorder. Psychiatr.
Clin. North Am. 25, 775.
Mundo E, Richter MA, Zai G et al. (2002) 5HT1Dbeta receptor gene implicated in the pathogen-
esis of obsessive–compulsive disorder: further evidence from a family-based association
study. Mol. Psychiatry 7, 805.
REFERENCES AND FURTHER READING 75
Murray J, Ehlers A, Mayou RA (2002) Dissociation and post-traumatic stress disorder two
prospective studies of road traffic accident survivors. Br. J. Psychiatry 180, 363.
Nutt D (2000) The psychobiology of posttraumatic stress disorder. J. Clin. Psychiatry 61, 24.
Nutt D, Ballenger J, Sheehan D, Wittchen H (2002) Generalized anxiety disorder: comorbidity,
comparative biology and treatment. Int. J. Neuropsychopharmacol. 5, 315.
Otto MW, Tuby KS, Gould RA, McLean RY, Pollack MH (2001) An effect-size analysis of the rela-
tive efficacy and tolerability of serotonin selective reuptake inhibitors for panic disorder.
Am. J. Psychiatry 158, 1989.
Overbeek T, Schruers K, Vermetten E, Greiez E (2002) Comorbidity of OCD and depression
prevalence, symptom severity, and treatment effect. J. Clin. Psychiatry 63, 1106.
Pariser SF, Jones BA, Pinta ER et al. (1979) Panic attacks: diagnostic evaluations of 17 patients.
Am. J. Psychiatry 136(1), 105.
Pereira A (2002) Combat trauma and the diagnosis of post-traumatic stress disorder in female
and male veterans. Mil. Med. 167, 23.
Perugi G, Toni C, Frare F (2002) Obsessive–compulsive bipolar comorbidity: a systematic explor-
ation of clinical features and treatment outcome. J. Clin. Psychiatry 63, 1129.
Phillips KA (2002) The obsessive–compulsive spectrums. Psychiatr. Clin. North Am. 25, 791.
Pigott TA (2003) Anxiety disorders in women. Psychiatr. Clin. North Am. 26, 621.
Pitman RK, Sander KM, Zusman RM et al. (2002) Pilot study of secondary prevention of post-
traumatic stress disorder with propranolol. Biol. Psychiatry 51, 189.
Pugh C, Trimble MR (1993) Psychiatric injury after Hillsborough. Br. J. Psychiatry 163, 425.
Rabios D, Batten SV, Keane TM (2002) Implications of biological findings for psychological
treatments of post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 443.
Rosario-Campos M, Leckman J, Mercadante M (2001) Adults with early-onset OCD. Am. J.
Psychiatry 158, 1899.
Rosenberg DR, MacMaster FP, Keshavan MS et al. (2000) Decrease in caudate glutamatergic
concentrations in pediatric obsessive–compulsive disorder patients taking paroxetine. J. Am.
Acad. Child Adolesc. Psychiatry 39, 1096.
Sachdev P, Hay P, Cumming S (1992) Psychosurgical treatment of obsessive–compulsive disorder.
Arch. Gen. Psychiatry 49, 582.
Saxena S, Brody AL, Ho ML et al. (2002) Differential cerebral metabolic changes with paroxetine
treatment of obsessive–compulsive disorder vs major depression. Arch. Gen. Psychiatry 59, 250.
Serpell L, Livingstone A, Neiderman M et al. (2002) Obsessive–compulsive disorder, obsessive–
compulsive personality disorder, or neither? Clin. Psychol. Rev. 22, 647.
Shear MK (2002) Building a model of posttraumatic stress disroder. Am. J. Psychiatry 159, 1931.
Shear MK, Houck P, Greeno C, Masters S (2001) Emotion-focused psychotherapy for patients
with panic disorder. Am. J. Psychiatry 158, 1993.
Sheikh JI, Leskin GA, Klein DF (2002) Gender differences in panic disorder: findings from the
National Comorbidity Survey. Am. J. Psychiatry 159, 55.
Solvason HB, Ernst H, Roth W (2003) Predictors of response in anxiety disorders. Psychiatr. Clin.
North Am. 26, 411.
Sorenson SB (2002) Preventing traumatic stress: public health approaches. J. Truama Stress 15, 3.
Stein MB, Jang KL, Taylor S (2002) Genetic and environmental influences on trauma exposure
and posttraumatic stress disorder symptoms: a twin study. Am. J. Psychiatry 159, 1675.
Stimpson NJ, Thomas HV, Weightman AL et al. (2003) Psychiatric disorder in veterans of the
Persian Gulf War of 1991: a systematic review. Br. J. Psychiatry 182, 391.
Swedo SE, Leonard HL, Kruesi MJ et al. (1992) Cerebrospinal fluid neurochemistry in children
and adolescents with obsessive–compulsive disorder. Arch. Gen. Psychiatry 49, 29.
Swedo SE, Pietrini P, Leonard HL et al. (1992) Cerebral glucose metabolism in childhood-onset
obsessive–compulsive disorder: revisualization during pharmacotheraphy. Arch. Gen.
Psychiatry 49, 690.
Thomas CS (2002) Psychological consequences of traumatic injury. Br. J. Psychiatry 180, 392.
76 NEUROTIC DISORDERS
True WR, Rice J, Eisen SA et al. (1993) A twin study of genetic and environmental contributions
to liability for post-traumatic stress symptoms. Arch. Gen. Psychiatry 50, 257.
Tuke R, Polat A, Ozdemir O et al. (2002) Comorbid conditions in obsessive–compulsive disorder.
Compr. Psychiatry 43, 204.
Ursano RJ (2002) Post-traumatic stress disorder. New Engl. J. Med. 346, 130.
Yehuda R (2002a) Current status of cortisol findings in post-traumatic stress disorder. Psychiatr.
Clin. North Am. 25, 341.
Yehuda R (2002b) Recent advances in the study of biological alterations in post-traumatic stress
disorder (PTSD). Psychiatr. Clin. North Am. 25, 76.
Yehuda T (2002c) Post-traumatic stress disorder. New Engl. J. Med. 346, 108.
Personality: development 6
and disorders
FREUD
• The oral stage relates to narcissism, dependence, envy, jealousy.
• The anal stage relates to obsessionality, orderliness, obstinacy, frugality; also rage
and sadomasochism.
• The phallic stage relates to competitiveness and ambition.
Character is that pattern of adaptation to instinctual and environmental forces
which is habitual for the individual. It results from a combination of: innate biological
predisposition, id forces, early ego defences, environmental influences and early iden-
tification and imitation. Character traits owe their existence to successful repression,
leading to persistence. Neurotic symptoms result from a failure of repression.
ADLER
Lifestyle is the individual’s active adaptation to the social milieu. The individual is motiv-
ated by a striving for superiority as a defence against the helplessness of inferiority.
HORNEY
Horney emphasizes the important effect of culture. There are three character types
depending on the predominant mode of relating to others: compliant/self-effacing,
aggressive/expansive, detached/resigned.
SULLIVAN
The individual has two major goals (and states): satisfactions (of biological needs) and
security (in relationships with others). Anxiety is the response to adult disapproval
and personality development is the process of learning to deal with this anxiety.
78 PERSONALITY: DEVELOPMENT AND DISORDERS
ERIKSON
Personality development takes place through (potentially) eight ‘stages’. These are a
series of alternative attitudes which develop into a ‘sense of the attribute’. ‘Epigenesis’
refers to the process of development of the ego through these stages.
1 Basic trust versus mistrust (oral/sensory) – awareness of consistency and continu-
ity, leading to ego identity.
2 Autonomy versus shame and doubt (muscular/anal) – self-control vs. loss of
self-esteem.
3 Initiative versus guilt (locomotor/genital) – planning tasks, but failure leads to guilt.
4 Industry versus inferiority (latency) – recognition is won by doing things, the dan-
ger is inferiority.
5 Identity versus role confusion (puberty) – may lead to the ‘identity crisis’, between
inner sense of continuity and outer vulnerability in one’s meaning for others.
6 Intimacy versus isolation (young adulthood) – the capacity to commit oneself to
others.
7 Generativity versus stagnation (adulthood) – productivity/creativity or self-absorption.
8 Integrity versus despair (maturity) – in the awareness of the closeness of death.
MEYER
Pathological personality reactions are regressions to former, previously protective phylo-
genetic reactions which are now maladaptive. Symptoms are the individual’s attempt to
cure himself or herself. Personality disorder results from disorganization of habits.
PIAGET
Piaget investigated the development of cognition in children. Human intelligence is
an extension of biological adaptation, has a logical substructure and develops in four
stages (another ‘epigenetic’ theory).
1 Sensorimotor (0–2 years) – learns object permanence, differentiates self from
objects, aware of effects of self on objects.
2 Preoperational (2–7 years) – uses symbols, language develops, egocentric.
3 Concrete operational (7–12 years) – capable of logical thought, develops concept of
conservation, classifies, relates.
4 Formal operational (12⫹) – capable of abstract thought, hypothesis, concerned
with ideologies.
PERSONALITY DISORDERS
DEFINITIONS
DSM-IV and ICD-10 presume a major category of personality disorders (PDs), with
features (see Table 6.1):
• Deeply ingrained, maladaptive patterns of behaviour.
• Recognizable in adolescence or earlier.
PERSONALITY DISORDERS 79
Cluster A
Paranoid Paranoid
Schizoid Schizoid
Schizotypal
Cluster B
Antisocial Dissocial
Emotionally unstable Borderline
Impulsive type Histrionic
Borderline type Narcissistic
histrionic
other specific (includes narcissistic)
Cluster C
Anxious (avoidant) Avoidant
Dependent Dependent
Anankastic Obsessive–compulsive
Pers. disorder unspecified Pers. disorder mixed
Pers. disorder NOS
EPIDEMIOLOGY
PD rates are variable, and unreliable, being very dependent on sampling, assessment
and definition:
• General population – 10 per cent.
• Epidemiological Catchment Area (ECA) study – 6 per cent.
• A prison population – 20–80 per cent.
• Psychiatry outpatient attenders – 10–40 per cent.
• Primary care attenders – 7 per cent (one-third of those with ‘conspicuous’ psychi-
atric morbidity will have PD).
DIMENSIONAL APPROACHES
The trait approach (Cloninger, 1987) considers personality as a constellation of traits –
a set of dimensions along each of which any individual will vary. Differences between
normal and abnormal are viewed as quantitative.
The dimensional approach is also applied along psychiatric ‘continua’; e.g. schizo-
phrenic spectrum disorders, borderline spectrum.
Approaches may show overlap on psychobiological measures.
Typical assessments
These include (see Chapter 1):
• Catell Sixteen Personality Factor Test (16PF).
• Minnesota Multiphasic Personality Inventory (MMPI).
• Eysenck Personality Inventory (EPI).
AETIOLOGICAL THEORIES
Theories are diverse. Many researchers tend to favour a specific theory, although the
biopsychosocial model may be a more appropriate and integrative approach.
PERSONALITY DISORDERS 81
PSYCHODYNAMIC THEORY
Defensive, non-adaptive personality patterns develop as a result of a disruptive early
environment. Under the personality dysfunctioning lies defective and infantile ego
functions (see Chapter 23); e.g. poor impulse control, defective object relations, intoler-
ance of affect, unstable identification and super-ego lacunae.
Borderline PD uses primitive defence mechanisms (splitting, projective identifica-
tion) which may result from pathological early object relations and difficulties at the
separation/individuation stage of development.
Reality testing is distorted by intense internal needs and conflicts, leading to habit-
ual distortion of thought, judgement and perception obvious to others but not the
individual.
Poor self-image is combined with infantile feelings of entitlement. Aggressive impulses
are poorly integrated, resulting in persistently disturbed relationships with others.
Such mechanisms develop as responses to early childhood relationships, and particu-
lar personality traits relate to particular disturbances of upbringing. Psychodynamic
development may be halted at a particular stage owing to environmental stress, or the
individual may regress to that stage under further stress later in life.
GENETICS
Diagnostic imprecision causes difficulties. Central markers include serotonin dysreg-
ulation in sociopathy, borderline PD and impulse disorders, sleep and dysregulation
and eye-tracking abnormalities (see Chapter 3). Peripheral markers include platelet
MAO, DST suppression.
• Polymorphisms in the COMT gene are associated with anger-related traits
(Rujescu et al., 2003).
• An association has been shown between a functional promoter polymorphism in
the dopamine D2 receptor gene and detached personality trait, as seen in schizoid
or avoidant behavior (Jonsson et al., 2003).
• Criminality, social introversion, pattern of crime (sexual, violent criminal career)
have all been shown to have higher MZ concordance.
• Danish adoption studies:
– Biological father criminal – 21 per cent criminality in adoptees.
– Neither father criminal – 10 per cent criminality in adoptees.
– Both fathers criminal – 36 per cent criminality in adoptees.
• XYY individuals show evidence of increased criminality independent of low IQ
and socioeconomic status.
• XY individuals show greater aggression and greater reported/detected criminality
than XX.
• There is a prominent influence in schizotypal (see Chapter 3), antisocial PD (see
Chapter 18).
82 PERSONALITY: DEVELOPMENT AND DISORDERS
SOCIOCULTURAL FACTORS
Social learning theory emphasizes personality traits of children derived from the
shaping influence of parents (direct reinforcement or modelling). Most likely this is a
complex interaction; e.g. match of temperament with parental expectations, subcul-
tural expectation.
TEMPERAMENT
The New York Longitudinal Study followed 133 subjects from infancy to adulthood.
Behaviour is said to consist of:
• Abilities (the ‘what’).
• Motivations (the ‘why’).
• Temperament (the ‘how’).
Nine categories of temperament are defined (e.g. biological rhythmicity, activity
level, mood, withdrawal, adaptability). Three temperamental constitutions are found:
• The easy child (40 per cent) – regular, positive, adaptable.
• The difficult child (10 per cent) – irregular, negative, not adaptable.
• The slow-to-warm-up child (15 per cent) – mildly negative, slow to adapt.
Temperament is partly governed by genetics, not by sex or parental attitudes
(except parental conflict, which related to early adult adjustment).
Continuity of temperament over time from infancy was very evident given stability
of the environment. The difficult child was most vulnerable to development of behav-
iour disorders. Optimal development depends on consonance between individual and
environment – ‘goodness of fit’.
Multidimensional
• Rule out any organic cause, such as focal or diffuse brain disorder, toxic or meta-
bolic disorder, seizure disorder.
• Rule out other or evaluate for co-morbid psychiatric disorder. Ensure that the
problem is persistent since adolescence, not episodic.
• Hospitalization is probably best avoided (brief if required for crisis such as
co-morbidity, suicidality/deliberate self-harm). The person may function better
in a partial hospitalization setting.
Pharmacotherapy
SSRI therapy decreases impulsivity in borderline personality and is useful for co-morbid
depression. Mood stabilizers are effective in managing mood lability, anger and aggres-
sion. Atypical antipsychotics are preferred for cognitive–perceptual disturbances.
Psychotherapy
There is some evidence for the role of dialectical behaviour therapy in deliberate
self-harm (DSH).
CAT therapy carries some weak evidence.
Group therapy may be more useful than individual for some PDs (not for paranoid
disorders).
PROGNOSIS
Coid JW (2003) Epidemiology, public health and the problem of personality disorder. Br. J.
Psychiatry 182 (Suppl. 44), s3.
Costa PT, Widiger TA (eds) (2002) Personality Disorders and the Five-factor Model of Personality,
2nd edn. American Psychological Association, Washington, DC.
Crandell LE, Patrick MP, Hobson RP (2003) ‘Still-face’ interactions between mothers with bor-
derline personality disorder and their 2-month-old infants. Br. J. Psychiatry 183, 239.
Davidson SE (2002) Principles of managing patients with personality disorder. Adv. Psychiatr.
Treat. 8, 1.
Duggan C, Milton J, Egan V et al. (2003) Theories of general personality and mental disorder.
Br. J. Psychiatry 182 (Suppl. 44), s19.
Frankenburg FR, Zanarini MC (2002) Divalproex sodium treatment of women with borderline
personality disorder and bipolar II disorder: a double-blind placebo-controlled pilot study.
J. Clin. Psychiatry 63, 442.
Fullerton J, Cubin M, Wang TH et al. (2003) Linkage analysis of extremely discordant and con-
cordant sibling pairs identifies quantitative-trait loci that influence variation in the human
personality trait neuroticism. Am. J. Hum. Genet. 72, 879.
Jonsson EG, Cichon S, Gustavsson JP et al. (2003) Association between a promoter dopamine D2
receptor gene variant and the personality trait detachment. Biol. Psychiatry 53, 577.
Kendell RE (2002) The distinction between personality disorder and mental illness. Br. J.
Psychiatry 180, 110.
Koenigsberg HW, Harvey PD, Mitropoulou V et al. (2002) Characterizing affective instability in
borderline personality disorder. Am. J. Psychiatry 159, 784.
Lewis G, Appleby L (1988) Personality disorder: the patients psychiatrists dislike. Br. J. Psychiatry
153, 44.
Linehan MM, Dimeff LA, Reynolds SK et al. (2002) Dialectical behavior therapy versus compre-
hensive validation therapy plus 12-step for the treatment of opioid dependent women meet-
ing criteria for borderline personality disorder. Drug Alcohol Depend. 67, 13.
Miller MC (2001) Personality disorders. Med. Clin. North Am. 85, 819.
Nagin DS, Tremblay RE (2001) Parental and early childhood predictors of persistent physical
aggression in boys from kindergarten to high school. Arch. Gen. Psychiatry 58, 389.
Nickell AD, Waudby CJ, Trull TJ (2002) Attachment parental bonding and borderline personality
disorder features in young adults. J. Pers. Disord. 16, 148.
Paris J (1993) Personality disorders: a biopsychosocial model. J. Pers. Disord. 7(3), 255.
Paris J (2002) Clinical practice guidelines for borderline personality disorder. J. Pers. Disord.
16, 107.
Paris J, Zweig-Frank H (2001) A 27-year follow-up of patients with borderline personality dis-
order. Compr. Psychiatry 42, 482.
Pfohl B, Coryell W, Zimmerman M et al. (1986) DSM-III personality disorder: diagnostic over-
lap and internal consistency of individual DSM-III criteria. Comp. Psychiatry 27, 21.
Rendu A, Moran P et al. (2002) Economic impact of personality disorders in UK primary care
attenders. Br. J. Psychiatry 181, 62.
Rinne T, van den Brink W, Wouters L, van Dyck R (2002) SSRI treatment of borderline personal-
ity disorder: a randomized, placebo-controlled trail for female patients with borderline
personality disorder. Am. J. Psychiatry 159, 2948.
Rujescu D, Giegling I, Gietl A et al. (2003) A functional single nucleotide polymorphism (V158M)
in the COMT gene is associated with aggressive personality traits. Biol. Psychiatry 54, 34.
Samuels J, Eaton WW et al. (2002) Prevalence and correlates of personality disorders in a com-
munity sample. Br. J. Psychiatry 180, 523.
Sanislow CA, Grilo CM, Morey LC et al. (2002) Confirmatory factor analysis of DSM-IV criteria
for borderline personality disorder: findings from the collaborative longitudinal personality
disorder study. Am. J. Psychiatry 159, 284.
REFERENCES AND FURTHER READING 85
Schmahl CG, McGlashan TH, Bremmer JD (2002) Neurobiological correlates of borderline per-
sonality disorder. Psychopharmacol. Bull. 36, 69.
Skodol AE, Gunderson JG, McGlashan TH et al. (2002a) Functional impairment in patients with
schizotypal, borderline, avoidant, or obsessive–compulsive personality disorder. Am. J.
Psychiatry 159, 276.
Skodol AE, Gunderson JG, Pfohl B et al. (2002b) The borderline diagnosis. I: Psychopathology,
comorbidity, and personality structure. Biol. Psychiatry 51, 936.
Skodol AE, Siever LJ, Livesley WJ et al. (2002c) The borderline diagnosis. II: Biology, genetics,
and clinical course. Biol. Psychiatry 51, 951.
Stone MH (1993) Long-term outcome in personality disorder. Br. J. Psychiatry 162, 299.
Torgersen S, Kringlen E, Cramer V (2001c) The prevalence of personality disorders in a commu-
nity sample. Arch. Gen. Psychiatry 58, 596.
Trull TJ (2001) Structural relations between borderline personality disorder features and puta-
tive etiological correlates. J. Abnorm. Psychol. 110, 471.
Tyrer P (1988) Personality Disorders: Diagnosis, Management and Course. Wright, London.
Tyrer P (2002) Practice guideline for the treatment of borderline personality disorder: a bridge
too far. J. Pers. Disord. 16, 13.
Tyrer P, Duggan C, Coid J (2003) Ramifications of personality disorder in clinical practice. Br.
J. Psychiatry 182, s1.
Verheul R, Van Den Bosch LMC et al. (2003) Dialectical behaviour therapy for women with
borderline personality disorder: 12-month randomised clinical trial in the Netherlands. Br.
J. Psychiatry 182, 135.
White CN, Gunderson JG, Zanarini MC, Hudson JI (2003) Family studies of borderline person-
ality disorder: a review. Harvard Rev. Psychiatry 11, 8.
Zanarini MC (2003) The longitudinal course of borderline psychopathology: 6-year prospective
follow-up of the phenomenology of borderline personality disorder. Am. J. Psychiatry 160, 274.
Zimmerman M (1994) Diagnosis of personality disorders: a review of issues and research
methods. Arch. Gen. Psychiatry 51, 225.
Eating disorders 7
OBESITY
Obesity has been defined as a body mass index (BMI) above 30. In England, 17
per cent of males and 21 per cent of females are obese. It is the most common nutri-
tional disorder in the UK. There has been an alarming increase in the number of chil-
dren who are obese. Obesity is most common in lower social class, middle-aged
females.
Obesity is associated with an increased risk of cardiovascular disorders (MI, CVA,
hypertension), diabetes, cancer (breast, ovarian, colon), osteoarthritis, sleep apnoea
and accidents.
AETIOLOGY OF OBESITY
MANAGEMENT OF OBESITY
Diet
A calorie-controlled diet to decrease energy balance by 500–600 kcal/day will result in
weight loss of about 0.5–1.0 kg/week. Numerous types of diets exist, but there is a high
relapse rate associated with dieting alone.
Psychotherapy
Group psychotherapy may be particularly helpful. Marital therapy may be necessary
to alter family patterns. Ultimately, management may require inpatient supervision in
a therapeutic milieu.
Behaviour therapy
Self-monitoring is the key to behaviour therapy. Regulation of environmental cues
for eating, alteration of eating behaviour and self-reinforcement in weight loss
(also group reinforcement, e.g. ‘Weight Watchers’) has proven effective. Cognitive fac-
tors are important: guilt and feelings of failure are common, so attempt to reduce
these.
Drug therapy
Orlistat (inhibits fat absorption by inhibiting lipase) and sibutramine (enhances sati-
ety via noradrenergic/serotonin reuptake inhibition) show effectiveness in promoting
weight loss.
Surgical therapy
Surgery is generally limited to those with morbid obesity (BMI ⬎ 40). Gastric bypass,
gastric banding, and vertical banded gastroplasty are effective in providing sustained
long-term weight loss.
EPIDEMIOLOGY OF AN
• Anorexia nervosa is the third most common chronic illness in teenage females
(Lucas et al., 1991).
• Annual incidence:
– 14.6/100 000 for females.
– 1.8/100 000 for males.
– Unclear whether incidence is increasing – some increase suggested for 15- to
24-year age-group.
• Prevalence – 0.5–3.7 per cent in adolescent/early adult females. There are higher
rates in certain groups; e.g. ballet dancers, gymnasts.
• AN is over-represented in higher social classes (I & II).
• 90 per cent of females have onset within 5 years of menarche.
• Seasonal pattern of onset (maximum May)?
88 EATING DISORDERS
Adverse life effects are more evident in ‘late onset’ (⬎25 years) AN. Eighty-four
per cent of AN patients have a lifetime diagnosis of another psychiatric disorder
(Halmi et al., 1991), with major depression in 68 per cent of patients.
AETIOLOGY OF AN
Psychological factors
There are inconsistent data on personality disorder – high rates of avoidant personality
have been described. A specific association with childhood sexual abuse is overestimated.
• Body image disturbance is a core feature – body shape misperception or
disparagement.
• Morbid fear of fatness, pursuit of thinness, weight phobia – body thinness is viewed
as a cognitive construct equated with self-worth and control. Twenty-five per cent
of AN patients are overweight before onset.
• Psychodynamics – regression to the ‘prepubertal’ state; fear of becoming a sexual-
ized adult; fixation at the oral (pregenital) stage.
Familial factors
There are high rates of psychiatric illness – particularly depression, alcoholism,
psychosexual disturbances and obsessive–compulsive disorder (OCD) in mothers
(Halmi et al., 1991).
Earlier descriptions emphasize the family as the site of pathology: a dominant, intru-
sive mother; a passive, ineffectual father; an enmeshed, overprotective, rigid family struc-
ture with conflict avoidance. It is unclear whether these characteristics are cause or effect.
Twin studies affirm genetic and non-genetic environmental contributions.
Cultural factors
• The western ‘thinness-conscious’ culture.
• Role conflict – changing expectations for and by women.
• Food as a form of communication.
Biological factors
• Familial aggregation – association with (unipolar) depression may suggest genetic
predisposition.
ANOREXIA NERVOSA (AN) 89
Differential diagnosis
• Psychiatric – depression, schizophrenia, OCD, psychotic disorder.
• Medical – hypopituitarism, thyrotoxicosis, diabetes mellitus, neoplasia, reticulosis,
malabsorption.
MANAGEMENT OF AN
General principles
• Use a multifaceted approach (APA, 2000; Royal College of Psychiatrists, 2000):
– Detect and treat medical complications.
– Encourage a ‘normal’ balanced diet to regain ‘normal’ weight.
– Educate about diet and exercise.
90 EATING DISORDERS
Table 7.3 IDC-10 and DSM-IV diagnostic criteria for anorexia nervosa
ICD-10 DSM-IV
Behavioural approaches
• Encourage a regular diet (3000 kcal daily) to attain 1.5 kg weekly weight gain;
smaller intake if severe weight loss (tube or IV feeding rarely necessary); restora-
tion to at/near ideal bodyweight as target – i.e. body mass index of 20–25.
• Nurse supervision during and after meals helps to avoid surreptitious vomiting,
disposal of food and/or over-exercising.
Psychological approaches
Cognitive–behavioural therapy (CBT), psychoanalytic psychotherapy and family
therapy are effective in producing weight gain (Dare et al., 2001).
Education: dietary, exercise; body function/sexual and psychological maturation;
life skills support.
Pharmacological approaches
There is a limited role. Atypical antipsychotics have been shown to result in weight
gain. Antidepressants and anxiolytics can be given as clinically indicated. SSRIs may be
beneficial.
PROGNOSIS FOR AN
The prognosis is generally poor. There are high drop-out rates from treatment, and no
consistent evidence that treatment clearly alters outcome.
One 20-year follow-up (Zipfel et al., 2000) showed:
• 50.6 per cent recovered.
• 10.4 per cent still had DSM-IV criteria.
• 15.6 per cent died.
There is a high mortality from complications of AN, including suicide. Even ‘recov-
ered’ anoretics show psychopathology.
BULIMIA NERVOSA (BN) OR ‘DIETARY CHAOS SYNDROME’ 91
Note that a further category has been proposed in DSM-IV – ‘binge-eating disorder’:
• Recurrent distressing episodes of uncontrolled overeating.
• Not satisfying the diagnostic criteria for BN.
It is unclear whether this group differs in pathophysiology, treatment outcome, etc.
EPIDEMIOLOGY OF BN
AETIOLOGY OF BN
Psychological factors
• There are high rates of depression/dysphoria, alcohol abuse, personality distur-
bance (borderline, labile).
• There is poor self-esteem and sense of personal control.
Familial factors
There are high rates of psychiatric disturbance, particularly depression.
Cultural factors
As for AN (see above).
Biological factors
• Twin studies – MZ:DZ ⫽ 22%:9%.
• Serotonin dysfunction is more extensively studied in BN:
– Deficits in CSF 5-HIAA persist after treatment.
– Blunted GH response to D-fenfluramine challenge.
92 EATING DISORDERS
CLINICAL FEATURES OF BN
MANAGEMENT OF BN
As with AN, the approach is multifaceted. Most are treated as outpatients. The criteria
for hospitalization are similar to AN (see above).
Psychological approaches
• Psychoeducation, nutritional counselling, relaxation training are all used.
• CBT:
– Intensive, weekly over 5 months.
– Many components include self-monitoring (diary-keeping).
• Self-reporting – establish cognitive and behavioural strategies to alter low frustra-
tion tolerance, poor impulse control, negative self-concept, poor recognition and
identifications of emotions.
• CBT is more effective than interpersonal therapy (Agras et al., 2000).
• CBT is most effective for attitudes to weight and shape.
• CBT is more effective in the short term than antidepressants. A combination of
CBT and antidepressants may be best.
• Group psychotherapy can be used. Family therapy also is helpful, where clinically
indicated. Self-help and support groups are beneficial.
REFERENCES AND FURTHER READING 93
Pharmacological approaches
SSRI antidepressants are effective independent of mood status, at dosages similar to
treatment of depression. Naltrexone and ondansetron may reduce binging and purging.
PROGNOSIS FOR BN
Overall the outlook is better than for AN, but there are high rates of relapse and psy-
chosocial impairment.
One prospective 5-year study of 102 BN females (Fairburn et al., 2000) showed:
• Continuously ill – half to two-thirds.
• Subsequent relapse after initial ‘recovery’ – 33 per cent.
Johnson JG, Cohen P, Kotler L et al. (2002) Psychiatric disorders associated with risk for the
development of eating disorders during adolescence and early adulthood. J. Consult. Clin.
Psychol. 70, 119.
Kaye WH, Gwirstman HE, George DT et al. (1991) Altered serotonin activity in anorexia nervosa
after long term weight restoration. Arch. Gen. Psychiatry 48, 556.
Kaye WH, Lilenfeld LR, Berrettini WH et al. (2000) A search for susceptibility loci for anorexia
nervosa: methods and sample description. Biol. Psychiatry 47, 749.
Keel P, Mitchell J, Miller K et al. (1999) Long term outcome of bulimia nervosa. Arch. Gen.
Psychiatry 56, 63.
Klump KL, Kaye WH, Strober M (2001a) The evolving genetic foundations of eating disorders.
Psychiatr. Clin. North Am. 24, 215.
Klump KL, Miller KB, Keel PK et al. (2001b) Genetic and environmental influences on anorexia
nervosa syndromes in a population-based twin sample. Psychol. Med. 31, 737.
Klump K, Wonderlich S, Lehoux P et al. (2002) Does environment matter? A review of non-
shared environment and eating disorders. Int. J. Eat. Disord. 31, 118.
Labib M (2003) The investigation and management of obesity. J. Clin. Pathol. 56, 17.
Lucas AR, Beard CM, O’Fallon WM et al. (1991) 50-year trends in the incidence of anorexia ner-
vosa in Rochester, Minnesota: a population-based study. Am. J. Psychiatry 148, 917.
McGuire MT, Jeffery RW, French SA (2002) The psychologic correlates of obesity. Clin. Fam.
Pract. 4, 319.
Mitchell JE, Peterson CB, Myers T, Wonderlich S (2001) Combining pharmacotherapy and psy-
chotherapy in the treatment of patients with eating disorders. Psychiatr. Clin. North Am. 24, 315.
Monteleone P, Brambilla F, Bortolotti F, Maj M (2000) Serotonergic dysfunction across the eating
disorders: relationship to eating behaviour, purging behaviour, nutritional status and general
psychopathology. Psychol. Med. 30, 1099.
Nielsen S (2001) Epidemiology and mortality of eating disorders. Psychiatry Clin. North Am. 24, 214.
Norman RJ, Davies MJ, Lord J, Moran LJ (2002) The role of lifestyle modification in polycystic
ovary syndrome. Trends Endocrinol. Metab. 13, 251.
Padwal R, Li SK, Lau DCW (2003) Long-term pharmacotherapy of overweight and obesity: a
systematic review and meta-analysis of randomized controlled trials. Int. J. Obesity 27, 1437.
Palmer RL, Birchall H et al. (2002) Self-help for bulimic disorders: a randomised controlled trial
comparing minimal guidance with face-to-face or telephone guidance. Br. J. Psychiatry 181, 230.
Paul T, Kirsten S et al. (2002) Self-injurious behavior in women with eating disorders. Am. J.
Psychiatry 159, 408.
Polivy J, Herman C (2002) Causes of eating disorders. Annu. Rev. Psychol. 53, 187.
Powers PS, Santana CA (2002) Eating disorders: a guide for the primary care physician. Prim.
Care 29, 81.
Pratt B, Woolfenden S (2002) Interventions for preventing eating disorders in children and ado-
lescents. Cochrane Database Syst. Rev. 2, CD002891.
Rome ES, Ammerman S, Rosen DS et al. (2003) Children and adolescents with eating disorders:
the state of the art. Pediatrics 111, e98.
Rosenblum J, Forman S (2002) Evidence-based treatment of eating disorders. Cur. Opin.
Pediatrics 14, 379.
Rosenblum J, Forman S (2003) Management of anorexia nervosa with exercise and selective
serotonergic reuptake inhibitors. Cur. Opin. Pediatrics 15, 346.
Royal College of Psychiatrists (2000) Eating Disorders in the UK: Policy for Service Development
and Training. RCP, London.
Rudolf M, Sahota P, Barth J et al. (2001) Increasing prevalence of obesity in primary school chil-
dren: a cohort study. BMJ 322, 1094.
Shea MT, Stout R et al. (2002) Short-term diagnositc stability of schizotypal, borderline,
avoidant, and obsessive–compulsive personality disorders. Am. J. Psychiatry 159, 2036.
Sigman GS (2003) Eating disorders in children and adolescents. Pediatr. Clin. North Am. 50, 1139.
REFERENCES AND FURTHER READING 95
Steinhausen H (2002) The outcome of anorexia nervosa in the 20th century. Am. J. Psychiatry
159, 1261.
Walsh BT, Agras WS, Devlin MJ et al. (2000) Fluoxetine for bulimia nervosa following poor
response to psychotherapy. Am. J. Psychiatry 157, 1332.
Westen D, Harnden-Fischer J (2001) Personality profiles in eating disorders: rethinking the dis-
tinction between axis I and axis II. Am. J. Psychiatry 158, 547.
World Health Organization (1998) Obesity: Preventing and Managing the Global Epidemic.
WHO, Geneva.
Yanovski SZ (2003) Binge eating disorder and obesity in 2003: could treating and eating disorder
have a positive effect on the obesity epidemic? Int. J. Eat. Disord. 34, s117.
Zabinski MG, Wilfley DE, Pung MA et al. (2001) An interactive internet-based intervention for
women at risk of eating disorders: a pilot study. Int. J. Eat. Disorder. 30, 129.
Zipfel S, Lowe B, Reas DL et al. (2000) Long-term prognosis in anorexia nervosa: lessons from a
21 year follow-up study. Lancet 355, 721.
Human sexuality 8
NORMAL BEHAVIOUR
EPIDEMIOLOGY
PHYSIOLOGY
NEUROPHYSIOLOGY
• Exact mechanism of orgasm unknown.
• Dopaminergic effects result in increased sexual activity. Antidopaminergic drugs
cause decreased sexuality and impotence.
• Noradrenergic effects (␣2 receptors) reduce sexual activity.
RELATIONSHIP BEHAVIOUR
Consider:
• Communication – within the relationship.
• Commitment – to the relationship.
• Conflict – within the relationship.
• Context – of the sexual encounter (culture, personal, surroundings).
SEXUAL DYSFUNCTIONS
DEFINITIONS
Male
• Erectiled dysfunction (‘impotence’) – inability to sustain an erection adequate for
penetration. Commonest disorder presenting in males at clinic.
• Ejaculatory impotence – inability to ejaculate despite adequate erection. Uncommon.
• Premature ejaculation – ejaculation before, during or immediately after penetration.
Usually in young men. Common.
Female
• Anorgasmia (‘frigidity’) – orgasm achieved rarely or never.
• Vaginismus – involuntary contraction of vaginal introitus in response to attempts
at penetration.
98 HUMAN SEXUALITY
Either sex
• Low sex drive.
• Dyspareunia – pain on intercourse.
CLASSIFICATIONS
Can be classified as:
• Primary or secondary; i.e. no history of normal function or onset later in life after a
period of normal functioning.
• Symptomatic or functional; i.e. due to organic or psychological cause.
Can be further classified as:
• Acute or insidious onset.
• Total or partial.
• Global or situational.
– or according to stage affected (see Table 8.2).
SEXUAL DYSFUNCTIONS 99
ASSESSMENT
AIMS OF ASSESSMENT
1 To define the dysfunction.
2 To assess whether it is organic, functional or both. Often a mild dysfunction due to
organic causes (e.g. diabetes mellitus) can lead to ‘performance anxiety’, and thus to
a much worse ‘functional’ disorder.
3 To determine the immediate causes.
4 To assess the couple’s resources and motivation.
5 To decide on the correct management and likely prognosis.
Always see the sexual partner; see both partners together also if possible.
The problem
• Exact nature of problem, precise examples sought.
• Frequency and timing of dysfunction.
• Total or partial? If partial, seek situational circumstances.
• Any sign of normal function, e.g. morning erections in male.
• Mode of onset: acute or insidious, primary or secondary?
• Duration of problem.
• Course of problem: constant or fluctuating?
Current influences
• Environmental conditions: sexual stress, relationship with partner, other stresses,
timing and setting of sexual encounters.
• Personal variables: sexual knowledge and experience, emotional reaction (guilt,
anxiety), cognitive avoidance, contraceptive habits, fear of conception.
• Organic condition: important in only about 10 per cent presenting to a psych-
iatrist. Age is often an important factor.
• Consequences of problem: avoidance of intercourse, partner’s reaction.
Resources
• Personal resources: motivation, honesty, flexibility, ability to verbalize, history of
sex drive.
• Sexual relationship: commitment, willingness to be involved in treatment, conflict.
In 30 per cent, both partners have dysfunctions.
• Professional resources: time and personnel available to treat the disorder.
100 HUMAN SEXUALITY
PROGRAMME OF ASSESSMENT
History
• Take a full history of the complaint: look for precise diagnosis, indication of aetiology
and prognostic signs.
• Family background and personal history: parental relationships, attitude to sex.
• Sexual and marital history: degree of sexual knowledge, past sexual experiences,
relationship with sexual partner, contraceptive methods, children, attitudes to
pregnancy.
• Drug and alcohol abuse.
Examination
• Assess mental state: depression, anxiety.
• Physical examination, including genitalia.
Investigations
Physical investigations may be indicated, particularly with impotence and if there is
total absence of any sign of erection in a man with previously normal sexual history.
Include urinalysis for sugar, liver function tests, testosterone level. The nocturnal penile
tumescence strain gauge is a useful diagnostic tool.
Intersexual disorders:
AETIOLOGY
Previous experiences
• Restrictive upbringing leading to intrapsychic conflict.
• Traumatic early sexual encounters.
• Abnormal family relationships.
SEXUAL DYSFUNCTIONS 101
Current circumstances
• Sexual stresses (e.g. concerning contraception or pregnancy).
• Non-sexual stresses (e.g. lack of privacy, recent childbirth).
• Relationship difficulties (e.g. partner rejection, sexual sabotage).
• Ignorance or guilt resulting in failure to engage in effective sexual behaviour.
• Psychiatric disorder (e.g. depression, schizophrenia with sexual delusions).
• ‘Performance anxiety’ – fear of failure arising from demand for performance by
partner or excessive need to please partner.
• ‘Spectatoring’ – observing own behaviour and not allowing automatic responses
or recognizing erotic sensations.
Organic factors
An organic cause of impotence is suggested by:
• Penis never fully turgid/generalized dysfunction (i.e. not situational).
• No associated significant life event.
• Previous uninterrupted period of normal sexual function.
• Sexual interest being maintained.
Age
Erectile dysfunction increases dramatically with age: 0.1 per cent under 20 years;
7 per cent 40–50 years; 75 per cent over 70 years.
General illness
• Endocrine – diabetes mellitus, thyroid disorder, HPA axis disorder.
• Cardiovascular – atheromatous, Leriche’s syndrome, heart failure.
• Hepatic – cirrhosis.
• Renal/urological – Peyronie’s disease, hydrocele, varicocele, renal failure.
• Others – respiratory failure, intersex disorders, congenital (severe) hypospadias.
Local disorders
Look for urethritis, balanitis, penile or vaginal trauma, chordee, castration, radical
surgery (prostatectomy, colostomy, etc.).
Drugs
• Decreased libido – antipsychotics, antiandrogens, antidepressants (most varieties
but SSRIs least likely); alcohol increases libido acutely but libido reduces with
chronic misuse.
• Impaired erection – antipsychotics, antidepressants, beta-blockers.
• Priapism – may occur with antipsychotics.
• Impaired ejaculation – antipsychotics, antidepressants.
• Hyperprolactinenia – secondary to antipsychotic therapy causes amenorrhoea in
females; sometimes also breast engorgement/galactorrhea.
Attend to any organic cause, if possible, but only 10 per cent of cases of impotence
presenting to psychiatrists (and a much lower proportion of other dysfunctions) have
102 HUMAN SEXUALITY
an organic cause, and this is often not reversible. Psychological factors almost always
play an important part, and these can be treated.
Behaviour therapy
This is the treatment of choice. ‘Masters and Johnson’ techniques are used. It is short-
duration, symptom-focused therapy, seeing the couple together after initial individual
interviews.
The aim is to reduce performance anxiety, reduce spectatoring and reduce the pressure
of sexual demands on the self and from the partner. Autonomic responses (erection,
orgasm, etc.) are not concentrated on. Instead, increased pleasure and confidence and
reduction of anxiety are aimed at, with the presumption that normal sexual activity
will follow.
Therapy may be performed intensely every day for 2 weeks, but under the NHS
weekly therapy sessions for 6–10 weeks are more common and almost as successful.
Sequence of therapy
1 Supply and discuss sexual information (anatomy, physiology, partner discord, erro-
neous beliefs).
2 Direct attempts to modify attitudes by explanation, by sanctioning behaviour, etc.
3 Establish effective communications, assumption of joint responsibility.
4 Explain ‘giving to get’ (i.e. mutual exchange of rewards).
5 Define and discuss precise goals of therapy.
6 Clear sexual assignments are given, explained and discussed (‘homework’). Couple
set aside a time each day for these and report back.
7 Homework starts with ‘non-demand pleasuring’ (or ‘sensate focus technique’).
Prohibit coition for the first week or more. Couple take turns in caressing each other,
avoiding genital areas initially. This is discovery of what is pleasurable, mutual
enhancement of non-orgasmic sexual pleasure, without being concerned about erec-
tions, orgasms or performance. This is therefore a form of desensitization.
8 Discuss resistances, guilt and anxieties when reporting back in therapy sessions.
Couple progress from caressing non-sexual areas (back, legs, etc.) to caressing sex-
ual areas (breasts, vulva, penis), but not aiming at orgasm or penetration.
9 Progress is made to specific techniques as appropriate:
– Erectile impotence – gradual introduction of penis with female superior or side
by side. Then male relaxes and enjoys it. Instruction given to focus on erotic sensa-
tions and stop rationalizing (‘get out of your head and into your body’). May
proceed to extravaginal orgasm before finally achieving intravaginal orgasm.
– Ejaculatory impotence – vigorous penile stimulation with lotion or cream, grad-
ually bringing penis nearer to vagina and continuing stimulation as inserted.
– Premature ejaculation – Seman’s technique. Female squeezes base of penis or
glans as orgasm approaches (initially extravaginally, then intravaginally), thus
preventing ejaculation, and then proceeds to arousal again. May be repeated
several times before ejaculation is allowed.
– Vaginismus – relaxation training, gradual approach to intercourse as for erectile
impotence. Vaginal dilators may be used initially.
– Anorgasmia– masturbation, use of vibrators, gradual progress to coitus with clit-
oral stimulation.
PARAPHILIAS 103
Psychotherapy
It is rarely useful to enter into prolonged analytic therapy unless sexual dysfunction is
part of an extensive neurotic or personality problem. Broader marital therapy sessions
may be indicated.
PARAPHILIAS
EXHIBITIONISM
EPIDEMIOLOGY
• Commonest single sexual offence.
• 3000 convictions per year in England and Wales.
• Peak age of onset is 15–25 years.
• Incidence in persons under 25 years has doubled since 1945.
• 75 per cent are under 40 years.
• 5 per cent are subnormal or psychotic.
AETIOLOGICAL FACTORS
• Personality factors – immature, passive, obsessional if type 1.
• Enjoyment of risk taking.
• Dissociative behaviour in response to stress or depression.
• Witness response (fear or disgust) may reinforce behaviour.
• Often poor sexual performance – with impotence or premature ejaculation and
increased masturbation.
• Possibly close ambivalent relationships with mother and poor distant relationship
with father.
MANAGEMENT
The first court appearance is often sufficient deterrent. Psychiatric management is
suggested if there has been more than one offence:
• Aversive behavioural techniques (e.g. covert sensitization).
• Group therapy with other exhibitionists may be helpful.
• Injections with antiandrogen compounds – long-acting agonists of luteinizing
hormone-releasing hormone – may help control sexual impulses.
PROGNOSIS
Good: 80 per cent only offend once.
• Heterosexual relationship.
• Sympathetic wife.
PAEDOPHILIA
INCEST
TRANSVESTISM
EPIDEMIOLOGY
There are possibly 30 000 transvestites in the UK. Fifty per cent are married. Thirty-
five per cent of men are homosexual (most of women are homosexual). Fifteen per
cent are permanent cross-dressers.
Transvestism is most common in social classes II and III.
CLINICAL FEATURES
• Usually evident before age 10.
• May develop increasingly prominent female interests.
• May use female clothing for fetishistic masturbation.
• Older transvestites often belong to clubs and act socially as females.
106 HUMAN SEXUALITY
TRANSSEXUALISM
Transsexualism is disturbance of the core gender identity, usually a biological male who
is convinced that he is female. It is not itself an offence, but the person may be charged
with ‘breach of the peace’.
CLINICAL FEATURES
• Many have been fetishistic transvestites before becoming fully transsexual and
homosexual in orientation.
• Usually convinced of ‘wrong sex’ before age 8.
• Often has poor work record, difficulty in forming relationships, low sex drive.
MANAGEMENT
Transsexualism tends to be intractable, but the person may fluctuate in the desire for
sex-change surgery. Surgery should be postponed until the person has lived as the
opposite-sex person for 2 years.
Pre- and post-surgical counselling is necessary. Success is related to premorbid per-
sonality, acceptance of surgical limitations, effectiveness and motivation to maintain
opposite-sex lifestyle.
Hormone therapy is mainly of cosmetic benefit.
HOMOSEXUALITY
Abel GG, Osborn C (1992) The paraphilias: the extent and nature of sexually deviant and crim-
inal behavior. Clin. Forensic Psych. 15, 675.
Adson PR (1992) Paraphilias and related disorders. Psych. Ann. 22(6).
Andersson KE (2003) Erectile physiological and pathophysiological pathways involved in erectile
dysfunction. J. Urol. 170, s6.
Bailey JM, Pillard RC, Neale NC, Agyei Y (1993) Heritable factors influence sexual orientation in
women. Arch. Gen. Psychiatry 50, 217.
Bancroft JHJ (1974) Sexual dysfunction in men. Medicine (Series 1) 30, 1790.
REFERENCES AND FURTHER READING 107
Baron M (1993) Genetic linkage and male homosexual orientation. BMJ 304, 12.
Berrios DC, Hearst N, Perkins LL (1992) HIV antibody testing in young, urban adults. Arch.
Intern. Med. 152, 397.
Blanker MH, Bosch JL, Groeneveld FP et al. (2001) Erectile and ejaculatory dysfunction in a
community-based sample of men 50 to 70 years old: prevalence, concern, and relation to sex-
ual activity. Urology 57, 763.
Blythe MJ, Rosenthal SL (2000) Female adolescent sexuality: promoting health sexual develop-
ment. Obstet. Gynec. Clin. North Am. 27, 125.
Brannon GE (2002) Paraphilias. Emedicine. www.emedicine.com/topic3127.htm.
Bridges LJ, Moore KA (2002) Religious involvement and children’s well-being: what research tells
us (and what it doesn’t). Child Trends: Research Brief, Washington, DC.
Briken P, Hill A, Berner W (2003) Pharmacotherapy of paraphilias with long-acting agonists of
luteinizing hormone-releasing hormone: a systematic review. J. Clin. Psychiatry 64, 890.
Brock GB, McMahon CG, Chen KK et al. (2002) Efficacy and safety of tadalafil for the treatment
of erectile dysfunction: results of integrated analyses. J. Urol. 168, 1332.
Byne W, Parsons B (1993) Human sexual orientation: the biologic theories reappraised. Arch.
Gen. Psychiatry 50, 228.
Centers for Disease Control and Prevention (2002) Trends in Sexual Risk Behaviors Among High
School Students, United States, 1991–2001. MMWR, 51, 856.
Cochran SD, Mays V (2000) Lifetime prevalence of suicide symptoms and affective disorders
among men reporting same-sex sexual partners: results from NIHANES III. Am. J. Pub.
Health 90, 578.
Duncan P, Dixon RR, Carlson J (2003) Childhood and adolescent sexuality. Pediatr. Clin. North
Am. 50, 765.
Feldmann, J, Middleman ABM (2002) Adolescent sexuality and sexual behaviour. Cur. Opin.
Obstetrics Gyn. 14, 489.
Ferguson KJ, Stapleton JT, Helms CM (1991) Physicians’ effectiveness in assessing risk for human
immunodeficiency virus infection. Arch. Intern. Med. 151, 561.
Frank E, Anderson C, Rubinstein D (1978) Frequency of sexual dysfunction in ‘normal’ couples.
New Engl. J. Med. 299, 111.
Goldstein I, Lue TF, Padma-Nathan H et al. (1998) Oral sildenafil in the treatment of erectile dys-
function. New Engl. J. Med. 338, 1397.
Green J, Miller D (1985) Male homosexuality and sexual problems. Br. J. Hosp. Med. 33, 353.
Gregoire A (1992) New treatments for erectile impotence. Br. J. Psychiatry 160, 315.
Hawton K (1985) Drug treatments in psychiatry: sexual dysfunction. Br. J. Hosp. Med. 34, 207.
Hawton K, Catalan J, Martin P et al. (1986) Long-term outcome of sex therapy. Behav. Res. Ther.
24, 665.
Johnson AM, Mercer CH, Erens B et al. (2001) Sexual behaviour in Britain: partnerships, prac-
tices and HIV risk behaviors. Lancet 358, 1835.
Jorm AF, Korten AE, Rodgers B et al. (2002) Sexual orientation and mental health: results from a
community survey of young and middle-aged adults. Br. J. Psychiatry 180, 423.
Kaplan HS (1978) The New Sex Therapy. Peregrine, London.
Kay DSG (1992) Masturbation and mental health: uses and abuses. Sexual Marital Ther. 7, 97.
King M, McKeown E, Warner J (2003) Mental health and quality of life of gay men and lesbians
in England and Wales: a controlled, cross-sectional study. Br. J. Psychiatry 183, 552.
Kinsey AC, Pomeroy WB, Martin CE (1948) Sexual Behaviour in the Human Male. WB Saunders,
Philadelphia.
Kinsey AC, Pomeroy WB, Martin CE et al. (1953) Sexual Behaviour in the Human Female.
WB Saunders, Philadelphia.
Laws DR, O’Donohue W (1997) Sexual Deviance: Theory, Assessment and Treatment. Guilford
Press, New York.
108 HUMAN SEXUALITY
• Alcohol abuse.
• Alcohol dependence (see Chapter 10 for definition).
• Alcohol intoxication.
• Alcohol withdrawal.
• Alcohol delirium.
• Alcohol persisting dementia.
• Alcohol persisting amnestic disorder.
• Alcohol psychotic disorder – with delusions or with hallucinations.
• Alcohol mood disorder.
• Alcohol anxiety disorder.
• Alcohol sexual dysfunction.
• Alcohol sleep disorder.
EPIDEMIOLOGY OF DEPENDENCE
National Institute on Alcohol Abuse and Alcoholism (NIAAA) (2000) guidelines for
safe use of alcohol:
Table 9.2 Per capita consumption of alcohol (litres of pure alcohol) by country
Country 1997 1998 1999 2000
Adapted from NTC Publications (2002). World Drink Trends. NTC Publications Ltd,
Henley-on-Thames, UK.
General surveys
See Table 9.1 for results of a national survey in the USA, and Table 9.2 for per capita
consumption in various countries.
The National Center for Social Research (2002) survey among secondary school
pupils in England showed that 4 per cent of 11- to 15-year-olds used alcohol in the
previous week.
Hospital/practice surveys
Thirty per cent of patients in general health care have alcohol-related disabilities.
Co-morbidity
Forty-seven per cent of alcoholics meet criteria for another psychiatric disorder (see
Table 9.3).
Curran et al. (2003) measured co-morbid substance use disorders in emergency
room patients who had a primary psychiatric diagnosis and found the following
rates:
Ethnic factors
Dependence is high in North American, Afro-Caribbean and Irish; low in Jewish and
in Chinese – may relate to different isoenzymes of acetaldehyde dehydrogenase.
112 ALCOHOL DEPENDENCE
AETIOLOGY OF DEPENDENCE
GENETICS
Family studies
• There is a sevenfold increase in risk of alcoholism among first-degree relatives of
alcoholics versus controls.
• Twin studies – MZ:DZ ⫽ 70%:43% for males (Pickens et al., 1991), 47%:32% for
females (Kendler et al., 1992).
Adoption studies
Danish, Swedish and US (Iowa) studies indicate:
• Sons of alcoholics are four times more likely to be alcoholic than sons of non-
alcoholic, whether raised by alcoholic biological parents or by non-alcoholic
adoptive parents.
• Sons of alcoholics raised by non-alcoholic adoptive parents are no more susceptible
to another non-alcoholic adult psychiatric disorder.
• There is a higher rate of childhood conduct disorder in male offspring of alcoholics.
• Alcoholism and antisocial personality are genetically independent disorders for
both males and females.
Cloninger (1987) proposed, on the basis of Swedish data, type I/II subgrouping of
alcoholism:
• Type I – predominantly female, later onset than type II, not associated with antisocial
behaviour, higher psychological dependency, more guilt, more related to environmen-
tal factors than genetic, abusers show high traits of dependency and harm avoidance.
• Type II – predominantly males, onset usually before 25 years, high genetic com-
ponent, parental alcoholism, parental antisocial behaviour, more alcohol-related
aggression, more legal problems, less likely to achieve abstinence, more impulsive/
antisocial personality traits.
Chromosomes
Variations in allele compositions for alcohol dehydrogenase and aldehyde dehydroge-
nase may contribute to risk patterns for alcoholism among oriental populations.
Vulnerability markers
Abnormalities in P3 event-related potential are associated with genetic risk for sub-
stance use disorders (Iacono et al., 2002).
MOLECULAR GENETICS
A number of alcohol-responsive genes have been found (Pandey et al., 2003).
Neuropeptide Y (NPY) is of particular interest; decreased expression of NPY has been
proposed as a substrate for the predisposition to alcohol-seeking behaviors and alco-
holism (Ilveskoski et al., 2001).
Mayfield et al. (2002) propose that alcohol alters genes expression involved in cAMP
signalling pathways that modulate alcohol sensitivity as well as withdrawal anxiety.
CLINICAL FEATURES 113
BIOCHEMICAL FACTORS
Alcohol has complex interactions with multiple systems (Ciraulo et al., 2003).
• Dopamine (DA) – Acute alcohol consumption stimulates DA release in nucleus
accumbens. Chronic alcohol use results in down-regulation of D2 receptors.
• Serotonin (5-HT) – Alcohol interferes with serotonin function. Greater reduction
of serotonin function is associated with impulsivity, aggression, suicidality and
psychiatric disorders.
• Growth homone (GH) – Chronic alcoholism is associated with reduced GH
response to stimulus challenge, and is reflective of severe dependence.
• Opioids – Endogenous opioid system mediates reinforcing effects of alcohol and
may be altered in those with high risk for alcoholism.
• Other receptor/neuropeptides.
PSYCHOLOGICAL FACTORS
Meszaros et al. (1999) used a ‘tridimensional personality questionnaire’ to measure
the three personality dimensions: novelty seeking (NS), harm avoidance (HA) and
reward dependence (Cloninger et al., 1987) in detoxified alcoholics and found that
NS is a strong predictor for relapse in detoxified males, and that HA predicts ‘early’
relapse (4 weeks) in females.
Operant conditioning: relief of withdrawal symptoms promotes further abuse.
SOCIOCULTURAL FACTORS
• Cultural values, role of alcohol in social activities.
• Per capita consumption and cultural patterns of alcohol usage correlate with
prevalence of alcohol-related disabilities.
• Peer-group pressures.
• Occupation-related factors.
CLINICAL FEATURES
6 Subjective awareness of compulsion to drink – The desire for a further drink is seen
as irrational, resisted, but the further drink is taken (analogous to classic descrip-
tion of compulsive disorder).
7 Reinstatement after abstinence – Many patients find abstinence surprisingly easy to
maintain in, say, a ward setting where drinking cues are removed. Relapse into the
earlier stage of dependence (reinstatement) is rapid (within 72 hours of drinking)
for those severely dependent and varies (weeks, months) for lesser degrees.
CNS EFFECTS
WITHDRAWAL SYMPTOMS
The spectrum of symptoms is wide: tremor, nausea (or retching), sweating (drenching
in early morning), mood disturbance (fearful, depressive), hyperacusis, tinnitus, itch-
ing, muscle cramps, sleep disturbance, perceptual distortions and hallucinations,
convulsions and fully developed syndrome of delirium tremens.
• Acute tremulousness – 34 per cent.
• Transient hallucinosis – 11 per cent.
• Auditory hallucinosis – 2 per cent.
• Convulsions – ⬍12 per cent.
• Wernicke–Korsakoff syndrome – ⬍3 per cent.
• Full-blown delirium tremens – 5 per cent.
Delirium tremens is typically seen 3–5 days after selective or absolute withdrawal,
although prodromal features occur earlier. Trauma or infection present from outset in
up to 50 per cent of cases and biochemical evidence of liver damage in up to 90 per cent.
There may be vivid hallucinations, delusions, profound confusion and inattention,
with agitation and restlessness, sleeplessness, autonomic overactivity and fearful affect.
Primary disorder of the reticular activating system is suggested by inattention, over-
arousal, insomnia and overactivity. There is a 10–20 per cent mortality rate related to
autonomic instability.
Alcoholic hallucinosis, in a restricted sense, applies to rare conditions in which audi-
tory hallucination occurs alone in clear consciousness. Voices are frequently offensive
and critical. This may be followed by secondary delusional interpretation. It usually
clears in a few days, where there is no evidence for association with schizophrenia.
WERNICKE–KORSAKOFF SYNDROME
Wernicke’s encephalopathy (also see Chapter 13)
This is caused by thiamine deficiency. There are acute degenerative changes in thalamus,
hypothalamus, mamillary bodies. Signs are:
• Confusion/clouding of consciousness.
• Ocular palsies and nystagmus.
COMPLICATIONS OF ALCOHOL DEPENDENCE 115
• Staggering gait.
• Peripheral neuropathy.
Treatment with thiamine is usually effective in promptly resolving ataxia and ocular
symptoms, but cognitive symptoms are slower to resolve.
Korsakoff syndrome
There are degenerative changes in upper brain stem, thalamus, hypothalamus and
mamillary bodies. Signs are:
Korsakoff’s syndrome
80%
Established Korsakoff’s
⫾ alcohol dementia
ALCOHOLIC DEMENTIA
There is debate as to whether this is actually a manifestation of evolving Korsakoff ’s.
There are mild to moderate cognitive deficits, including impaired memory and judge-
ment, social and personal neglect, and paranoia.
Dementia rarely occurs before age 40 years. Females may be more at risk. It is usu-
ally accompanied by other CNS and liver evidence of alcohol damage. It is associated
with CT/MRI evidence of ‘atrophy’, especially in the frontal lobes.
In a small number of patients without full dementia who maintain abstinence, radio-
logical ‘atrophy’ reverses with time (see Chapter 15).
116 ALCOHOL DEPENDENCE
PSYCHIATRIC EFFECTS
Respiratory
• Orofacial/laryngeal carcinoma.
• COPD/lung cancer related to 80 per cent smoking rate in alcoholics.
• Klebsiella pneumonia in alcoholics.
• Reactivation of primary TB focus in alcoholics.
Cardiovascular
• Cardiomyopathy.
• Hypertension – alcohol-associated may not respond well to antihypertensives.
• Sinus tachycardia with intoxication and withdrawal.
Gastrointestinal
• Gastritis.
• Barrett’s oesophagitis.
• Oesophageal varices.
• Mallory–Weiss oesophageal rupture.
• Peptic/gastric ulceration – in 20 per cent of alcoholics. Bleeding may be exacerbated
by vitamin K deficiency secondary to cirrhosis.
• Carcinoma of stomach.
• Possible association with large bowel/rectal carcinoma.
• Pancreatitis.
• Diabetes mellitus.
COMPLICATIONS OF ALCOHOL DEPENDENCE 117
Liver damage
Liver damage is related to lifetime intake, enhanced by nutritional deficiences. Fatty
infiltration is the earliest feature – decreased fatty acid oxidation.
• Alcoholic hepatitis – Acute episode resembles viral hepatitis: 10–30 per cent die, a
proportion go on to cirrhosis. Occurs usually after 10 years’ abuse.
• Cirrhosis – Up to20 per cent of chronic alcoholics suffer. Eighty per cent of all cases
of cirrhosis are related to alcohol abuse. Women are more susceptible. Vulnerability
may be due in part to histocompatibility antigen HLA-B8, found in approximately
25 per cent of the population. Alternatively, HLA-A28 may have a protective effect.
Note that hepatotoxicity may occur at ‘therapeutic’ doses of acetaminophen.
Haematological
• Macrocytosis – folate deficiency and direct toxic effect of alcohol.
• Anaemia:
– Iron deficiency – absorption, blood loss.
– B12 – nutritional deficiency.
– Malabsorption.
– Liver stores.
• Thrombocytopenia – splenic sequestration due to enlarged spleen secondary to
liver disease; suppression of platelet formation due to toxic effect of alcohol.
Neoplasm
May be orofacial, GI, respiratory, liver.
Endocrine
There may be sexual problems and feminization in males – erectile impotence due to
impaired metabolism of estrogen by liver and suppression of testosterone production.
Menstrual irregularities occur in females.
Disabilities may precede the psychological and physical by several years. Family/mari-
tal difficulties include:
• Physical/sexual abuse of partner, ‘reactive’ psychiatric disorder (usually depres-
sion) in partner.
118 ALCOHOL DEPENDENCE
• Increased divorce.
• Increased abuse of children.
• Increased risk of later alcoholism in children, developing other psychiatric disorders,
later marrying an alcoholic.
EFFECTS IN SOCIETY
GENERAL GUIDELINES
Make an initial comprehensive, multidimensional assessment of alcohol-related dis-
abilities. Involve the spouse/significant relationship.
MANAGEMENT OF ALCOHOL DEPENDENCE 119
DETOXIFICATION
• Give attention to hydration and electrolyte balance; multivitamin, folic acid, and
thiamine given. Intramuscular/vascular thiamine should be given prior to any
glucose load to avoid depletion of thiamine stores and subsequent precipitation/
exacerbation of Wernicke–Korsakoff syndrome.
• Give attention to general medical conditions and the risk of respiratory depression/
infection. Co-morbid physical illness/sepsis are associated with high mortality in
acute Wernicke–Korsakoff syndrome.
• Benzodiazepines are the mainstay of withdrawal treatment, in tapering dose or
as-needed dose per CIWA scale (Sullivan et al., 1989); they are the treatment of choice
for withdrawal seizures/DT. Lorazepam or oxazepam (no metabolites/renal clear-
ance) are favoured in patients with liver dysfunction or the elderly.
• Give antipsychotics as needed for alcoholic hallucinosis.
• An ␣2-adrenergic blocker (clonidine) is useful to lessen noradrengergic symptoms.
• Anticonvulsants carbamazepine and divalproex have shown efficacy for detoxifica-
tion but are not in widespread use.
PSYCHOSOCIAL REHABILITATION
Principles of treatment
• ‘No cure’ – achieving abstinence ⫽ remission.
• All efforts are aimed at motivating the patient towards abstinence.
• Education is essential about addiction, compulsive behaviours, medical complications.
• Emotional insight is stressed.
• Involvement of family/significant relationships is critical to treatment.
• Induction into AA’s Twelve-Step Facilitation (TSF) Therapy is especially helpful
for alcoholics who drink heavily in social situations.
• Group/individual therapy aims at self-understanding and realization of the effect
of addiction on the patients’ life.
• Continued participation in support/follow-up programme, AA, etc., should be
encouraged.
Modalities
• Individual therapy:
– Cognitive–behavioral therapy (CBT) (see Chapter 23) is shown to have durable
effects.
– Motivational enhancement therapy (MET) motivates individuals to utilize their
own resources to effect change in their behaviour. It is most effective in alco-
holics with high levels of anger.
– Coping skills training.
• Group therapy.
• Couples therapy.
• Family therapy.
Patient attributes rather than treatment factors are a better predictor of outcome.
There is a poor prognosis with:
• Established brain damage.
• Co-morbid psychiatric illness, especially antisocial personality disorder.
• Criminal history.
• Low IQ.
• Poor support.
• Low motivation.
Follow-up
• Sixty per cent with ‘good’ outcome at 20.8 months; 40 per cent in remission and
19 per cent with no more than three relapses and continuous sobriety 6 months
prior to survey (Castle Craig Hospital Extended Care Unit Follow-up Study, 1999).
• Self-reports for follow-up study are about 90 per cent reliable (Secades-Villa and
Fernandez-Hermida, 2003).
REFERENCES AND FURTHER READING 121
Anderson P, Cremona A, Paton A et al. (1993) The risk of alcohol. Addiction 8, 1493.
Babor TF, Hofmann M, DelBoca JK et al. (1992) Types of alcoholics. I: Evidence for an empiric-
ally derived typology based on indicators of vulnerability and severity. Arch. Gen. Psychiatry
49, 599.
Bolnick JM, Rayburn WF (2003) Substance use disorders in women: special considerations dur-
ing pregnancy. Obstet. Gynecol. Clin. North Am. 30, 545.
Brook DW, Brook JS, Zhang C et al. (2002) Drug use and the risk of major depressive disorder,
alcohol dependence, and substance use disorders. Arch. Gen. Psychiatry 59, 1039.
Brun A, Andersson J (2001) Frontal dysfunction and frontal cortical synapse loss in alcoholism:
the main cause of alcohol dementia? Dement. Geriatr. Cogn. Disord. 12, 289.
Castle Craig Hospital (1999) Castle Craig Hospital Extended Care Unit Follow-up Study 1999.
www.castlecraig.co.uk/treatment/ecu_followup_1999p.htm (accessed 1 January 2004).
Chasnoff IJ (1991) Drugs, alcohol, pregnancy, and the neonate: pay now or later. JAMA
266, 1567.
Chick J (1993) Benno Pollack Lecture, (1992) Alcohol dependence: an illness with a treatment?
Addiction 8, 1481.
Ciraulo DA, Piechniczek-Buczek J, En I (2003) Outcome predictors in substance use disorders.
Psychiatr. Clin. North Am. 26, 381.
Cloninger CR (1987) Neurogenic adaptive mechanisms in alcoholism. Science 23, 410.
Collins GB (1993) Contemporary issues in the treatment of alcohol dependence. Psychiatr. Clin.
North Am. 16, 33.
Condren RM, O’Connor J, Browne R (2001) Prevalence and patterns of substance misuse in
schizophrenia: a catchment area case–control study. Psychiatr. Bull. 25, 17.
Curran GM (2003) Emergency department use of persons with comorbid psychiatric and sub-
stance abuse disorders. Ann. Emerg. Med. 41, 659.
Edwards G, Gross MM (1976) Alcohol dependence: provisional description of a clinical syn-
drome. BMJ 1, 1058.
Enoch MA, Goldman D (2002) Problem drinking and alcoholism: diagnosis and treatment. Am.
Fam. Physician 65, 441.
Faculty of Public Health Medicine (1991) Alcohol and the Public Health. Macmillan, London.
Fleming MF, Mundt MP, French MT et al. (2002) Brief physician advice for problem drinkers:
long-term efficacy and benefit–cost analysis. Alcohol Clin. Exp. Res. 26, 36.
Gelernter J, Goldman D, Risch N (1993) The Al allele at the D2 dopamine receptor gene and alco-
holism. JAMA 269, 1673.
Greenfield S, Manwani SG, Nargiso JE (2003) Epidemiology of substance use disorders in
women. Obstet. Gynecol. Clin. North Am. 30, 413.
Hearne R, Connolly A, Sheehan J (2002) Alcohol abuse: prevalence and detection in a general
hospital. J. Royal Soc. Med. 95, 84.
Heath DB (2001) Culture and substance abuse. Psychiatr. Clin. North Am. 24, 479.
Heilig M, Thorsell A (2002) Brain neuropeptide Y (NPY) in stress and alcohol dependence. Rev.
Neurosci. 13, 85.
Helzer JE, Pryzbeck TR (1991) The co-occurrence of alcoholism with other psychiatric disorders
in the general population and its impact on treatment. J. Stud. Alcohol 49, 219.
Hopfer CJ, Crowley TJ, Hewitt JK (2003) Review of twin and adoption studies of adolescent sub-
stance use. J. Am. Acad. Child Adolesc. Psychiatry 42, 710.
Iacono WG, Carlson SR, Malone SM, McGue M (2002) P3 event-related potential amplitude and
the risk for disinhibiroty disorders in adolescent boys. Arch. Gen. Psychiatry 59, 750.
Ilveskoski E, Kajander OA, Lehtimäki T et al. (2001) Association of neuropeptide Y polymorph-
ism with the occurrence of type 1 and type 2 alcoholism. Alcohol Clin. Exp. Res. 10, 1420.
122 ALCOHOL DEPENDENCE
Jackson KM, Sher KJ, Wood PK, Bucholz KK (2003) Alcohol and tobacco use disorders in a gen-
eral population: short-term and long-term associations from the St Louis Epidemiological
Catchment Area Study. Drug Alcohol Depend. 71, 239.
Johnson BA, Roache JD, Ait-Daoud N et al. (2002) Ondansetron reduces the creving of biologic-
ally predisposed alcoholics. Psychopharmacology 160, 408.
Kendler KS, Heath AC, Neale MC et al. (1992) A population-based twin study of alcoholism in
women. JAMA 268, 1877.
Kiefer F, Jahn H, Tarnaske T (2003) Comparing and combing naltrexone and acamprosate in
relapse prevention of alcoholism: a double-blind, placebo-controlled study. Arch. Gen.
Psychiatry 60, 92.
Koren G, Nulman I, Chudley AE, Loocke C (2003) Fetal alcohol spectrum disorder. CMAJ 169, 1181.
Lingford-Hughes A, Nutt D (2002) Neurobiology of addiction and implications for treatment.
Br. J. Psychiatry 182, 97.
Litt MD, Babor TF, DelBoca FK et al. (1992) Types of alcoholics. II: Application of an empirically
derived typology to treatment matching. Arch. Gen. Psychiatry 49, 609.
Madden JS (1993) Depression: alcohol and depression. Br. J. Hosp. Med. 50(5), 265.
Markianos M, Lykouras L, Moussas G et al. (2001) Changes in dopamine receptor responsivity
during alcohol detoxification may predict relapse. Drug Alcohol Depend. 64, 363.
Martin SE (2001) The links between alcohol, crime and the criminal justice system: explanations,
evidence and interventions. Am. J. Addict. 10, 136.
Mayfield RD, Lewohl JM, Dodd PR et al. (2002) Patterns of gene expression are altered in the
frontal and motor cortices of human alcoholics. J. Neurochem. 81, 802.
McGovern MP, Carroll KM (2003) Evidence-based practices for substance use disorders.
Psychiatr. Clin. North Am. 26, 991.
Meszaros K, Lenzinger E, Hornik K et al. (1999) The tridimensional personality questionnaire as
a predictor of relapse in detoxified alcohol dependents. The European Fluvoxamine in
Alcoholism Study Group. Alcohol. Clin. Exp. Res. 23, 483.
Monterosso JR, Flannery BA, Pettinati HM et al. (2001) Predicting treatment response in nal-
trexone: the influence of craving and family history. Am. J. Addict. 10, 258.
National Institute on Alcohol Abuse and Alcoholism (2000) NIH publication no. 00-1583.
National Survey on Drug Use and Health, Substance Abuse and Mental Health Services Adminis-
tration (SAMHSA) (2002). www.samhsa.gov/oas/nhsda/2k2nsduh/Results/2k2Results.htm.
Overman GP, Teter CJ, Guthrie SK (2003) Acamprosate for the adjunctive treatment of alcohol
dependence. Ann. Pharmacother. 37, 1090.
Pandey SC, Carr LG, Heilig M et al. (2003) Neuropeptide y and alcoholism: genetic, molecular,
and pharmacological evidence. Alcohol. Clin. Exp. Res. 27, 149.
Pettinati HM, Volpicelli JR, Pierce JD et al. (2000) Improving naltrexone response: an interven-
tion for medical practicioners to enhance medication compliance in alcohol dependent
patients. J. Addict. Dis. 19, 71.
Pickens RW, Svikis DS, McGue M et al. (1991) Heterogeneity in the inheritance of alcoholism: a
study of male and female twins. Arch. Gen. Psychiatry 48, 19.
Rice DP, Kelman S, Miller LS (1991) Estimates of economic costs of alcohol and drug abuse and
mental illness, 1985 and 1988. Public Health Rep. 106, 280.
Sattar SP, Petty F, Burke WJ (2003) Diagnosis and treatment of alcohol dependence in older alco-
holics. Clin. Geriatr. Med. 19, 743.
Secades-Villa R, Fernandez-Hermida JR (2003) The validity of self-reports in a follow-up study
with drug addicts. Addict. Behav. 28, 1175.
Shivani R, Goldsmith RJ, Anthenelli RM (2002) Alcoholism and psychiatric disorders: diagnostic
challenges. Alcohol Res. Health 26, 90.
Sullivan JT, Sykora K, Schneiderman J et al. (1989) Assessment of alchol withdrawal: the revised
clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br. J. Addict. 84, 1353.
Drug dependence and 10
gambling
SUBSTANCE DEPENDENCE
Substance misuse which results in clinically significant impairment or stress, as evi-
dent by ⭓3 of the following during a 12-month period:
Lifetime illicit drug use in the USA (SAMHSA Household Survey on Drug Abuse,
2002):
Of the US population 8.3 per cent actively used illicit drugs in 2002; 3.3 per
cent needed treatment in 2002 for a drug problem, of which 0.6 per cent actually
received help.
Co-morbidity
• 45 per cent of patients with alcohol abuse/dependence have at least one other psy-
chiatric disorder.
• 72 per cent of patients with drug abuse/dependence have at least one other psychi-
atric disorder.
• Co-occurrence of substance and psychiatric disorders portends negatively for suc-
cessful treatment of either.
• Over half of schizophrenic patients in the USA have substance use disorder.
Possible associations:
1 Vulnerability hypothesis – SA may precipitate schizophrenia in predisposed indi-
viduals. It is unlikely as a primary cause.
2 Self-medication hypothesis:
– SA counteracts negative symptoms, depressed mood.
– SA counteracts side-effects of treatment.
Pattern of abuse
• Episodic abuse generally seen with less addictive drugs, continuous course with
highly addictive drugs.
• Cannabis is the first drug of abuse in 70 per cent of opiate addicts.
• Polysubstance abuse is common: 90 per cent of opiate abusers also abuse benzodi-
azepines (especially diazepam or temazepam, oral and IV).
• Other drug use is more ‘contained’:
– Volatile SA is often experimental; only 20 per cent become chronic abusers and
polysubstance abusers.
– Ecstasy (NMDA) is used mainly for recreational purposes – dance parties or
‘raves’.
• Only one-third of opiate users are in contact with treatment agencies at any time.
• Average duration of use before seeking treatment is 9 years.
• Average duration of intravenous use before seeking treatment is 4 years.
GENETICS
Twin studies in adolescents suggest a modest influence of genetics in conveying liabil-
ity for non-alcohol substance use disorders (Hopfer et al., 2003).
Drugs Pharmacology Route of administration Psychic effects Physical effects Withdrawal effects Dependence Treatment
Opioids: Bind to opioid receptors; Oral, IV, IM, Euphoria, relaxation, Miosis, bradycardia, Craving, agitation, Yes Overdose:
heroin naltrexone, naloxone – subcutaneously drowsiness, personality itching, nausea, restlessness, cardiorespiratory
morphine competitive antagonists change, hypoactivity, constipation tachycardia, dilated support, naloxone
meperidine Tolerance develops with ↓ appetite, ↓ libido pupils, perspiration, Detoxification:
methadone usage; also cross-tolerance yawning, diarrhoea, methadone
pentazocine within opioid group abdominal cramps, buprenorphine,
Withdrawal commences ‘goose flesh’ clonidine
4–6 hours after last dose,
peaks 28–48 hours, lasts
7–10 days
Cocaine Blocks re-uptake of Chewing, sniffing, Euphoria, excitement, Mydriasis, tremor, ‘Crash’: craving, Yes ↓ Craving:
serotonin and smoking, IV confusion, paranoid tachycardia, depression, amantadine,
catecholamines, especially psychosis, formication perforated insomnia, propranolol for
dopamine – inhibits (‘cocaine bugs’) nasal septum, psychomotor severe craving
transporter uptake site; fever, seizures, agitation
various dopamine agonists/ cardiorespiratory
autoreceptors studied for arrest, CVA
↓ craving
Crack-cocaine – Smoking Extreme agitation, – – Yes –
psychosis
Amphetamines Sympathomimetics, Oral, IV Euphoria, excitement, Mydriasis, tachycardia, Dysphoria, anergia Yes Overdose:
detected by urinalysis hyperalertness, hyperreflexia sedation,
toxicology if ⭐48 hours irritability/aggression, Overdose: cardiac antiarrhythmic,
after last dose paranoia, psychosis, arrhythmia, acidify urine
hallucinosis hyperpyrexia Detoxification:
self-resolution;
neuroleptic only
if psychosis
prolonged
Hallucinogens Sympathomimetic; 5-HT Oral Depersonalization, Red eyes, mydriasis, None No Abstinence,
lysergic acid agonist; onset of effects in derealization, ataxia, tachycardia rehabilitation
diethylamide 1 hour, last 8–12 hours; hyperperceptualization,
(LSD) flashback may occur false sense of ability,
mescaline spontaneously even 1 year anxiety, ideas of
psilocybin after stopping LSD reference, impaired
(‘magic judgement, flashbacks,
mushrooms’) psychotic or
mood disturbance
Phenylcyclidine Receptor sites located Oral, IV, sniffing, smoking Hallucinations, paranoid Nystagmus, ↑ blood Craving, depression, Yes Desipramine for
(PCP) in calcium ion schizophreniform pressure anergia craving; haloperidol
channel of NMDA psychosis, depressed for agitation/
subtype of glutamate consciousness psychosis, avoid
aggression chlorpromazine
Overdose: with
hypertension ataxia,
adrenergic crisis
Cannabis Active compound is Smoking Euphoria, relaxation, Conjunctival – Yes Abstinence
marijuana tetrahydocannabinol; heightened perceptual infection, dry
‘hashish’ G-protein receptor for awareness, Cannabis mouth, tachycardia,
cannabinoids recently psychosis – disputed respiratory tract
discovered; onset of effect entity irritation
is minutes to 1 hour; effect
lasts 6–12 hours
Barbiturates CNS depressants Oral, IM, IV Anxiolytic/respiratory Cellular signs, Restlessness, insomnia, Yes Withdrawal with
CNS, depression with respiratory anorexia, nausea, benzodiazepine
higher doses depression in seizures, delirium and anti-convul-
overdose sant cover
Benzo- CNS depressants; bind Oral, IV Anxiolytic; impaired Ataxia, nausea, Agitation, insomnia, Yes Gradual
diazepines to benzodiazepines-GABA concentration, respiratory tremor, withdrawal
receptor complex; also judgement; memory depression restlessness
see Chapter 21 disturbance
(Continued)
Table 10.1 Continued
Drugs Pharmacology Route of administration Psychic effects Physical effects Withdrawal effects Dependence Treatment
PHARMACOLOGICAL TREATMENTS
• Methadone – long-acting synthetic opiate used in opiate addiction for mainten-
ance or detox.
– Maintenance therapy at doses of 20–70 mg, with regular urine monitoring for
abuse of other drugs.
– Moderate/high dosage of methadone required to maintain abstinence.
– There is a variable drop-out from maintenance programmes. Persistence is asso-
ciated with better outcome, less physical morbidity, slower progression of HIV
infection.
• Levomethadyl acetate (LAAM) – long-acting synthetic opiate agonist used in opi-
ate addiction.
– Potential for life-threatening arrhythmias due to QT prolongation limits its use
to opiate addicts who fail other treatments.
• Naltrexone – opiate antagonist used in detoxification and maintenance.
– Generally less acceptable to abuser than methadone. Compliance limits its use-
fulness.
• Buprenorphine – mixed opioid agonist–antagonist.
– As effective as methadone in opiate detoxification and maintenance.
– Also available combined with naloxone.
– Does not require special licensing to prescribe in the USA as with methadone/
LAAM.
• Clonidine – used in opiate withdrawal for autonomic suppression but does not
help withdrawal symptoms of insomnia or muscular aches.
• Benzodiazepines – used as an adjunct to opioid withdrawal for anxiety/
insomnia.
• Other agents not yet in routine clinical use/under investigation. Numerous agents
are currently being investigated for treating cocaine and marijuana use disorders
but their use is not supported by convincing evidence.
PSYCHOSOCIAL TREATMENTS
Aim to tackle underlying psychological/social/environmental factors perpetuating
SA. Increase awareness, and develop alternative coping mechanisms. Foster cognitive–
behavioural strategies to manage craving and eliminate reinforcing behaviours.
Biopsychosocial treatments combined with pharmacological therapy improve
treatment outcomes (Albanese and Shaffer, 2003).
130 DRUG DEPENDENCE AND GAMBLING
There is a high initial relapse after treatment. Follow-up shows high psychiatric mor-
bidity, continued use, high mortality (suicide, accidents, physical complications of
SA, AIDS).
Therapeutic communities are associated with better outcomes than methadone
treatment alone in opiate dependence.
PATHOLOGICAL GAMBLING
PHASES OF ADDICTION
There are four phases: winning, losing, desperation, giving up. Stress-related physical
illness, depression, deliberate self-harm and criminal behaviour are common sequelae
of the final two phases.
Two-thirds of Gamblers Anonymous members have committed some illegal activ-
ity to support their gambling.
Albanese MJ, Shaffer HJ (2003) Treatment considerations in patients with addictions. Prim.
Psychiatry 10, 55.
Cairney S, Maruff P, Burns C, Currie B (2002) The neurobehavioural consequences of petrol
(gasoline) sniffing. Neurosci. Biobehav. Rev. 26, 81.
Carroll KM, Ball SA, Nich C et al. (2001) Targeting behavioral therapies to enhance naltrexone
treatment of opioid dependence. Arch. Gen. Psychiatry 58, 755.
Carruthers S (2003) The ins and outs of injecting. J. Subst. Use 8, 11.
Centers for Disease Control and Prevention. HIV/AIDS surveillance report 2000. 12, 14.
Chander G, McCaul ME (2003) Co-occurring psychiatric disorders in women with addictions.
Obstet. Gynecol. Clin. North Am. 30, 469.
Ciraulo DA, Piechniczek J, Iscan EN (2003) Outcome predictors in substance use disorder.
Psychiatr. Clin. North Am. 2, 381.
Cohn JA (2002) HIV-1 infection in injection drug users. Infect. Dis. Clin. North Am. 16, 745.
D’Aunno T, Pollack HA (2002) Changes in methadone treatment practices: results from a
national panel study, 1988–2000. JAMA 288, 850.
Dettmer K, Saunders B, Strang J (2001) Take home naloxone and the prevention of deaths from
opiate overdose: two pilot schemes. BMJ 322, 895.
Dyer JE, Roth B, Hyma BA (2001) Gamma-hydroxybutyrate withdrawal syndrome. Ann. Emerg.
Med. 37, 147.
Ernst M, Grant SJ et al. (2002) Decision making in adolescents with behavior disorders and
adults with substance abuse. Am. J. Psychiatry 160, 10.
Farre M, Mas A, Torres M et al. (2002) Retention rate and illicit opioid use during methadone
maintenance interventions: a meta-analysis. Drug Alcohol Depend. 65, 283.
Ferentzy P, Skinner W (2003) Gamblers Anonymous: a critical review of the literature. The
Electronic Journal of Gambling Issues: eGambling [on-line serial], 9. Available: www.camh.net/
egambling/issue9/research/index.html.
132 DRUG DEPENDENCE AND GAMBLING
National Research Council Committee on Data and Research on Illicit Drugs (2002) For debate:
executive summary of the National Research Council’s report: informing America’s policy on
illegal drugs: what we don’t know keeps hurting us. Addiction 97, 647.
Pennings EJM, Leccese AP, de Wolff FA (2002) Effects of concurrent use of alcohol and cocaine.
Addiction 97, 773.
Pollack HA (2001) Cost-effectiveness of harm reduction in preventing hepatitis C among injec-
tion drug users. Med. Decis. Making 21, 357.
Ricaurte GA, Yan J, Hatzidimitriou G et al. (2002) Severe dopaminergic neurotoxicity in primates
after a common recreational dose regimen of MDMA (‘ecstasy’). Science 297, 2260.
Rounsaville BJ, Petry NM, Carroll KM (2003) Single versus multiple drug focus in substance
abuse clinical trails research. Drug Alcohol Depend. 70, 17.
Silberg J, Rutter M, D’Onofrio B, Eaves L (2003) Genetic and environment risk factors in adoles-
cent substance use. J. Child Psychol. Psychiatry 44, 664.
Sinha R, Easton C, Renee-Aubin L, Carroll KM (2003) Engaging young probation-referred
marijuana-abusing individuals in treatment: a pilot trial. Am. J. Addict. 12, 314.
Substance Abuse and Mental Health Services Administration (2002) Results from the 2001
National Household Survey on Drug Abuse. Vol. I: Summary of National Findings. Office of
Applied Studies, Rockville, MD.
Toneatto T, Skinner W (2000) Relationship between gender and substance use among treatment-
seeking gamblers. The Electronic Journal of Gambling Issues: eGambling [on-line serial],
1. Available: www.camh.net/egambling/issue1/research/index.html.
Van Ree JM, Gerritis MAFM, Vanderschuren LJMJ (1999) Opioids, reward and addicts: an
encounter of biology, psychology, and medicine. Pharmacol. Rev. 51, 341.
Volkow ND, Chang L, Wang G-J et al. (2001) Higher cortical and lower subcortical metabolism
in detoxified methamphetamine abusers. Am. J. Psychiatry 158, 383.
Suicide and non-fatal 11
deliberate self-harm
SUICIDE
DEFINITIONS
• Kessel – suicide and ‘deliberate self-poisoning/injury’. ‘Deliberate self-injury’ substi-
tuted for ‘attempted suicide’ because many patients ‘performed their acts in the
belief that they were comparatively safe’.
• Kreitman – suicide and parasuicide: ‘Parasuicide’ refers to ‘a behavioural analogue
of suicide but without considering a psychological orientation towards death being
in any way essential to the condition’.
• Morgan – non-fatal deliberate self-harm (DSH): ‘A deliberate non-fatal act,
whether physical, drug overdose or poisoning, done in the knowledge that it was
potentially harmful, and in the case of drug overdosage, that the amount taken was
excessive.’
• Beck – suicide: ‘A wilful self-inflicted life-threatening act which has resulted in death.’
• Durkheim: proposed three forms of suicide:
– Egoistic.
– Anomic.
– Altruistic.
EPIDEMIOLOGY OF SUICIDE
• Figures from the Centers for Disease Control and Prevention (2001):
– Suicide is the eleventh leading cause of death in the USA and the third major
cause of death in the 15–34 year age-group.
– Males complete suicide at a rate four times that of females.
– Whites commit suicide at twice the rate of blacks.
• In the UK, suicide is the second leading cause of death in the 15–34 year age-group.
• Methods of suicide: firearms 55.1 per cent, suffocation 20.2 per cent, poisoning
17.0 per cent, fall 2.1 per cent, cut/pierce 1.5 per cent, drowning 1.1 per cent.
PSYCHIATRIC ILLNESS AND SUICIDE 135
• Worldwide, almost one million suicides and over ten million suicide attempts
occur annually. See Table 11.1.
• Highest rates are in the spring, lowest in December.
VICTIM CHARACTERISTICS
• A psychiatric diagnosis is evident in over 90 per cent of victims; 60 per cent suffer
from a mood disorder. Alcohol and other substance use, schizophrenia, bipolar
disorder and personality disorder are commonly seen in suicide victims. Males
exceed females for all age-groups.
• Rates are highest in the divorced or widowed. Married have lowest rates.
• Urban dwellers exceed rural.
• Socioeconomic class – higher in lowest and highest groups, lower in middle
groups.
• Religion – strong religious affiliation is a protective factor.
• Occupation – higher-risk groups are doctors, lawyers, police officers, hotel and bar
trade owners.
• Unemployment – there is a strong statistical association, especially for males.
DEPRESSION
Fifteen per cent of patients hospitalized for mood disorder will kill themselves.
Greater risk of suicide is seen with psychotic depression. Risk factors include:
ALCOHOLISM
Fifteen per cent of alcoholics kill themselves. Risk factors are (Preuss et al., 2003):
• Separated or divorced.
• Drug dependence.
• Substance-induced psychiatric disorder.
• More severe course of alcoholism.
PERSONALITY DISORDER
Co-morbidity with other psychiatric disorders; risk highest in antisocial and border-
line personalities.
PHYSICAL ILLNESS
CNS disorders carry a high risk; AIDS, multiple sclerosis, epilepsy (especially TLE),
head injury, peptic ulcer disease, cancer.
The risk of suicide is reported to be higher in people with low cholesterol, particu-
larly for males. The relationship is poorly understood.
PSYCHIATRIC ILLNESS AND SUICIDE 137
SPECIAL POPULATIONS
Adolescents
• Rare before age 14 years; rate increasing in adolescents.
• Risk factors include psychiatric illnesses, substance use (especially alcohol), male
gender, disrupted family relations, availability of lethal means, involvement in legal
system, lack of religious involvement.
Elderly
• The rate is increasing in the elderly.
• Up to 74 per cent of elderly suicide victims visited a primary care provider within
1 month of death.
• Comprising only 13 per cent of the US population, those 65 years and older
accounted for 18 per cent of deaths by suicide in 2000.
• In 2000, death by suicide for white males over 84 years was 59 per 100 000, greater
than five times the national rate.
• 80–90 per cent of elderly suicides have depressive illness.
– Often the first episode of depression.
– Deliberate self-harm in elderly more closely associated with completed suicide.
– Denial of suicide more common.
– Physical illness is more associated, especially if debilitating physical illness.
Prison inmates
• Rates are three to four times higher than in the general population.
• Remand prisoners are at particular risk; also prisoners convicted of murder/
violent/sexual crimes.
• One-half of suicides occur in the first 3 months of imprisonment; one-half have
have seen the doctor in the week prior to suicide.
• 90 per cent occur by hanging.
• One-third have a previous psychiatric history, almost one-half a history of DSH.
NEUROCHEMISTRY
Research shows a general lack of serotonergic activity in the prefrontal cortex of sui-
cide victims, which would confer less behavioral inhibition and make them more
likely to act on suicidal thoughts.
• Lower CSF 5-HIAA levels are associated with more lethal suicide attempts.
• Decreased CSF 5-HIAA is the most consistent finding in patients with DSH.
138 SUICIDE AND NON-FATAL DELIBERATE SELF-HARM
GENETICS
• Twin studies – MZ:DZ ⫽ 11.3%:1.8% (Roy et al., 1991).
• Suicidal behaviour clusters in families. Familial clustering probably represents an
inherited genetic variation in the serotonin-related genes, which are the object of
ongoing research.
RISK FACTORS
• Childhood trauma.
• Teenage to early adulthood.
• Female.
• Eating disorder.
• Marital status: divorced ⬎ single ⬎ widowed; least for married.
• Urban/rural: urban ⬎ rural; high rates in ‘inner city’ areas associated with over-
crowding, lack of facilities, less social cohesion.
• Social class: inverse relationship; strong association with unemployment both for
males (relative risk 12.1) and for females (13.6).
NON-FATAL DELIBERATE SELF-HARM 139
• Psychiatric illness:
– Most attempters have symptoms of psychological distress, but definite psychi-
atric illness found in under one-third.
– Most common diagnoses are ‘reactive’ depression, alcoholism, panic disorder (high
rates from ECA study now disputed), personality disorder (borderline, sociopathic).
• Most commit DSH as an impulsive act.
• 65 per cent followed some major life event.
• 50 per cent followed a serious argument with partner/friend.
Predictors of repetition
• Number of previous episodes of DSH.
• Features of personality disorder.
• History of violence.
• Alcoholism.
• Unmarried, lowest social class.
• Females equivalent to males.
MANAGEMENT OF DSH
Treatments
• Psychotherapy; dialectical behavior therapy, family therapy.
• Social support.
• Treat mood disorder, thought disorder, substance use disorder.
• Pharmacology – lithium reduces suicide risk; well–managed depression will
reduce risk.
• ECT may reduce suicidality in a manic or several depressed state.
For those with repeated DSH, the above interventions have been of limited effectiveness.
REPEATED SELF-MUTILATION
EPIDEMIOLOGY
• Types:
– Repeated minor lacerations (usually of the wrist) – the largest group.
– Psychotic patients.
– Seriously suicidal.
• Incidence:
– 3–4 per cent in the general psychiatric population within 1 month.
– 15 per cent of the subnormal population within 1 month.
• Age and sex – younger; women more than men in hospital populations.
SYMPTOMS
• Mounting tension, sense of emptiness/loss.
• Depressive feeling described less commonly.
• Emotional relief on self-injury.
CORRELATES
• The ‘typical’ wrist-cutter is described as young, female, aged 16–24.
– May have nursing or other medical connections.
– Low self-esteem, expressing dislike of own body.
– May have associated anorexia/bulimia nervosa.
– Around 50 per cent have used alcohol or drugs to excess.
– Some research has shown increased incidence of menstrual irregularity.
– Poor verbalizer.
• Childhood – increased incidence of broken homes and hospitalization before
age 5.
• Precipitants – recent loss, rejection or impasse in relationships.
MANAGEMENT
Management is difficult. A carefully coordinated team response is needed to mutilat-
ing behaviour (minimize ‘gain’). Therapy explores areas of self-image/esteem. Tension
reduction might be achieved by relaxation techniques.
REFERENCES AND FURTHER READING 141
Agerbo E, Nordentoft M, Mortensen PB (2002) Familial, psychiatric, and socioeconomic risk fac-
tors for suicide in young people: nested case–control study. BMJ 325, 74.
Appleby L, Shaw J, Sherratt J et al. (2001) Safety First: Five-Year Report of the National
Confidential Inquiry into Suicide and Homicide by People with Mental Illness. Department of
Health, London.
Austin MC, Witehead RE, Edgar CL et al. (2002) Localized decrease in serotonin transporter-
immunoreactive axons in the prefrontal cortex of depressed subjects committing suicide.
Neuroscience 114, 807.
Bennewith O, Stocks N, Gunnell D et al. (2002) General-practice based intervention to prevent
repeat episodes of deliberate self harm: cluster randomized controlled trial. BMJ 324, 1254.
Bostwick JM. Pankratz VS (2000) Affective disorders and suicide risk: a reexamination. Am. J.
Psychiatry 157, 1925.
Brent DA, Oquendo M, Birmaher B et al. (2002) Familial pathways to early-onset suicide
attempt: risk for suicide behavior in offspring of mood-disordered suicide attempters. Arch.
Gen Psychiatry 59, 801.
Cavanagh JT, Carson AJ, Sharpe M, Lawrie SM (2003) Psychological autopsy of suicide: a sys-
tematic review. Psychol. Med. 33, 395.
Centers for Disease Control and Prevention (2000) National Vital Statistics. CDCP, Washington, DC.
Centers for Disease Control and Prevention (2001) National Vital Statistics. CDCP, Washington, DC.
Conner KR, Cox C, Buberstein PR et al. (2001) Violence, alcohol, and completed suicide: a
case–control study. Am. J. Psychiatry 158, 1701.
Conwell Y (2001) Suicide in later life: a review and recommendations for prevention. Suicide Life
Threaten Behav 31 (Suppl.) 32.
Coryell W, Schlesser M (2001) The dexamethasone suppression test and suicide prediction.
Am. J. Psychiatry 158, 748.
Daigle M (2003) Death in our prisons. CMAJ 168, 830.
De Leo D (2002) Why are we not getting any closer to preventing suicide? Br. J. Psychiatry 181, 372.
Dieserud G, Roysamb E, Ekeberg O, Kraft P (2001) Toward an integrative model of suicide
attempt: a cognitive psychological approach. Suicide Life Threaten Behav 31, 153.
Dooley E (1990) Prison suicide in England and Wales 1972–1987. Br. J. Psychiatry 156, 40.
Esposito CL, Clum GA (2002) Psychiatric symptoms and their relationship to suicidal ideation in
a high-risk adolescent community sample. J. Am. Acad. Child Adolesc. Psychiatry 41, 44.
Fawcett J (1993) Predicting and preventing suicide. Psych. Ann. 23(5).
Gairin I, House A, Owens D (2003) Attendance at the accident and emergency department in the
year before suicide: retrospective study Br. J. Psychiatry 183, 28.
Green AI, Canuso CM, Brenner MJ, Wojcik JD (2003) Detection and management of comorbid-
ity in patients with schizophrenia. Psychiatr. Clin. North Am. 26, 115.
Grupp-Phelan J (2003) The suicidal pediatric patient: an emergency medicine focus. CPEM 4, 141.
Haw C, Hawton K, Houston K, Townsend E (2001) Psychiatric and personality disorders in
deliberate self harm patients. Br. J. Psychiatry 178, 48.
Hawton K, Houston K, Haw E et al. (2003a) Comorbidity of axis I and axis II disorders in
patients who attempted suicide. Am. J. Psychiatry 160, 1494.
Hawton K, Zahl D, Weatherall R (2003b) Suicide following deliberate self-harm: long-term
follow-up of patients who presented to a general hospital. Br. J. Psychiatry 182, 537.
Horrocks J, Price S, House A, Owens D (2003) Self-injury attendances in the accident and emer-
gency department: clinical database study. Br. J. Psychiatry 183, 34.
Hsiung SC, Adlersberg M, Arango V, Mann JJ et al. (2003) Attenuated 5-HT1A receptor signaling
in brains of suicide victims: involvement of adenylyl cyclase, phosphatidylinositol 3-kinase,
Akt and mitogen-activated protein kinase. J. Neurochemistry 87, 182.
142 SUICIDE AND NON-FATAL DELIBERATE SELF-HARM
Inskip HM, Harris EC, Barraclough B (1999) Lifetime risk of suicide for affective disorder, alco-
holism and schizophrenia. Br. J. Psychiatry 172, 35.
Jenkins GR, Hale R, Papanastassiou M et al. (2002) Suicide rate 22 years after parasuicide: cohort
study. BMJ 325, 1155.
Kelly BD, McLoughlin DM (2002) Euthanasia, assisted suicide and psychiatry: a Pandora’s box.
Br. J. Psychiatry 181, 278.
Kessler RC, Borges G, Walters EE (1999) Prevalence of and risk factors for lifetime suicide
attempts in the national comorbidity study. Arch. Gen. Psychiatry 56, 617.
Klonsky ED, Oltmanns TF, Turkheimer E (2003) Deliberate self-harm in a nonclinical popula-
tion: prevalence and psychological correlates. Am. J. Psychiatry 160, 1501.
Koller GP, Preuss UW, Bottlender M et al. (2003) Impulsivity and aggression as predictors of sui-
cide attempts in alcoholics. Eur. Arch. Psychiaty Clin. Neruoscience 252, 155.
Luoma JB, Martin CE, Pearson JL (2002) Contact with mental health and primary care providers
before suicide: a review of the evidence. Am. J. Psychiatry 159, 909.
Mann JJ (2002) A current perspective of suicide and attempted suicide. Ann. Intern. Med. 136, 302.
Mann JJ (2003) Neurobiology of suicidal behavior. Nat. Rev. Neurosci. 4, 819.
Mann JJ, Malone KM, Psych MR et al. (1996) Attempted suicide characteristics and cerebrospinal
fluid amine metabolites in depressed inpatients. Neuropsychopharmacology 15, 576.
Mann JJ, McBride PA, Brown MP et al. (2000) A serotonin transporter gene promoter poly-
morphism (5-HTTLPR) and prefrontal cortical binding in major depression and suicide.
Arch. Gen. Psychiatry 57, 729.
Marttunen MJ, Hillevi MA, Henriksson MM, Lonngvist JK (1991) Mental disorder in adolescent
suicide. Arch. Gen. Psychiatry 48, 834.
McGlure GMG (2001) Suicide in children and adolescents in England and Wales 1970–1998.
Br. J. Psychiatry 178, 469.
Munroe J, O’Sullivan D, Andrews C et al. (1999) Active monitoring of 12 760 clozapine recipients
in the UK and Ireland: beyond pharmacovigilance. Br. J. Psychiatry 175, 576.
National Institute of Mental Health (2003) Older Adults: Depression and Suicide Facts.
www.nimh.nih.gov/publicat/elderlydepsuicide.cfm (accessed 22 December 2003).
Oquendo MA, Kamali M, Ellis SP et al. (2002) Adequacy of antidepressant treatment after dis-
charge and the occurrence of suicidal acts in major depression: a prospective study. Am. J.
Psychiatry 159, 1746.
Owens D, Horrocks J, House A (2002) Fatal and non-fatal repetition of self-harm. a systematic
review. Br. J. Psychiatry 181, 193.
Preuss UW, Schucket MA, Smith TL et al. (2003) Predictors and correlates of suicide attempts
over 5 years in 1237 alcohol-dependent men and women. Am. J. Psychiatry 160, 56.
Purselle DC, Nemeroff CB (2003) Serotonin trasporter: a potential substrate in the biology of
suicide. Neuropsychopharmacology 28, 613.
Raymont V (2001) Suicide in schizophrenia: how can research influence training and clinical
practice? Psychiatr. Bull. 25, 46.
Reed J (2002) Delivering psychiatric care to prisoners: problems and solutions. Advan. Psychiatr.
Treat. 8, 117.
Reed J (2003) Mental health care in prisons. Br. J. Psychiatry 182, 287.
Roy A, Segal NI, Centerwall BS, Robinette CD (1991) Suicide in twins. Arch. Gen. Psychiatry
48, 29.
Rucci P, Frank E, Kostelnik B, Gagiolini A et al. (2002) Suicide attempts in patients with bipolar i
disorder during acute and maintenance phases of intensive treatment with pharmacotherapy
and adjunctive psychotherapy. Am. J. Psychiatry 159, 1160.
Souery D, Oswald P, Linkowski P, Mendlewicz J (2003) Molecular genetics in the analysis of
suicide. Ann. Med. 35, 191.
REFERENCES AND FURTHER READING 143
Spivak B, Shabash E, Sheitman B et al. (2003) The effects of clozapine versus haloperidole on
measures of impulsive aggression and suicidality in chronic schizophrenia patients: an open,
nonrandomized, 6-month study. J. Clin. Psychiatry 64, 755.
Tomassini C, Juel K, Holm NV et al. (2003) Risk of suicide in twins: 51 year follow up study.
BMJ 327, 373.
Turvey CL, Conwell Y, Jones MP et al. (2002) Risk factors for late-life suicide: a prospective,
community-based study. Am. J. Geriatr. Psychiatry 10, 398.
UK Government (1992) The Health of the Nation: A Strategy for Health in England. HMSO,
London.
Vythilingam M, Chen J, Bremner JD et al. (2003) Psychotic depression and mortality. Am. J.
Psychiatry 160, 574.
Walker BF (2003) Risk of suicide remains high fifteen years after deliberate self-harm. Evidence
Based Ment. Health 6, 106.
Wilkinson S, Taylor G, Templeton L et al. (2002) Admissions to hospital for deliberate self-harm
in England 1995–2000: an analysis of hospital episode statistics. J. Public Health Med. 24, 179.
World Health Organization (2001) The World Health Report 2001. Mental Health: New
Understanding, New Hope. www.who.int/whr2001/2001/main/en/chapter2/002g.htm (accessed
22 December 2003).
Wright JH, Beck AT (1994) Cognitive therapy. In: Hales RE, Yudofsky SC, Talbott JA (eds),
Textbook of Psychiatry, 2nd edn. American Psychiatric Press, Washington, DC.
Uncommon psychiatric 12
syndromes
DELUSIONAL MISIDENTIFICATION
CLINICAL FEATURES
This is the belief that a person known to the patient has been replaced by an exact double.
Usually the person implicated is a close relative, particularly spouse. This is not part of
organic confusion, but repeated misidentification of a specific person or people.
AETIOLOGY
It is usually part of a paranoid disorder, particularly schizophrenic, but may be affective
or as a primary delusional disorder. It could be the result of an ambivalent attitude to
the person implicated. It may occur in the presence of organic brain disease, particu-
larly frontal lobe dysfunction.
MANAGEMENT
Treat the underlying disorder; support the relative.
OTHER CONDITIONS
When unassociated with any other secondary psychiatric or organic disorder, the
primary condition is considered a subtype of delusional disorders (see Chapter 3).
DE CLÉRAMBAULT’S SYNDROME
CLINICAL FEATURES
This is the delusional belief that another person (the object), often of unattainably
higher social status, loves the patient (the subject) intensely. The subject is usually
female. There may be sudden onset of delusion. ‘Pure’ erotomania is an isolated phe-
nomenon. ‘Secondary’ erotomania is much more common and occurs in the setting of
paranoid, manic or other disorder. The subject may be importunate and disrupt the
object’s life and, after rejection, the love may turn to hatred.
AETIOLOGY
If the ‘pure’ form, it may be projection of denied, narcissistic self-love.
MANAGEMENT
Treat the underlying disorder if secondary. It can be very resistant to physical treat-
ments and psychotherapy if in the ‘pure’ form.
CLINICAL FEATURES
This is the delusion of infidelity on the part of the sexual partner. Normal phenomena
are interpreted to fit in with this conviction. The patient may examine underwear, sex-
ual organs, etc., in an attempt to find proof. There is a desire to extract a confession,
which may lead to severe aggression and murder.
AETIOLOGY
It may be associated with alcoholism (in a jealous, insecure personality), organic psycho-
sis, schizophrenia (particularly paranoia) or with paranoid, obsessional personality.
It might be a projection of the patient’s own desires for infidelity or of repressed
homosexuality, or the result of other feelings of inadequacy.
MANAGEMENT
Treat the underlying condition. Antipsychotic medications may help. Geographical
separation from the partner is often advisable.
146 UNCOMMON PSYCHIATRIC SYNDROMES
CLINICAL FEATURES
Hypochondriacal delusions may take various forms; e.g. skin infestation by insects
(Ekbom’s syndrome), internal parasitosis, delusion of lumps under the skin (leading
to excoriation), conviction of personal ugliness or emission of foul smell, delusional
body image disturbance, delusional pain.
Some are coenaesthopathic states with exaggeration or distortion of subjective experi-
ence and sensation.
The patient is convinced of the physical cause and gathers ‘evidence’ for this. Multiple
opinions are sought and bizarre treatments are suggested by the patient. Increasing
anger and paranoia may be expressed. The delusional system may remain ‘encapsulated’
for years, without general thought disorder or personality deterioration.
COUVADE SYNDROME
CLINICAL FEATURES
The husband (usually) develops extreme anxiety and various physical symptoms, as of
pregnancy, when his wife is pregnant. He may have morning sickness, abdominal
pains, constipation, food cravings, etc. It tends to present in the third or ninth month
of the wife’s pregnancy. The name ‘couvade’ refers to the ancient ritual of the husband
retiring to bed and simulating labour pains during the wife’s labour.
AETIOLOGY
This may be a manifestation of understandable anxiety in an anxious father-to-be.
It could be expression of frustrated creativity, jealousy of attention paid to wife or
over-identification with wife.
MANAGEMENT
Simple reassurance is usually adequate.
CLINICAL FEATURES
The patient gives approximate answers (absurdly wrong but almost correct, such as
‘a horse has five legs’), which are inconsistent. There may also be hysterical conver-
sion symptoms (e.g. ataxia), dissociative amnesia (altered level of consciousness) and
HYSTERIA – ALLIED SYNDROMES 147
AETIOLOGY
There is an hysterical twilight state. Occasionally, it is post-epileptic or associated with
depression. It may be similar to the ‘buffoonery state’ of acute or catatonic schizophrenia.
MANAGEMENT
The person usually recovers when the stressor is removed.
This rare condition is now termed dissociative identity disorder. The patient has two or
more distinct personalities. with dramatic changes from one personality to another.
There is amnesia for existence and events during the other personality.
There is a history of childhood sexual abuse in more than 70% of patients. Epilepsy
was noted in 25 per cent in one study. There is a wide range of psychopathology (Ross
et al., 1990).
DIFFERENTIAL DIAGNOSIS
Malingering; dissociative fugue; dissociative amnesia; schizophrenia.
MÜNCHAUSEN SYNDROME
This is classified under ‘other disorder of adult personality and behaviour’ in ICD-10.
In DSM-IV it is factitious disorder.
Symptoms are generated intentionally under voluntary will, motivated to assume
the sick role, with absence of external incentives (economic gain, avoiding criminal
prosecution, etc.). DSM-IV emphasizes whether there are predominantly psychological
or physical symptoms, or both.
CLINICAL FEATURES
The patient gives plausible, often dramatic, history and symptoms of acute physical
illness in the absence of that illness. He/she may inflict self-injury or simulate symptoms
148 UNCOMMON PSYCHIATRIC SYNDROMES
in a bizarre way (e.g. insert needles into chest, swallow blood, etc.). A common com-
plaint is of abdominal symptoms. There is a history of multiple hospital admissions
and multiple operations. Lying is pathological with a lack of personal rapport.
Variants of the syndrome present with psychiatric symptoms or false bereavements. It
may present with factitious illness in a child or dependent (Münchausen by proxy).
AETIOLOGY
There is hysterial behaviour in severely disordered personality. The person is
masochistic, attention-seeking, and may seek analgesic drugs.
MANAGEMENT
Sufferers frequently abscond from psychiatric treatment. Occasionally there is a degree
of treatable depression. There is a need to limit behaviour – keep a hospital registry of
such patients.
CLINICAL FEATURES
Usually one member of a couple is psychotic and the other comes to share the delu-
sional beliefs. It may occur in families or groups (folie à plusieurs). Persecutory or
hypochondriacal delusions may become shared by the submissive member of an over-
involved pair. There may not be evidence of this dominance and submission, however,
and it may be difficult to decide which members are primarily psychotic. It most
frequently occurs in a mother and daughter relationship.
AETIOLOGY
Often there is over-identification with the psychotic person in a submissive, over-
dependent personality. The person may have low IQ.
MANAGEMENT
Treat the psychotic member, if identifiable. Supportive and family therapy is often indi-
cated. Psychosis will need treatment if is co-morbid and independent; i.e. folie simultanée.
CLINICAL FEATURES
There are delusions of negation, to a varying degree. The patient may believe that
his/her body or self has disappeared and he/she no longer exists, even that the whole
universe no longer exists. This occurs more commonly in women. Often it is associated
REFERENCES AND FURTHER READING 149
with anxiety and irritability. It may be associated with mutism, delusions of self-
blame, hallucinations (e.g. of rotting smells), refusal to eat.
AETIOLOGY
It is frequently a depressive symptom, but may have a basis in organic brain disease
(acute or chronic). Depersonalization is frequently the underlying phenomenon.
Treat as per underlying condition.
DIFFERENTIAL DIAGNOSIS
DEMENTIA
Auditory functions
• Impaired auditory sensation – verbal (dominant), musical (non-dominant), auditory
agnosia.
• Sensory dysphasia (Wernicke’s area – dominant).
Visual functions
• Contralateral, upper quadrant, homonymous hemianopia (optic radiation).
• Prosopagnosia (inability to recognize faces).
Memory
• Bilateral lesions – global amnesia with normal immediate recall (includes
Korsakoff ’s psychosis).
• Unilateral lesions – dominant: impaired verbal memory; non-dominant: impaired
non-verbal (spatial) memory.
Personality/psychosis
• Related to temporal lobe epilepsy.
• Dominant – ? schizophreniform.
• ? Emotional lability, aggressive behaviour.
• Reduced sexual activity usually.
• Klüver–Bucy syndrome – extensive bitemporal lesions.
NEUROPSYCHIATRIC ASSESSMENT 153
• Korsakoff-type amnesia.
• Hypersomnia.
• Emotional lability.
• Hypothalamus:
– Polydipsia and polyuria.
– Appetite disturbance.
– Elevation of temperature.
Anterior cerebral
• Contralateral lower-limb paresis and sensory deficits.
• Clouding of consciousness.
Middle cerebral
• Clouding of consciousness.
• Contralateral hemiplegia, hemianaesthesia and hemianopia.
• Motor and sensory aphasia if dominant.
Posterior cerebral
• As for middle cerebral.
• Contralateral hemianalgesia and spontaneous pain (thalamus).
Posterior inferior cerebellar artery
• Ipsilateral – facial analgesia, Horner’s syndrome, ataxia, weakness of vocal cords
and tongue.
• Dissociated or contralateral analgesia.
Basilar artery Headache, vertigo, coma, flaccid quadriplegia or monoplegia, total
anaesthesia, hyperpyrexia, ipsilateral cranial nerve palsies and cerebellar signs.
NEUROPSYCHIATRIC ASSESSMENT
Assess
Attention, memory, language, visuospatial functions, calculation, abstract thinking,
handedness, facial asymmetry, abnormal movements, primitive reflexes (e.g. palmo-
mental/grasp/snout reflexes), ‘soft signs’.
154 ORGANIC PSYCHIATRY
History
• No history of depression.
Investigations
• Psychometry – verbal performance discrepancy.
• Sulcal widening on CT scan (and ventricular dilatation to a lesser extent).
• EEG abnormalities.
DELIRIUM
Between 10 per cent and 30 per cent of all medical/surgical inpatients have had delir-
ium. There is a higher prevalence in the elderly or seriously ill. Risk factors include
increasing age, underlying dementia or physical illness.
Aetiology
There are multifactorial aetiological mechanisms, but relative similarity of individual
clinical pictures. Aetiology is undetermined in 5–20 per cent of the elderly delirious.
Dementia coveys increased risk.
Most common causes are CVA, UTI, diabetes, ischaemic heart disease, metabolic
abnormalities, major organ failure, drug toxicity (prescribed or alcohol or illicit).
There is significant mortality – up to 76 per cent of elderly, hospitalized delirious
patients die during hospitalization.
Management
• Adequate investigation – history from staff, relatives.
• Baseline laboratory tests, EEG, CT/MRI.
• Treat underlying cause, if known.
• Treat any (other) reversible component; e.g. infection, anaemia, dehydration.
• Nurse in well-lit room, avoid under/overstimulation from environment.
• Agitation – use lowest effective dosage of atypical antipsychotics.
THE DEMENTIAS
This historically refers to presenile dementia before 65 years, but now also includes
dementia after age 65.
EPIDEMIOLOGY
About 3 per cent of the population aged over 65 years have AD, 50 per cent over
85 years. Age is the most important risk factor for AD, but AD is not just a form of
accelerated aging!
There is a higher prevalence in females (2:1), even when controlled for greater
longevity in females and increased CVA in males.
AETIOLOGY
See the diagram on page 156.
Genetics
• Trisomy 21 – There is an association between AD and Down syndrome. All develop
the typical histopathological lesions of AD (amyloid plaques, neurofibrillary tan-
gles before age 40 years).
156 ORGANIC PSYCHIATRY
Clinical syndrome
• Chromosome 21 – Mutations are found in the gene encoding for ‘amyloid precursor
protein’ (APP), seen in familial AD.
• Chromosome 14 – Early-onset AD.
• Chromosome 19 – Sporadic, late-onset AD.
Risk factors
• Head trauma (some similarity in neuropathology findings in punch-drunk
syndrome).
• Low educational level.
Neuropathology
The ‘amyloid hypothesis’ Either increased amyloid -peptide synthesis or decreased
amyloid clearance in the brain results in aggregation of these peptides to form amy-
loid plaques (AP). APs are seen particularly in the outer three layers of cortex, but all
layers are affected – hippocampus, parietal regions usually first affected. The deposi-
tion of these neuritic plaques precedes AD.
The extent of APs correlates with severity of clinical illness, and are hypothesized to
be the pathogenesis of AD.
Apolipoprotein E (APOE) APOE is a cell membrane protein that transports choles-
terol into the cell. Homozygotes for APOE 4 on chomosome 19 have a higher risk of
AD than heterozygotes. APOE 4 is thought to increase the risk for AD by either
increasing the sythesis of AP, or decreasing the clearance of amyloid -peptides.
Neurofibrillary tangles (NFTs) NFTs are intracellular hyperphosphorylated pro-
teins that accumulate and form paired helical filaments. The extent of NFTs serves as
a marker of severity of illness.
Other abnormalities:
• Glial proliferation.
• Granulovascular degeneration – especially in hippocampus.
• Hirano inclusion bodies.
THE DEMENTIAS 157
Immunology
Immunohistochemistry shows:
• Localized inflammatory reaction in AD.
• Complement in SPs.
• Neuroglial reaction to amyloid.
• Increased acute-phase reactants.
However, these are probably not primary events because there is little evidence for an
autoimmune or infectious process.
Classification of AD
See Table 13.1. Features of Klü ver–Bucy syndrome (hyperorality, hypersexuality,
placidity, increased touching) are seen in type I AD, reflecting bitemporal damage.
CLINICAL FEATURES
There is generally an insidious onset. Memory failure is usually the presenting feature,
often accompanied by lability of mood, anxiety, depression or apathy, with impaired
attention.
158 ORGANIC PSYCHIATRY
MANAGEMENT
See Chapter 17. There should be a thorough initial assessment. Clarify the diagnosis,
rule out any medical cause, treat all/any reversible component (e.g. hypoxia, mild
heart failure, anaemia).
Education Intensive family and psychosocial support is necessary.
Psychotherapy Reality orientation, reminescence therapy are useful.
Drug pharmacotherapy
• Acetylcholinesterase inhibitors target cognitive symptoms – memory and attention –
and may delay but not alter disease progression. Commonly used drugs include
donepezil, galantamine and rivastigmine. No clear evidence at present for superior
efficacy between these drugs, but there may be advanages in dosing and tolerabil-
ity. Drugs stabilize functioning in the first year and make subsequent decline
more gradual. Uncertainty as to how early to start treatment and how long to
continue.
• NMDA receptor antagonists (e.g. memantine) slow the rate of cognitive and func-
tional decline.
• Experimental treatments include NSAIDs, oestrogen, statins, heavy metal chelators
(may enhance amyloid clearance); amyloid vaccine is also under investigation.
• Vitamin E and selegiline may delay but not alter disease progression.
• Antipsychotics may be used to target behavioral symptoms and psychosis.
• Antidepressants can be given for depressive symptoms.
Future treatments Research is under way involving vaccination with antibodies to
amyloid -peptide.
THE DEMENTIAS 159
PROGNOSIS
Severity of cognitive impairment is a crude index of survival time. Deterioration to
death is within 2–5 years of hospital admission.
The cognitive ability of the elderly naturally declines with age. The term MCI refers to
a state between normal age-related cognitive decline and dementia. MCI is marked by
objective evidence of memory deficits but with intact general cognitive and activity
functioning.
A significant proportion of individuals diagnosed with MCI will progress to
Alzheimer’s disease – up to 36 per cent per year. More research is needed to ascertain
whether MCI represents an early stage of AD.
The rate of death for those diagnosed with MCI is about 1.7 times that of those
without the diagnosis.
EPIDEMIOLOGY
VaD represents 5–15 per cent of dementias. As with AD, prevalence increases with age.
AETIOLOGY
VaD is caused by either ischemic injury from embolic and or atherothrombotic vessel
occlusions. An autosomal dominant gene on chromosome 19 conveys small vessel dis-
ease which results in VaD in 50 per cent of carriers.
CLINICAL FEATURES
There is acute onset with patchy, stepwise deterioration. There is fluctuating cognitive
impairment with episodes of nocturnal confusion. Depression and ‘emotional incon-
tinence’ may be prominent.
Personality is often preserved until late, and insight is often intact.
Focal neurological deficits are common, and hypertension is present in most cases.
Frequently, there is evidence of arteriosclerosis elsewhere.
The Hatchinski index (using the above clinical features) may give a diagnostically
indicative score.
Binswanger’s chronic progressive subcortical encephalopathy with white matter
degeneration may be caused by arteriosclerosis.
PICK’S DISEASE
EPIDEMIOLOGY
The peak age of onset is 40–60 years, and it is most common in men. It accounts for
about 5 per cent of dementias.
AETIOLOGY
A minority of cases are due to an autosomal dominant gene with variable penetrance.
Pathology
• Frontal and temporal lobes are particularly affected.
• ‘Knife-blade’ atrophy is seen due to neuronal loss.
• Pick’s cells are present. These are swollen cells with silver-staining inclusion bodies
(‘balloon cells’).
• Fibrous gliosis is present.
• SPs or NFTs are absent.
CLINICAL FEATURES
Personality deterioration occurs early, with a ‘frontal lobe’ syndrome of disinhibition.
Perseveration and dysphasia are characteristic.
There is a less generalized cognitive decline than in AD. Hyperalgesia is experienced
late in illness in some patients.
PROGNOSIS
There is a slower time-course than in Alzheimer’s disease, being 2–10 years to death.
The average is 5 years from diagnosis.
HUNTINGTON’S CHOREA
EPIDEMIOLOGY
The prevalence is 2–10 cases per 100 000 population. The age at onset is usually 25–50
years.
AETIOLOGY
• There is a single autosomal dominant gene on chromosome 4 with almost
100 per cent penetrance. The gene is located on proximal arm of chromosome 4
(Gusella et al., 1993).
• There is selective loss of GABA neurones, particularly in basal ganglia.
• GABA and glutamic acid decarboxylase have been shown to be reduced, resulting
in dopamine hypersensitivity.
• Glutamate excitotoxicity a possible mechanism?
Pathology
There is atrophy of caudate and putamen in particular, but also of cortex (especially
frontal).
THE DEMENTIAS 161
CLINICAL FEATURES
• May present with chorea or with mental changes. Often they develop independ-
ently. Psychiatric illness may precede chorea.
• Personality change is often realized retrospectively. Characteristically the person
becomes irritable, distractable, apathetic and depressed.
• Psychotic disorders, particularly a paranoid psychosis, may develop.
• Insidious onset of global dementia may develop.
• Chorea, initially of face and upper limbs, may develop. There may also be intention
tremor, ataxic gait, dysarthria and rigidity.
• In children, rigidity, tremor and fits are more common and there is more rapid
deterioration.
• There is a high rate of suicide among (unaffected) relatives.
• CT/MRI – show dilated ventricles, caudate atrophy.
• PET/SPECT – show frontal and basal ganglia hypometabolism.
• EEG – ‘flat’.
PROGNOSIS
In adults, death occurs within 13–16 years; within 8 years in children.
EPIDEMIOLOGY
CJD is rare and occurs equally in males and females. Onset is usually within the range
50 to 70 years of age for the sporadic form; the average is 30 years with the variant
form (vCJD) – thought to be an animal crossover from eating beef from cows infected
with bovine spongiform encephalopathy.
Sporadic CJD accounts for 80–85 per cent of cases; inherited form, 5 per cent;
iatrogenic form, 5 per cent; other forms, 5–10 per cent.
AETIOLOGY
It is a prion disorder – neurodegenerative infective protein pathogens which are
encoded on human chromosome 20. It also appears as an inherited autosomal dom-
inant form.
Disease may be transmitted iatrogenically from infected CNS stereotactic needles,
or corneal transplant.
Pathology
There is spongiform, neuronal degeneration with astrocytic glial proliferation.
CLINICAL FEATURES
• Personality change, apathy, depression, anxiety, fatigue, withdrawal, slowness,
memory loss, organic psychosis.
• Seizures, myoclonic jerks, cortical blindness.
• CT/MRI – cortical atrophy, worse frontally.
• Abnormal EEG in 90 per cent – periodic triphasic complexes seen in CJD but
not vCJD.
162 ORGANIC PSYCHIATRY
PROGNOSIS
CJD is rapidly progressive over 6 months to 2 years.
LEWY-BODY DEMENTIA
This is a recently described dementia which may be the second most common. It is
characterized by confusional states, fluctuating cognitive impairment, psychotic
symptoms (hallucinations, delusions, depression), mild/variable short-term memory
loss, some mild extrapyramidal features or extreme sensitivity to EPS effects with neu-
roleptic treatment.
The pathological hallmark is the Lewy-body (LB) – intracellular inclusion bodies of
ubiquitin, protein, and other proteins.
LBs are classically seen in Parkinson’s disease, especially in substantia nigra.
They are also seen cortically and subcortically in LB dementia, especially in
hippocampus.
HYDROCEPHALUS
Types
1 Non-obstructive and communicating – secondary to brain atrophy
2 Obstructive and non-communicating – secondary to obstruction of CSF flow within
the ventricular system.
3 Obstructive and communicating (‘normal pressure hydrocephalus’) – secondary to
obstruction of CSF flow in the subarachnoid space or failure of normal absorp-
tion. Fifty per cent of cases may be due to subarachnoid haemorrhage, meningitis,
head injury.
CLINICAL FEATURES
• Memory impairment.
• Slowness and apathy.
• Unsteady gait.
• Incontinence.
SUBCORTICAL DEMENTIA
CLINICAL FEATURES
• Forgetfulness.
• Slowing of thought processes – delayed answers (‘bradyphrenia’).
• Personality change – apathy, irritability, depression.
• Decreased ability to manipulate acquired knowledge.
PUNCH-DRUNK SYNDROME
This is usually the result of repeated mild head injuries (e.g. in boxers). There is cere-
bral atrophy with brain stem and hippocampal–limbic damage.
CLINICAL FEATURES
• Cerebellar lesions – ataxia, festinant gait.
• Pyramidal lesions – spasticity.
• Extrapyramidal lesions – tremor.
• Intellectual and personality deterioration.
VITAMIN DEFICIENCIES
Wernicke’s encephalopathy
• Acute onset of:
– Ophthalmoplegia and nystagmus.
– Clouding of consciousness.
– Ataxia.
– Peripheral neuropathy.
In 84 per cent of cases this results in Korsakoff ’s psychosis.
164 ORGANIC PSYCHIATRY
AETIOLOGY
• Korsakoff ’s psychosis:
– Thiamine deficiency.
– Head injury.
– Carbon monoxide (CO) poisoning.
– Tumour.
– Anaesthetic accident.
• Thiamine deficiency:
– Alcoholism.
– Starvation.
– Hyperemesis.
Pathology
• Parenchymal loss.
• Proliferation of blood vessels.
• Petechial haemorrhages.
CLINICAL FEATURES
• Very poor retention of recent memories, sometimes with confabulation.
• Retrograde amnesia.
• Apathy or euphoria.
Anticholinergics Amphetamines
Isoniazid Hallucinogens
Cycloserine Corticosteroids
Mecamylamine Barbiturates
Bromides Digoxin
Almost all psychotropics in the elderly
INFECTIONS
CLASSIC PICTURES
• Simple dementing – 20–40 per cent.
• Depressive – 25 per cent.
• Grandiose – 10 per cent.
• Also seen:
– Manic elation.
– Paranoid schizophreniform.
– Neuraesthenia.
Treatment
Penicillin is the only proven effective treatment.
INFECTIONS 167
Onset is rapid. There are severe inflammatory changes which may be necrotizing and
haemorrhagic. Infection especially affects medial temporal and orbital regions.
The viral aetiology of this disorder may also imply latent infection in other psychi-
atric disorders.
CLINICAL FEATURES
• Pyrexia.
• Focal signs (temporal lobe).
• Delirium, often with marked hallucinations.
PROGNOSIS
In 15 per cent there are severe sequelae – dementia, focal deficits, amnesic syndrome.
Seventy per cent of cases are fatal.
• Typhus.
• Trypanosomiasis (sleeping sickness).
• Cerebral malaria (Plasmodium falciparum, malignant tertiary malaria).
• Encephalitis lethargy – delirium followed by fatigue, parkinsonism, personality
change.
• Acute disseminated encephalomyelitis.
AETIOLOGY
This is multifactorial
• Cytopathic effects of virus on CNS (e.g. AIDS dementia).
• Secondary to CNS infection.
• Secondary to systemic illness/metabolic derangement.
• Secondary/exacerbation of pre-existing mental co-morbid illness (e.g. substance
abuse, depression).
• Secondary to psychosocial stressors (stigma, withdrawal of social support, finan-
cial insecurity).
AIDS dementia complex (ADC)
This is the most common neuropsychiatric complication of human immunodefi-
ciency virus (HIV) infection and can occur before AIDS develops.
It is associated with initially poor concentration, mental and motor slowing, apathy –
subcortical dementia features; later, profound dementia, frontal release signs.
In the early stages it is difficult to detect cognitive impairment on neuropsycho-
logical testing.
168 ORGANIC PSYCHIATRY
MRI shows subcortical involvement, widespread changes in cortical grey and white
matter and possibly vacuolation in the spinal cord. Post-mortem studies have shown:
• An encephalitic process.
• HIV-infected multinucleated giant cells and endothelial cells.
• Decreased neuronal density.
Psychosis
This may be paranoid, schizophrenia-like, affective-like, organic psychosis (CNS
involvement, opportunistic infection, CNS lymphoma, zidovudine or other
medication-related).
Affective disorder
There were reports of major depression and of mania which appeared secondary
to HIV infection; this responded to zidovudine treatment. Many symptoms of
depression overlap with clinical features of AIDS itself. Depression also is a grief
reaction.
Suicide is 66 times more common than in the general population (Marzuk et al., 1988).
Adjustment disorders
The most prominent adjustment disorders are anxiety and depression. Worries con-
cern illness progression, impact on family and friends, social status, and work.
MANAGEMENT
• Full evaluation:
– Immunology (CD4 count is best marker in illness progression).
– Neuropsychological tests.
– Neuroimaging.
– CSF, biochemistry.
– Full psychiatric and psychosocial evaluation.
• Psychosocial:
– Education.
– Supportive psychotherapy.
– Counselling.
– Information for patient and family about illness before cognitive deficits appear.
– Mobilize family and financial support.
• Medical:
– Treat infection, metabolic derangements, dehydration, drug toxicity.
• Pharmacological:
– ‘Highly active anti-retroviral therapy’ (HAART) has improved survival follow-
ing diagnosis of ADC.
– Zidovudine (AZT) partially ameliorates cognitive deficits.
– Antidepressants – use lower doses, agents with less anticholinergic toxicity.
– Neuroleptics – atypical antipsychotics for hallucinations/delusions.
– Psychostimulants – methylphenidate is worthy of consideration with psy-
chomotor retardation.
– Lithium – used in some HIV-mania cases, also helpful in leucopenia secondary
to AZT.
– ECT – if no response to mood stabilizers or antidepressants.
METABOLIC DISORDERS (PSYCHIATRIC ASPECTS) 169
HEPATIC FAILURE
This may present with psychiatric disturbance. Exacerbations and remissions are
typical. Non-specific EEG changes are often an early sign; triphasic waves are seen later.
CLINICAL FEATURES
• Delirium, confusion, irrational and uninhibited behaviour.
• Hypersomnia, coma.
• Labile mood.
• Memory impairment.
• Neurological abnormalities.
URAEMIA
CLINICAL FEATURES
• Memory impairment.
• Malaise, fatigue, drowsiness.
• Depression.
• Occasionally functional psychosis.
• Acute delirium in 30 per cent.
• Seizures in 30 per cent.
ELECTROLYTE DISTURBANCE
CLINICAL FEATURES
• Abdominal – colicky pain, vomiting, constipation.
• Neurological – peripheral neuropathy, bulbar palsies, epilepsy.
• Psychiatric:
– Delirium in 50 per cent, depression and emotional lability.
– Psychosis, especially paranoid.
– ‘Hysteria’ – may be diagnosed.
170 ORGANIC PSYCHIATRY
MULTIPLE SCLEROSIS
Injury may be focal (haemorrhage, infarct, contusion) or diffuse (diffuse axonal injury;
DAI):
1 Primary (at time of impact).
2 Secondary (oedema, hypoxia, increased intracranial pressure).
Prognosis is worsened by:
• Long post-traumatic amnesia (see below).
• Penetrating injury.
• Intracranial bleeding.
Impaired consciousness
Long duration of impaired consciousness suggests a poor prognosis. If longer than
1 month:
• 40 per cent die without regaining consciousness.
• 20 per cent return to work.
Retrograde amnesia
Retrograde amnesia covers the period between injury and the last clear memory from
before the injury. Initially, the period is lengthy but it shrinks over time. The final
duration is often less than 1 minute. This is not a good prognostic indicator.
A duration of less than 12 hours suggests probable full recovery; more than
48 hours – probably some residual damage.
AETIOLOGICAL FACTORS
• Amount of brain damage – correlates closely with sequelae.
• Location of brain damage – especially left temporal lobe.
• Development of epilepsy – 5 per cent of closed injuries; 30 per cent of penetrating
injuries.
• Premorbid personality.
• Family history of psychiatric disorder.
• Past history of psychiatric disorder.
• Emotional factors and the ‘meaning’ of the injury to the patient.
• Insecure convalescent environment.
• Compensation and litigation factors.
CLASSIFICATION
Neuroses (‘post-concussional syndrome’)
Neuroses are the commonest psychiatric sequelae (11–22 per cent of severe injuries)
and are often underestimated.
• Mild depression.
• Fatigue – frequently self-limiting but may not disappear for 1 year.
• Anxiety, phobias, hypochondriasis.
• Irritability and sensitivity to noise.
• Somatic complaints – headache, dizziness, impotence.
• Hysterical symptoms.
• Loss of sexual interest.
Personality changes
These are common (6–18 per cent of severe injuries).
• Injuries with brain damage:
– As part of dementia.
– Due to frontal lobe damage.
– As reduced control over aggression.
• Injuries without brain damage:
– Usually an exaggeration of previous traits.
Psychoses
These occur in 5–8 per cent of severe injuries.
• Affective:
– Usually depressive psychosis.
– Associated with right hemisphere and frontal damage.
172 ORGANIC PSYCHIATRY
• Schizophreniform:
– Especially paranoid, may be with morbid jealousy.
– Rarely show ‘process’ schizophrenia.
• Associated with temporal lobe damage.
Cognitive impairment
This occurs in 3 per cent of severe injuries. It is more likely with:
• Long post-traumatic amnesia.
• Left parietal or left temporal lobe damage.
• Penetrating injury.
• Haemorrhage or infection.
• Increasing age.
Recovery may progress over 10 or more years.
Bennett DA, Wilson RS, Schneider JA et al. (2002) Natural history of mild cognitive impairment
in older persons. Neurology 59, 18.
Bouman WP, Pinner G (2002) Use of atypical antipsychotic drugs in old age psychiatry. Adv.
Psychiatr. Treat. 8, 49.
Bullock R, Hammond G (2003) Realistic expectations: the management of severe Alzheimer dis-
ease. Alzheimer Dis. Assoc. Disord. 17, s80.
Burns A, Dening T, Baldwin R (2001) Care of older people: mental health problems. BMJ 322, 789.
Butler R, Fleminger S (2001) Creutzfeldt–Jacob disease and its implications for psychiatric man-
agement. Adv. Psychiatr. Treat. 7, 50.
Clifford DB (2002) AIDS dementia. Med. Clin. North Am. 86, 537.
Coffey CE, Cummings JL (1994) Textbook of Geriatric Neuropsychiatry. American Psychiatric
Press, Washington, DC.
REFERENCES AND FURTHER READING 173
Marzuk PM, Tierney H, Tardiff K et al. (1988) Increased risk of suicide in persons with AIDS.
JAMA 259, 1333.
Mayou R, Bryant B (2002) Psychiatry of whiplash neck injury. Br. J. Psychiatry 180, 441.
McKeith IG (2002) Dementia with Lewy bodies. Br. J. Psychiatry 180, 144.
Misra S, Ganzini L (2003) Delirium, depression, and anxiety. Crit. Care Clin. 19, 771.
Morris JC, Storandt M, Miller P et al. (2001) Mild cognitive impairment represents early-stage
Alzheimer’s disease. Arch. Neurol. 58, 397.
O’Brien JT, Erkinjuntti T, Reisberg B et al. (2003) Vascular cognitive impairment. Lancet Neurol.
2, 89.
Pisani MA, McNicoll L, Inouye SK (2003) Cognitive impairment in the intensive care unit. Clin.
Chest. Med. 24, 727.
Romain GC (2002) Vascular dementia revisited: diagnosis, pathogenesis, treatment, and preven-
tion. Med. Clin. North Am. 86, 477.
Rosenburg RN (2000) Wartenberg Lecture. The molecular and genetic basis of AD: the end of
the beginning. Neurology 54, 2045.
Roth M (1986) The association of clinical and neurobiological findings and its bearing on the
classification and aetiology of Alzheimer’s disease. Br. Med. Bull. 42(1), 42.
Schupf N, Sergievsky GH (2002) Genetic and host factors for dementia in Down’s syndrome. Br.
J. Psychiatry 180, 405.
Sharma N, Standaert DG (2002) Inherited movement disorders. Neurol. Clin. 20, 759.
Shumaker SA, Legault C, Rapp SR et al. (2003) Estrogen plus progestin and the incidence of
dementia and mild cognitive impairment in postmenopausal women. The Women’s Health
Initiative memory study: a randomized controlled trial. JAMA 289, 2651.
Skegg K (1993) Multiple sclerosis presenting as a pure psychiatric disorder. Psychol. Med. 23, 909.
Skuster DZ, Digre KB, Corbett JJ (1992) Neurologic conditions presenting as psychiatric dis-
orders. Psychiatr. Clin. North Am. 15, 311.
St George-Hyslop PH, Haines JL, Ferrer LA et al. (1990) Genetic linkage studies suggest that
Alzheimer’s disease is not a single homogeneous disorder: FAD Collaborative Study Group.
Nature 347, 194.
Stanton LR, Coetzee RH (2004) Down’s syndrome and dementia. Adv. Psychiatr. Treat. 10, 50.
Stevens T, Livingston G, Kitchen G et al. (2002) Islington study of dementia in the community.
Br. J. Psychiatry 180, 270.
Stevens T, Livingston G, Kitchen G et al. (2002) Islington study of dementia subtypes in the com-
munity. Br. J. Psychiatry 180, 270.
Sy MS, Gambetti P, Wong B (2002) Human prion disease. Med. Clin. North Am. 86, 551.
Terry RD, Masliah E, Salmon DP et al. (1991) Physical basis of cognitive alterations in
Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann. Neurol.
30, 572.
Psychiatric aspects of epilepsy 14
and sleep disorders
EPILEPSY
CLASSIFICATIONS
Classification may be according to:
• Symptoms and signs of the seizure.
• Anatomical and electrophysiological evidence of the source of the seizure.
• Aetiology or precipitant of seizures.
Classification of seizure type is more straightforward than classification of ‘the
epilepsies’.
b. Myoclonic seizures.
c. Clonic seizures.
d. Tonic seizures.
e. Tonic–clonic seizures (‘grand mal’).
f. Atonic seizures (‘drop attacks’).
3 Unclassified seizures.
EPIDEMIOLOGY
• Lifetime prevalence – About 10 per cent of the population will experience at least
one seizure in their lifetime. About 3–4 per cent will develop epilepsy.
• Prevalence of active epilepsy is 5 per 1000.
• It is more prevalent in males; M:F ⫽ 1.5:1.
• Highest incidence is in young children and the elderly.
• Estimated 29 per cent of people with epilepsy overall show conspicuous psycho-
logical problems (50 per cent if temporal lobe epilepsy).
Age at onset
• 0–10 years – 30 per cent.
• 11–20 years – 25 per cent.
• 21–30 years – 20 per cent.
Seizure type
• Partial – 60 per cent (mostly complex, 90 per cent arising in temporal lobes).
• Generalized – 35 per cent.
• Mixed – 13 per cent.
AETIOLOGY
• Post-traumatic – 7 per cent.
• Cerebrovascular – 9 per cent.
• Other – 9 per cent.
• Unknown – 75 per cent.
PROGNOSIS
Eighty per cent of those having a first seizure will have further seizures. Fifty per cent
of those will have 10 or fewer seizures, usually as a short burst over a few months. If
free for 5 years on medication, they have 30 per cent chance of having further fits
if medication is stopped.
There is an increased risk of death due to accidents, especially drowning. The risk of
unexplained sudden death is 20 times greater than that of the general population.
GENETIC COUNSELLING
The recurrent risk is 1 in 25 if one parent has had epilepsy, 1 in 10 if parent and grand-
parent do. Certain epilepsies have a strong genetic component (e.g. juvenile myoclonic
epilepsy).
EPILEPSY 177
PREICTAL PHASE
• Prodromal features:
– Irritability, tension, insomnia, restlessness, occasionally suicidal depression.
– May occur days or hours before fit.
• Aura:
– Usually precedes a fit by only a few seconds, and lasts a few seconds – acute
perceptual change, depersonalization, acute mood change, etc.
– In itself a focal fit, reflecting abnormal electrical discharge.
– Indicates focal disturbance in cerebral cortex.
– Temporal lobe aura typically a rising epigastric feeling; déjàvu.
Diagnosis
• This is essentially on clinical grounds. An abnormal EEG may confirm, but a nor-
mal EEG in-between episodes does not exclude. Seek evidence from a witness –
sudden onset, impaired awareness.
• There is no retrograde amnesia.
• If an offence is committed, seek evidence that it was unpremeditated and there was
no attempt at concealment.
Differential diagnosis
• Hysterical amnesia and fugue. (Often covert conflict with purposeful escape.
Amnesia of longer duration.)
• Malingering (marked variability and inconsistency).
• Stress reaction (inhibited individual exercising denial mechanisms).
• Alcohol, drug intoxication.
• Sleepwalking (stage IV; rarely repetitive or stereotyped; behaviour usually well
integrated).
POST-ICTAL PHASE
• Automatism (see above).
• Twilight states.
• Transient paranoid–hallucinatory states (post-ictal psychosis).
INTER-ICTAL PERIODS
Aggressive behaviour
There is a higher prevalence of epilepsy in the British prison population but violence
is not more common in epileptics than in other prisoners; automatism could not account
for the majority of crimes.
Possibilities are:
1 Organic brain disorder is responsible for both epilepsy and offence behaviour.
2 Organic brain disorder causes epilepsy with consequent social rejection and sense
of inferiority, leading to offensive behaviour.
3 Adverse social factors lead to both epilepsy and antisocial behaviour (e.g. battered
child).
4 A tendency to reckless and antisocial behaviour leads to offences and accidents
which could injure the brain and cause post-traumatic epilepsy.
Serious violence as an epileptic phenomenon is very rare; any violence is usually
short-lived, fragmentary, unsustained, purposeless.
‘Episodic dyscontrol syndrome’ This is controversial. There are episodes of senseless,
poorly remembered unprovoked violence. Temporal lobe EEG abnormalities may be
present. It may be helped by carbamazepine.
It is associated with:
Suggested mechanisms
• Epiphenomena – ? There is a common brain disorder responsible for both schizo-
phrenic symptoms and epilepsy.
• Psychodynamic – ? Symptoms are a response to social rejection, etc., associated
with epilepsy, and to abnormal mental experiences produced by it.
• Pathophysiological – ? Schizophrenic symptoms are produced by physiological
changes consequent on abnormal electrical or neurotransmitter activity.
Dementia
A small proportion develop progressive decline in intellectual ability, with diffuse
cerebral atrophy. This may develop after many years’ functioning at adequate level.
It is also associated with deterioration in personality.
Dementia is more common where epilepsy is secondary to a known brain lesion,
and where epilepsy is early-onset, severe, chronic and temporal-lobe.
Exclude:
TREATMENT OF EPILEPSY
Drug treatments
Remember:
Specific drugs:
Surgery
Consider temporal lobectomy for treatment-resistant epilepsy (after adequate trials)
with a definite EEG focus. This usually requires extensive workup – neurophysiology
and imaging. Up to 60–70 per cent are seizure-free after surgery.
With other brain regions, up to 50 per cent are seizure-free afterwards (e.g.
callosotomy).
Ketogenic diet
By maintaining a ketoacidotic state, seizures may be suppressed by an unknown
mechanism. However, it is difficult to maintain a ketogenic state. It has only been
demonstrated to be effective in children.
Psychosocial
Be aware of the family, social and personal context.
• Family – Overprotection may foster dependency.
• Personal – Is there poor self-esteem, inadequate social skills and social repertoire?
• Societal – Be aware of negative attitudes, discrimination.
SLEEP DISORDERS
See Table 14.1. The normal physiology/normal sleep EEG is covered in Chapter 15.
INSOMNIA
Insomnia is a symptom, not a disease. Thirty-five per cent of the population experi-
ence some insomnia; in 10–15 per cent it is clinically significant.
SLEEP DISORDERS 181
Dyssomnias
Primary insomnia
Primary hypersomnia
Sleep–wake schedule disorders
Jet lag
Sleep delay
Other
Disorders of excessive sleep
Breathing-related sleep disorder (obstructive sleep apnoea)
Narcolepsy
Parasomnias
Nightmares
Sleep terrors
Sleepwalking
REM sleep behaviour disorder
Other
Sleep disorder related to other mental disorder
Sleep disorder related to general medical condition
Risk factors are: female, elderly, anxious, depressed, multiple health problems, lower
social group.
It is most prevalent in the elderly because of changes in the sleep pattern: ↓ REM,
↓ REM latency, ↑ number and duration of awakenings, ↑ shift through sleep stages,
↑ daytime napping; also increased physical and psychiatric morbidity.
Forty per cent of insomniacs self-medicate with over-the-counter drugs or alcohol;
20 per cent take prescription sedatives/hypnotics.
MANAGEMENT
There should be a thorough initial evaluation to rule out secondary (physical/psychiatric)
or situational (stress-related/environmental) causes.
Sleep hygiene
Encourage: regular bedtimes and rise times; a bedtime ritual (e.g. short read); diet
(avoid hunger or overeating at night); avoid caffeine; avoid alcohol; no daytime naps;
regular exercise. The bedroom should be dark, quiet, at normal temperature. Avoid
‘clock watching’ – use bed to sleep.
Cognitive–behavioural therapy
This is useful as a means of treating, possibly curing, primary insomnia as well as
achieving discontinuation of hypnotic drug use.
rebound insomnia with discontinuation (see Chapter 21). Abuse and dependency
are problematic.
• Non-benzodiazepines: zolpidem and zopiclone – Although associated with lower
abuse than benzodiazepines, those with a history of substance abuse or depend-
ence, or psychiatric illness may be at increased risk to abuse these agents.
NARCOLEPSY
Narcolepsy has a population prevalence of about 0.05 per cent. The ‘narcoleptic
tetrad’ is:
1 Hypersomnia.
2 Cataplexy (sudden loss of muscle tone) in 80 per cent of cases.
3 Sleep paralysis (marked loss of muscle tone on awakening).
4 Hypnagogic hallucinations (i.e. on going to sleep) or hypnopompic (on waking).
Only 25 per cent of patients have the complete tetrad.
Two-thirds have fallen asleep while driving, 80 per cent fallen asleep while at work.
AETIOLOGY
There is an abnormality on chromosome 6 (HLA DQB1 and DQA1 alleles) seen in over
85 per cent of patients. An association with human leukocyte antigen (HLA) allele sug-
gests an autoimmune link. Neurochemical studies show absence of hypocretin in CSF.
DIAGNOSIS
Use the multiple sleep latency test (MSLT) EEG during the day – rapid onset of REM
(⬍10 mins after onset of sleep), ⭓2 sleep-onset REM periods during MSLT is virtually
diagnostic; also HLA testing.
REFERENCES AND FURTHER READING 183
Night terrors 3% children, First Non-REM, Terrified, screaming, None Reassurance and
commonest in 1–2 hours stage 4 thrashing, can’t be practical advice
ages 4–7; often of sleep easily aroused, for parents;
family history ‘trance-like’, may behavioural
last 10–20 minutes waking schedule
if persistent
Sleepwalking 1–15%, normally First Non-REM, May last minutes None Safety precautions;
8–15 years old, 1–2 hours stage 4 to 1 hour avoid sleep
but also in adults of sleep deprivation
TREATMENT
• Allow only scheduled daytime naps.
• Use of stimulants – modafinil, dexamphetamine and methylphenidate. Cataplexy
may be effectively treated with clomipramine or an SSRI.
OTHER CONDITIONS
ELECTROENCEPHALOGRAPHY (EEG)
Frequency ranges
• Delta – less than 4 Hz. May occur as regular waves or irregularly. Diffusely distrib-
uted over scalp in sleeping adults and in children but invariably abnormal in non-
sleeping adults.
• Theta – 4–7 Hz. Transient are components found in 15 per cent of the normal
population.
• Alpha – 8–13 Hz. Prominent over occipital region, accentuated by eye closure and
attenuated by attention. A consistent difference of 1 Hz or more between hemi-
spheres is pathological. Slowing seen in early phenytoin toxicity.
• Beta – 14 Hz and above. Principally frontocentral. May be enhanced by anxiety,
alcohol and some drugs (barbiturates, benzodiazepines).
• Mu – Arch-like 7–11 Hz waves over precentral areas, attenuated by contralateral
limb movements.
• Lambda – Single sharp waves in occipital region, usually associated with visual
‘scanning’.
• Vertex waves – Electronegative sharp waves over vertex, evoked by auditory stimulus.
DEVELOPMENT
Infants have slower and usually higher-amplitude rhythms. They are asynchronous at
first and easily disturbed. Mature rhythms develop at between 2 and 6 years.
186 EEG AND BRAIN IMAGING IN PSYCHIATRY
Adults usually show either alpha posteriorly and beta anteriorly but generalized
low-amplitude beta may be present – established by puberty. When the subject is
drowsy, alpha becomes intermittent and theta appears.
Alpha frequency tends to slow in old age, and delta activity is decreased; by 60 years,
Stage 4 represents 10 per cent of total sleep. There is decreased rapid eye movement
(REM) latency, with increased frequency and duration of nocturnal arousals.
NORMAL SLEEP
• Stage 1 (lightest) – low-voltage, desynchronized activity and sometimes low
voltage-regular activity at 4–6 Hz. Undulating low-frequency deflections seen due
to rolling eye movements.
• Stage 2 – frequent spindle-shaped tracings at 13–15 Hz (sleep spindles) and high-
voltage K complexes (high-voltage slow waves plus short episode of fast activity
over vertex, response to sound).
• Stage 3 – high-voltage delta waves begin to appear.
• Stage 4 – delta waves occupy more than 60 per cent of record.
Abnormalities include:
• Reduced amount and amplitude of normal frequencies (generalized or localized).
• Increased slow frequencies (generalized or localized).
ABNORMAL EEG PATTERNS 187
• Abnormal waveforms – spikes (duration less than 80 ms), sharp waves (duration
80–200 ms), spike and wave complexes.
Abnormal forms may occur spontaneously or may be provoked by photic stimula-
tion, sleeping, or hyperstimulation.
Diffuse abnormalities
• Rhythmic slowing.
• Occasionally periodic discharges.
Focal abnormalities
• Polymorphic, arrhythmic unreactive delta.
• Periodic lateralized epileptiform discharges.
Epilepsy
• Initial interictal EEG is abnormal in 75 per cent of suffers.
• With repeated recordings, 90–95 per cent will show abnormalities.
• 2 per cent of normal population have abnormalities considered to be epileptiform.
• Absence seizures:
– 3/second spike and wave in infancy.
– 4/second spike and wave in a juvenile.
• Primary generalized tonic–clonic seizures:
– Interictal – bursts of spike and wave.
– Ictal – 10-Hz fast activity during tonic phase, followed by lower-frequency spike
and wave complexes during clonic phase.
– Postictal – generalized slowing ␦ range.
• Myoclonic epilepsy:
– Polyspike and wave.
• Partial (focal) epilepsy:
– Interictal – focal spikes or sharp waves.
– Ictal – focal rhythmic discharge.
Periodic complexes
• Herpes simplex encephalitis (look for localized temporal complexes).
• Creutzfeldt–Jakob disease (occurs in late stages).
• Subacute sclerosing panencephalitis.
Triphasic waves
These indicate liver, renal, hypoxic or metabolic encephalopathies.
Alpha coma
There is widespread, non-reactive alpha-range activity. It occurs in generalized
encephalopathy.
188 EEG AND BRAIN IMAGING IN PSYCHIATRY
Burst-suppression
There are high-voltage bursts, followed by periods of extreme suppression (flattening).
It occurs with bihemispheric insult and deep anaesthesia.
STUPOR
Non-organic stupor due to depression, schizophrenia or hysteria shows a preservation
of alpha rhythm.
BRAIN IMAGING
Structural Functional
Recent developments
• Voxel-based quantitative morphometry, for more sophisticated volume
measurements.
• Shape morphometrics, for examining shape rather than volume.
• Diffusion tensor imaging (DTI), which is MRI of myelin traits.
• Magnetoencephalography (MEG) a very recent technique using measurement of
alteration in cerebral magnetic fields to provide detailed information on cortical
activity. It may be combined with MRI and is good for studying deeper brain
structures.
XENON INHALATION
• This is another index of rCBF. There is well-documented hypofrontality in schizo-
phrenia, with failure of activation during performance of the Wisconsin Card
Sorting Test (WCST).
• There have been similar reports in affective disorder, but this may be a less consis-
tent finding.
MR SPECTROSCOPY (MRS)
This uses similar principles to structural MRI, but the tuning of the head coil at
particular frequencies will allow information to be obtained on phosphorus and ATP
metabolism (31P-MRS), glutamate, N-acetyl asparate (1H proton MRS), or pharma-
cology (19F MRS for neuroleptics or fluoxetine; Li+ MRS for lithium concentration in
brain).
• Schizophrenic patients show decreased phosphomonoesterases and ATP meta-
bolism in dorsolateral prefrontal cortex.
• Alzheimer’s disease patients show increases in phosphomonoesterases, even early
in the illness.
Bostwick JM, Philbrick KL (2002) The use of electroencephalography in psychiatry of the med-
ically ill. Psychiatr. Clin. North Am. 25, 17.
Bullmore E, Fletcher P (2003) The eye’s mind: brain mapping and psychiatry. Br. J. Psychiatry
182, 381.
Burton EJ, Karas G, Paling SM et al. (2002) Patterns of cerebral atrophy in dementia with Lewy
bodies using voxel-based morphometry. Neuroimage 17, 618.
Chance SA, Esiri MM, Crow TJ (2002) Amygdala volume in schizophrenia: post-mortem study
and review of magnetic resonance imaging findings. Br. J. Psychiatry 180, 331.
Du AT, Schuff N, Amend D et al. (2001) Magnetic resonance imaging of the entorhinal cortex
and hippocampus in mild cognitive impairment and Alzhiemer’s disease. J. Neurol.
Neurosurg. Psychiatry 71, 441.
Gilbert DL, Sethuraman G, Kotagal U, Buncher CR (2003) Meta-analysis of EEG test perform-
ance shows wide variation among studies. Neurology 60, 564.
Gross-Isseroff R, Hermesh H, Zohar J, Weizman A (2003) Neuroimaging communality between
schizophrenia and obsessive compulsive disorder: a putative basis for schizo-obsessive dis-
order? World J. Biol. Psychiatry 4, 129.
Grossman R, Buchsbaum MS, Yehuda R (2002) Neuroimaging studies I post-traumatic stress
disorder. Psychiatr. Clin. North Am. 25, 317.
Hambrecht M, Lammertink M, Klosterkotter J (2002) Subjective and objective neuropsycho-
logical abnormalities in a psychosis prodrome clinic. Br. J. Psychiatry 181, s30.
Hull AM (2002) Neuroimaging findings in post-traumatic stress disorder: a systematic review.
Br. J. Psychiatry 181, 102.
Kim J, Lee MC, Kim J et al. (2001) Grey matter abnormalities in obsessive–compulsive disorder:
statistical parametric mapping of segmented magnetic resonance images. Br. J. Psychiatry
179, 330.
Lacerda AL, Dalgalarrondo P, Caetano D et al. (2003) Elevated thalamic and prefrontal regional
cerebral blood flow in obsessive–compulsive disorder: a SPECT study. Psychiatry Res. 123, 125.
Lawrie SM, Whalley HC, Abukmeil SS (2002) Temporal lobe volume changes in people at high
risk of schizophrenia with psychotic symptoms. Br. J. Psychiatry 181, 138.
Lawrie SM, Whalley HC, Job DE, Johnstone EC (2003) Structural and functional abnormalities
of the amygdala in schizophrenia. Ann. NY Acad. Sci. 985, 445.
Martin R, Burneo JG, Prasad A et al. (2003) Frequency of epilepsy in patients with psychogenic
seizures monitored by video-EEG. Neurology 61, 1791.
O’Brien JT, Wiseman R, Burton EJ et al. (2002) Cognitive associations of subcortical white mat-
ter lesions in older people. Ann. NY Acad. Sci. 977, 436.
Phan KL, Wager T, Taylor SF et al. (2002) Functional neuroanatomy of emotion: a meta-analysis
of emotion activation studies in PET and FMRI. Neuroimage 16, 331.
Raush SL (2003) Neuroimaging and neurocircuitry models pertaining to the neurosurgical treat-
ment of psychiatric disorders. Neurosurg. Clin. North Am. 14, 213.
Scheltens P, Fox N, Barkhof F, De Carli C (2002) Structural magnetic resonance imaging in the
practical assessment of dementia: beyond exclusion. Lancet Neurol. 1, 13.
Shergill SS, Brammer MJ, Fukuda R et al. (2003) Engagement of brain areas implicated in pro-
cessing inner speech in people with auditory hallucinations. Br. J. Psychiatry 182, 525.
194 EEG AND BRAIN IMAGING IN PSYCHIATRY
CONCEPTS
These are disorders in which the onset and exacerbation of organic change are often
seen in association with emotional distress – e.g. asthma.
Before 1950, Alexander’s concept of psychosomatic medicine dominated: ‘a causal
link between a specific constellation of unconscious conflicts, of psychological methods
of coping with them … and the development of one of several organic diseases’.
Psychophysiological disorders (involvement of autonomic nervous system, smooth
muscles) were then separated from conversion disorders (sensorimotor, skeletal muscle).
Between 1951 and 1965, the postulated ‘psychosomatic specificity hypothesis’ was
tested against bronchial asthma, rheumatoid arthritis, ulcerative colitis, dermatitis, essen-
tial hypertension, peptic ulcer and thyrotoxicosis by the Chicago Institute for
Psychoanalysis. Investigations concluded that it is possible to differentiate between illness
on the basis of psychological patterns associated with them – but neither the specificity
nor the direction of causality is established. Four possible models of the relationship are
show in the diagram below.
1. No relationship
2. Soma Psyche
3. Soma Psyche
Psyche
4. Constitution
Soma
3 Clinical activities at the interface of medicine and the behavioural sciences, gener-
ally termed ‘consultation–liaison psychiatry’.
RECENT CONCEPTS
Recent concepts shift away from searching for psychodynamic formulations associated
with specific organic pathology, rather to increased interest in social/environmental
events and their effects on psychophysiological functioning, and relationship with
onset, course and outcome of various diseases.
• Murray Parkes (1970) has demonstrated vulnerability to physical illness in the first
year after death of the spouse.
• Recent research demonstrates superior outcome in cancer therapy among patients
who are psychologically minded and have less anxiety/depression (Spiegel, 2001).
• There is a large literature supporting a major role for depression in predicting
morbidity and mortality in patients with ischemic heart disease (Blumenthal et al.,
2003; Jiang et al., 2003).
Liaison psychiatry There has been growth of this concept in the last 60 years, facili-
tated by broader concepts of disease and location of psychiatric units in general
hospitals (Kornfeld, 2002):
PATTERNS OF RESPONSE
• Therapeutic adaptation – to the symptoms.
• Anxiety – usually the first response.
• Depression – commonest psychiatric disorder in medical inpatients (see Chapter 4
for notes).
• Paranoid reaction – especially if deaf or blind. May blame relatives or doctors.
• Denial of illness – may be a helpful defence but may delay seeking help.
• Preoccupation with illness – ‘vigilant focusing’ on the symptoms.
• Prolongation of the sick role – for secondary gain.
SOMATOFORM DISORDERS
SOMATIZATION DISORDER
that the symptoms have no physical basis. If any physical disorders are present, they
are insufficient to explain the severity of symptoms or patient distress/preoccupation.
These people are extensive users of healthcare resources. For example, the manage-
ment cost of treating chronic pelvic pain accounts for 0.6 per cent of UK health
expenditure. Claims of gastrointestinal, dermatological, sexual or menstrual symp-
toms are most common.
Prevalence rates vary. ECA reports 0.03–0.4 per cent (Escobar et al., 1987); approx-
imately 10 per cent rate in medical outpatients. The male:female ratio is 1:20.
There is a familial component. Between 10 and 20 per cent of first-degree female
relatives are somatizers. First-degree male relatives are prone to substance abuse, anti-
social personality disorder.
It is associated with other psychiatric disorders: depression, substance abuse, anti-
social and histrionic personality disorder.
MANAGEMENT
• It is a chronic disorder with a fluctuating course.
• Establish the absence of an underlying physical cause.
• Limit ‘window-shopping’ for doctors.
• Supportive psychotherapy is helpful.
• Pharmacotherapy is indicated for secondary complications (e.g. anxiety, depres-
sion) but has limited use otherwise (especially benzodiazepines because of poten-
tial for abuse).
CONVERSION DISORDER
There is loss of motor or sensory function without an identifiable physical cause. Both
primary and secondary gain encourage the persistence of the symptoms.
‘Classic’ conversion symptoms are those that suggest neurological disease, such as
paralysis, aphonia, convulsions, coordination disturbances, etc. Vomiting as a conver-
sion symptom may represent revulsion or disgust. Pseudocyesis (false pregnancy) may
represent both a wish for, and fear of, pregnancy.
Conversion symptoms can complicate true organic disease: Slater (1965) followed up
85 patients diagnosed as hysterical, after 9 years. One-third were found to have developed
organic disease not initially detected, but probably having played a part in initial symp-
toms; 12 patients had died, of whom 3 had symptoms which could account for the previ-
ous ‘hysterical’ symptoms. Of 33 patients who had no significant organic disease, 13 had
developed significant psychiatric illness.
Conversion symptoms may be distinguished from organic symptoms by:
• Their variability.
• A typical nature, often reflecting a patient’s concept of the disability.
• Inconsistency (e.g. apparently paralysed muscles may show synergistic power).
EPIDEMIOLOGY
There is no definite information on age. Female:male ratio ⫽ 2–10:1. The condition
accounts for about 3–4 per cent all psychiatric consultations.
SOMATOFORM DISORDERS 199
The estimated annual incidence is 11–22 cases per 100 000. Lower socioeconomic
groups may be most affected (Stefansson).
AETIOLOGY
Genetics
There is an incidence among first-degree relatives of about 5 per cent (lower in
fathers, higher in mothers and daughters). This level most likely reflects family
learning. There is some evidence of monozygotic twin-pair concordance, but not
dizygotic.
Psychophysiological aspects
Evoked responses in patients with hysterical anaesthesias suggest two underlying
mechanisms:
• A lowering of peripheral receptor sensitivity.
• A central mechanism of inhibition along different pathways.
Psychoanalytic aspects
Repressed anxiety leads to hysterical symptoms, often having symbolic meaning and
secondary gain. ‘Direct coping’ with conflict is avoided. Unresolved oedipal conflicts
are often a prominent source of anxiety.
Psychological/social aspects
Both primary and secondary gain encourage the persistence of the symptoms.
Hysterical symptoms have been viewed (Pilowsky) as a form of non-verbal communi-
cation in the doctor–patient relationship. (May particularly apply to those less
effective in verbal communication, e.g. those perceiving themselves in a dependent
inferior role.)
TREATMENT
• Explain and reassure as to nature of the symptom.
• Investigate as far as necessary to exclude organic cause, not merely as a method of
reassurance.
• Detect and treat associated emotional disorder, psychotherapy.
• Interviewing with sodium amytal administration is sometimes useful diagnos-
tically as well as therapeutically.
200 PSYCHOPHYSIOLOGICAL, SOMATOFORM, DISSOCIATIVE AND RELATED DISORDERS
PAIN DISORDER
This is defined as the complaint of pain in the absence of adequate physical findings and
in association with evidence of the aetiological role of psychological factors. Common
sites are head and neck, abdomen, lower back and genitals.
Patients may be any age, peaking around middle age. It is more common in women.
The course is variable and depends on reinforcement factors, including
secondary gain.
CLINICAL FEATURES
• Inconsistent with anatomical distribution of the nervous system.
• Continuous over long periods by day.
• May prevent getting off to sleep but not cause wakening.
• May have symbolic significance; e.g. chest pain where father died of a heart attack.
• Insight into role of psychological factors is often restricted.
• Responds better to psychotropics than analgesics.
HYPOCHONDRIASIS
It is more common in men, young and old, in lower socioeconomic classes and
those closely associated with disease.
MANAGEMENT
• Exclude organic pathology.
• If secondary to primary illness (e.g. depression), treat this. Hypochondriacal
symptoms may then fade.
• If primary:
– Follow firm policy regarding further investigations.
– Educate over role of psychological factors in symptoms. Avoid equation of psy-
chological with ‘faking’. Use cognitive and distraction techniques.
– Search for meaning of symptoms in the social/family setting, where appropriate.
– Exercise caution where symptoms serve a powerful defensive purpose.
– Some advocate a trial of tricyclics in all patients.
PROGNOSIS
The outcome is variable, but poor in more chronic and established cases. Those asso-
ciated with depressive illness or anxiety disorder have better prognosis.
EPIDEMIOLOGY
The prevalence is between 0.7 and 2.3 per cent in the general population, 11.9 per cent
in a dermatology setting (Phillips et al., 2000). There is a wide range of sex ratios, but
probably M ⫽ F. Seventy-five per cent have never been married.
TREATMENT
The condition is often chronic and difficult to treat. BDD is thought by some to be a
type of obsessive–compulsive disorder and treatment is similar. When patients agree
to psychopharmacological treatment, improvement is seen with SSRI or SRI therapy.
Cognitive–behavioural therapy has also been shown to help.
DISSOCIATIVE DISORDERS
Dissociative fugue
Like dissociative amnesia, there is a sudden alteration in memory, especially import-
ant personal information, which is also accompanied by unexpected travel away from
the person’s usual setting.
It is important to distinguish dissociative fugue from fugue states that may occur
after head injury, in epilepsy, during depressive illness and in the context of heavy
drinking (alcohol amnesic episodes). Often it is difficult to decide whether a fugue is
an act of malingering or genuinely beyond the patient’s control.
Depersonalization disorder
This is characterized by periods of feeling detached from one’s own body, identity or
mental processes.
MANAGEMENT
• Rule out any medical cause for the symptoms.
• In a supportive therapeutic relationship, memory usually returns with dissociative
amnesia and dissociative fugue. With DID, long-term therapy is usually needed.
• Most dissociative disorders are not responsive to medications. With depersonaliza-
tion disorder, SSRIs may be helpful.
REFERENCES AND FURTHER READING 203
This is severe, disabling fatigue of uncertain aetiology associated with a variable extent
of somatic and/or neuropsychiatric symptoms. Presentation is between ages 20 and
50 years, and females predominate.
The prevalence is 7.4 per 100 000. There is no clear association with socioeconomic
status.
AETIOLOGY
Patarca (2001) postulates immune dysfunction along with psychological vulnerability,
but the evidence is inconclusive. There are immunological abnormalities, especially
cell-mediated. T-lymphocyte mechanisms are common, but their significance is
unclear.
There is a high prevalence (⬎60 per cent) of antecedent/lifetime psychiatric illness,
especially minor depression, anxiety and somatization.
MANAGEMENT
• Cognitive–behavioural therapy has been beneficial (Whiting et al., 2001).
• There is no effective medical treatment. Medications are given for symptomatic
treatment – antidepressants, analgesics. Non-steroidal anti-inflammatory agents
are ineffective.
Barsky AJ, Ahern DK, Bailey ED et al. (2001) Hypochondriacal patients’ appraisal of health and
physical risks. Am. J. Psychiatry 158, 783.
Barsky AJ, Fama JM, Bailey ED, Ahern DK (1998) A prospective 4- to 5-year study of DSM-III-R
hypochondriasis. Arch Gen Psychiatry 55, 737.
Blumenthal JA, Lett HS, Babyak MA et al. (2003) Depression as a risk factor for mortality after
coronary artery bypass surgery. Lancet 362, 604.
Breitbart W, Gibson C, Tremblay A (2002) The delirium experience: delirium recall and delirium-
related distress in hospitalized patients with cancer, their spouses/caregivers, and their
nurses. Psychosomatics 43, 183.
Carson AJ, Best S, Postma K et al. (2003) The outcome of neurology outpatients with medically
unexplained symptoms: a prospective cohort study. J. Neurol Neurosurg Psychiatry 74, 897.
Crimlisk HL, Bhatia K, Cope H et al. (1998) Slater revisited: 6-year follow-up study of patients
with medically unexplained motor symptoms. BMJ 316, 582.
Escobar JI, Burnam MA, Karno M et al. (1987) Somatization in the community. Arch. Gen.
Psychiatry 44, 713.
Hickie I, Davenport T, Issakidis C, Andrews G (2002) Neurasthenia: prevalence, disability and
health care characteristics in the Australian community. Br. J. Psychiatry 181, 56.
Hollander E, Neville D, Frenkel M et al. (1992) Body dysmorphic disorder: diagnostic issues and
related disorders. Am. J. Psychiatry 33, 156.
Horwitz BJ, Fisher RS (2001) Current concepts. The irritable bowel syndrome. New Engl. J. Med.
344, 1846.
204 PSYCHOPHYSIOLOGICAL, SOMATOFORM, DISSOCIATIVE AND RELATED DISORDERS
Jiang W, Babyak MA, Ronzanski A et al. (2003) Depression and increased myocardial ischemic
activity in patients with ischemic heart disease. Am. Heart J. 146, 55.
Kornfeld DS (2002) Consultation–liaison psychiatry: contributions to medical practice. Am. J.
Psychiatry 159, 1964.
Lipowski ZJ (1988) Somatization: the concept and its clinical applications. Am. J. Psychiatry
145, 1358.
Martin JB (2002) The integration of neurology, psychiatry, and neuroscience in the 21st century.
Am. J. Psychiatry 159, 695.
Medical Journal of Australia (2002) Clinical practice guidelines. Chronic fatigue syndrome. Med.
J. Aust. 176, s23.
Mehendale AW (2002) Fibromyalgia syndrome, idiopathic widespread persistent pain or syn-
drome of myalgic encephalomyelopathy (SME): what is its nature? Pain. Prac. 2, 35.
Musselman DL, Tomer A, Manatunga AK et al. (1996) Exaggerated platelet reactivity in major
depression. Am. J. Psychiatry 153, 1313.
Ness DE (2002) Discussing treatment options and risks with medical patients who have psychi-
atric problems. Arch Intern. Med. 162, 2097.
Nimnuan C, Rabe-Hesketh S et al. (2001) How many functional syndromes? J. Psychosom. Res.
51, 549.
Patarca R (2001) Cytokines and chronic fatigue syndrome. Ann. NY Acad. Sci. 933, 185.
Phillips KA, Dufresne RG (2002) Body dysmorphic disorder: a guide for primary care physicians.
Prim. Care 29, 99.
Phillips KA, Dufresne RG, Wilkel C et al. (2000) Rate of body dysmorphic disorder in dermatol-
ogy patients. J. Am. Acad. Dermatol. 42, 436.
Richards SC, Scott DL (2002) Prescribed exercise in people with fibromyalgia: parallel group
randomised controlled trial. BMJ 325, 185.
Roelofs K, Keijsers PJ et al. (2002) Childhood abuse in patients with conversion disorder. Am.
J. Psychiatry 159,1908.
Slater E (1965) The diagnosis of hysteria. BMJ 1, 1395.
Spiegel D (2001) Mind matters: coping and cancer progression. J. Psychosom. Res. 50, 287.
Van der Pompe G, Antoni MM, Duivenvoorden HJ et al. (2001) An exploratory study into the
effect of group psychotherapy on cardiovascular and immunoreactivity to acute stress in
breast cancer patients. Psychother. Psychosom. 70, 307.
Wessely S, Pariante C (2002) Fatigue, depression and chronic hepatitis C infection. Psychol.
Med. 32, 1.
Whiting P, Bagnall AM, Sowden AJ et al. (2001) Interventions for the treatment and management
of chronic fatigue syndrome: a systematic review. JAMA 286, 1360.
Wise MG, Rundell JR (2002) Textbook of Consultation–Liaison Psychiatry: Psychiatry in the
Medically Ill, 2nd edn. American Psychiatric Press, Washington, DC.
Yudofsky SC, Hales RE (2002) Neuropsychiatry and the future of psychiatry and neurology. Am.
J. Psychiatry 159, 1261.
Psychogeriatrics 17
PSYCHIATRIC DISORDER
EPIDEMIOLOGY
• In 2000, 15.6 per cent of the population of the UK was over 65 years of age, and is
projected to be 20.4 per cent in 2025.
• In 2000, 12.4 per cent of the population of the USA was over 65 years of age, and is
projected to be 18.2 per cent in 2025.
• 45 per cent aged over 65 live alone in the USA.
• About a 25 per cent increase in the population over 75 years of age is expected by
the year 2025 in both the USA and the UK.
• Over one-quarter of the elderly have a mental disorder (16 per cent with a psychi-
atric disorder and 10 per cent with dementia). This number is expected to increase
as the proportion of population over 65 years increases (Jeste et al., 1999; see also
Table 17.1).
AFFECTIVE DISORDER
EPIDEMIOLOGY
• First admissions for affective disorders fall over 65 years, although inception rates
for depressive psychosis in elderly men remain high.
AETIOLOGICAL FACTORS
An increased prevalence is seen if:
• Female.
• Past psychiatric history – depressive or neurotic disorder.
• ‘Personality deviation’.
• Social isolation.
• Presence of physical ill-health.
• Early loss of parent.
• Smoking.
• Lack of satisfaction with life, loneliness.
Genetic factors
There is much less evidence of familial incidence in late-onset (over 50) compared
with early-onset (before age 40) depression. The risk of affective illness in relatives
decreases with increasing age of the proband.
Organic factors
No aetiological connection with senile dementia has been confirmed, although
depressive features may be a reaction to early dementia.
Cerebrovascular disease may act as a precipitant of depression, but depressed
patients may show increased incidence of cerebrovascular disease at follow-up.
Depression may include a subgroup who have delayed auditory-evoked responses,
evidence of ventricular dilatation on CT scan, more white matter hyperintensities on
MRI, and a higher mortality rate than other depressives. In some cases depression may
be a symptom of ‘general systems failure’.
Causes of symptomatic depression include antihypertensive drugs, myxoedema,
and potassium deficiency (see Chapter 4).
Environmental factors
It is widely held that environmental factors (bereavements, retirement, deprivation)
are aetiological factors, yet there is little proof of causal relationships. A significant
excess of losses in late-onset depression compared with early-onset has not been
demonstrated.
In the year following the death of a spouse there is increased incidence of suicide,
death and psychiatric referral, but most elderly people adapt to the loss well: 16 per
cent are still depressed at 13 months (Zisook and Shuchter, 1993). Prolonged grief
AFFECTIVE DISORDER 207
reaction is seen more commonly in the socially isolated, the poor and those with little
experience of death in earlier life.
Personality factors
Unipolar neurotic depression may be related to obsessional premorbid personality.
Psychotic depression is less clearly related to this personality type.
CLINICAL FEATURES
Agitation is much more common than retardation. The condition is often accompan-
ied by:
• Histrionic, importunate behaviour.
• Hypochondriacal preoccupations or delusions.
• Delusions of guilt, poverty, nihilism, persecution.
• Pseudodementia – with a tendency to answer ‘Don’t know’ rather than confabulate.
Suicide is a particular danger in elderly depressed, socially isolated men (see Chapter 11).
There is little evidence for a distinction between ‘reactive’ and ‘endogenous’ groups.
Indeed, many with clear reactive features have marked ‘endogenous’ symptoms.
Depression in the elderly is divided into:
• Agitated depression – characterized by apparently shallow affect, bizarre delusions,
importunate behaviour, somatic interpretations of anxiety and a high risk of suicide.
• Senile melancholia – severe agitated depression with delusions of nihilism, guilt,
grandiosity and hypochondriasis.
• Organic depression – depressive disorder precipitated or exposed by cerebral dis-
ease in a predisposed person.
• Depressive pseudodementia – depressive illness with perplexity, loss of interest, loss
of concentration and low self-esteem, leading to approximate answers or lack of
answers and the appearance of impaired awareness and memory. It is character-
ized by relatively acute onset, prominent complaints of cognitive difficulty, com-
munication of distress, patchy deficits, inattention, mental slowing and absence of
focal signs. Abreaction or sleep deprivation may clarify the diagnosis.
• Masked depression – depression expressed as physical symptoms or worsening of
longstanding neurotic symptoms. There is little apparent depressive affect but
many somatic symptoms of depression (anorexia, sleep disturbance, poor concen-
tration, etc.).
This may be a useful descriptive classification but it does not carry aetiological
implications.
Apathetic depression is also seen, in which self-neglect, loss of interest and social
withdrawal are marked features.
Manic–depressive psychosis
• Very rarely presents initially at ages over 65 years (Young, 1992).
• 5 per cent of affective episodes in over-65s are diagnosed as mania or hypomania.
Mixed affective states are more common.
• Hypomania in the elderly is characterized by:
– Irritability.
– Garrulousness, anecdotal speech with little flight of ideas.
208 PSYCHOGERIATRICS
MANAGEMENT
Hospital admission is necessary if the patient is agitated and a suicide risk. Make a full
assessment of social factors, isolation, housing, family support. Investigate and treat
any intercurrent physical illness which may form a focus of distress as well as a pos-
sible aetiological factor.
Drug treatment
Response to SSRI antidepressants is often very effective for the depression. Lower
dosages and careful timing of doses may be indicated. Introduction of medication
should be careful and increase should be gradual. Explanation and reassurance are
especially necessary.
Delusional depression does not respond well to SSRI therapy and usually requires
additional antipsychotic therapy.
Social therapies
Rehabilitation measures are vital in all cases. Occupational therapy, home assessment,
improvement of social support and development of ‘second careers’ are all of great
importance. Support of the family and reassurance and discussion with them is neces-
sary. Slow discharge with increasing periods at home to build confidence is indicated.
Day hospital, day centre or residential home supervision may be indicated.
PROGNOSIS
Overall, there is a similar pattern to depression in younger patients.
• 88 per cent are discharged from hospital, but only 30 per cent remain symptom-
free for 6 years.
• 17 per cent remain chronically depressed; i.e. initial prognosis is good but relapse
rate is high.
• 30 per cent die within 6 years.
Poor prognosis indicators are:
PARANOID SYNDROMES
There is much debate concerning the relationship between pure paranoid psychosis
and schizophrenia. Paranoid psychoses developing in late life may be distinguishable
from paranoid schizophrenia and are often called ‘paraphrenias’.
EPIDEMIOLOGY
• 4 per cent of schizophrenic disorders in men and 14 per cent in women arise after
age 65.
• 5.6 per cent of all psychiatric first admissions after age 65 are for paranoid
psychosis.
• Prevalence – 0.2–0.3 per cent of the population aged over 65 are affected. It is more
common in females.
AETIOLOGY
Genetics
There is an increased risk of schizophrenia in relatives of late paraphrenics when com-
pared with the general population, but a reduced risk compared with early-onset
schizophrenia.
There is an increased incidence of personality disorder in families, but not of
manic–depressive psychosis.
Sensory defects
Between 30 and 40 per cent of paranoid psychotics have impaired hearing. There is an
increased prevalence of visual defects also.
Organic causes
Cerebral lesions, especially of temporal lobe and diencephalon, are more common
(e.g. cerebrovascular disease). Other physical disorders may present with para-
noia; e.g. Parkinson’s disease, Huntington’s chorea and other dementias, metabolic
disorders.
Personality features
• Sufferers are often withdrawn and suspicious, with sensitive premorbid personality –
paranoid or schizoid type.
• Occasionally there is a history of schizophreniform illness in earlier life with per-
sonality defect since then.
• Patients are socially isolated, usually unmarried. They frequently live in self-
created social isolation.
• They are said to have been cold, unloving parents.
Environmental factors
Factors which appear to be precipitants are often merely uncovering pre-existing
psychosis. The condition occasionally does seem to be precipitated by life events.
There may be a sudden paranoid reaction to stress in a sensitive personality.
210 PSYCHOGERIATRICS
CLINICAL FEATURES
• Usually, there is insidious onset of increasingly secluded, isolated and suspicious
personality with episodes of bizarre behaviour, abuse of neighbours, self-neglect,
complaints to police, suicide attempt, etc.
• Often, once recognized, a well-organized paranoid delusional system is found to be
present. This often concerns plots to kill the patient, who may feel hypnotized,
drugged, spied upon and show other passivity phenomena.
• Hallucinations may not be present or may be bizarre (e.g. taste or smell of poison,
gases, etc.).
• Mood is often congruous, may be angry and excited or fearful and depressed.
Seventy per cent of paranoid patients appear depressed.
• Personality is frequently well preserved.
Differential diagnosis
• Depression – especially if associated with ideas of guilt and retribution.
• Organic cerebral disease – especially if associated with marked misinterpretations,
lack of systematized delusions and visual hallucinations.
PROGNOSIS
The natural course is of chronic illness with only minor fluctuations in intensity. The
person may become mute, withdrawn, flat, characterless.
With treatment the illness usually becomes less florid, though the delusional system
is often maintained, but may not interfere with life.
• Best prognosis – short duration of illness, good initial response.
• Worse prognosis – severe personality difficulties, deafness, cerebrovascular disease,
non-compliance with medication.
TREATMENT
• Investigate and treat any intercurrent physical illness which may be an aetiological
factor.
• Hospital admission may be necessary if the patient is disorganized, lacks capacity
of self-care, or is at risk for harm to self or others.
• Antipsychotics, atypicals have a lower side-effect burden and require lower
doses.
• Consider cognitive–behavioral therapy or supportive psychosocial therapy.
• Social/environmental assessment is required.
• Modify the environment where necessary.
• Provide education and support for the care-giver.
DEMENTIA
PRINCIPLES
Family support is the most important factor here, and families must themselves be
supported, with their problems explained and discussed. High rates of physical and
psychiatric illness occur among carers.
Maximize home support with community nurses, social workers, practical help
(meals on wheels, home helps, laundry service, attendance allowance) and ensure correct
accommodation (warden-controlled flats, residential home, etc.). However, when
dementia patients cannot be managed on their own at home, support in this circum-
stance paradoxically accelerates institutionalization (O’Connor et al., 1990).
Outpatient clinic support of patient and relatives may be very helpful. Day hospital,
day centre or luncheon club attendance is beneficial. The day hospital needs to have a
high staff/patient ratio and multidisciplinary input. However, cost-effectiveness is
somewhat disputed.
Admission to a short-stay psychogeriatric unit for full physical, psychological and
mental state assessment may be indicated.
TREATMENT POSSIBILITIES
Use of drugs
• Beware of overmedication or undertreatment.
• Assess the physical condition (heart, lungs, kidneys, liver) and presence of other
drugs (including alcohol).
• Treat with the lowest effective dose.
• Use a limited range of familiar drugs.
• Introduce medication slowly and carefully, to avoid side-effects and to increase
compliance. Assess with plasma drug levels if available.
• If at home, give small quantities with each prescription and supply large written
instructions.
• Explain the treatment to the patient and carers and involve relatives as appropriate.
212 PSYCHOGERIATRICS
Use of psychotherapy
• The person may need longer-term therapy, but with shorter individual sessions
than for younger age-groups.
• Cognitive–behavioural therapy is effective in the elderly.
• There is an increased need for support and encouragement, attention to self-
esteem and practical issues.
Inpatient issues
Aim for a high staff/patient ratio. Build and maintain morale and interest in the unit.
Treat patients with respect, and avoid institutionalization.
Administration on Aging (2001) Older Adults and Mental Health Issues and Opportunities.
Department of Health and Human Services, Rockville, MD.
Beekman ATF, Geerlings SW, Deeg DJH, Smit JH et al. (2002) The natural history of late-life
depression. Arch. Gen. Psychiatry 59, 605.
REFERENCES AND FURTHER READING 213
Benbow SM, Jolley D (2002) Home assessments in old age psychiatry. Adv. Psychiatr. Treat. 8, 316.
Blazer DG (2003) Depression in late life: review and commentary. J. Gerontol. A. Biol. Sci. Med.
Sci. 58, 249.
Bouman WP, Pinner G (2002) Use of atypical antipsychotic drugs in old age psychiatry. Adv.
Psychiatr. Treat. 8, 49.
Brodaty H, Sachdev P, Koschera A et al. (2003) Long-term outcome of late-onset schizophrenia:
5-year follow-up study. Br. J. Psychiatry 183, 213.
Brown GK, Bruce ML, Pearson JL et al. (2001) High risk management guidelines for elderly with
suicidal patients in primary care settings. Int. J. Geriatr. Psychiatry 16, 593.
Bruce ML, McAvay GJ, Raue PJ et al. (2002) Major depression in elderly home health care
patients. Am J. Psychiatry 159, 1367.
Burns A, Dening T, Baldwin R (2001) Care of older people: mental health problems. BMJ
322, 789.
Burns A, Lawlor B, Craig S (2002) Rating scales in old age psychiatry. Br. J. Psychiatry 180, 161.
Cohen-Mansfield J (2001) Nonpharmacologic interventions for inappropriate behaviors in
dementia. Am. J. Geriatr. Psychiatry 9, 361.
Dewey ME, Saz P (2001) Dementia, cognitive impairment and mortality in personas aged 65 and
over living in the community: a systematic review of the literature. Int. J. Geriatr. Psychiatry
16, 751.
Evans M, Mottram P (2000) Diagnosis of depression in elderly patients. Adv. Psychiatr. Treat.
6, 49.
Furniss L (2002) Use of medicines in nursing homes for older people. Adv. Psychiatr. Treat. 8, 198.
Geller B, Craney JL, Bolhofner K et al. (2002) Two-year prospective follow-up of children with a
prepubertal and early adolescent bipolar disorder phenotype. Am. J. Psychiatry 159, 927.
Hybels CF, Blazer DG (2003) Epidemiology of late-life mental disorders. Clin. Geriatr. Med. 19, 663.
Jeste DV, Alexopoulos GS, Bartels SJ et al. (1999) Consensus Statement on the Upcoming Crisis in
Geriatric Mental Health: research agenda for the next 2 decades. Arch. Gen. Psychiatry 56, 848.
Kawas CH, Brookmeyer R (2001) Aging and the public health effects of dementia. New Engl. J.
Med. 344, 1160.
Lawlor B (2002) Managing behavioural and psychological symptoms in dementia. Br. J.
Psychiatry 181, 463.
Lenze EJ, Dew MA, Mazumdar S, Begley AE (2002) Combined pharmacotherapy and psychotherapy
as maintenance treatment for late-life depression: effects on social adjustment. Am. J. Psychiatry
159, 466.
Mather AS, Rodriguez C, Guthrie MF et al. (2002) Effects of exercise on depressive symptoms in
older adults with poorly responsive depressive disorder: randomised controlled trail. Br. J.
Psychiatry 180, 411.
Nebes RD, Vora IJ, Meltzer CC et al. (2001) Relationships of deep white matter hyperintensities
and apolipoprotein E genotype to depressive symptoms in older adults without clinical
depression. Am. J. Psychiatry 158, 878.
O’Connor DW, Pollitt PA, Roth M et al. (1990) Problems reported by relatives in a community
sample of dementia. Br. J. Psychiatry 156, 835.
Olin JT, Katz IR, Meyers BS et al. (2002) Provisional diagnostic criteria for depression of
Alzheimer disease. Am J. Geriatr. Psychiatry 10, 129.
Ormel J, Oldehinkel AJ, Brilman E et al. (2001) The interplay and etiological continuity of neur-
oticism, difficulties, and life events in the etiology of major and subsyndromal, first and
recurrent depressive episodes in later life. Am. J. Psychiatry 158, 885.
Ostling S, Skoog I (2002) Psychotic symptoms and paranoid ideation in a nondemented population-
based sample of the very old. Arch. Gen. Psychiatry 59, 53.
Oyebode J (2003) Assessment of carer’s psychological needs. Adv. Psychiatr. Treat. 9, 45.
Richardson B, Orrell M (2002) Home assessments in old age psychiatry. Adv. Psychiatr. Treat. 8, 59.
214 PSYCHOGERIATRICS
Salib E, El-Nimr G (2003) Gender in elderly suicide: analysis of coroner’s requests of 200 cases of
elderly suicide in Cheshire 1989–2001. Int. J. Psychiatry Clin. Pract. 18, 1082.
Smith D, Dempster C, Glanville J et al. (2002) Efficacy and tolerability of venlafaxine compared
with selective serotonin reuptake inhibitors and other antidepressants: a meta-analysis. Br. J.
Psychiatry 180, 396.
Snowden J, Arie T (2002) Old age psychiatry services: long-stay care facilities in Australia and the
UK. Psychiatr. Bull. 26, 24.
Spector A, Thorgrimsen L, Woods B et al. (2003) Efficacy of an evidence-based cognitive stimu-
lation therapy programme for people with dementia: randomised controlled trail. Br. J.
Psychiatry 183, 248.
Unutzer J, Patrick DL, Marmon T, Simon GE, Katon WJ (2002) Depressive symptoms and mor-
tality in a prospective study of 2558 older adults. Am. J. Geriatr. Psychiatry 10, 521.
Waern M, Runeson BS, Allebeck P, Beskow J et al. (2002) Mental disorder in elderly suicides: a
case – control study. Am. J. Psychiatry 159, 450.
Whalley LJ (2002) Brain ageing and dementia: what makes the difference? Br. J. Psychiatry 181, 369.
Wilson KCM, Mottram PG, Ashworth L, Abousaley MT (2003) Older community residents with
depression. Long-term treatment with sertraline: a randomised, double-blind, placebo-
controlled study. Br. J. Psychiatry 182, 492.
Wolfson C, Wolfson DB, Asgharian M et al. (2001) A reevaluation of the duration of survival
after the onset of dementia. New Engl. J. Med. 344, 1111.
Young RC (1992) Geriatric mania. Clin. Geriatr. Med. 8, 387.
Zisook S, Schucter SR (1993) Uncomplicated bereavement. J. Clin. Psychiatry 54, 365.
Forensic psychiatry 18
HISTORICAL DEVELOPMENT
• Pinel (1801) – Manie sans délire:
– Disturbance of emotions and volition; reason intact.
• Rush (1812) – Moral derangement:
– Innate, constitutional moral depravity, amenable to medical treatment.
• Pritchard (1835) – Moral insanity:
– Intellectually unimpaired, but affective and moral faculties disturbed.
• Koch (1891) – Psychopathic inferiority:
– Constitutional predisposition to mental disturbances of all kinds.
EPIDEMIOLOGY
There is a 2–3 per cent lifetime prevalence in Western societies (Coid, 2003a). Males
are more affected than females (ratio 5:1), and urban dwellers more than rural.
Highest rates are in 25- to 44-year-olds.
AETIOLOGY
Organic causes
• Twin studies – MZ:DZ concordance ⫽ 60%:30%.
• Adoption studies confirm a genetic component.
• There is an excess of obstetric complications, minor physical anomalies,
neuropsychological impairments – a form of minimal brain damage or
dysmaturation?
• EEG abnormalities:
– Generalized slow-wave abnormalities (but normal in 50 per cent of aggressive
criminals) which may be localized to the temporal region.
– Posterior slow and sharp waves.
– Immature ‘EEG’.
• Corpus callosum abnormalities may reflect atypical neurodevelopmental
pressesses and help explain abnormal interhemispheric transfer seen in psycho-
pathic individuals (Raine et al., 2003).
• Low serotonin is found in impulse disorders/ASP.
VIOLENCE IN THE CONTEXT OF MENTAL ILLNESS 217
Sociocultural factors
• Lower socioeconomic status families, single/divorced parents.
• History of parental sociopathy.
• Physical/sexual abuse.
Psychodynamic factors
Interference with early bonding may result in defective socialization and immaturity
of emotional and moral development. Defective superego development may result in:
• Abnormal, stereotyped antisocial behaviour under stress.
• Excessive anxiety at any perceived threat, so that all anxiety is ignored and there is
a lack of anxiety to reinforce morality.
• Failure to acquire social behaviour at critical learning periods.
MANAGEMENT
Primary prevention
• Prenatal care can lessen intrauterine insults to the brain.
• Parenting classes can establish a nurturing environment in infancy as well as effect-
ive parenting styles.
• Early identification of at-risk children (i.e. conduct disorder) can lead to interven-
tion in the home or at school.
Active management
• Pharmacological – control of aggressive and sexual impulses; treatment of
co-morbid illness (depression, DSH, substance abuse).
• Psychological:
– Supportive psychotherapy; advice to help avoid stressful situations; environ-
mental manipulation.
– Cognitive–behavioural therapy to heighten awareness of consequences of
behaviour; reshape to appropriate behaviour.
Hospitalization
Psychiatric hospitalization is of little benefit. More appropriate is a specialized inpa-
tient or day care unit. A therapeutic prison (e.g. Grendon Underwood, UK) may be
effective for aggressive psychopaths.
Incarceration limits damage to society by the offender.
PROGNOSIS
The more numerous the risk factors in early life, the greater likelihood of antisocial
personality developing. ‘Protective factors’ may offset risk factors; i.e. positive social
orientation, good family support system, structure and rules in the household.
Patients may become less aggressive and antisocial in later life. They tend to become
depressed and self-blaming later. There is an increased incidence of alcoholism and
suicide.
The relationship between violence and mental illness is poorly understood and
overestimated by the public and media. In societies, violent behaviour is the result of
218 FORENSIC PSYCHIATRY
PATIENT ASSESSMENT
• May depend on type and quality of violence. Aggressive sex offenders and the
morbidly jealous are particularly liable to reoffend with violence. Threats of vio-
lence and frequent violence when drunk may indicate further danger. Repeated
violence implies further violence.
• May depend on environmental factors – if stress remains or if potential victims are
still available.
• Disinhibiting factors (e.g. alcohol, drugs, fatigue) which may occur must be
assessed.
• Lack of remorse may indicate increased dangerousness.
• Widespread aggressive behaviour appearing at an early age (arson, cruelty to ani-
mals) and continuing, especially if also present in the family, indicates recurrence.
• Fear engendered in the examiner may well indicate dangerousness.
• Regressive, infantile behaviour during and after an offence may indicate
dangerousness.
• Sadistic fantasy life is an ominous finding.
KILLING
DEFINITIONS
EPIDEMIOLOGY
• 500 per year in England and Wales.
• Murderers have a male:female ratio of 11:1.
• 75 per cent of victims have a previous relationship with their murderer.
• 50 per cent of victims are a relative or lover.
• In the USA, homicide is the 11th most common cause of death.
• Up to 30 per cent of homicide suspects kill themselves following murder (espe-
cially women).
• Alcohol is involved in up to 50 per cent of cases.
• 50 per cent of murderers are mentally abnormal – particularly with severe person-
ality disorder.
• Fewer than 1 per cent recommit murder.
220 FORENSIC PSYCHIATRY
Thus the most common combination of factors leading to murder are: an irritable
and violent husband, alcohol and family disharmony.
Sadistic murderers are described as: usually male, under 35, solitary, emotionally
blunted, reserved, with a rich fantasy life (fascism, black magic, sadistic pornography).
RAPE
DEFINITION
Rape is sexual intercourse (i.e. penetration) with a woman who does not consent, the man
knowing that she did not consent or being reckless as to whether or not she consented.
A CLASSIFICATION
• Aggressive aim – sexual assault is primarily destructive and sadistic. May be
displaced anger (e.g. to mother). May humiliate the victim.
• Sexual aim – aggression with the aim of achieving sexual intercourse. Part of
general hedonism.
• Explosive – forcible expression of sexual drives in an over-controlled man. May
have compulsive quality.
• Aggressive and sexual aim – resistance and humiliation are essential for sexual
satisfaction.
EPIDEMIOLOGY
Most rapists are aged under 25 years, single, have a record of non-sexual crime and are
not mentally disordered. There is an increased incidence in summer, in the first half of
night and at weekends.
Thirty per cent of victims are neighbours or acquaintances. Twenty per cent of vic-
tims have a criminal record (especially soliciting).
OUTCOMES
• 80 per cent of rapists are sentenced to prison.
• 85 per cent of aggressive rapists later commit non-sexual crimes and 20 per cent
recommit sexual offences.
• 28 per cent of non-aggressive rapists later commit non-sexual crimes and 3
per cent recommit sexual offences.
ARSON
DEFINITION
Arson is to damage or destroy any property by fire, without lawful excuse.
A CLASSIFICATION
• Motivated arson:
– No psychotic disorder; insurance fraud, bankruptcy, revenge, political, to cover
up another crime, vagrant.
– Suicidal.
FEATURES OF VIOLENT CRIMES 221
EPIDEMIOLOGY
Arson accounts for 0.1 per cent of all serious crime (one-third the incidence of
murder or rape). There is a peak incidence at 17 years in men, at 45 years in women
(85 per cent of offenders are men). There is an increased incidence of mental retardation
(up to 50 per cent) and alcoholism.
OUTCOMES
• Fewer than 4 per cent repeat arson.
• There is an increased likelihood of recurrence with:
– History of previous arson.
– Presence of psychosis, severe abnormality or dementia.
– Marked pleasure or sexual excitement associated.
– Awareness by arsonist of overwhelming urge to start fires to relieve tension.
DEFINITIONS
• In 1962 Kempe introduced the term battered child syndrome to describe the signs
and symptoms characteristic of physical abuse.
• In 1972 Caffey introduced the term shaken baby syndrome to describe the signs and
symptoms of violent shaking of an infant that results in tearing of intracranial
veins with the degree of brain damage corresponding to the intensity of shaking.
• An overall definition is ‘the killing of, physical violence towards, persistent abuse of
or neglect of a child, by those in charge of the child’.
A CLASSIFICATION (SCOTT)
• Elimination – of an unwanted encumbrance.
• Euthanasia – mercy killing (e.g. of handicapped child).
• Psychotic – the result of delusions.
• Displaced anger – from elsewhere on to the child.
• Anger – arising from within the child–parent relationship.
222 FORENSIC PSYCHIATRY
EPIDEMIOLOGY
Possibly 0.5 per cent of children aged under 3 years are involved (considerable under-
reporting). Underweight and ill children are particularly likely to be battered.
• 1 in 1000 children aged under 4 years suffers major injury each year in England
and Wales.
• The death rate is 10 per cent in 2 years, and 25 per cent are intellectually damaged.
• 2–4 per cent of children are in subnormality hospitals.
• There is a 60 per cent chance of further battering.
• 19 per cent of siblings have also been battered.
PAEDOPHILIA
Paedophilia is the erotic attraction to children. There are three characteristic groups:
• Immature adolescents.
• Middle-aged men with marital difficulties.
• Elderly, socially isolated men.
Fifty per cent of perpetrators are relatives or friends. Once discovered, most do not
reoffend.
INCEST
There is a variable extent of sexual activity, from fondling to intercourse. In 75 per cent
cases it is between a father/stepfather and daughter.
Five per cent of the adult female population report being abused by their father.
Forty-four per cent of incest perpetrators have also committed extrafamilial offences.
Child sexual abuse is a general term that includes incest. A range of definitions results
in wide reported prevalence rates: 12–36 per cent of females and 3–29 per cent of
males report some sexual abuse in childhood.
CSA may occur at any age, but the peak occurrence is after age 12 years. The mean
duration of abuse before detection is 2 years.
Boys tend to be abused at an earlier age, and the offender is more likely to be a
stranger. Absence of one or both parents and the presence of a stepfather in the home
conveys greater risk of CSA.
Poverty is associated with greater reporting of CSA but not necessarily greater
incidence.
EVALUATION
• Attempt to confirm CSA.
• Many cases of ‘suspected abuse’ demonstrate incomplete evidence, and the family
declines investigation.
• Use of anatomical dolls is controversial. There is overlap in play behaviour of non-
abused and abused children, so this is not a good diagnostic tool.
• If CSA is confirmed in a minor, or strongly suspected by a health professional,
social services must by law be informed in the UK and USA.
• Children as witnesses – Younger children are suggestible; overall, children are com-
petent witnesses; most do not lie.
• Multidisciplinary evaluation – Legal involvement must be early on to protect the
child from ongoing CSA.
MANAGEMENT
This must be multimodal:
• Cognitive–behavioural therapy.
• Social skills education, stress management.
• Family intervention therapy, if appropriate.
• Legal action and a programme to prevent further CSA.
OUTCOMES
There is a drop-out rate of 18 per cent for incest families in therapy. However, with
therapy, 60 per cent of families are safe from further abusive behaviours.
Long-term sequelae for the abused child
Emotional: Anxiety/fear, low self-esteem, anger, guilt.
Psychiatric:
• Depression, deliberate self-harm.
• Personality disturbance (borderline, multiple personality).
• Substance abuse.
• PTSD symptoms.
• Eating disorders.
• Somatization.
Behavioural:
• Early sexual activity.
• Promiscuity, teenage prostitution.
• Adult sexual dysfunctional disorders.
EPIDEMIOLOGY
Figures in the early 1970s showed that most offenders were women. Ninety per cent
did not reoffend when caught. Fifteen per cent of British-born offenders showed a
psychiatric disorder.
Recent changes
• There has been an increase in young shoplifters (ages 10–18) – now the majority.
• There has also been an increase in male shoplifters – now the majority.
• The incidence of psychiatric disorder is reduced – now estimated at 5 per cent.
• The offence may be regarded by some as an ‘accepted perk’ of shopping.
Approximately 5 per cent shoplift at each shop they visit.
LEGAL ASPECTS
Plan of report
– Name, address and age of person charged.
– Charge.
– When and where interviewed.
– All other sources of information (notes, other doctors, relatives, etc.).
– Short description of person charged.
– Concise, relevant family history.
– Concise, relevant personal history.
– Past medical, psychiatric and criminal history.
– Brief account of circumstances of offence and any relevant psychiatric disturb-
ances, sources of tension, etc.
– Findings at interview, including assessment of personality.
– Findings of further investigations (EEG, psychological testing, etc.).
– Opinion – All the above information is merely an explanation of the basis of the
opinion. Comment on fitness to plead, responsibility for offence, mitigating fac-
tors, prognosis.
– Recommendations – for treatment and further management, if appropriate.
– Psychiatrist’s name, qualifications, professional address and approval under the
Mental Health Act.
Aim at accuracy, understandability, relevance and impartiality.
Diminished responsibility
This defence can be used only if the charge is murder. If found, it reduces the charge of
murder (carrying a mandatory life sentence) to manslaughter (sentencing at the dis-
cretion of the judge).
The defendant must be suffering from ‘such abnormality of mind … as substantially
to impair his mental responsibility for his acts’. ‘Abnormality of mind’ is a state of mind
so different from that of ordinary human beings that the reasonable person would term
it abnormal. It could include severe personality disorder, extreme intoxication, etc.
Possible results at sentencing
• The law takes its normal course – prison, fine, etc.
• Conditional or absolute discharge – possibly with voluntary psychiatric treatment.
• Probation order, under Powers of Criminal Courts Act 1973. An approved psych-
iatrist (s.12 of the Mental Health Act) takes on the responsibility for treatment, as
an inpatient or outpatient. The offender must agree to this.
• Detention in hospital under s.60 of the Mental Health Act, with or without s.65.
• Offenders aged under 17 years may be committed to the care of the local authority.
CRIMINAL RESPONSIBILITY (APPLIES TO UK ONLY)
AGE
• A child under 10 years is held to be incapable of forming a guilty intent (mens rea).
• A child of 10–13 years is so capable if he/she is able to discern good from evil.
• A child of 14 years and over is presumed to be fully responsible for his/her actions.
INTENT
Some offences require that specific guilty intent (mens rea) be proved present as well
as the unlawful act (actus reus) – e.g. murder, arson, rape, assault with intent to cause
grevious bodily harm.
Other offences do not require proof of guilty intent – e.g. manslaughter, indecent
assault, assault occasioning actual bodily harm.
LEGAL ASPECTS 227
Complicating factors
• Multiple intention.
• Unconscious intention.
• Changing intention during the crime.
• Overwhelming tension, stress or emotion.
• Amnesia, including that due to alcohol.
• Alien intention (as in schizophrenic passivity).
• Self-induced intoxication
Simple drunkenness is no defence. A person may not, however, be held to have com-
mitted a crime requiring mens rea if that person was too drunk to form an intent. The
person may, however, be held to have committed a crime not requiring proof of mens rea.
A person may make a will if he/she is ‘of sound disposing mind’ and:
1 Knows the nature and extent of his/her property.
2 Knows the persons having a claim on it and the relative strengths of their claims.
3 Can express himself/herself clearly and without ambiguity.
INFORMED CONSENT
Informed consent, which may be verbal or written, includes:
1 Disclosure of information.
2 Competency.
3 Understanding.
4 Voluntariness.
5 Decision.
COMPETENCY
Does the patient understand:
1 The condition for which treatment is proposed?
2 The nature and purpose of the treatment?
3 The risks and benefits of undergoing the treatment?
4 The risks and benefits of not undergoing the treatment?
NEGLIGENCE
Negligence results in unintentional wrong to a person. To be found it requires the Four D’s:
1 A duty to a client.
2 A dereliction (breach) of duty.
3 The breach is a direct cause of the damage.
4 Actual damages result from the breach of duty.
228 FORENSIC PSYCHIATRY
TARASOFF DOCTRINE
In the USA, courts have decided that a psychiatrist who knows or should know of a
patient’s dangerousness to a third person must take all reasonable steps to protect (not
just inform) potential victims.
INVOLUNTARY COMMITMENT
There is wide variation across countries and mental health systems on terms and pro-
cedures for commitment. Common elements include:
• Commitment due to the presence of mental disorder which poses grave and immi-
nent risk to self or others.
• Certification by a health professional (not exclusively by a psychiatrist).
• Limitation on duration of involuntary hold.
• A review process (tribunal, court, etc.) prior to the end of the time limitation,
linked to patient appeal process.
Commitment must be for a defined mental disorder. Sexual deviancy, immorality,
excesses of drugs/alcohol, violence (without mental disorder ⫽ legal problem) are not
mental disorders and reasons per se for commitment. Commitment represents a deli-
cate balance between the protection of society and protecting personal autonomy.
In some systems, commitment procedures allow containment only for assessment,
there being a separate (secondary) procedure for involuntary treatment. Most systems
invoke both assessment and treatment.
Most commitment statutes are for inpatient hospitalization, but there is a growing
trend towards outpatient commitment. The patient is ordered to follow a ‘community
treatment order’, or else revocation of community tenure with rehospitalization. This
is difficult to enforce and monitor.
New initiatives
There is a broad move to enhance appropriate diversion of mentally ill offenders into
mental heath care rather than jails. In a jail diversion programme, for example, mental
health professionals might be called out to assist police at the time of disturbance of
the peace due to a patient’s psychotic behavior; the patient receives hospitalization
rather than jail.
Mental health courts are another initiative.
Two types of directive are available to specify the wishes of an individual should
he/she no longer have the capacity to make decisions on his/her own behalf.
MANAGEMENT OF DANGEROUS MENTALLY DISTURBED PERSONS 229
AT A POLITICAL LEVEL
Possible policies
1 Mental hospitals should provide secure facilities on an area or regional basis; i.e. a
return to traditional roles.
2 There should be better provision for the mentally disturbed within prisons. This
requires a change of policy: prisons are for punishment, hospitals for treatment.
Grendon Underwood, for people with severe personality disorders, is the only such
prison in England and Wales.
– Between 20 and 40 per cent of prisoners are found to be psychiatrically disturbed
(2 per cent are psychotic, 11 per cent have alcohol and drug addictions, 14 per cent
are mentally handicapped), and the suicide rate is three times higher than normal.
In Western societies the size of the prison population is inversely related to the
size of the mental hospital population.
4 There needs to be more provision of special hospitals (e.g. Broadmoor, UK). But
these may be expensive, institutionalized and have difficulty discharging patients
because other hospitals will not accept them. They are part of the Health Service
and are under the direct control of the Secretary of State for Health.
5 There can be provision of regional secure units and, more recently advocated,
development of smaller, more widely distributed units: 1500 medium secure units
and 750 long-term medical secure beds are recommended for England and Wales
(Reed Report; UK Government, 1992).
230 FORENSIC PSYCHIATRY
AT WARD LEVEL
Architectural considerations
• Adequate but unobtrusive security.
• Ease of arousal of alarm.
• Available space for exercise, expression of anger, etc.
Staff policies
• Develop a clear violence-prevention policy of which all staff are aware.
• Adequate training of staff in coping with violent behaviour.
• Adequate numbers of staff (1:1 ratio) in units with violent patients.
• Acceptance of responsibility of dealing with violence by all staff, teamwork.
• Effective communication of dangers.
• Rapid availability of more staff and of medical staff.
Management of the violent incident
• Raise the alarm.
• Free any victim, remove weapons as soon as possible.
• Assess diagnosis (e.g. alcohol, psychosis).
• Remain calm and non-critical.
• Use minimum necessary force; avoid force if possible.
• ‘Talk patient down’ – done by the most skilled staff member or member most
trusted by the patient. Involves listening, agreeing, reassuring.
• If force is necessary, ensure adequate numbers of staff.
• If sedation is needed (IV or IM), use carefully. Can be given even to informal
patients in an emergency.
• Ensure adequate reporting and ward discussions afterwards.
LONG-TERM MANAGEMENT
Psychotherapy
• Detainees need a place to call at times of stress.
• There should be attention to self-esteem and masculinity.
• Exploration of violent fantasies in a controlled setting can be beneficial.
• Increase the patient’s understanding of feelings behind violence.
• Counselling and behavioural techniques may help the patient to avoid stressful
situations.
Drug therapy Numerous drugs are claimed to be anti-aggressive (Corrigan et al.,
1993): lithium, antipsychotics, valproate, carbamazepine. Use of benzodiazepines may
result in paradoxical aggression due to disinhibition.
American Psychiatric Association (2002) Psychiatric Services in Jails and Prisons: a Report of the
Task Force to Revise the APA Guidelines on Psychiatric Serviecs in Jails and Prisons. American
Psychiatric Association, Washington, DC.
Applebaum P (2001) Thinking carefully about outpatient commitment. Psychiatr. Serv. 52, 347.
Blair RJR (2003) Neurobiological basis of psychopathy. Br. J. Psychiatry 182, 5.
Bluglass R (1990) Forensic Psychiatry: a Comprehensive Textbook. Churchill Livingstone, Edinburgh.
REFERENCES AND FURTHER READING 231
Buchanan A, Leese M (2001) Detention of people with dangerous severe personality disorders:
a systematic review. Lancet 358, 1955.
Buckley PF, Noffsinger SG, Smith DA et al. (2003) Treatment of the psychotic patient who is violent.
Psychiatr. Clin. North Am. 26, 231.
Carpenter WT (1999) The challenge to psychiatry as society’s agent for mental illness treatment
and research. Am. J. Psychiatry 156, 1307.
Chen YH, Aria AM, Anthony JC (2003) Firesetting in adolescence and being aggressive, shy, and
rejected by peers: new epidemiologic evidence from a national sample survey. J. Am. Acad.
Psychiatry Law 31, 44.
Coid J (2003a) Epidemiology, public health and the problem of personality disorders. Br. J.
Psychiatry 182, s3.
Coid J (2003b) Formulating strategies for the primary prevention of adult antisocial behaviour:
‘high risk’ or ‘population’ strategies? In: Farrington DP, Coid JW (eds), Early Prevention of
Adult Antisocial Behaviour, pp. 32–78. Cambridge University Press, Cambridge.
Coid J, Petruckevitch A, Bebbington P et al. (2002a) Ethnic differences in prisoners. 1: Criminality
and psychiatric morbidity. Br. J. Psychiatry 181, 473.
Coid J, Petruckevitch A, Bebbington P et al. (2002b) Ethnic differences in prisoners. 2: Risk factors
and psychiatric service use. Br. J. Psychiatry 181, 481.
Corrigan PW, Yudovsky SC, Silver JM (1993) Pharmacological and behavioural treatments for
aggressive psychiatric patients. Hosp. Commun. Psychiatry 44, 125.
Cottle CC, Lee RJ, Heilbrun K (2001) The prediction of criminal recidivism in juveniles. Crim.
Just. Behav. 28, 367.
Dolan M, Millington J, Park I (2002) Personality and neuropsychological function in violent,
sexual and arson offenders. Med. Sci. Law 42, 34.
Earthrowl, M, O’Grady J, Birmingham L (2003) Providing treatment to prisoners with mental
disorders: development of a policy: selective literature review and expert consultation exer-
cise. Br. J. Psychiatry 182, 299.
Fazel S, Danesh J (2002) Serious mental disorders in 23,000 prisoners: a systematic review of 62
surveys. Lancet 349, 545.
Feeney A (2003) Dangerous severe personality disorder. Adv. Psychiatr. Treat 9, 349.
Gesch CB, Hammond SM et al. (2002) Influence of supplementary vitamins, minerals and essen-
tial fatty acids on the antisocial behaviour of young adult prisoners: randomised, placebo-
controlled trial. Br. J. Psychiatry 181, 22.
Glasser M, Campbell KD, Glasser A et al. (2001) Cycle of child sexual abuse: links between being
a victim and becoming a perpetrator. Br. J. Psychiatry 179, 482.
Gordon H, Grubin D (2004) Psychiatric aspects of the assessment and treatment of sex offend-
ers. Adv. Psychiatr. Treat. 10, 73.
Haque Q, Cumming I (2003) Intoxication and legal defences. Adv. Psychiatr. Treat 9, 144.
Harty MA, Thomas S, Parrot J (2001) HM prison healthcare needs assessment. J. Forens.
Psychiatry 12, 639.
Hawkins JD, Herrenkohl TI (2002) Prevention in the school years. In: Farrington DP, Coid JW
(eds), Early Prevention of Adult Antisocial Behaviour, pp. 265–291. Cambridge University
Press, Cambridge.
Herpertz SC, Wenning B, Mueller B et al. (2001) Psychophysiological responses in ADHS boys
with and without conduct disorder: implications for adult antisocial behavior. J. Am. Acad.
Child Adolesc. Psychiatry 40, 1222.
Hill J (2003) Early identification of individuals at risk for antisocial personality disorder. Br. J.
Psychiatry 182 (Suppl. 44), s11.
Hodgins S (1992) Mental disorder, intellectual deficiency, and crime: evidence from a birth
cohort. Arch. Gen. Psychiatry 49, 476.
Honberg RS (2003) Advance Directives. www.nami.org/Content/ContentGroups/Legal/
Advance_Directives.htm (accessed 28 December 2003).
232 FORENSIC PSYCHIATRY
Kennedy HG, Ivenson RC, Hill O (1999) Violence, homicide and suicide: strong correlation and
wide variation across districts. Br. J. Psychiatry 175, 462.
Lamb HR, Bachrach LL (2001) Some perspectives on deinstitutionalization. Psychiatr. Serv. 52, 1039.
Lane WG (2003) Diagnosis and management of physical abuse in children. Clin. Fam. Pract. 5, 493.
Litwack TR (2001) Actuarial versus clinical assessments of dangerousness. Psychol. Pub. Pol.
Law 7, 409.
Macpherson R, Cornelius F, Kilpatrick D, Blazey K (2002) Outcome of clinical risk management
in the Gloucester rehabilitation service. Psychiatr. Bull. 26, 449.
Monahan J, Bonnie RJ, Applebaum PS et al. (2001) Mandated community treatment: beyond
outpatient commitment. Psychiatr. Serv. 52, 1198.
Monahan J, Steadman H, Silver E et al. (2001) Rethinking risk assessment: the MacArthur study
of mental disorder and violence. Oxford University Press, New York.
Mowbray CT, Grazier KL, Holter M (2002) Managed behavioral health care in the public sector:
will it become the third shame of the States? Psychiatr. Serv. 53, 157.
Munro E, Rumgay J (2000) Role of risk assessment in reducing homicides by people with mental
illness. Br. J. Psychiatry 76, 116.
Nestor PG (2002) Mental disorder and violence: personality dimensions and clinical features.
Am. J. Psychiatry 159, 1973.
Putnam FW (2003) Ten-year research update review: child sexual abuse. J. Am. Acad. Child
Adolesc. Psychiatry 42, 269.
Raine A (2002) Biosocial studies of antisocial and violent behavior in children and adults: a
review. J. Abnorm. Child Psychol. 30, 311.
Raine A, Lentz T, Taylor K et al. (2003) Corpus callosum abnormalities in psychopathic antisocial
individuals. Arch. Gen. Psychiatry 60, 1134.
Ramchandani P, Jones DPH (2003) Treating psychological symptoms in sexually abused chil-
dren: from research findings to service provision. Br. J. Psychiatry 183, 484.
Reed J (2003) Mental health care in prisons. Br. J. Psychiatry 182, 287.
Roberts LW (2002) Informed consent and the capacity for voluntarism. Am J. Psychiatry 159, 233.
Rock M (2001) Emerging issues with mentally ill offenders: causes and social consequences.
Admin. Policy Ment. Health 28, 165.
Rutter M (2003) Causal processes leading to antisocial behaviour (commentary). Dev. Psychol. 39, 372.
Tardiff K (1992) The current state of psychiatry in the treatment of violent patients. Arch. Gen.
Psychiatry 49, 493.
Taylor JL, Thorne I, Robertson A, Avery G (2002) Evaluation of a group intervention for convicted
arsonists with mild and borderline intellectual disabilities. Crim. Behav. Ment. Health 12, 282.
Taylor PY, Leese M, Williams D et al. (1998) Mental disorder and violence. Br. J. Psychiatry 172, 218.
Tremblay RE, Japel C (2003) Prevention during preganancy, infancy and the preschool years. In:
Farrington DP, Coid JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 205–242.
Cambridge University Press, Cambridge.
Trowell J, Kolvin I, Weeramanthri H et al. (2002) Psychotherapy for sexually abused girls: psy-
chopathological outcome findings and patterns of change. Br. J. Psychiatry 180, 234.
UK Government (1992) Review of Health and Social Services for Mentally Disordered Offenders
and Others Requiring Similar Services (Reed Report). HMSO, London.
Uting D (2003) Prevention through family and parenting programmes. In: Farrington DP, Coid
JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 243–264. Cambridge University
Press, Cambridge.
Volavka J (2002) The Neurobiology of Violence. American Psychiatric Press, Washington, DC.
Walsh E, Buchanan A, Fahy T (2002) Violence and schizophrenia: examining the evidence. Br. J.
Psychiatry 180, 490.
Wasserman GA (2003) Mental health assessments in juvenile justice: report on the consensus
conference. J. Am. Acad. Child Adolesc. Psychiatry 42, 752.
Wettstein RM (2002) Ethics and forensic psychiatry. Psychiatr. Clin. North Am. 25, 623.
World Health Organization (2002) World Report on Violence and Health. WHO, Geneva.
Child psychiatry 19
OVERVIEW
EPIDEMIOLOGY
The Mental Health Evaluation and Community Consultation Unit at the University of
British Columbia (2002) reported on the prevalence of mental disorders in youth and
found a 15 per cent prevalence of any type of mental disorder. Of these, 6.5 per cent
had an anxiety disorder, 3.3 per cent conduct disorder, 3.3 per cent attention-
deficit/hyperactivity disorder (ADHD), 2.1 per cent depression.
TREATMENT CONSIDERATIONS
Psychopharmacology
• Research on psychopharmacology in the young is limited.
• There is frequent ‘off label’ use of prescribed medications, frequently treat target
symptoms.
• Appropriate consent for treatment is needed.
• Extended-release medications avoid school dosing.
• Children require lower dosing of dopamine antagonists.
• There is highly efficient hepatic metabolism in the young.
Other considerations
• Need for family involvement in assessment and treatment.
• Role of peer influence.
• School teachers/counsellors are important.
234 CHILD PSYCHIATRY
Table 19.1 Main groups of childhood psychiatric disorders as classified in ICD-10 and DSM-IV
ICD-10 DSM-IV
MATERNAL DEPRIVATION
Bowlby has expounded the theory that a warm, intimate and continuous mother–child
relationship is essential for subsequent mental health of the child. There are two
components:
1 Bonding describes the relationship formed between mother and baby, usually
over the first few days of life. This process may be impaired by illness, separation,
ambivalence towards the pregnancy, etc.
2 Attachment describes the relationship of child to mother. This is presumed not to
be formed until after the first 6 months.
CLINICAL FEATURES
• Onset before 30 months of age.
• Major deficits in language development (echolalia, pronomial reversal, perseveration).
• Disturbance of normal social interaction.
• Bizarre responses to environment; e.g. resistance to change, irrational attachment
to various objects, rituals and routines.
• Absence of delusions, hallucinations, loosening of associations as in schizophrenia.
Associated features
• Unpredictable fears, screaming or laughter.
• Abnormal movements (stereotypies, etc.).
• Hyperkinesis.
• Self-destructive behaviour.
• Difficulties learning manipulative tasks.
• Isolated skills (e.g. rote memory).
• Up to two-thirds have IQs in the MR range.
EPIDEMIOLOGY
• By definition, onset is before age 30 months.
• Boy:girl ratio ⫽ 3.8:1.
• There is a normal socioeconomic distribution.
• There are 34 cases per 10 000 in the USA (Yeargin-Allsopp et al., 2003).
• There are 62.6 cases per 10 000 in the UK (Chakrabarti and Frombonne, 2001).
AETIOLOGY
Genetics
• Concordance rate – MZ:DZ twins ratio ⫽ 36:0.
• There is a 3 per cent prevalence among siblings of autistics.
• About 5 per cent of autistic patients have fragile X syndrome.
236 CHILD PSYCHIATRY
Non-genetic factors
Autism is (uncommonly) associated with PKU, congenital rubella, tuberous sclerosis,
Rett’s syndrome. There is a high prevalence of mental retardation and cognitive
impairments, even in ‘mild’ autistics. One-third of autistics develop seizures during
adolescence.
Neurochemistry
• Increased CSF HVA associated with autistic stereotypies.
• Increased 5-HIAA associated with symptom severity.
Other factors
There is an excess of perinatal complications, minor physical anomalies, abnormal
dermatoglyphics – suggesting a neurodevelopmental basis. Some MRI findings (cere-
bellar hypoplasia, polymicrogyria) are consistent with this, although there has been
overall inconsistency in neuroimaging findings to date.
Psychosocial factors
Emotional factors are not causative. The hypothesis of ‘refrigerator parents’ is now
discounted.
DIFFERENTIAL DIAGNOSIS
Exclude: deafness, childhood schizophrenia, mental retardation with behavioural
symptoms, disintegrative psychosis, developmental language disorder, CNS disorders
(tuberous sclerosis, etc.).
MANAGEMENT
There is no ‘specific’ treatment. Modalities cover:
ASPERGER’S DISORDER
Asperger’s disorder begins in the third year of life. Males are affected more than
females (6:1 ratio).
There are not the cognitive or verbal deficits as seen in autism. There is abnormal
social reciprocity – the child often appears odd or eccentric. He/she often exhibits
restricted obsessional, ritualistic or idiosyncratic interests/activities.
This disorder is said to have a better social prognosis than autism, but their separate
status is disputed by some.
CHILDHOOD-ONSET SCHIZOPHRENIA
Twenty-five per cent of schizophrenia has an onset before age 15 years. There are
prominent brain changes on MRI.
Medication treatment is complicated by the greater sensitivity to antipsychotic
medication side-effects, so lower doses are indicated. The prognosis is poor.
DISINTEGRATIVE PSYCHOSIS
There is severe and sustained impairment in social relationships, speech and language.
Onset is after 24 months.
BIPOLAR DISORDER
MANAGEMENT
As with adults, manage with mood stabilizers, atypical antipsychotics, or a combination of
atypical antipsychotics with a mood stabilizer. However, treatment resistance is common.
Depressive symptoms are common in emotionally disturbed children, but earlier stud-
ies suggested that typical depressive disorder of adulthood was uncommon. Rutter et al.
(1970) found depressive disorders in only 1–2 children per 1000 of 10- to 11-year-olds.
A broader view suggests that masked depression (presenting as behaviour disorders)
and depressive equivalents (presenting with somatic symptoms) are much more com-
mon. However, these concepts are so over-inclusive that nearly all childhood disorders
could be included.
There are high rates (40 per cent) of co-morbidity, especially of anxiety disorder
and conduct disorder.
• Depression, irritability and social withdrawal are prominent features.
• Childhood depression is usually self-limiting, but may become chronic and
presage recurrent depression in adulthood.
• Suicide is extremely rare before puberty, but the incidence rises during adolescence.
SCHOOL REFUSAL
The term ‘school phobia’ is now rarely used. Some classify school refusal under
‘separation anxiety disorders’ (ICD-10). Probably it is not an entity – possibly in some
cases it is a variant of childhood depression.
Other features
• Anxiety symptoms are seen more often than depressive symptoms.
• Onset is more often gradual than sudden.
• The child may be timid and fearful outside, demanding and wilful at home.
• Academic attainments good or superior.
EPIDEMIOLOGY
Age at presentation is most commonly 11 years but is distributed over a wide range.
Boys and girls are equally affected. They tend to be in a higher social class. They
account for 3 per cent of all child psychiatric referrals.
AETIOLOGY
There are three broad categories:
• Younger age.
• Stability of the home.
• ‘Psychological sophistication’ of the parents.
Probably one-third of school refusers later present as adult ‘neurotics’. Twenty per
cent of agoraphobics interviewed had had ‘school phobia’, but this is the same as in
neurotics in general.
INAPPROPRIATE SOILING
ENURESIS
ASSOCIATED FEATURES
The majority do not have a coexisting mental disorder, but psychiatric disorder is
twice as common in this group as the general population (especially among girls).
With functional encopresis, sleepwalking and night terrors may also be present.
Typically, disturbance occurs during the first third of the night, during non-REM sleep.
INAPPROPRIATE SOILING 241
Urinary-tract-infection (UTI) Five per cent of enuretics (usually girls) have signifi-
cant bacteriuria. Fifteen per cent of children with UTI are consequently enuretic.
EPIDEMIOLOGY
• Primary after age 4 years, secondary between ages 5 and 8.
• Boys are more affected than girls (3:1 ratio, but varies with age).
• Lower social classes are over-represented.
• At age 7 – about 7 per cent for boys, 3 per cent for girls.
• At age 15 and older – 2 per cent for boys, almost non-existent for girls.
AETIOLOGY
Any hypothesis must explain the following facts:
• Greater concordance in MZ than DZ twins.
• Higher incidence in relatives.
• Higher incidence in social classes IV and V.
• Larger families.
• Institutional upbringing.
• Male predominance.
• Below-average IQ.
• Stress events in early childhood (illness and hospitalization, maternal death).
• Small functional bladder capacity.
• No association with any specific syndrome, except encopresis.
Possible mechanisms
• Enuresis is secondary to a psychiatric disorder; or
• The same factors (e.g. stress) produce both psychiatric disorder and enuresis; or
• Psychiatric disorder is secondary to negative parental reactions to enuresis.
ENCOPRESIS
MANAGEMENT
• Exclude physical reasons for soiling, such as retention, constipation with overflow
leakage (possibly due to anal fissure, Hirschsprung’s disease) and/or diarrhoea.
• Reassure the child and support the parents, with explanations.
• Start retraining if necessary.
NIGHT-TIME INCIDENTS
SLEEPWALKING
Sleepwalking is repeated episodes of arising from bed during sleep, walking about for
several minutes and remaining unresponsive to the efforts of others to influence sleep-
walking, or to communicate. The child can be awoken only with great difficulty, and is
amnesic on waking.
It usually occurs between 30 and 180 minutes after onset of sleep (EEG: delta activity,
stages 3 and 4).
Between 1 and 4 per cent of children experience the disorder at some time. Isolated
episodes are even more frequent. Adolescence usually sees the disorder disappear.
NIGHT TERRORS
Night terrors are repeated episodes of abrupt awakening lasting 1–10 minutes, occur-
ring between 30 and 180 minutes after onset of sleep (typically occurs during stages 3
and 4). They usually begin with a panicky scream. There are then signs of autonomic
arousal – tachycardia, rapid breathing, dilated pupils, etc. There is confusion, dis-
orientation and perseveration of movements. The person is relatively unresponsive
to others.
SRR applies to children whose reading ability falls significantly below the average for
their age, schooling and IQ. It must be distinguished from ‘reading backwardness due
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD) 243
to low IQ’. There is a prevalence of 4–10 per cent (higher in inner-urban areas), with a
male predominance of 3–4:1.
It is a broader concept than dyslexia, which implies localized cerebral immaturity.
ASSOCIATED FEATURES
• Large family size.
• Low socioeconomic status.
• Poor concentration and attention.
• Increased prevalence in epileptic children, but overall no overt prevalence of neuro-
logical abnormalities.
Conduct disorder
One-third of 10-year-olds with SRR in an Isle of Wight study were diagnosed as ‘con-
duct disorder’. There was a family history of reading difficulties, spelling difficulties,
speech delay, clumsiness and poor left–right differentiation.
This is the leading neurobehavioural disorder among the young. Some will improve
with maturity, others persist into adulthood. Criteria include:
• There is inattention and/or hyperactivity–impulsivity.
• Behaviour occurs in at least two settings, e.g. home and school.
• It causes impairment in social, academic, or occupational functioning.
• Symptoms are evident before age 7 years.
• Behaviour is not due to other another disorder.
ADHD is classified into three subtypes:
1 Predominantly inattentive.
2 Predominantly hyperactive–impulsive.
3 Combined.
ASSOCIATED FEATURES
• Dyssocial behaviour, difficulty disciplining, temper episodes.
• Family discord.
• Injuries.
• Low self-esteem.
• Low frustration threshold.
• Learning difficulties common.
• Under-achiever at school even when IQ is taken into account.
244 CHILD PSYCHIATRY
• Soft neurological signs (motor coordination, perceptual and attention tests), EEG
abnormalities (dysmaturation EEG) have been described.
DIFFERENTIAL DIAGNOSIS
There is much overlap. Chief differentials are:
EPIDEMIOLOGY
Onset is typically before age 3 years, though it may not present before school age. Boys
outnumber girls (3:1 ratio). Prevalence estimates in school-aged children range from
3 to 7 per cent.
AETIOLOGY
The aetiology is probably multifactorial. The heterogeneity view suggests a group of
syndromes which have a common clinical phenotype.
Genetics
It seems to be biological, although adoptive parents of hyperactive children show
increased rates of alcoholism and sociopathy. Biological fathers were likely to have been
overactive.
Recent risk analysis studies suggest a shared familial vulnerability for ADHD and
affective disorders.
Other factors
• Neurological soft signs, EEG, clinical evidence of maturational lags (e.g. associated
learning disabilities) may suggest in utero damage.
• fMRI studies indicate subnormal acitivation in prefrontal brain regions as well as
decreased putaminal blood flow (Yitzchak and Pavlakis, 2001).
• Noradrenergic dysfunction has been demonstrated.
• Other neurotransmitters are implicated.
It has been hypothesized that such children have under-aroused CNS with insuffi-
cient cortical inhibitory control. Hence, stimulants are said to stimulate the reticular
activating system (RAS) and increase cortical inhibition.
MANAGEMENT
The main focus for treatment is to maximize functioning.
‘SYMPTOMATIC’ DISORDERS
TICS
DIFFERENTIAL DIAGNOSIS
• Choreiform movements – uncoordinated, irregular, non-repetitive.
• Athetiod movements – slow, writhing and irregular, frequently in fingers and toes.
• Myoclonic movements – brief, shock-like muscle contractions that may affect part
or whole of a muscle (not muscle groups).
• Dystonic movements – slower, more sustained movements.
• Dyskinesias – especially those such as tardive dyskinesia, which are oral, buccal,
lingual masticatory movements in the face and choreoathetiod movements in the
limbs.
• Hemiballismic movements – coarse, intermittent and unilateral movements of
the limbs.
• Spasmodic torticollis.
ASSOCIATED FEATURES
• Development disorders.
• Other psychiatric disorders.
• IQ normally distributed.
246 CHILD PSYCHIATRY
EPIDEMIOLOGY
Age at onset is nearly always during childhood and adolescence and may be as early as
2 years. Boys are more affected than girls (3:1 ratio). Between 10 and 20 per cent of
children are reported as having transient tic-like movements at some stage. There is a
normal social class distribution (?).
AETIOLOGY
There is association with other developmental disorders. Stress, temperamental fea-
tures and psychiatric disorder may act as precipitants.
MANAGEMENT
• Relaxation exercises, with massed practice, have been proposed. Evidence for their
effectiveness is unclear.
• Minor tranquillizers and haloperidol are sometimes effective.
• Individual and family counselling, including reassurance, is aimed at minimizing
stress.
This is a disorder characterized by multiple motor and at least one vocal tic. Onset is
before age 21 years. The site, frequency and pattern of tics change over time.
There is substantial overlap between GTS and obsessional disorders. About 40 per
cent of GTS patients exhibit obsessive–compulsive behaviours. First-degree relatives
of GTS patients have high rates for diagnosis of oppositional defiant disorder (ODD).
EPIDEMIOLOGY
The exact prevalence is unknown but a figure of 0.5 per 1000 has been suggested.
There are no known associations with race or social class. Males are more affected
than females (4:1 ratio).
AETIOLOGY
Genetics
A major autosomal dominant gene is likely. Linkage studies show preliminary evi-
dence: 18 per cent of first-degree relatives have GTS.
Non-genetic factors
• EEG abnormalities (non-specific) are seen in 10–40 per cent of GTS cases.
• PET and SPECT show hypermetabolism in frontal and basal ganglia regions.
CONDUCT DISORDER 247
CLINICAL FEATURES
• Age at onset is 2–15 years, with mean 7 years.
• Vocal tics have mean age at onset of 11 years.
• Motor tics are most commonly facial. Others are squatting, jumping, gait
abnormalities.
• Vocal tics may be coughing, barking, throat-clearing grunting.
• Coprolalia (shouting obscenities) is seen in 30 per cent of GTS cases; mean onset
13–14 years.
• Echolalia is seen in 20–40 per cent.
• 40 per cent of GTS patients show associated disturbances, including attention deficits,
aggressive, antisocial or inappropriate sexual behaviour, and deliberate self-harm.
CONDUCT DISORDER
Subclassification
1 Socialized – behaviour is viewed as normal within the context of the child’s subcul-
tural group (e.g. truancy and gang membership).
248 CHILD PSYCHIATRY
EPIDEMIOLOGY
Onset is usually before puberty for the unsocialized type, and pubertal or postpuber-
tal for the socialized type. There is a 5 per cent point prevalence in middle childhood.
It was the most common psychiatric disorder in an Isle of Wight study.
It is far more common in boys than girls (ratios range from 4:1 to 12:1). Lower
social classes appear to be most affected.
AETIOLOGY
Possible important factors:
• Unsocialized type – parental rejection, inconsistent management with harsh dis-
cipline, early institutionalization, frequent change of parent figures (e.g. fostering)
and being illegitimate.
• Socialized type – large family size, membership of a gang, absent father.
• Generally – disorder more common in children of alcoholic parents and parents
with antisocial personality disorder.
• Child factors – male, biological vulnerability, difficult temperament (see Chapter 6),
early behavioural problems, school failure.
• One-third show severe retardation of reading.
MANAGEMENT
Management is aimed at reversing significant aetiological factors:
• Conjoint family therapy; behavioural training for parents.
• Remedial teaching.
• Individual counselling or group counselling.
• Alternative peer-group provision (e.g. adventure clubs, etc.).
Intoxication can lead to injuries and death, and impairment in social, educational and
psychological development and wellbeing.
There is variability over time in the popularity of different substances. Surveys show
that half of 12- to 15-year-olds have consumed alcohol. By age 15, almost two-thirds
REFERENCES AND FURTHER READING 249
had tried cigarettes and about one-quarter had tried marijuana. Over half of
12th-graders indicated they had used an illicit drug.
The most commonly used substances from greatest to least are as follows: (Kaul and
Coupey, 2002): marijuana; amphetamines; inhalants; hallucinogens; ecstasy; barbit-
urates; tranquilizers; cocaine; heroin.
RISK FACTORS
• Behavior and mood disorders at an early age.
• Previous diagnosis of ADHD, conduct disorder, personality disorder.
• A history of sexual or physical abuse.
• Inherited genetic factors.
• Association with drug-using peers.
• No after-school supervision.
• Broken family.
• Poverty.
Cote S, Tremblay RE, Nagin DS et al. (2002) Childhood behavioral profiles leading to adolescent
conduct disorder: risk trajectories for boys and girls. J. Am. Acad. Child Adolesc. Psychiatry
41, 1086.
Dale RC, Heyman I (2002) Post-streptococcal autoimmune psychiatric and movement disorders
in children. Br. J. Psychiatry 181, 188.
Dalsgaard S, Mortensen PE et al. (2002) Conduct problems, gender and adult psychiatric out-
come of children with attention-deficit hyperactivity disorder. Br. J. Psychiatry 181, 416.
Dekker MC, Koot HM, van der Ende J, Verhulst FC (2002a) Emotional and behavioral problems
in children and adolescents with and without intellectual disability. J. Child Psychol.
Psychiatry 43, 1087.
Dekker MC, Nunn RJ, Koot HM (2002b) Psychometric properties of the revised developmental
behaviour checklist scales in Dutch children with intellectual disability. J. Intellect. Disabil.
Res. 46, 61.
Delbello MP, Schwiers ML, Rosenberg HL, Strakowski SM (2002) A double-blind, randomized,
placebo-controlled study of quetiapine as adjunctive treatment for adolescent mania. J. Am.
Acad. Child Adolesc. Psychiatry 41, 1216.
Dunn DW, Kronenberger WG (2003) Attention-deficit/hyperactivity disorder in children and
adolescents. Neurologic Clinics 21, 933.
Egger HE, Costello EJ, Angold A (2003) School refusal and psychiatric disorders: a community
study. J. Am. Acad. Child Adolesc. Psychiatry 42, 797.
Emslie GJ, Mayes TL (2001) Mood disorders in children and adolescents: psychopharmacologi-
cal treatment. Biol. Psychiatry 49, 1082.
Emslie GJ, Mayes TL, Laptook RS, Batt M (2003) Predictors of response to treatment in children
and adolescents with mood disorders. Psychiatr Clin North Am. 26, 435.
Essex MJ, Klein MH, Cho E, Kraemer HC (2003) Exposure to maternal depression and marital
conflict: gender differences in children’s later mental health symptoms. J. Am. Acad. Child
Adolesc. Psychiatry 42, 728.
Fishman L, Rappaport L, Schonwald A, Nurko S (2003) Trend in referral to a single encopresis
clinic over 20 years. Pediatrics 111, e604.
Fombonne E, Tidmarsh L (2003) Epidemiological data on Asperger disorder. Child Adolesc.
Psychiatr. Clin. North Am. 12, 15.
Ford T, Goodman. R, Meltzer H (2003) The British Child and Adolescent Mental Health Survey
1999: the prevalence of DSM-IV disorders. J. Am. Acad. Child Adolesc. Psychiatry 42, 1203.
Frombonne E, Wostear G, Cooper V, Harrington R, Rutter M (2001) The Maudsley long-term
follow-up of child and adolescent depression. 1: Psychiatric outcomes in adulthood. Br. J.
Psychiatry 179, 210.
Frombonne E, Wostear G, Cooper V, Harrington R, Rutter M (2001) The Maudsley long-term
follow-up of child and adolescent depression. 2: Suicidality, criminality and social dysfunc-
tion in adulthood. Br. J. Psychiatry 179, 218.
Geller B, Craney JL, Bolhofner K et al. (2002) Two-year prospective follow-up of children with a
prepubertal and early adolescent bipolar disorder phenotype. Am. J. Psychiatry 159, 6.
Goodman T, Ford T, Meltzer H (2002) Mental health problems of children in the community: 18
month follow-up. BMJ 324, 1496.
Goodyer IM (2002) Social adversity and mental functions in adolescents at high risk of psy-
chopathology: position paper and suggested framework for future research. Br. J. Psychiatry
181, 383.
Grella CE, Hser Y-I, Joshi V, Rounds-Bryant J (2001) Drug treatment outcomes for adolescents
with comorbid mental and substance use disorders. Mental Dis. 189, 384.
Guilleminault C, Palombini L et al. (2003) Sleepwalking and sleep terrors in prepubertal chil-
dren: what triggers them? Pediatrics 111, e17.
Hazell PL, Stuart JE (2003) A randomized controlled trial of clonidine added to psychostimulant
medication for hyperactive and aggressive children. J. Am. Acad. Child Adolesc. Psychiatry 42, 886.
REFERENCES AND FURTHER READING 251
Hofstra MB, van der Ende J, Verhulst FC (2002) Child and adolescent problems predict DSM-IV
disorder in adulthood: a 14-year follow-up of a Dutch epidemiological sample. J. Am. Acad.
Child Adolesc. Psychiatry 41, 182.
Kaminski KM, Garber J (2002) Depressive spectrum disorders in high-risk adolescents: episode
duration and predictor of time to recovery. J. Am. Acad. Child Adolesc. Psychiatry 41, 410.
Kaul P, Coupey SM (2002) Clinical evaluation of substance abuse. Pediatr. Rev. 23, 85.
Keenan K, Wakschlag LS (2002) Can a valid diagnosis of disruptive behavior disorder be made in
preschool children? Am. J. Psychiatry 159, 351.
King M, Coxell A, Mezey G (2002) Sexual molestation of males: associations with psychological
disturbance. Br. J. Psychiatry 181, 234.
Klin A, Warren J, Schultz R et al. (2002) Defining and quantifying the social phenotype in autism.
Am. J. Psychiatry 159, 153.
Kolvin I, Ounsted C, Humphrey M et al. (1971) Studies in the childhood psychoses. II: The phe-
nomenology of childhood psychoses. Br. J. Psychiatry 118, 385.
Kowatch RA, Suppes T, Carmody TJ et al. (2000) Effect size of lithium, divalproex sodium, and
carbamazepin in children and adolescents with bipolar disorder. J. Am. Acad. Child Adolesc.
Psychiatry 39, 713.
Kuperman S, Schlosser SS, Kramer JR et al. (2001) Developmental sequence from disruptive
behavior diagnosis to adolescent alcohol dependence. Am. J. Psychiatry 158, 2022.
Kurlan R, Como PG, Miller B et al. (2002) The behavioral spectrum of tic disorders: a
community-based study. Neurology 59, 414.
Kurlan R, McDermott MP, Deeley C et al. (2001) Prevalence of tics in school children and associ-
ation with placement in special education. Neurology 57, 1383.
Lord C, Volkmar F (2002) Genetics of childhood disorders: XLII. Autism part 1: diagnosis and
assessment in autistic spectrum disorders. J. Am. Acad. Child Adolesc. Psychiatry 41, 1134.
McCracken JT, McGough J, Shah B et al. (2002) Risperidone in children with autism and serious
behavioral problems. New Engl. J. Med. 347, 314.
Meltzer H, Gatward R, for the Office for National Statistics (2000) Mental Health of Children and
Adolescents in Great Britain. The Stationery Office, London.
Mental Health Evaluation and Community Consultation Unit (2002) Prevalence of Mental
Disorders in Children and Youth. University of British Columbia, Vancouver. Available
online at www.mheccu.ubc.ca/publications/cy/MHECCU_Prevalence_Oct02.pdf (accessed
10 November 2003).
Michelson D, Allen AJ, Busner J et al. (2002) Once-daily atomoxetine treatment for children and
adolescents with attention-deficit hyperactivity disorder: a randomized, placebo-controlled
study. Am. J. Psychiatry 159, 1896.
Moreau D, Weissman MM (1992) Panic disorder in children and adolescents: a review. Am. J.
Psychiatry 149, 1306.
Pappadopulos E, Jensen S, Schur SB et al. (2002) ‘Real world’ atypical antipsychotic prescribing
practices in public child and adolescent inpatient settings. Schizophr. Bull. 28, 111.
Pappadopulos E, MacIntyre JC, Crismon ML et al. (2003) Treatment recommendations for the
use of antipsychotics for aggressive youth (TRAAY): II. J. Am. Acad. Child Adolesc. Psychiatry
42, 145.
Patel NC, Sanchez RJ, Johnsruc MT, Crismon ML (2002) Trends in antipsychotic use in a Texas
Medicaid population of children and adolescents: 1996 to 2000. J. Child Adolesc.
Psychopharmacol. 12, 1219.
Pickles A, Rowe R, Somonoff E et al. (2001) Child psychiatric symptoms and psychosocial
impairment: relationship and prognostic significance. Br. J. Psychiatry 179, 230.
Rosenberg DR, MacMillan SN, Moore GJ (2001) Brain anatomy and chemistry may predict treat-
ment response in paediatric obsessive–compulsive disorder. Int. J. Neuropsychopharmacol. 4, 179.
Rutter M (2002) The interplay of nature, nurture, and developmental influences: the challenge
ahead for mental health. Arch. Gen. Psychiatry 59, 996.
252 CHILD PSYCHIATRY
Rutter M, Caspi A, Moffitt TE (2003) Using sex differences in psychopathology to study causal
mechanisms: unifying issues and research strategies. J. Child Psychol. Psychiatry 44, 1092.
Sayal K, Taylor E et al. (2002) Pathways to care in children at risk of attention-deficit hyperactiv-
ity disorder. Br. J. Psychiatry 181, 43.
Schur SB, Sikich L, Findling RL et al. (2003) Treatment recommendations for the use of antipsy-
chotics for aggressive youth (TRAAY). I: A review. J. Am. Acad. Child Adolesc. Psychiatry 42, 132.
Silberg J, Rutter M, D’Onofrio B, Eaves L (2003) Genetic and environmental risk factors in ado-
lescent substance use. J. Child Psychol. Psychiatry 44, 664.
Simpkin DR (2002) Adolescent substance use disorders and comorbidity. Pediatr. Clin. North
Am. 49, 463.
Stein MA, Sarampote CS, Waldman ID et al. (2003) A dose–response study of oral methylphenidate
in children with attention-deficit/hyperactivity disorder. Pediatrics 112, e404.
Szatmari P, Merette C, Bryson SE et al. (2002) Quantifying dimensions in autism: a factor-
analytic study. J. Am. Acad. Child Adolesc. Psychiatry 41, 467.
Tourette’s Syndrome Study Group (2002) Treatment of ADHD in children with tics. Neurology
58, 527.
Trowell J, Kolvin I, Weeramanthri T et al. (2002) Psychotherapy for sexually abused girls: psy-
chopathological outcome findings and patterns of change. Br. J. Psychiatry 180, 234.
Tuchman R (2003) Autism. Neuro Clin. 21, 915.
US Department of Health and Human Services (2001) Mental Health: Culture, Race and
Ethnicity (supplement to Mental Health: a Report of the Surgeon General). Department of
Health and Human Services, Substance Abuse and Mental Health Services Administration,
Center for Mental Health Services, National Institutes of Health, National Institute of Mental
Health; Rockville, MD.
Volkow ND, Wang G, Fowler JS et al. (2001) Therapeutic doses of oral methylphenidate signifi-
cantly increase extracellular dopamine in the human brain. J. Neuroscience 21, rc121.
Wagner KD, Ambrosini P, Rynn M (2003) Efficacy of sertraline in the treatment of children and
adolescents with major depressive disorder: two randomized controlled trials. JAMA 290, 1033.
Wakefield JC, Pottick KJ, Kirk SA (2002) Should the DSM-IV diagnostic criteria for conduct dis-
order consider social context? Am. J. Psychiatry 159, 380.
Watson S, Porter R, Birmaher B et al. (2002) The role of hypothalamic–pituitary–adrenal axis
dysfunction in the attenuated growth hormone response in adolescents with familial loading
for affective disorder. Arch. Gen. Psychiatry 59, 186.
Weiner DA, Abraham ME, Lyons J (2001) Clincial characteristics of youths with substance use
problems and implications for residential treatment. Psychiatr. Serv. 52, 793.
Yeargin-Allsopp M, Karapurkar RC, Boyle DN et al. (2003) Prevalence of autism in a US metro-
politan area. JAMA 289, 49.
Yitzchak F, Pavlakis SG (2001) Brain imaging in neurobehavioral disorders. Pediatr. Neurol. 25, 278.
Zito JM, Safer DJ, dosReis S et al. (2000) Trends in the prescribing of psychotropic medications
to preschoolers. JAMA 283, 1025.
Mental retardation 20
OVERVIEW
DEFINITIONS
World Health Organization
• Impairment – any loss or abnormality of psychological, physiological or anatom-
ical structure or functions.
• Disability – any reduction or lack (resulting from impairment) of ability to
perform an activity in the manner or within the range considered normal for a
human being.
• Handicap – a disadvantage for the individual, resulting from impairment or dis-
ability, that limits the fulfilment of a role that is normal (depending on age, sex,
culture) for that individual. May be in dimensions of physical independence,
mobility, occupations, social integration, economic self-sufficiency, orientation
or other.
ICD-10
Mental retardation (MR) A condition of arrested or incomplete development of the
mind, which is especially characterized by impairment of skills manifested during the
developmental period, which contribute to the overall level of intelligence; i.e. cogni-
tive, language motor and social abilities.
DSM-IV-TR
Coding See Table 20.1. The criteria are those of social competence. Precise classification
by IQ is not always possible. IQ of less than 50–55 usually denotes major impairment,
254 MENTAL RETARDATION
Mild MR 55–60 to 70
Moderate MR 35–40 to 50–55
Severe MR 20–25 to 35–40
Profound MR ⬍20–25
EPIDEMIOLOGY
• Severe impairment has a prevalence of 3·5 per 1000 population. Between 2 and
3 per cent of the population have an IQ less than 70.
• It is more common in males, who have a larger variance in IQ.
• Of inpatient populations:
– 10 per cent have severe psychiatric disorders.
– 20 per cent have defects of vision or hearing.
– 20 per cent have severe speech defects.
AETIOLOGY
Severe impairment
• Nearly all cases have gross cerebral pathology at post mortem.
• Between 33 and 85 per cent have an organic aetiology diagnosed during life.
• 33 per cent are due to Down syndrome.
• 19 per cent are due to other inherited conditions or associated congenital
malformations.
• 18 per cent are due to perinatal injury.
• 14 per cent are due to infections.
• 4 per cent are due to biochemical disorders (inborn error of metabolism).
• 15 per cent are of unknown aetiology.
Mental impairment
• Fewer than 33 per cent have an organic aetiology diagnosed during life.
• Mental impairment shows a ninefold increase in the lower social class.
• A proven organic aetiology is more likely if the handicapped child is from a higher
social class.
Social factors (i.e. ‘subcultural problems’, poor education, poor home environment,
poor diet, etc.) therefore play a much larger part in the aetiology of impairment than
of severe impairment.
The lower end of the normal distribution curve of IQ (excluding the excess caused
by organic disease) will account for a proportion of the handicapped group.
CHROMOSOMAL ABNORMALITIES 255
CHROMOSOMAL ABNORMALITIES
TRISOMIES
FRAGILE X SYNDROME
Fragile X syndrome is the second most common known cause of MR in males; it is
thought to account for 6 per cent of severe MR, 10 per cent of mild MR in males.
Clinical features
These include MR, floppy ears, prognathism, macro-orchidism, hypertelorism,
blue eyes, single palmar crease. Female carriers have physical stigma and somewhat
reduced IQ.
GENETIC ABNORMALITIES
Most are autosomal recessive except Hunter’s and Lesch–Nyhan syndromes and
nephrogenic diabetes insipidus, which are X-linked.
258 MENTAL RETARDATION
OVERFLOW AMINOACIDURIAS
• Phenylketonuria – This is the most common inborn metabolic error (1 per 12 000
live births). Phenylalanine hydroxylase deficiency leads to build-up of phenylalan-
ine in blood and phenylpyruvate in urine. All newborn babies in the UK are tested
(Guthrie test) at 6–14 days for phenylalanine, which promotes the growth of Bacillus
subtilis in a quantitative fashion. Subjects tend to be fair-haired, blue-eyed and prone
to eczema. They may be epileptic and severely handicapped if untreated. Treat with
a phenylalanine-free diet.
• Homocystinuria – There is a deficiency of cystathionine synthetase leading to
raised homocystine and methionine. Clinically there is fair hair and skin, eye and
skeletal abnormalities, poor peripheral circulation, liver degeneration, epilepsy
and mental deterioration. Treat with a methionine-free diet.
• Argininosuccinic acidura – There is deficiency of argininosuccinase leading to
raised argininosuccinic acid and ammonia. Subjects have short brittle hair, epilepsy,
chorea and variable handicap.
• Maple syrup disease – There is a deficiency of ketoacid decarboxylase leading to
abnormalities of branched chain amino acids. There is epilepsy, spasticity, paralysis
and very early death if untreated. Treat with a diet low in leucine, isoleucine and valine.
MUCOPOLYSACCHARIDOSES
• Nutritional/toxic:
– Placental insufficiency.
– Malnutrition.
– Infantile hypoglycaemia.
– Fetal alcohol syndrome (20–50 per cent risk with alcoholic mother).
– Lead encephalopathy.
• Anoxia:
– Perinatal.
– In infancy.
260 MENTAL RETARDATION
• Maternal infection:
– Rubella at up to 16 weeks of pregnancy. Leads to microcephaly, eye, ear and head
abnormalities and subnormality.
– Cytomegalovirus.
– Syphilis.
– Toxoplasmosis.
– Listeria.
• Child infection:
– Encephalitis.
– Meningitis.
• Trauma:
– Non-accidental injury – possibly one of the most important causes of mental
handicap.
– Accidental injury.
– Birth trauma.
• Rhesus factor incompatibility.
INDIVIDUAL SYNDROMES
Schizophrenia
Between 3 and 6 per cent of handicapped inpatients suffer with schizophrenia. They
are characterized by childish behaviour and stereotypies, poverty of thought, perplex-
ity and ‘confusion’, loss of drive and ill-formed hallucinations and delusions.
SERVICES REQUIRED 261
Neurotic disorders
Hysterical symptoms tend to be more common than in the normal population.
Bereavement and adjustment reactions are underestimated.
Epilepsy
Epilepsy is found in 30 per cent of the severely handicapped. Hypsarrhythmia,
Lennox–Gastaut syndrome and West’s syndrome are associated. Incidence generally
reduces with age but may develop later in autism, Down’ syndrome and progressive
disorders (e.g. lipidoses).
SERVICES REQUIRED
OVERALL GUIDELINES
ASSESSMENT SERVICES
EDUCATIONAL SERVICES
These are the responsibility of the local education authority, no matter how handi-
capped the child is, if under 19 years.
There is considerable debate about whether handicapped children are best
taught in special schools or in ordinary schools, integrated with normal children
(‘mainstreaming’).
Structured, active teaching with precise measurable goals is most effective, based on
careful developmental assessment.
Behaviour modification techniques are particularly useful for severely handicapped
people. Prolonged face-to-face care and teaching are important and more time needs
to be spent with the child. Education may need to go on for longer (e.g. into early 20s).
After this, sheltered workshops are often needed. Adult training and social education
centres provide continuing assessment and training for adults.
RESIDENTIAL SERVICES
MANAGEMENT PRINCIPLES
MEDICAL
Medical management is rarely useful, as in phenylketonuria and cretinism. Severe
physical handicaps may required medical or surgical treatment.
PREVENTION OF MENTAL RETARDATION 263
PSYCHIATRIC
Psychotropic medication may be required for agitation, depression, etc. Individual
and family psychotherapy may be appropriate. Behaviour therapy may be useful.
Behavioural modification involves detailed analysis of unwanted behaviour and the
supplying of immediate appropriate rewards for required behaviour.
PRIMARY PREVENTION
• Avoid development of the condition.
• Give genetic counselling.
• Manipulate the environment.
SECONDARY PREVENTION
Detect and treat the condition early.
TERTIARY PREVENTION
Avoid additional disability by good care and early intervention.
1 Genetic counselling:
– Unknown-cause severe handicap – 30 per cent recurrence risk.
– Balanced translocation – mother, 20 per cent risk; father, 5 per cent risk.
264 MENTAL RETARDATION
Ivanov D, Kirov G, Norton N et al. (2003) Chromosome 22q11 deletions, velo-cardio-facial syn-
drome and early-onset psychosis: molecular genetic study. Br. J. Psychiatry 183, 409.
Kahng SW, Iwata BA, Lewin AB (2000) Behavioral treatment of self-injury, 1964 to 2000. Am. J.
Ment. Retard. 107, 212.
Linhorst DM, Bennet L, McCutchen T (2002) Development and implementation of a program
for offenders with developmental disabilities. Ment. Retard. 40, 41.
McCarthy J, Boyd J (2001) Psychopathology and young people with Down syndrome: childhood
predictors and adult outcome of disorder. J. Intellect. Disabil. Res. 45, 99.
Moss SC, Emerson E, Kiernan C et al. (2000) Psychiatric symptoms in adults with learning dis-
ability and challenging behaviour. Br. J. Psychiatry 177, 452.
Murphy KC, Owen MJ (2001) Velo-cardio-facial syndrome: a model for understanding the
genetics and pathogenesis of schizophrenia. Br. J. Psychiatry 179, 397.
Sanderson TL, Doody GA, Best GA et al. (2001) Correlations between clinical and historical vari-
ables and cerebral structural variables in people with mild intellectual disabilities. J. Intellect.
Disabil. Res. 45, 89.
Schupf N (2002) Genetic and host factors for dementia in Down’s syndrome. Br. J. Psychiatry
180, 405.
Simpson MK, Hogg J (2001) Patterns of offending among people with intellectual disabilty: a
systematic review. I: Methodology and prevalence data. J. Intellect. Disabil. Res. 45, 384.
Surgeon General (2001) Closing the Gap: a National Blueprint to Improve the Health of Persons
with Mental Retardation. Washington, DC.
Szymanski L, King GH (1999) Practice parameters for the assessment and treatment of children,
adolescents, and adults with mental retardation and comorbid mental disorders. J. Am. Acad.
Child Adolesc. Psychiatry 38, s5.
Thompson CL, Reid A (2002) Behavioural symptoms among people with severe and profound
intellectual disabilities: a 26-year follow-up study. Br. J. Psychiatry 181, 67.
Thorpe L, Davidson P, Janicki M (2001) Healthy ageing – adults with intellectual disabilities:
biobehavioural issues. J. Appl. Res. Intellect. Disabil. 14, 218.
Turk J (1992) The fragile X syndrome: on the way to a behavioural phenotype. Br. J. Psychiatry
160, 24.
Van Narrden Braun K, Yeargin-Allsopp M, Schendel D, Fernhoff P (2003) Long-term develop-
mental outcomes of children identified through a newborn screening program with a meta-
bolic or endocrine disorder: a population-based approach. J. Pediatrics 143, 236.
Warren ST, Nelson DL (1994) Advances in molecular analysis of fragile X syndrome. JAMA
271(7), 536.
Young ID (1993) Diagnosing fragile X syndrome. Lancet 342, 1004.
Drug therapy 21
• Pharmacokinetics – What the body does to the drug. Time-course of drug absorption
(distribution, metabolism, excretion) and drug transport (to and from receptors).
• Pharmacodynamics – What the drug does to the body. Relationship between drug
concentration and efficacy (tolerability, drug effects at receptor level.)
ABSORPTION
Absorption depends on:
1 Nature of the drug – Particle size, diluents, coating materials, etc., affect rate of
absorption.
2 Gastric emptying and gut motility – Anticholinergic effects of many psychotropic
drugs slow absorption.
3 Gut mucosa – Malabsorption syndromes.
4 Liver enzymes – May be inhibited (e.g. by MAOIs) or induced (e.g. by barbitu-
rates). All drugs absorbed from the GI pass through the liver first and are partly
destroyed (about 15 per cent chlorpromazine reaches systemic circulation).
Compare IV, IM or sublingual preparations, which quickly reach the brain.
PROTEIN BINDING
Most drugs bind to plasma and tissue proteins. Only unbound drug is biologically
active. Binding may be influenced by:
1 Displacement by other drugs.
2 Change in concentration of plasma proteins.
METABOLISM
Metabolism is mostly in the liver, but also in lung, gut, kidney and placenta.
Metabolism in the liver is mostly through the cytochrome P450 hepatic microenzyme
system (e.g. CYP2D6, CYP3A3/4).
PHARMACOKINETICS AND PHARMACODYNAMICS 267
Liver metabolism produces derivatives of increasing polarity, which are less lipid-
soluble and so more readily excreted by the kidney. The rate of metabolism is an
important factor in influencing serum levels.
DRUG EXCRETION
This is mostly through the kidney by passive diffusion. Some drugs, particularly glu-
curonide conjugates, are excreted in bile.
• Age (increasing age reduces liver metabolism, affects cerebral circulation, reduces
renal clearance).
• Sex.
• Proportion of body fat.
Young ↑ ↑ ⫽
Old ↓ ⫽↓ ⫽
Pregnant ↑ ⫽ ↓↑ ⫽↓
Renal disease ↓ ↓ ↓
Liver disease ⫽↓ ↓ ⫽↓
Omeprazole MAOIs
Carbamazepine Fluoxetine, fluvoxamine, paroxetine
Phenytoin Nefazodone
Barbiturates ‘Azole’ antifungals (ketoconazole)
Co-trimoxazole
Macrolides
Cimetidine
Quinidine
Cigarettes
268 DRUG THERAPY
Genetic polymorphisms
• CYP2D6 – poor metabolizers, autosomal recessive, more in Asians.
– N-acetyltransferase – slow acetylators, autosomal recessive, more in Caucasians.
PHARMACOGENETICS
Pharmacogenetics is the study of genetically based, interindividual variability in
response to drugs and in susceptibility to drug-induced adverse effects. It focuses on
genetic polymorphisms influencing structure or function of proteins for which a
given gene codes. Examples include:
• Polymorphism of dopamine D3 receptor gene exists – homozygotes (serine–serine;
glycine–glycine) versus heterozygotes (serine–glycine) – DRD3 glycine–glycine phe-
notype associated with higher risk of tardive dyskinesia with antipsychotic therapy
(Lerer et al., 2002).
• Genetic variation in serotonin transporter gene predicts response to antidepressant
(especially SSRIs; see page 275) therapy (Lever and Marciardi, 2002) – still at
research stage but likely to influence clinical practice in coming years.
PRESCRIBING IN PREGNANCY
RISKS TO FETUS
• Increased incidence of dysmorphogenesis, especially cardiac anomalies with
lithium.
• Possible increased risk with other psychotropics, but no clear evidence.
• Do not use any drug during pregnancy, especially in first 12 weeks, except when
risks of relapse outweigh other risks. If necessary, give a minimum dosage.
RISKS TO NEWBORN
• May be born ‘flat’.
• May show withdrawal symptoms if mother dependent on opiates or alcohol.
• May be limp or goitrous if mother takes lithium.
• Most drugs cross the placental barrier. This is probably unimportant in pheno-
thiazines, tricyclics, hypnotics and anticonvulsants. Avoid breast feeding with
lithium and high doses of diazepam.
ANTIPSYCHOTIC DRUGS
Phenothiazine
– Aliphatic class Chlorpromazine 100
– Piperidine class Thioridazine 100
– Piperazine class Trifluoperazine 10
Butyrophenone Haloperidol 5
Thiozanthene Fluphenthixol ?
Diphenylbutylpiperidine Pimozide 1
Substituted benzamide Sulpiride ?
Dibenzodiazepine Clozapine
Benzisoxazole Risperidone
Thienobenzodiazepine Olanzapine
Dibenzothiazepine Quetiapine
Benzisothiazolyl Ziprasidone
Phenylindol Aripiprazole
Phenylindol Sertindole
Dibenzothiepine Zotepine
Acute dystonia Acute hypodopaminergic Young, male, high dose, Immediate: Oral/IM
– oculogyric crisis in basal ganglia high potency, typical anticholinergic
– torticollis antipsychotics Subsequent: decrease
– dysarthria dosage, add anticholinergic,
– dysphagia or change to atypical.
Parkinsonism Basal ganglia D2 blockage Dose related, more with Reduce dose or add oral
– tremor typical antipsychotics anticholinergic, or change to
– cog-wheel rigidity atypical.
– bradykinesia
Akathisia Basal ganglia D2 blockage Low serum iron Reduce dose, or add
– subjective and Low iron also relevant? Dose related, more with benzodiazepines or
motor restlessness typical antipsychotics betablocker.
Change to atypical.
ANTIPSYCHOTIC DRUGS 271
Typ ⫽ typical antipsychotics; Clz ⫽ clozapine; Ris ⫽ risperidone; Olz ⫽ olanzapine; Qtp ⫽ quetiapine; Zip ⫽ ziprasidone;
a
⫽ dose-related; ⫾ ⫽ none to minimal; ⫹ ⫽ mild; ⫹⫹ ⫽ moderate; ⫹⫹⫹ ⫽ marked compared with placebo rate.
ANTIDEPRESSANT DRUGS
The pharmacological action of antidepressant drugs (a few hours) does not correlate
with mood effect (2–4 weeks). The exact mechanism of altering mood is uncertain,
but the therapeutic effect occurs after manipulation of central neurotransmitters.
Unlike the older TCAs and MAOIs, most of the newer antidepressants have high
therapeutic indexes. Ensure maximum dose and adequate length of trial before aban-
doning a particular agent/class.
Side-effects can be used as therapeutic effects.
SIDE-EFFECTS
General
All antidepressants – with the exception of mirtazapine, bupropion and nefazodone –
have sexual side-effects which include impotence, anorgasmia and delayed ejaculation.
There have been rare cases of priapism with trazodone.
Gastrointestinal upset is associated to some degree with almost all antidepressants
except mirtazapine, TCAs and MAOIs.
Serotonin syndrome
With overstimulation of central serotonin receptors, the patient my appear agitated,
confused, and exhibit myoclonus, diaphoresis, nausea, vomiting, diarrhoea, syncope,
tachycardia and elevated blood pressure.
Ventricular tachycardia, seizures, disseminated intravascular coagulation, renal fail-
ure, coma and hypotension are complications seen in severe cases.
Aetiology Caused by serotonergic medication use – additive effect.
Treatment Discontinue serotonergic agents. With supportive treatment the syndrome
will usually resolve within 24 hours.
ANTIDEPRESSANT DRUGS 273
SSRIs
Fluoxetine S – ⫹⫹⫹ – 330 20–80
Paroxetine S ⫹ ⫹ ⫹ 21 20–50
Fluvoxamine S – ⫹ ⫹ 16 100–300
Sertraline S – ⫹⫹ ⫾ 26 50–200
Citalopram S – ⫾ ⫾ 35 10–60
Escitalopram S – ⫾ ⫾ 27–32 10–20
Other
Bupropion D, N, S – ⫹⫹⫹ – 20 150–450
Trazodone S ⫾ – ⫹⫹⫹ 6 300–800
Nefazodone N, Sb – ⫾ ⫹⫹ 3 100–600
Mirtazapine Nb, Sb – – ⫹⫹ 30 15–45
Venlafaxine D, N, S – ⫹⫹ ⫹ 5 75–350
TCAs 2nd
Desipramine N ⫹⫹ ⫾ ⫹⫹ 14–25 50–300
Nortriptyline N, S ⫹⫹ – ⫹⫹ 18–35 20–150
TCAs 3rd
Amitriptyline N, S ⫹⫹⫹ – ⫹⫹⫹ 9–25 50–300
Clomipramine N, S ⫹⫹⫹ – ⫹⫹⫹ 19–37 50–300
Doxepine N, S ⫹⫹⫹ – ⫹⫹⫹ 6–8 50–300
Imipramine N, S ⫹⫹⫹ – ⫹⫹ 8–16 50–300
MAOIs
Phenelzine ⫹⫹ ⫾ ⫹ 15–90
Tranylcypromine ⫹⫹ ⫹ – 20–90
These are the first-line medical treatment for depression. They have a more
favourable side-effect profile than TCAs and MAOIs and a negligible mortality risk in
overdose. A report of increased suicidal ideation/behaviour in children is under
investigation.
USES OF SSRIs
• Depression.
• OCD.
• Bulimia nervosa.
• PTSD.
274 DRUG THERAPY
• Social phobia.
• Generalized anxiety disorder.
• Panic disorder.
• Premenstrual dysphoric disorder.
Side-effects of SSRIs Nausea; loose stools; headache; insomnia (best given in morning
dosage regime); nervousness, agitation; sweating; weight gain; withdrawal syndrome
(associated with agents with short half-lives).
Bupropion
Bupropion primarily inhibits the re-uptake of dopamine and norepinephrine, and sero-
tonin to a lesser extent. It has no sexual side-effects, so it is used as an adjunct to SSRIs
to counter those side-effects. It has been associated with weight loss. Otherwise, the side-
effects are similar to those of SSRIs.
Trazodone
• Blocks 5-HT2 receptors at low dosage, stimulates at higher dosage, and is a weak
inhibitor of serotonin re-uptake.
• Low therapeutic index due to sedation.
• Low anticholinergic effect, and reported to be non-cardiotoxic (mixed agonist effects).
• Side-effects include sedation, orthostatic hypotension, dizziness, headache, dry mouth.
Nefazodone
Similar to trazodone – weak inhibitor of norepinephrine and serotonin reuptake and
blocks 5-HT2 serotonin receptors. Side-effects also similar to trazodone, with the
exception of less sedation/sexual side-effects.
Mirtazapine
• Antagonizes ␣2-adrenergic and serotonin 5-HT2 receptors.
• Moderate therapeutic index owing to sedation.
• Has significant antihistamine activity, which accounts for its sedating effects – more
so at lower doses.
• No sexual or SSRI-like side-effects.
• Side-effects include sedation, increased appetite and weight gain, dizziness, dry
mouth, constipation.
• Rare cases of blood dyscrasias reported, but all recovered after cessation of this drug.
ANTIDEPRESSANT DRUGS 275
Venlafaxine
• Inhibits re-uptake of serotonin at low doses and norepinephrine and dopamine at
high doses.
• Extended-release formulation is indicated for generalized anxiety disorder as well
as depression.
• Side-effect profile similar to SSRIs.
• Monitor for increased blood pressure (dose related).
SIDE-EFFECTS OF TRICYCLICS
• Anticholinergic (dry mouth, blurred vision, worsening glaucoma, urinary hesi-
tancy, constipation).
• Hypotension (central effect – anti-␣1-noradrenergic).
• Drowsiness, sedation (anti-histamine/ ⫾ anti-acetylcholine).
• Cardiovascular:
– Palpitations.
– Tachycardia.
– ECG changes (‘R on T phenomenon’), quidine-like effect; QT prolongation,
decreased ST interval; myocardial sensitization to catecholamines.
– Ventricular tachyarrhythmias.
– Cardiomyopathy or heart failure (decreased inotropic effect following depletion
of catecholamines from myocardium).
– Distal conduction defects in bundle of His following overdosage.
• Weight gain/increased appetite (serotonergic ?).
• Confusional reactions in the elderly – probably due to anticholinergic effects, espe-
cially where phenothiazine (weak anticholinergic) and a strong antiparkinson drug
are combined.
• Tremor.
• Convulsions (rare).
• Sexual dysfunction, impotence, anorgasmia (especially clomipramine), delayed
ejaculation.
• Withdrawal syndrome – symptoms of noradrenergic and cholinergic ‘overdrive’.
276 DRUG THERAPY
OTHER TRICYCLICS
• Dothiepin – derivative of amitriptyline, with fewer autonomic side-effects.
• Doxepin – derivative of amitriptyline, strongly anxiolytic, with less cardiotoxicity.
• Mianserin – blocks ␣2-adrenergic receptors; effectively no re-uptake blocking activity
or anticholinergic activity. Minimal cardiotoxicity. Rarely causes convulsions; risk of
leucopenia requires careful monitoring.
Monamine oxidase is an enzyme that degrades tyramine, serotonin, dopamine and nor-
epinephrine, and its inhibition causes an increase in these monamines.
MAO inhibition reaches a maximum in 5–10 days. Restoration of MAO stores takes
2 weeks after stopping MAOIs. Drug and dietary restrictions are necessary to avoid
hypertensive crises (see below).
MAOIs are thought to be effective in refractory and atypical depressive states –
especially those with mixed anxiety, phobic, obsessional features.
SIDE-EFFECTS OF MAOIs
• Anticholinergic.
• Postural hypotension.
• Tremor.
MOOD STABILIZERS USED IN BIPOLAR ILLNESS 277
• Ankle oedema.
• Paraesthesia in limbs.
• Confusional states and possible precipitation of mania.
• Hypertensive crisis:
– Headache and neck pain.
– Throbbing neck veins.
– Palpitations.
– Hyperpyrexia.
– Convulsions, coma, death.
– Reverse with phentolamine 5–10 mg IV; chlorpromazine (PO) also used.
• Insomnia.
• Nausea.
• Myoclonus.
• Tranylpromine has amphetamine-like properties.
Mood stabilizers used for bipolar illness include lithium, antiepileptic drugs (AED)
and, more recently, atypical antipsychotics. These agents are used with varying success
to delay or treat the onset of mood episodes.
Lithium has long been known to exert suicide-protective effects in bipolar patients.
Recent studies also suggest that AED mood stabilizers are associated with reduced sui-
cide ideation and attempts (Yerevanian et al., 2003).
Atypical antipsychotics have been shown to be useful both alone and in combina-
tion with mood stabilizers in the treatment of acute mania. Benzodiazepines are also
useful in the treatment of acute mania.
LITHIUM
Lithium is prescribed in the form of its simple salts. It was introduced into medicine in
1859 as a treatment for gout, but later abandoned because of toxicity. It was reintroduced
278 DRUG THERAPY
as a treatment for mania by John Cade in 1949, in Australia. Its use was generally estab-
lished by 1965.
KINETICS OF LITHIUM
Absorption is rapid following an oral dose and complete within 6–8 hours. Plasma level
peaks in 30 minutes to 2 hours. It is distributed in total body water, shifting slowly to
cells. There is no protein-binding. The therapeutic index is low due to neurotoxicity.
There is no metabolism – the substance is excreted unchanged by the kidney. Between
one- and two-thirds of the oral dose appears in urine after 8–12 hours; the rest is
excreted slowly over days. Once lithium therapy is established, the clearance rate is
fairly constant.
Rates of lithium clearance between different persons may differ fourfold. It depends
on renal function: the amount of fluid passing through the kidney and its sodium con-
tent. Lithium tends to follow sodium in reabsorption at proximal tubules; hence:
• Increased sodium intake produces decreased reabsorption, with decreased reabsorp-
tion of lithium.
• A sodium-restricted diet produces increased reabsorption, and lithium levels may
become toxic.
• Thiazide diuretics decrease lithium clearance by 24 per cent, owing to compensatory
reabsorption of sodium in proximal tubules.
ACTIONS OF LITHIUM
The therapeutic action is not understood, but the following effects have been noted.
Neurotransmitters
• Synapses – Lithium is thought to increase presynaptic destruction of catecholamines,
inhibit release of neurotransmitter, decrease sensitivity of postsynaptic receptors.
• Ions – Lithium influences sodium and calcium ion transfer across cell membranes.
These ions affect neurotransmitter release and receptor activity.
• Cyclic AMP – Lithium inhibits prostaglandin E-stimulated cyclic AMP.
• Lithium stimulates sodium and magnesium-dependent ATPase.
Cations and water Lithium stimulates exit of sodium from cells, probably by stimu-
lating the pump mechanism, where intracellular Na is elevated (as in depression).
Lithium stimulates entry of sodium into cells where intracellular Na is low (as may be
the case in mania).
Cell membranes Lithium may interact with both calcium and magnesium and increase
cell membrane permeability.
Other actions
• Lithium restores diurnal rhythm of corticosteroids to normal in mania (but may
simply reflect changes in behaviour as mania ameliorates).
• In depressed patients, there is restoration of normal slow-wave EEG rhythms during
sleep, and decreases in stage 1 and REM sleep correlate with plasma levels.
• Changes in magnesium and calcium may be the secondary effects of altered
carbohydrate metabolism. Lithium influences this by releasing insulin and increas-
ing transport of glucose and muscle glycogen formation. This may be the cause of
weight gain.
MOOD STABILIZERS USED IN BIPOLAR ILLNESS 279
USES OF LITHIUM
1 Control of mania (3–4 days for therapeutic effect).
2 Prophylaxis of recurrent bipolar and unipolar disorder.
3 Schizoaffective disorder.
4 Augmentation of antidepressant therapy.
5 Treatment of impulsive and aggressive behaviour.
There are significant reductions in aggressive behaviour among prisoners and men-
tally retarded on lithium compared with placebo treatment.
SIDE-EFFECTS OF LITHIUM
Early
• Nausea, vomiting, diarrhoea (related to ‘peak’ serum levels).
• Tremor, especially on voluntary movement.
• Dryness of mouth, slight thirst.
• Fatigue, drowsiness.
• Stuffy nose, metallic taste in mouth.
At any time Toxicity – tremor, ataxia, incoordination, slurred speech, confusion,
disorientation convulsion, coma and death. Symptoms begin to appear with blood
levels ⬎2.0 mmol/L.
Longer-term
• Nephrogenic diabetes insipidus. Polyuria and polydipsia may occur at therapeutic
plasma concentrations. The distal tubule becomes resistant to the influence of
antidiuretic hormone (ADH), possibly owing to blockade of ADH-sensitive adenyl
cyclase. This is reversible but may take weeks.
– Treatment: Reduce/stop lithium; use indomethacin or amiloride.
• Hypothyroidism occurs in about 3 per cent of chronic lithium-takers, females more
than males. The lithium ion interferes with production of thyroid hormones and
the action of TSH. This is reversible but will recur on restarting lithium.
• Oedema.
• Weight gain (not accounted for by water retention).
• Neurological – choreoathetosis, ataxia, dysarthria, tardive dyskinesia (rare), neuro-
toxicity with neuroleptics or carbamazepine, NMS.
• Cardiac T-wave flattening on ECG.
• Arrhythmias – possibly caused by reduction of intracellular potassium.
• Poor memory short-term.
• Nephropathy – association unclear; 5–10 per cent develop nephropathy, but this
does not invariably cause ‘clinical’ renal insufficiency.
280 DRUG THERAPY
• Dermatological/alopecia.
• SLE/myasthenia gravis.
MONITORING
• Baseline – examination; routine lab tests including urea, electrolytes, creatinine,
urine tests, thyroxine and TSH; weight; ECG; pregnancy test, if female of child-
bearing age.
• During treatment:
– Lithium – 8-weekly once stabilized.
– Chemistry, T4, TSH, creatinine, urea, urine – 6–12 months.
– ECG examination – annually.
VALPROIC ACID
The therapeutic level for bipolar disorder is 50–100 micrograms for both maintenance
and acute mania. It is better tolerated than lithium. It is equal to lithium in the treat-
ment of acute mania, and more effective for rapid cycling and mixed states.
The mechanism of action is unknown, but it is shown to increase central GABA levels
by inhibiting its degradation/enhancing its synthesis.
Valproic acid has a moderate therapeutic index gastrointestinal symptoms and
neurotoxicity. It is metabolized in the liver.
CARBAMAZEPINE
USES OF CARBAMAZEPINE
• Acute mania.
• Prophylaxis of bipolar illness.
• Rapid cycling mania – more effective than lithium.
• Trigeminal neuralgia.
• Epilepsy.
• Alcohol withdrawal.
SIDE-EFFECTS OF CARBAMAZEPINE
Dizziness, sedation, ataxia, dry mouth; generalized erythematous rash (Steven Johnson
syndrome); leucopenia/agranulocytosis occurring in early stages of treatment; hypona-
tremia; neural tube/craniofacial defects during pregnancy.
LAMOTRIGINE
Lamotrigine is used for maintenance therapy in bipolar disorder. It delays the onset of
manic/hypomanic as well as depressive episodes in bipolar illness. It is not effective for
acute mania.
Lamotrigine is thought to work by stabilization of neurons via inhibition of sodium
and calcium channels in presynaptic cell membranes.
It does not require serum level monitoring like lithium, valproic acid and
carbamazepine.
Valproic acid increases lamotrigine levels while carbamazepine lowers levels. It is
not associated with weight gain.
USES OF LAMOTRIGINE
• Maintenance therapy for bipolar illness.
• Epilepsy.
SIDE-EFFECTS OF LAMOTRIGINE
Headache; nausea; insomnia; rash (higher risk with rapid titration, higher doses,
younger age).
Gabapentin, tiagabine, oxcarbazepine and topiramate are used for mood stabilization
with promising reports, but studies do not fully support their use in this manner.
282 DRUG THERAPY
BENZODIAZEPINES
MODE OF ACTION
There is enhancement of GABA effects, probably via benzodiazepine (bz) receptors
localized on neurones throughout brain, but with highest density in cortical and lim-
bic areas.
The bz receptors are closely tied to GABA receptors, which explains the CNS
inhibitory actions of the benzodiazepines.
Benzodiazepines are safe in overdoses, producing drowsiness or stupor, and
rebound insomnia in the next few days.
USES OF BENZODIAZEPINES
• Anxiety disorders.
• Insomnia.
• Withdrawal symptoms.
• Psychosis induced by hallucinogens.
• Status epilepticus.
• Abreactive techniques.
• Premedication and minor operative procedures.
• Muscle relaxant.
• Acute agitation.
SIDE-EFFECTS OF BENZODIAZEPINES
• Sedation.
• Ataxia/motor impairment.
Long-acting
Clorazepate 40–50 Nordiazepam
Chlordiazepoxide 24–30 Desmethylchlordiazepoxide
Clonazepam 30–40 None
Diazepam 20–100 Nordiazepam
Flurazepam 47–100 N-hydroxyethyl-flurazepam
Intermediate-acting
Estazolam 10–24 4-hydroxy estazolam (weak)
Lorazepam 13 None
Oxazepam 6–11 None
Temazepam 3.5–18.4 None
Short-acting
Alprazolam 11.2 None
Triazolam 1.5–5.5 None
SEDATIVES AND ANXIOLYTICS 283
• Cognitive blunting.
• Memory impairment.
• Apnoea on IV administration.
• Slight respiratory depression (important in patients with obstructive airways disease).
• Dependency – psychological and physical, associated with chronic use.
• Amnesia in large doses.
• Confusion in the elderly.
WITHDRAWAL EFFECTS
On withdrawal (placebo-controlled) of long-term normal-dose benzodiazepine
treatment, there is:
• Rebound insomnia, REM rebound.
• Tremor, anxiety, restlessness.
• Weight loss, appetite disturbance, sweating.
Symptoms usually subside after several days, but may last months in some cases.
Withdrawal is possibly aided by substituting long-acting bz, gradual titration, and
supportive/counselling measures.
Convulsions have been reported on abrupt withdrawal of long-term, very-high-dose
treatment.
NON-BENZODIAZEPINE HYPNOTICS
Zaleplon 1 None
Zolpidem 2.6 None
Zopiclone 3.5–6.5 None
AZAPIRONES (BUSPIRONE)
BARBITURATES
Barbiturates are rarely used now because of the high risk of psychological and phys-
ical dependence. There is tolerance and liver enzyme induction, drug accumulation
causing confusional states (especially in the elderly). Respiratory depression is another
drawback, as is the withdrawal syndrome (see Chapter 10).
Barbiturates are used sometimes in abreaction, for narcosis in a severely disturbed
patient.
ADRENERGIC AGENTS
ALPHA AGONISTS
BETA BLOCKERS
If disulfiram is taken with alcohol, the person experiences severe headache, nausea,
facial flushing and general malaise. Severe reaction can be treated by oxygen, dextrose
drip or parenteral antihistamine. Effectiveness is limited by compliance issues.
Disulfiram interferes with metabolism of other drugs, especially barbiturates,
phenytoin, warfarin and paraldehyde.
Citrated calcium carbimide has fewer side-effects and milder reaction.
SIDE-EFFECTS OF DISULFIRAM
Nausea, constipation, fatigue; breath odour, metallic taste in mouth; psychotic and
confusional states; reduction in libido; hypothyroidism.
CONTRAINDICATIONS
• Cardiac failure or ischaemic heart disease.
• Pregnancy.
• Psychosis (may exacerbate schizophrenic psychosis).
STIMULANTS
PSYCHOSTIMULANTS
Pemoline has similar effects but is structurally different from the prototype stimu-
lants and sees only limited use because of excessive morbidity and mortality associated
with liver complications.
USES OF PSYCHOSTIMULANTS
• ADHD (first-line treatment).
• Narcolepsy.
• Obesity.
• Augmentation of antidepressants.
SIDE-EFFECTS OF PSYCHOSTIMULANTS
Insomnia; appetite suppression; growth suppression; unmasking of latent tic disorder;
hallucinations; agitation, excitement; tolerance and dependency; rebound depression
on stopping or after prolonged use; paranoid psychosis; hypertension.
NON-PSYCHOSTIMULANTS (ATOMOXETINE)
PHARMACOECONOMICS
Pharmacoeconomics examines drug utilization, risks and benefits, access, and afford-
ability in mental health delivery systems. It is increasingly playing a role in availability/
rationing of new (invariably more expensive) medications.
Kohen D (2004) Psychotropic medication in pregnancy. Adv. Psychiatr. Treat. 10, 59.
Lambert M, Conus P, Lambert T, McGorry PD (2003) Pharmacotherapy of first-episode psych-
osis. Expert Opin. Pharmacother. 4, 717.
Lerer B, Macciardi F (2002) Pharmacogenetics of antidepressant and mood-stablizing drugs: a
review of candidate-gene studies and future research directions. Int. J. Neuropsychopharmacol.
5, 255.
Lerer B, Segman RH, Fangerau H et al. (2002) Pharmacogenetics of tardive dyskinesia: combined
analysis of 780 patients association with D3 receptor gene ser9Gly Polymorphism.
Neuropsychopharmacology 27, 105.
Licht RW (2002) Limits of the applicability and generalizability of drug trials in mania. Bipolar
Disord. 4 (Suppl. 1), 66.
Lin K, Smith MW, Ortiz V (2001) Culture and psychopharmacology. Psychiatr. Clin. North. Am.
24, 523.
Mason PJ, Morris VA, Balcezak TJ (2000) Serotonin syndrome: presentation of two cases and
review of the literature. Medicine 79, 201.
Meltzer HY, Alphs L, Green AI et al. (2003) Clozapine treatment for suicidality in schizophrenia:
International Suicide Prevention Trail. Arch. Gen. Psychiatry 60, 82.
Michelson D, Adler L, Spencer T et al. (2003) Atomoxetine in adults with ADHD: two random-
ized, placebo-controlled studies. Biol. Psychiatry 53, 112.
Michelson D, Faries D, Wernicke J et al. (2001) Atomoxetine in the treatment of children and
adolescents with attention-deficit/hyperactivity disorder: a randomized, placebo-controlled,
dose–response study. Pediatrics 108, e83.
Paton C, Okocha C (2004) Risperidone long-acting injection: the first 50 patients. Psychiatr. Bull.
28, 12.
Pickar D (2003) Pharmacogenomics of psychiatric drug treatment. Psychiatr. Clin. North Am. 26, 303.
Schatzberg AF, Nemeroff CB (2001) Essentials of Clinical Psychopharmacology. American
Psychiatric Press, Washington, DC.
Smith D, Dempster C, Glanville J et al. (2002) Efficacy and tolerability of venlafaxine compared
with selective serotonin reuptake inhibitors and other antidepressants: a meta-analysis.
Br. J. Psychiatry 180, 396.
Terzano MG, Rossi M, Palomba V et al. (2003) New drugs for insomnia: comparative tolerability
of zopiclone, zolpidem, and zaleplon. Drug Safety 26, 261.
Thase ME (2002) Comparing the methods used to compare antidepressants. Psychopharmacol.
Bull. 36 (Suppl. 1), s1.
Thase ME, Bhargava M, Sachs GS (2003) Treatment of bipolar depression: current status, con-
tinued challenges, and the STEP-BD approach. Psychiatr. Clin. North Am. 26, 495.
Yatham LN, Grossman F, Augustyns I et al. (2003) Mood stabilizers plus risperidone or placebo
in the treatment of acute mania: international, double-blind, randomized controlled trial.
Br. J. Psychiatry 182, 8.
Yerevanian BI, Koek RJ, Mintz J (2003) Lithium, anticonvulsants and suicidal behavior in bipolar
disorder. J. Affect. Disord. 73, 223.
Zarate CA, Quiroz JA (2003) Combination treatment in bipolar disorder: a review of controlled
trails. Bipolar Disord. 5, 217.
Zhang Z, Yao Z, Liu W et al. (2004) Effects of antipsychotics on fat deposition and changes in
leptin and insulin levels: magnetic resonance imaging study of previously untreated people
with schizophrenia. Br. J. Psychiatry 184, 58.
Zimmerman M, Posternak MA (2002) Are subjects in pharmacological treatment trials of
depression representative of patients in routine clinical practice? Am. J. Psychiatry 159, 469.
Physical treatments 22
HISTORY
Camphor-induced convulsions were first used by W. Oliver in 1785 for melancholia.
The effect was slow and produced fits inconsistently. In the 1930s, Meduna used IV
injections of metrazol, based on a belief that there is an antagonism between schizo-
phrenia and epilepsy. Cerletti, on the basis of the same notion in 1938, administered
an electrically induced fit to a catatonic vagrant found wandering in a Rome railway
station.
Later, anaesthesia was introduced and convulsions modified using muscle-relaxing
agents.
PRESENT INDICATIONS
In depressive illness
• Poor response to adequate pharmacotherapy.
• Person unable to tolerate side-effects of pharmacotherapy (especially the elderly).
• Depressive stupor, not eating or drinking.
• Severe suicide risk.
• ‘Severe’ depression with delusions, psychomotor retardation.
• Severe post-partum depression.
The presence of delusions and severe psychomotor agitation or retardation are the
main ‘reliable’ clinical predictors of response to ECT.
Numerous studies of real ECT versus simulated ECT confirm the therapeutic efficacy
of ECT. It is more effective than antidepressant medications (UK ECT Review Group,
2003). Up to 90 per cent show improvement in depressive symptoms.
In mania
• Quicker response and ‘better social response’ in ECT-treated patients.
• Equally efficacious but more rapid response with ECT ⫹ neuroleptics.
• Use generally reserved for acute treatment-‘refractory’ mania.
290 PHYSICAL TREATMENTS
Schizophrenia
ECT is useful when schizophrenia is superimposed with catatonia or major depression.
SIDE-EFFECTS OF ECT
Early reported side-effects are:
• Headache.
• Slight and temporary confusion.
• Short-term memory loss, increasing with the number used.
• Tachycardia and hypertension immediately after ECT.
At 6 months after the course, there is no significant difference in memory between
those receiving ECT and those receiving simulated ECT.
MORTALITY
Deaths are estimated 4.5 per 100 000 ECT treatments – similar to rates for minor
anaesthesia. The majority of deaths have been caused by cardiovascular complications
(arrhythmias, sudden cardiac arrest secondary to vagal inhibition).
ADMINISTRATION OF ECT
Before administration
1 Full physical examination.
2 Discuss any significant organic pathology with the anaesthetist.
3 Ensure an empty stomach in patient, and full resuscitatory equipment for the
anaesthetist.
Application of anaesthetic
1 Induction – methohexitole (most commonly).
2 Atropine – reduces secretions, counters cholinergic effects of muscle relaxants.
3 Muscle relaxant – succinylcholine; rarely, prolonged paralysis produced due to
pseudocholinesterase deficiency.
4 Oxygenate – will also facilitate seizure activity.
the seizure threshold is critical for efficacy in unilateral ECT in particular, and for the
speed of response in unilateral or bilateral ECT.
If there is no convulsion, repeat the stimulation up to a maximum of three times
(ensure good skin contact, oxygenation). Increasing the stimulation, decreasing con-
comitant benzodiazepines, and giving caffeine will help to maximize seizure activity
in a seizure-refractory patient.
• Unilateral – on non-dominant hemisphere, produces less cognitive impairment:
– Between frontotemporal and mastoid region.
– Lancaster position – between frontotemporal position and vertically to vertex.
• Bilateral – frontotemporal position.
Post-ictal
1 Oxygenate.
2 Nurse in prone position with airway in situ.
3 Reassure the patient during recovery of consciousness.
Do not prescribe ECT in set courses, although the average number is 6–8. Continue
applications twice to three times weekly (UK and US practices respectively) until
euthymic, up to a maximum of 10–12.
Transient elevation of mood on recovery after the first 1–2 treatments predicts good
response. If no response whatsoever by the sixth treatment, then prognosis is poor.
Daily application does not improve response, and seriously increases memory
disturbance.
Maintenance treatment is usually pharmacological; but some recent evidence
suggests reduced relapses with maintenance ECT.
EFFECTS OF ECT
Cardiovascular
• Brief asystole on passage of current.
• Bradycardia during the tonic phase, tachycardia during the clonic phase and occa-
sional arrhythmias in the post-ictal period.
• Brief blood pressure decrease during the early tonic phase followed by a rapid rise
above normal level. The rise persists through the clonic phase.
• Blood pressure rise apparently is centrally stimulated, independent of peripheral
convulsive activity. It is exacerbated by atropine. ?? Related to memory impairment.
Neurological
• Immediate loss of consciousness (if given without anaesthesia).
• Flattening of EEG, followed by slow waves, and waves reappear as consciousness
recovers, with gradual return to normal pattern over 30 minutes. Frontal areas are
slowest in resuming normal activity.
• Very rarely post-ictal automatisms.
Neuropathological (neuroendocrine)
• There are complex effects, and the overall mechanism of action is unclear.
• Increase in blood–brain barrier permeability and capillary leakage in CNS: transi-
tory cerebral oedema. Absence of MRI changes disputed.
292 PHYSICAL TREATMENTS
Patient refusal
What happens if the patient refuses treatment or is unable to understand what is pro-
posed? The patient’s right to refuse treatment must be weighed against his/her right to
receive treatment, where the ability to make a rational decision about his/her well-
being is impaired.
PSYCHOSURGERY 293
Under s.58 of the Mental Health Act 1983, ECT is a treatment requiring consent or a
second opinion, in the case of detained patients. A second opinion must be sought if
the patient is unable to give informed consent, refuses or withdraws consent. The opin-
ion is given by a medical practitioner appointed by the Mental Health Commission.
SIDE-EFFECTS OF VNS
• Mild voice hoarseness (related to the electric current intensity); headache; dyspha-
gia; neck pain; coughing; dyspnoea on exertion (related to the electric current
intensity).
• Overall, VNS is well tolerated and the side-effects not related to current intensity
resolve after time in the majority of patients.
• Unlike ECT, VNS has no associated cognitive side-effects.
DBS is used for the treatment of tremor in Parkinson’s disease. Electrodes are
implanted into the subthalamic nucleus or thalamus. Stimulation is via a pacemaker-
like device inserted on the anterior chest wall. High-frequency electrical stimulation
deactivates basal ganglia regions.
This provides non-invasive electrical stimulation of the brain, is well tolerated and has
been shown to improve depressive symptoms in numerous studies. A recent study on
bipolar depression showed no separation from sham treatment (Nahas et al., 2003).
Research continues into the treatment parameters and patient populations for TMS.
PSYCHOSURGERY
DEFINITIONS
• WHO – The selective surgical removal or destruction … of nerve pathways … with
a view to influencing behaviour.
294 PHYSICAL TREATMENTS
HISTORY
• 1875 – Ferrier removed frontal lobes of monkeys and noticed marked changes in
animal’s ‘disposition’ and ‘character’ with no effect on motor or sensory abilities.
• 1936 – Moniz performed a localized division of prefrontal tracts in a series of 20
patients. There was a claimed reduction in severe and chronic agitation without
marked side-effects.
• 1942 – Freeman and Watts introduced the ‘standard’ cut leucotomy involving wider
severing of prefrontal connections. It was an imprecise, nearly ‘blind’ operation,
with serious side-effects: epilepsy, incontinence, marked apathy with flattened
affect, disinhibition, intellectual impairment and aggression. Mortality was 6 per cent.
– At least 10 000 were performed between 1942 and 1952 in the UK, usually for
chronic illness with disturbed behaviour, unresponsive to other treatments –
66 per cent schizophrenia, 33 per cent affective disorder.
– ‘Modified’ operations were later designed to ablate more specific brain targets
without producing side-effects associated with the cruder ‘standard’ procedure.
• 1949 – Scoville introduced orbital undercutting. A modified form was used exten-
sively in the UK by Knight, who restricted orbital undercut to medial half of lobe.
• 1950s – The advent of effective psychotropic drugs with fuller documentation of
side-effects led to rapid decline of psychosurgery.
• 1961 – Only 11 British hospitals reported performing more than 10 leucotomies.
MODERN PROCEDURES
Modern surgery is highly selective, most often using radioisotopes (yttrium implants),
ultrasound, or electrocautery under stereotactic guidance by MRI and CT.
• Procedures for anxiety/OCD – cingulotomy, subcaudate tractotomy, limbic leuko-
tomy, capsulotomy.
• Procedure for depression with anxiety – subcaudate tractotomy.
• Procedures for Parkinson’s disease – thalamotomy, pallidotomy.
• Also for Parkinson’s disease – transplantation of embryonic mesencephalic or
genetically engineered autologous cells into the basal ganglia which synthesize
tyrosine hydroxylase.
Chronic intractable OCD is currently the main indication. There must be compre-
hensive presurgical evaluation including further pharmacological trials if indicated.
Psychosurgery is contraindicated if there is substance abuse, organic brain damage,
co-morbid personality disorder, insufficient evaluation or prior treatment.
American Psychiatric Association Task Force on ECT (1990) The Practice of ECT: Recommendations
for Treatment, Training and Privileging. APA, Washington, DC. (Summary of recommendations
in Convulsive Therapy (1990) 6, 85–120.)
Bridges PK, Bartlett JR, Hale AS (1994) Psychosurgery: stereotactic subcaudate tractomy, an
indispensable treatment. Br. J. Psychiatry 165, 599.
Brodaty H, Berle D, Hickie I, Mason C (2001) ‘Side effects’ of ECT are mainly depressive phe-
nomena and are independent of age. J. Affec. Disord. 66, 237.
Conway CR, Chinbnall JT, Li X, George MS (2002) Changes in brain metabolism in response to
chronic vagus nerve stimulation in depression. Biol. Psychiatry 51, 85.
Cosgrove GR, Rauch SL (2003) Stereotactic cingulotomy. Neurosurg. Clin. North Am. 14, 225.
Dougherty DD, Baer L, Cosgrove GR et al. (2002) Prospective long-term follow-up of 44 patients
who received cingulotomy for treatment-refractory obsessive–compulsive disorder. Am. J.
Psychiatry 159, 269.
Eranti SV, McLoughlin DM (2003) Electroconvulsive therapy: state of the art. Br. J. Psychiatry 182, 8.
George MS, Nahas Z, Bohning DE et al. (2002) Vagus nerve stimulation therapy: a research
update. Neurology 59 (Suppl. 4), s56.
George MS, Nahas Z, Lisanby SH et al. (2003) Transcranial magnetic stimulation. Neurosurg.
Clin. North Am. 14, 283.
Gershon AA, Dannon PN, Grunhaus L (2003) Transcranial magnetic stimulation in the treatment
of depression. Am. J. Psychiatry 160, 835.
296 PHYSICAL TREATMENTS
GENERAL ASPECTS
PSYCHOANALYSIS
Components of repression
• Dissociation from the self of the unconscious idea leads to –
• Failure of comprehension of the enacted idea, so there is then –
• Unresponsiveness to feedback, and acts are not regulated (leading to repetition
compulsion).
But there is still the:
• Abnormal motivational state – since unconscious motivation still drives the acts.
There is also:
• Repression of memory – but the data are preserved in the unconscious and normal
forgetting is prevented.
3 The patient must have adequate ‘ego strength’ – the ability to cope with the ten-
sions arising from inner conflict.
4 The patient must be able to form and sustain a psychotherapeutic relationship.
SEXUAL DEVELOPMENT
See Table 23.1.
• Oedipal complex – after the Greek tragedy in which Oedipus unknowingly killed
his father and married his mother. Signifies rivalry between son and father for
mother’s affection. The son imagines he will be castrated as a punishment.
• Electra complex – equivalent rivalry between daughter and mother, arising out of
daughter’s fear that she has been castrated.
Castration anxiety in males resolves the Oedipal complex and leads to the latency
period. Castration anxiety in females begins the Electra complex.
• Primary process thinking is unconscious and is based on the pleasure principle (the
libidinal drive for satisfaction).
• Secondary process thinking is conscious and is based on the reality principle (which
takes into account the social pressures).
There are two basic theories: instinct (libido) theory versus object relations theory;
i.e. the need to reduce instinctual drives versus the importance of the subject’s need to
relate to objects.
EARLY THEORISTS
Freud (1856–1939)
Development of his theories:
1 The cathartic model (‘psychic abscess’) – therapy releases the blocked emotions. See
Studies in Hysteria (Breuer and Freud, 1895).
IMPORTANT PSYCHOANALYTICAL THEORISTS 301
The persona is the outer crust of the personality, which is the opposite of the per-
sonal unconscious on dimensions of:
• Thinking/feeling.
• Sensuousness/intuition.
• Extrovert/introvert (related to direction of flow of mental energy).
Archetypes are generalized symbols and images within the collective unconscious.
They include:
Wilhelm Reich
• Neurosis results from sexual frustration.
• Body armour. Orgone energy accumulator.
• Recently developed into bioenergetics.
Otto Rank
• Neurosis originates in the trauma of birth.
302 PSYCHOTHERAPY
NEO-FREUDIANS (USA)
Horney
Horney attributed sexual difficulties (especially female difficulties) to social rather
than biological causes.
Fromm/Stack-Sullivan
The self consists of:
• The ‘reflected appraisals’ of others.
• The roles it has to play in society.
In therapy there is ‘consensual evaluation’ – therapist and patient interact to valid-
ate each other’s experience.
BRITISH SCHOOLS
Anna Freud
• Ego psychology and the importance of ego defence mechanisms.
• Psychotherapeutic relationship with the child is more educational.
Melanie Klein
• Worked with pre-oedipal children using play analysis. Ego and its defence mech-
anisms are present from birth and the superego before the age of 2 years.
• Paranoid position develops first. There is splitting of good and bad aspects. The
good aspects of mother are introjected but are threatened by the externalized bad
aspects – leads to rage, fear and hatred.
• Depressive position develops next. The realization that mother is both good and
bad leads to guilt and fear of destroying the loved one with the hatred.
Bowlby
Bowlby’s work on maternal depreviation pointed to the importance of separation anx-
iety, with stages of:
• Protest.
• Despair.
• Detachment.
IMPORTANT PSYCHOANALYTICAL THEORISTS 303
Winnicot (1896–1971)
• Development of object relations theory, with Fairbairn, Guntrip and others.
Satisfaction is sought in relationships, not only in sexual relief.
• Personality develops from internalized early relationships, particularly with the
mother (‘good-enough mother’). Transitional objects are intermediate between
oral eroticism and true object relationships.
Erikson
Erikson underlined the importance of psychosocial development and the adolescent
identity crisis.
Others
• Ellis – rational–emotive therapy.
• Assagioli – psychosynthesis.
• Moreno – psychodrama.
• Janov – primal therapy.
• Maslow – self-actualization.
An international approach has developed from the ideas of Adler, Stack-Sullivan and
Bateson and also from studies of control systems in physics and physiology.
304 PSYCHOTHERAPY
GROUP THERAPIES
ANALYTIC GROUPS
THERAPEUTIC COMMUNITIES
• Main, of the Northfield Clinic, made first use of the term in 1946.
• Maxwell-Jones – Henderson Hospital.
• Rapoport – basic features are:
– Democratization – abolition of hierarchy.
– Permissiveness – tolerance of disturbed behaviour.
– Reality confrontation – regular feedback to individuals of the results of their
behaviour.
– Communalism – equal shares for all.
306 PSYCHOTHERAPY
BEHAVIOURAL TREATMENTS
These two strands were brought together by Mowrer: the double learning theory (see
diagram below).
CS
Reward
Pavlovian Skinnerian
BEHAVIOURAL TREATMENTS
These involve:
• Learning theory principles.
• Precise observation of behaviour.
• Concentration on symptoms.
• An empirical approach.
• Directive treatment methods.
• Clear goals.
• Objective evaluation of results.
SOME PRINCIPLES
Premack principle Any frequently performed piece of behaviour can be used as a
positive reinforcer of the desired behaviour.
COGNITIVE THERAPY 307
COGNITIVE THERAPY
‘COGNITIVE RESTRUCTURING’
Depressive cognitions (‘automatic thoughts’) are identified from present or recent
experiences. The patient is then encouraged to challenge those assumptions and
express alternatives. The person keeps a record of automatic thoughts and possible
alternatives. Reality testing, graded test assignments, role rehearsal (trying out the new
cognitions and behaviour), activity scheduling with experience of success and social
skills training are all used to support the cognitive restructuring.
VARIATIONS
Interpersonal therapy (IPT ) Initially developed for depression (see Chapter 4). The
focus is on grief, interpersonal role disputes, interpersonal skill, life role and
transitions; also useful in bulimia nervosa.
Dialectic behavioral therapy (DBT) A form of cognitive behavioural therapy used
for borderline personality disorder (see Chapter 6). The focus is on emotional regula-
tion, distress tolerance and validation.
Motivational enhancement therapy (MET) Used for substance abuse (see Chapters
9 and 10). The focus is on the client’s motivation to change and plan for change.
PSYCHOTHERAPY RESEARCH
METHODOLOGICAL PROBLEMS
Methodological problems have proven almost insuperable. There are many possible
confounding variables:
• Patients – diagnosis, severity, age, IQ, culture, personality type, motivation, expect-
ation of therapy, attendance, current life circumstances, spontaneous recovery rates.
Appropriate controls are required.
• Therapists – precise techniques used, personality type, level of experience, length of
therapy. The interaction of patient and therapist variables.
• Outcome – assessed by whom (patient, therapist, observer) and how (self-report,
family report, video observation, MMPI, PSE, etc.)? Length of follow-up?
Multicentre trials particularly have failed either because of insufficient standardiza-
tion or because rigorous standardization has prevented progress (e.g. Maudsley/
Tavistock study of 1972).
Several large-scale ‘meta-analyses’ of outcome research have been published.
OUTCOMES
Given the above provisos, all forms of psychotherapy seem to give a general remission
rate of 65 per cent.
Bloch (1979) suggests seven factors are predictive of good progress in therapy:
1 A reasonable degree of personality integration and functioning.
2 Motivation for change.
3 Realistic expectations based on psychological mindedness (this can be improved
by preparatory interviews).
4 At least average intelligence.
5 Neuroses and mild personality disorders (not psychoses).
6 Strong affect is present (especially anxiety or depression).
7 Life circumstances are free of unresolvable crises.
PSYCHOTHERAPY RESEARCH 309
Compare this list with the traditional (YAVIS): young, attractive, verbal, intelligent,
successful.
Freud and others advocated a ‘trial interpretation’ to assess acceptance.
Sloane et al. (1975) conducted a comparative trial of (i) behaviour therapy, (ii) psy-
choanalysis and (iii) waiting list in anxiety states. Behaviour therapy showed 93 per
cent improved at the end of therapy. Short-term psychoanalysis showed 73 per cent
improved. On the waiting list, again, 73 per cent improved.
In 101 studies of outcome of psychotherapy up to 1970, 81 showed favourable out-
come and 20 did not.
Eysenck (1952) reported a spontaneous remission rate of 70 per cent in 2 years.
Analysts’ recovery rates were between 44 and 64 per cent in 2 years.
Malan (1977) proposed that ‘spontaneous remission’ after a first interview may be
due to:
• Insight gained.
• Realization of personal responsibility.
• Genuine reassurance.
• Joining with ‘significant other’.
THE PROCESS
Most studies show the personality, enthusiasm and involvement of the therapist and
the therapist–patient interaction to be far more important than the theoretical form
of therapy.
Therapist skills
A trained analyst may do no better than concerned, intelligent, thoughtful people (e.g.
college professors). Accurate empathy, unconditional positive regard and genuineness
(congruity) are said to be related to good outcome, but are unreliably measured
(Truax and Carkhuff, 1967).
Yalom (1985) found negative group therapy factors: ‘aggressive stimulator’ type of
leader, attack by the leader, rejection by the group. Exploitiveness and disinterest from
the therapist are negative factors.
Transference
Malan found early development of therapist/parent transference, encouraged by inter-
pretations relating to early parent relationships, to predict good outcome. Working
through termination of therapy is important.
Arousal
Sifneos and other proponents of brief psychotherapy regard emotional arousal as vital
to success. Jerome Frank has pointed to its relevance in all forms of psychotherapy.
Assessment by patients
Malan wrote that patients valued warmth and individual attention. Patients disliked
therapists who did not support or advise. No patient remembered an analytic-group
interpretation.
310 PSYCHOTHERAPY
Olfsen M, Marcus SC, Druss B, Pincus HA (2002) National trends in the use of outpatient psy-
chotherapy. Am. J. Psychiatry 159, 1914.
Perls F, Hefferline RF, Goodman P (1973) Gestalt Therapy. Penguin, Harmondsworth.
Pilkonis PA, Imber SD, Lewis P, Rubinsky P (1984) A comparative outcome study of individual,
group and conjoint psychotherapy. Arch. Gen. Psychiatry 41, 431.
Rogers CR (1951) Client Centred Psychotherapy. Houghton-Mifflin, Boston.
Ryle A (1976) Group psychotherapy. Br. J. Hosp. Med. 15, 239.
Sandler J, Dare C, Holder A (1973) The Patient and the Analyst: the Basis of the Psychoanalytic
Process. Allen & Unwin, London.
Schulberg HC, Raue PJ, Rollman BL (2002) The effectiveness of psychotherapy in treating
depressive disorders in primary care practice: clinical and cost perspectives. Gen. Hosp.
Psychiatry 24, 203.
Segal H (1964) Introduction to the Works of Melanie Klein. Heinemann, London.
Shear MK, Pilkonis PA, Cloitre M, Leon AC (1994) Cognitive behavioural treatment compared
with nonprescriptive treatment of panic disorder. Arch. Gen. Psychiatry 51, 395.
Skynner ACR (1976) One Flesh: Separate Persons. Constable, London.
Sloane RB, Staples FR, Cristol AH et al. (1975) Psychotherapy versus Behaviour Therapy. Harvard
University Press, Cambridge, MA.
Soldz S, Budman S, Demby A, Feldstein M (1990) Patient activity and outcome in group psy-
chotherapy: new findings. Int. J. Psychother. 40, 53.
Truax CB, Carkhuff R (1967) Towards Effective Counselling and Psychotherapy. Aldine, Chicago.
Vaillant GE (1971) Theoretical hierarchy of adaptive ego mechanisms. Arch. Gen. Psychiatry 24, 107.
Waldron G (1984) Crisis intervention: is it effective? Br. J. Hosp. Med. 31, 283.
Walton H (1971) Small Group Psychotherapy. Penguin, Harmondsworth.
Whitfield G, Williams C (2003) The evidence base for cognitive–behavioural therapy in depres-
sion: delivery in busy clinical settings. Adv. Psychiatr. Treat. 9, 21.
Willner P (1984) Cognitive functioning in depression: a review of theory and research. Psychol.
Med. 14, 807.
Yalom ID (1985) The Theory and Practice of Group Psychotherapy, 3rd edn. Basic Books,
New York.
Community-orientated 24
psychiatry
HISTORICAL REVIEW
DECARCERATION
The modern concept of reorientation of care away from large institutions was based
on principles of community mental health care:
• Locally based, accessible services.
• A comprehensive and integrated range of therapeutic interventions and resources
for range of mental health needs.
• Services delivered by locally based community mental health teams (CMHT).
Multidisciplinary teamwork involves medical and nursing staff, behaviour ther-
apists, psychologists, occupational therapists and social workers.
• Mental health teams work closely with, or integrated with, primary care teams.
RECENT DEVELOPMENTS IN COMMUNITY CARE 313
POLICY INITIATIVES
An estimate of inpatient bed requirements per 100 000 population in the UK is:
• Acute – 25.
• Substance abuse – 3.
• Medium-stay – 8.
• Long-stay and rehabilitation – 20.
Resources (as a percentage of gross domestic product) have not changed dramatically:
Mental disorders are a major cause of morbidity. They account for 14 per cent
reported days off work and for 23 per cent of British National Health Services inpa-
tient costs.
There are national and international efforts to:
• Continuity of care.
• Implementation of evidence-based mental health best practice.
• Cost containment and resource allocation (distinguishing clinical ‘effectiveness’
from efficacy).
• Providing integrated (mental health and addiction) services for persons with dual
diagnosis (co-occurring mental disorder and alcohol/drug addiction).
• Development and integration of recovery model services, including peer support
programs.
• Multidisciplinary teamwork with the consultant seen as a fundamental part of the
service.
• Need for more community psychiatric nurses and clinical psychologists.
• Need for greater integration of social workers and occupational therapists within
the multidisciplinary team.
HOMELESSNESS
Cohen and Thompson (1992) – Is it that the mentally ill are homeless or that the
homeless are mentally ill?
PSYCHIATRY AND GENERAL PRACTICE/PRIMARY CARE 315
There are high rates of psychiatric and physical morbidity. Marshall (1989)
reported that 29/46 hostel residents in Oxford showed psychosis. Susser et al. (1989)
reported that 17 per cent of new arrivals at New York shelters were psychotic and 58
per cent were substance abusers.
NEEDS ANALYSIS
Needs are multifaceted. Steps in care include:
1 Identification of those in need through outreach programmes.
2 Systematic evaluations – mental and physical health, support, familial needs.
3 Integration of care – treatment of psychosis, depression, substance abuse, physical
conditions.
4 Housing requirements.
5 Continued support and rehabilitative care.
6 Continued research and audit.
7 Refinement of local and national policy.
At present, care is poorly coordinated. In the USA, the case management system is
not focused towards the homeless; a bureaucratic process of health delivery ‘discour-
ages’ re-entry of the homeless into the health system (Bachrach, 1992).
Many homeless people deny any mental illness, are non-compliant with medication
and avoid mental health care. The US system protects personal rights, possibly aggra-
vating the plight of the homeless. An alternative view maintains that mental health sys-
tems cannot understand the real needs of these individuals without adopting their
perspective.
REHABILITATION ASSESSMENT
1 To determine the kinds of mental and physical disability present and their severity.
2 To discover potential talents that could be developed.
3 To specify short-term and longer-term objectives and design plans to achieve
them. In the UK, operation of care programme and care management approaches.
4 To seek appropriate forms of professional, voluntary and family help and involve-
ment of patient advocacy.
5 To monitor progress and tailor care plans as necessary.
6 Specifically to assess:
– Chronic symptoms and liability to relapse (psychiatrist, community psychiatric
nurse (CPN)).
– Behavioural analysis (nurses, occupational therapist (OT), psychologist).
– Self-care and domestic skills (OT).
– Occupational skills and work assessment (work rehabilitation programmes).
– Social skills training (develop interpersonal skills and ability to develop and
maintain relationships).
Primary care physicians or general practitioners (GPs) are in a prime position to detect
and begin early treatment of psychiatric illness. Twenty-five per cent of GP attenders
316 COMMUNITY-ORIENTATED PSYCHIATRY
have a psychiatric element to their consultation, yet only 43 per cent of GPs have had
training or experience in a psychiatric setting. Emphasis is on the role of primary care
physicians in multidisciplinary teams, and joint models of such care are now being
practised.
Bachrach LL (1992) Psychsocial rehabilitation and psychiatry in the care of long-term patients.
Am. J. Psychiatry 149, 1455.
Berzins KM, Petch A, Atkinson JM (2003) Prevalence and experience of harassment of people
with mental health problems living in the community. Br. J. Psychiatry 184, 526.
Christensen RC (2002) The ethics of cost shifting in community psychiatry. Psychiatr. Serv.
53, 921.
Clark C, Rich AR (2003) Outcomes of homeless adults with mental illness in a housing program
and in case management only. Psychiatr. Serv. 54, 78.
Cohen CI (2003) The future of community psychiatry. Commun. Ment. Health J. 39, 459.
Cohen CI, Thompson KS (1992) Homeless mentally ill or mentally ill homeless? Am. J. Psychiatr.
149, 816.
Compton SN, Swanson JW, Wagner HR et al. (2003) Involuntary outpatient commitment and
homelessness in persons with severe mental illness. Ment. Health Serv. Res. 5, 27.
Davies S (2002) Compulsory treatment in the community: current legal powers. Adv. Psychiatr.
Treat. 8, 180.
Desai MM, Rosenheck RA, Kasprow WJ (2003) Determinants of receipt of ambulatory medical
care in a national sample of mentally ill homeless veterans. Med. Care 41, 275.
Drury LJ (2003) Community care for people who are homeless and mentally ill. J. Health Care
Poor Underserved 14, 194.
Felton BJ (2003) Innovation and implementation in mental health services for homeless adults: a
case study. Commun. Ment. Health J. 39, 309.
Fiander M, Burns T et al. (2003) Assertive community treatment across the Atlantic: comparison
of model fidelity in the UK and USA. Br. J. Psychiatry 182, 248.
Gilmer TP, Folsom DP, Hawthorne W et al. (2003) Assisted living and use of health services
among Medicaid beneficiaries with schizophrenia. J. Ment. Health Policy Econ. 6, 59.
Hassett A, George K (2002) Access to a community aged psychiatry service by elderly from non-
English-speaking backgrounds. Int. J. Geriatr. Psychiatry 17, 623.
Jones K, Colson PW, Holter MC et al. (2003) Cost-effectiveness of critical time intervention to
reduce homelessness among persons with mental illness. Psychiatr. Serv. 54, 884.
Linsley K, Slinn R, Nathan R et al. (2001) Training implications of community-oriented psychi-
atry. Adv. Psychiatr. Treat. 7, 208.
Manderscheld RW, Henderson MJ, for the Center for Mental Health Services (2000) Mental
Health, United States 2000. DHHS, Washington, DC.
Marshall M (1989) Collected and neglected: are Oxford hostels for the homeless filling up with
disabled psychiatric patients? BMJ 299, 706.
Marshall M, Creed F (2000) Assertive community treatment: is it the future of community care
in the UK? Int. Rev. Psychiatry 12, 191.
Marshall M, Lockwood A (2000) Assertive community treatment for people with severe mental
disorders. Cochrane Database Syst. Rev. 2, CD-ROM.
Metraux S, Marcus SC, Culhane DP (2003) The New York-New York housing initiative and use of
public shelters by persons with severe mental illness. Psychiatr. Serv. 54, 67.
Moncrieff J (2003) The politics of a new Mental Health Act. Br. J. Psychiatry 183, 8.
REFERENCES AND FURTHER READING 317
Morrissey JP, Calloway MO, Thakur N et al. (2002) Integration of service system for homeless
persons with serious mental illness through the ACCESS program. Psychiatr. Serv. 53, 949.
Muijen M, Marks I, Connolly J et al. (1992) Home-based care and standard hospital care for
patients with severe mental illness: a randomized controlled trial. BMJ 304, 749.
Nose Michela, Garbui C (2003) Clinical interventions for treatment non-adherence in psychosis:
meta-analysis. Br. J. Psychiatry 183, 197.
Park MJ, Tyrer P, Elsworth E et al. (2002) The measurement of engagement in the homeless men-
tally ill: the Homeless Engagement and Acceptance Scale – HEAS. Psychol. Med. 32, 855.
Pijl YJ, Sytema S, Barels R, Wiersma D (2002) Costs of deinstitutionalization in a rural catchment
area in the Netherlands. Psychol. Med. 32, 1435.
Prigerson HG, Desai RA, Liu-Mares W, Rosenheck RA (2003) Suicidal ideation and suicide
attempts in homeless mentally ill persons: age-specific risks of substance abuse. Soc.
Psychiatry Psychiatr. Epidemiol. 38, 213.
Randolf F, Blasinsky M, Morrissey JP et al. (2002) Overview of the ACCESS program. Psychiatr.
Serv. 53, 945.
Readhead C, Henderson R, Hughes G, Nickless J (2002) Accredited accommodation: an alterna-
tive in-patient care in rural north Powys. Psychiatr. Bull. 26, 264.
Roberts G, Wolfson P (2004) The rediscovery of recovery: open to all. Adv. Psychiatr. Treat. 10, 37.
Rosenheack RA, Lam J, Morrissey JP et al. (2002) Service systems integration and outcomes for
mentally ill homeless persons in the ACCESS program. Psychiatr. Serv. 53, 958.
Simmons S, Coid J, Joseph P et al. (2001) Community mental health team management in severe
mental illness: a systematic review. Br. J. Psychiatry 178, 497.
Susser E, Conover M, Struering E (1989) Problems of epidemiologic method in assessing the type
and extent of mental illness among homeless adults. Hosp. Commun. Psychiatry 40, 261.
Swenson JR, Bradwejn J (2002) Mental health reform and evolution of general psychiatry in
Ontario. Can. J. Psychiatry 47, 644.
Trieman N, Leff J (2002) Long-term outcome of long-stay psychiatric in-patients considered
unsuitable to live in the community: TAPS Project 44. Br. J. Psychiatry 181, 428.
Turrer T, Priebe S (2002) Forget community care, reinstitutionalisaton is here. Br. J. Psychiatry
181, 253.
Wing JK, Brown GW (1970) Institutionalism and Schizophrenia: a Comparative Study of Three
Mental Hospitals 1960 to 1968. Cambridge University Press, Cambridge.
Ziguras SJ, Stuart GW, Jackson AC (2002) Assessing the evidence on case management. Br. J.
Psychiatry 181, 17.
Specific psychiatric 25
problems of women
EPIDEMIOLOGY
GENERAL
There is an increasing focus on women’s healthcare needs. Systems of care arrange to
promote comprehensive care to women – women’s Health Centers of Excellence – in
which mental health services play a major role.
In most Western societies, psychiatric disorders are more common in women.
Suggested reasons for this include:
• Genetic differences.
• Societal pressures.
• Differences of rearing patterns.
• Cultural expectations.
In general practice, the prevalence of mental disorders in females is three times that
in males. The inception rate is twice as high in females, suggesting a worse prognosis
in females.
SPECIFIC DISORDERS
Neuroses
• Women have twice the risk of developing neurotic depression.
• Interpersonal problems are reported more commonly in women.
• Anxiety states and obsessional disorders are equally distributed, but anxiety states
are more commonly reported by women.
Affective disorders
• The risk of developing unipolar psychotic depression is increased in women up to
the age of 75 (male, 3.5 per cent; female, 5.8 per cent).
• The risk of developing bipolar affective psychosis is evenly distributed.
• Women tend to report more somatic and psychic anxiety and more general
somatic symptoms.
EPIDEMIOLOGY 319
• Men tend to report more hypochondriacal fears and are more likely to lack insight.
• The oral contraceptive pill is not associated with a higher risk of depression in
females.
Schizophrenia
• The lifetime risk is equal in males and females.
• There is increased incidence in females aged under 16 years compared with males
under 16 and in females over 35 compared with males over 35.
• There is an increased incidence in males aged 16–35 compared with females aged
16–35.
• Process schizophrenia may be more common in men, while schizoaffective dis-
orders may be more common in women.
Suicidal behaviour
• Completed suicide is more common in men (11 per 100 000 per year) compared
with women (6 per 100 000).
• Deliberate self-harm is more common in women.
• Repeated deliberate self-harm seems to be slightly more common in men.
• The use of violent means of self-harm (knives, guns, etc.) is more common
in men.
Anorexia nervosa
• More common in females (female:male ratio about 9:1).
• More severe and with worse prognosis in males.
Mental handicap
More common in males (male:female ratio ⫽ 4:3).
Senile dementia
More common in females, but this may be due to the greater longevity of women.
Criminal behaviour
• Of children taken into care under the age of 13, 50 per cent of the boys have com-
mitted offences compared with 13 per cent of the girls.
• Adult males are convicted nine times more commonly than women. This figure
relates to reportability and sentencing policies as well as actual prevalence of
crime.
• Males commit more violent crime, while women tend to be convicted of offences
related to prostitution.
Alcoholism
Alcoholism is eight times more common in men (in a survey of south-east London).
320 SPECIFIC PSYCHIATRIC PROBLEMS OF WOMEN
PREMENSTRUAL SYNDROME
DEFINITIONS
There is no universally agreed definition.
• Physical symptoms – feeling bloated, weight gain, tender breasts, headache, back-
ache, cramps.
• Psychological symptoms – tension, irritability, depression, tiredness, forgetfulness.
There is recurrence of symptoms between ovulation and menstruation. They sub-
side during menstruation and are absent between menstruation and ovulation.
During this period there is said to be an increase in violent crimes, suicide and parasui-
cide, illness behaviour, accidents and poor academic performance. Many of these studies
are methodically flawed. Mental hospital admissions for all forms of disorder are higher
during the premenstrual period, suggesting that patients with pre-existing disorder feel
worse at this time. The relationship (if any) to mental disorder is unclear (Halbreich, 1995).
EPIDEMIOLOGY
Prevalence ranges from 20 to 95 per cent in studies, demonstrating diagnostic
unreliability.
Premenstrual complaint is found more commonly in those with psychiatric ill-
health. This may be because psychiatric distress sensitizes the women to the additional
premenstrual changes (Clare, 1983).
AETIOLOGY
Various unproven theories include:
• A relative deficiency of progesterone, raised prolactin levels, fluid retention, exces-
sive aldosterone, pyridoxine deficiency, raised MAO activity and ‘psychological’
effect.
• Premenstrual decline in circulating -endorphin.
TREATMENT
Selective serotonin re-uptake inhibitors have been shown to be effective in reducing the
symptoms of severe premenstrual syndrome (Dimmock et al., 2000). Progesterones
(e.g. dydrogesterone) show some improvement in symptoms. Supportive psychother-
apy, information giving and relaxation therapy may be beneficial.
EPIDEMIOLOGY
Women are less likely to be admitted to a psychiatric ward or to commit suicide dur-
ing pregnancy than at other times. This is in spite of the major life event which preg-
nancy forms.
POSTPARTUM PSYCHIATRIC DISORDERS 321
MANAGEMENT
• Increased support by medical, nursing and other services, as well as by family, may
reduce the need to contact psychiatric services. Clear and informed reassurance,
antenatal classes and discussion with other mothers should help.
• Interpersonal psychotherapy can be effective in the treatment of depression during
pregnancy (Spinelli and Endicott, 2003).
• Conjoint marital therapy or separate counselling of the husband may be indicated.
Drugs
Drug treatment with SSRIs or TCAs appears to be safe during pregnancy (Kohen,
2004).
Between 10 and 35 per cent of women take psychotropic drugs at some time during
their pregnancy. All psychotropics that can cross the blood–brain barrier (i.e. are
lipophilic) can cross the placenta. Higher blood levels may develop in the fetus than in
the mother. During the immediate antenatal period, psychotropics may lead to
oversedation of the neonate.
PUERPERAL PSYCHOSIS
EPIDEMIOLOGY
Psychoses occur following 1.5 per 1000 deliveries. They are associated with primi-
gravida status. A history of manic–depressive psychosis predicts 20 per cent chance of
developing puerperal psychosis.
Lack of specification of puerperal psychosis in ICD-10 and DSM-IV reflects con-
tinued confusion regarding the nosological status of puerperal disorders.
AETIOLOGY
• Genetic factors appear to play a part, since a family history of major psychiatric dis-
order predisposes to puerperal psychosis.
• Biochemical causes have been postulated for the functional psychoses, relating the
precipitation of psychosis to the effects of sudden decreases of progesterone and
oestrogen on tryptophan metabolism.
322 SPECIFIC PSYCHIATRIC PROBLEMS OF WOMEN
• There has been little evidence of an excess of psychological stresses in the peri-
natal period in the psychotic mother, although death of the baby may be a clear
precipitant.
• Psychodynamic factors may well be important and will include the patient’s relation-
ship with her own mother, her feelings about the responsibility of motherhood, her
reaction to this assertion of her female role, her relationship with her husband and
his personality (over-passive or over-dominant).
The relationship between lack of effective ‘bonding’ between mother and baby (due
to early separation, emotionally or physically) and the development of psychosis is
unclear.
CLINICAL FEATURES
Puerperal psychoses are widely held not to be a distinct and unitary form of psychosis
but to be divided into affective psychoses (70 per cent), schizophrenia (25 per cent)
and organic psychoses (very rare now in the UK).
The affective psychoses are primarily depressive. The few organic psychoses are par-
ticularly due to cerebral thrombophlebitis.
The evidence for suggesting that puerperal psychoses are not a distinct entity is:
1 Family history of psychotic disorder is as commonly present as in non-puerperal
psychosis.
2 There is an increased incidence of psychosis before and after the pregnancy and
puerperal period also.
3 Manic depressives have 10 times the risk of developing a puerperal psychosis com-
pared with the normal population.
4 The clinical syndromes resemble psychoses occurring at other times.
PROGNOSIS
Seventy per cent recover fully, affective psychosis having a better prognosis than schizo-
phrenic. The risk of psychosis in future puerperal periods is 14–20 per cent. The risk
of psychosis at any future time is up to 50 per cent.
Poor prognosis is indicated by a positive family history, schizophrenia, neurotic
personality and the presence of severe marital problems.
POSTPARTUM PSYCHIATRIC DISORDERS 323
PUERPERAL DEPRESSION
EPIDEMIOLOGY
Ten per cent (range 3–16 per cent) of women develop a non-psychotic depressive dis-
order in the postpartum period. Onset is usually within the first postpartum month,
often on return home and usually between day 3 and day 14.
It is associated with increased age, childhood separation from the father, problems
in relationships with mother- and father-in-law, marital conflict, mixed feelings about
the baby, physical problems in the pregnancy and perinatal period, a tendency to more
neurotic and less extroverted personalities.
AETIOLOGY
Possible aetiological factors include a postulated hormonal effect on tryptophan
metabolism.
Social and situational changes make the woman particularly vulnerable at this time.
Having a baby is an important life event involving changes in financial, social and
marital status. Lack of support from the partner or family may increase vulnerability
to depression.
CLINICAL FEATURES
Typically, the woman is tearful and irritable. Associated symptoms may include feeling
tired, despondent and anxious, with worry about ability to cope with baby, fear for
own and baby’s health and feeling generally inadequate.
There is often poor appetite, decreased libido and difficulty in sleeping. These
patients often have difficulty concentrating and may complain of feeling confused,
although cognitive testing is normal.
PROGNOSIS
Most symptoms (90 per cent) last less than 1 month, even without treatment. In 4 per
cent of cases they last longer than a year.
POSTPARTUM ‘BLUES’
EPIDEMIOLOGY
Fifty per cent of women have a short-lived emotional disturbance commencing on the
third day and lasting for 1–2 days. It is more common in primigravidae and in those
who complain of premenstrual tension.
CLINICAL FEATURES
Common features are: episodic weeping, feeling depressed and irritable, feeling sep-
arate and distant from the baby, insomnia and poor concentration. This coincides
with sudden weight loss, decreased thirst and increased urinary sodium secretion.
The syndrome would appear to have a biochemical basis.
324 SPECIFIC PSYCHIATRIC PROBLEMS OF WOMEN
Postpartum disorders are important to detect. There should be an early high index of
suspicion – don’t assume ‘baby blues’ – with use of rating scales (e.g. Edinburgh post-
natal depression scale). Postnatal depression may have enduring emotional and cogni-
tive sequelae for the infant. Young mothers particularly need support.
PSYCHOSIS
Admission to hospital is frequently required, owing to the potential danger to the baby
(of violence, neglect or mishandling) and to the difficulty of dealing with a behav-
iourally disturbed and psychotic mother at home.
Admission of both mother and baby together is always advisable, if possible (mother
and baby units). This allows for the development of bonding, reduction in the emo-
tional deprivation of the child and reduction in the guilt of the mother. It also allows for
the supervision of mother and baby, and their relationship. By gentle advice, encourage-
ment and reassurance the mother’s confidence can be built up. Breast-feeding can be
continued where possible and desired. The father should be free to visit and keep his
contact with his family.
Mothers admitted with their babies tend to stay in hospital for less time and are less
disturbed on discharge than mothers admitted without their babies.
Drugs and other physical treatments should be given as appropriate to the symptoms. If
the baby is breast-fed, major tranquillizers will be present in the milk and the baby should
be observed for over-sedation. If this occurs, the needs of the mother for sedation and
those of the baby for breast-feeding must be balanced. It may be necessary to stop breast-
feeding for a short period while the mother’s symptoms are brought under control.
Psychotherapy, usually of a supportive kind, is always required. Discussion will
centre on the mother’s relationship with the baby and her feelings about herself. Her
relationship with her partner and family may also be necessary to explore. Psychotherapy
will be aimed at reducing her guilt and feelings of inadequacy and hostility and at fos-
tering maternal feeling.
Couple therapy is often a critical component of recovery.
DEPRESSION
Since this is usually self-limiting, supportive measures of encouragement and reassurance
are usually all that are required. If the depression lasts for more than 1 month, an anti-
depressant may be indicated, as well as more active psychotherapy and marital therapy.
‘BLUES’
This does not require any more than simple reassurance and explanation, both to the
mother and to her partner.
TERMINATION OF PREGNANCY
About one in five pregnancies in the UK are terminated for therapeutic reasons. Sixty-
three per cent of females seeking abortion are single, 32 per cent are aged 20–24 years.
MENOPAUSE 325
STILLBIRTH
Psychiatric symptoms are rare after tubal ligation – 71–99 per cent are completely satis-
fied with the operation. Between 2 and 5 per cent greatly regret having the operation,
especially if aged less than 26, with a small family size and under pressure to be sterilized.
The incidence of psychiatric symptoms in the 18 months after sterilization is about
1 per cent and is no higher than the general population rate.
Sterilization has been shown to improve the mental state, social adjustment, general
health and marital and sexual relationships of the woman.
Although it was originally reported that hysterectomy is associated with increased
psychiatric illness, especially depression, subsequent studies have discounted this
claim.
MENOPAUSE
Angst J, Sellaro R, Merikangas KR, Endicott J (2001) The epidemiology of perimenstrual psycho-
logical symptoms. Acta Psychiatr. Scand. 104, 110.
Bhatia SC, Bhatia SK (2002) Diagnosis and treatment of premenstrual dysphoric disorder. Am.
Fam. Physician 66, 1239.
Birtchnell J (2001) The nature of grief: the evolution and psychology of reactions to loss. Br. J.
Psychiatry 178, 580.
Chandran M, Tharyan P, Muliyil J, Abraham S (2002) Post-partum depression in a cohort of
women from a rural area of Tamil Nadu, India: incidence and risk factors. Br. J. Psychiatry
181, 499.
Clare AW (1983) Psychiatric and social aspects of premenstrual complaint. Psychol. Med.,
Monograph Suppl. 4.
Cooper PJ, Murray L et al. (2003) Controlled trial of the short- and long-term effect of psycho-
logical treatment of post-partum depression. 1: Impact on maternal mood. Br. J. Psychiatry
182, 412.
Dimmock PW, Wyatt KM, Jones PW (2000) Efficacy of selective-serotonin-reuptake inhibitors
in premenstrual syndrome: a systematic review. Lancet 356, 1131.
Domoney CL, Vashisht A, Studd JW (2003) Premenstrual syndrome and the use of alternative
therapies. Ann. NY Acad. Sci. 997, 330.
Essex MJ, Klein MH, Miech R, Smider NA (2001) Timing of initial exposure to maternal major
depression and children’s mental health symptoms in kindergarten. Br. J. Psychiatry 179, 151.
Evans J, Heron J, Francomb H et al. (2001) Cohort study of depressed mood during pregnancy
and after childbirth. BMJ 323, 257.
Facchinetti F (2001) Female depression and menopause. Psychother. Psychosom. 70, 166.
Girman A, Lee R, Kligler B (2003) An integrative medicine approach to premenstrual syndrome.
Am. J. Obstet. Gynecol. 188, s56.
Grady-Weliky TA (2003) Premenstrual dysphoric disorder. New Engl. J. Med. 348, 433.
Halbreich U (1995) Premenstrual dystrophic disorders, anxiety and depressions: vulnerability
traits or comorbidity? Arch. Gen. Psychiatry 52, 606.
Howard LM, Goss C, Leese M, Thornicoft G (2003) Medical outcome of pregnancy in women
with psychotic disorders and their infants in the first year after birth. Br. J. Psychiatry 182, 63.
Huttner RP, Shepherd JE (2003) Gonadal steroids, selective serotonin reuptake inhibitors, and
mood disorders in women. Med. Clin. North Am. 87, 1065.
Iles S, Gath D (1993) Psychiatric outcome of termination of pregnancy. Psychol. Med. 23, 407.
Kessler RC (2003) Epidemiology of women and depression. J. Affect. Disord. 74, 5.
Kirkcaldy B, Siefen G, Furnham A (2003) Gender, anxiety-depressivity and self-image among
adolescents. Eur. Psychiatry 18, 50.
Kohen D (2003) Psychiatric illness in women: emerging treatment and research. Br. J. Psychiatry
B, a460.
Kohen D (2004) Psychotropic medication in pregnancy. Adv. Psychiatr. Treat. 10, 59.
Korstein SG, Wojcik BA (2002) Depression. In: Kornstein SG, Clayton AH (eds), Women’s Mental
Health: a Comprehensive Textbook. Guilford Press, New York.
Lee DTS, Yip ASK, Leung TYS, Chung TKH (2004) Ethnoepidemiology of postnatal depression:
prospective multivariate study of sociocultural risk factors in a Chinese population in
Hong Kong. Br. J. Psychiatry 184, 34.
Lehtinen V, Michalak E, Wilkinson C et al. (2003) Urban–rural differences in the occurrence
of female depressive disorder in Europe: evidence from the ODIN study. Soc. Psychiatry
Psychiatr. Epidemiol. 38, 283.
Lovett KF (2001) PTSD and stillbirth. Br. J. Psychiatry 179, 367.
REFERENCES AND FURTHER READING 327
MacArthur C, Winter HR, Bick DE et al. (2002) Effects of redesigned postnatal care on women’s
health 4 months after birth: a cluster randomized controlled trial. Lancet 359, 378.
Martin N (2001) Feminist bioethics and psychiatry. J. Med. Phil. 26, 431.
Miller LJ (2002) Postpartum depression. JAMA 287, 762.
Miller MN, Miller BE (2001) Premenstrual exacerbations of mood disorders. Psychopharmacol.
Bull. 35, 135.
Morris-Rush JK, Freda MC, Bernstein PS (2003) Screening for postpartum depression in an
inner-city population. Am. J. Obstet. Gynecol. 188, 1217.
Murray L, Cooper PJ et al. (2003) Controlled trial of the short- and long-term effect of psycho-
logical teatment of post-partum depression. 2: Impact on the mother–child relationship and
child outcome. Br. J. Psychiatry 182, 420.
Nonacs R, Cohen LS (2003) Assessment and treatment of depression during pregnancy: an
update. Psychiatr. Clin. North Am. 26, 547.
O’Connor TG, Heron J, Glover V (2002) Antenatal anxiety predicts child behavioral/emotional
problems independently of postnatal depression. J. Am. Acad. Child Adolesc. Psychiatry
41, 1470.
Petrou S, Cooper P et al. (2002) Economic costs of post-natal depression in a high-risk British
cohort. Br. J. Psychiatry 181, 505.
Reardon DC, Cougle JR, Rue VM et al. (2003) Psychiatric admissions of low-income women fol-
lowing abortion and childbirth. CMAJ 168, 1253.
Ross LE, Steiner M (2003) A biopsychosocial approach to premenstrual dysphoric disorder.
Psychiatr. Clin. North Am. 26, 529.
Sajatovic M, Rosenthal MB, Plax MS et al. (2003) Mental illness and menopause: a patient and
family perspective. J. Gend. Specif. Med. 6, 31.
Spinelli MG, Endicott J (2003) Controlled clinical trial of interpersonal psychotherapy versus
parenting education program for depressed pregnant women. Am. J. Psychiatry 160, 555.
Steiner M, Born L (2002) Psychiatric aspects of the menstrual cycle. In: Kornstein SG, Clayton
AH (eds), Women’s Mental Health: a Comprehensive Textbook. Guilford Press, New York.
Stotland NL (2002) Psychiatric issues related to infertility, reproductive technologies, and abor-
tion. Prim. Care 29, 13.
Turton P, Hughes P, Evans CDH, Fainman D (2001) Incidence, correlates and predictors of post-
traumatic stress disorder in the pregnancy after stillbirth. Br. J. Psychiatry 178, 556.
Warnock JK, Clayton AH (2003) Chronic episodic disorders in women. Psychiatr. Clin. North
Am. 26, 725.
Wyatt K, Dimmock P, Jones P et al. (2001) Efficacy of progesterone and progestogens in manage-
ment of premenstrual syndrome: systematic review. BMJ 323, 776.
Zolese G, Blacker CVR (1992) The psychological complications of therapeutic abortion. Br. J.
Psychiatry 160, 742.
Transcultural psychiatry 26
CULTURAL CONTEXT
Evidence exists for both views. Patterns of ‘pathological’ behaviour may mirror and
exaggerate the patterns of normal behaviour in a culture, but still fall into the same
very broad diagnostic categories in all countries – the ‘pathoplastic’ effect of culture.
Delusions and hallucinations are recognized as abnormal in almost all cultures (e.g.
Yoruba of Nigeria, West Indians, Asians). Inhabitants of developing countries tend to
discriminate differently between different emotional states from inhabitants of developed
countries.
Reaction to mental disorder by the local community varies greatly; greater acceptance
may reduce social incapacity.
SPECIFIC DISORDERS
SCHIZOPHRENIA
Schizophrenia was originally noted to have increased incidence in the USA compared
with the UK, as well as reduced incidence in developing countries. Neither view is correct
(see Chapter 3).
Use of the PSE in the International Pilot Study of Schizophrenia showed that
reliable diagnosis of schizophrenia could be made throughout the world by local
psychiatrists in nine different countries, including India, Colombia, Nigeria, the Soviet
Union, the USA and the UK. Prevalence was similar in all countries, although the USA
SPECIFIC DISORDERS 329
and Soviet Union had apparently higher prevalence of locally (but not PSE-) diag-
nosed ‘schizophrenia’.
Confusion, excitement, transient hallucinations and unsystematized (often para-
noid) delusions are more common in Africa. Catatonic symptoms are more common
in India.
Outcome is consistently shown to be better in developing countries, in terms of
reduced social disability and psychopathology, even when single acute episodes are
discounted. The reason is unknown (Jablensky et al., 1992).
DEPRESSION
NEUROSES
‘CULTURE-BOUND’ DISORDERS
ORGANIC PSYCHOSYNDROMES
AFFECTS OF MIGRATION
Astrup C, Ødegaard O (1960) Internal migration and mental disease. Psychiatr. Q. Suppl. 34, 116.
Baer RD, Weller SC, de Alba Garcia JG et al. (2003) A cross-cultural approach to the study of the
folk illness nervios. Culture, Med. Psychiatry 27, 315.
Bhui K, Stansfeld S, Hull S et al. (2003) Ethnic variations in pathways to and use of specialist
mental health services in the UK: a systematic review. Br. J. Psychiatry 182, 105.
Boydell J, van Os J, McKenzie K et al. (2002) Incidence of schizophrenia in ethnic minorities.
I: London – ecological study into interactions with environment. BMJ 323, 1336.
Caracci G, Mezzich JE (2001) Culture and urban mental health. Psychiatr. Clin. North Am. 24, 581.
Coker EM (2003) Narrative strategies in medical discourse: constructing the psychiatric ‘case’ in
a non-western setting. Social Sci. Med. 57, 905.
Fabrega H (2001) Culture and history in psychiatric diagnosis and practice. Psychiatr. Clin. North
Am. 24, 391.
Fabrega H (2001) Cultural psychiatry: international perspectives. Epilogue. Psychiatr. Clin.
North Am. 24, 595.
Fabrega H (2001) Mental health and illness in traditional India and China. Psychiatr. Clin. North
Am. 24, 555.
Harrison G (1991) Migration and Mental Disorders. Med. Internat., 3978. The Medicine
Group (UK).
Harrison G, Eaton W (2002) Migration and the social epidemiology of schizophrenia. In:
Hafner H (ed.), Risk and Protective Factors in Schizophrenia. Steinkopff, Darmstadt.
Harrison G, Owens D, Holton T et al. (1988) A prospective study of severe mental disorder in
Afro-Caribbean patients. Psychol. Med. 18, 643.
332 TRANSCULTURAL PSYCHIATRY
USEFUL WEBSITES
GOVERNMENTAL
• US National Library of Medicine, creator of MEDLINE/PubMed:
– www.nlm.nih.gov
• National Institute of Mental Health (NIMH), the leading Federal agency for
research on mental and behavioral disorders in the USA:
– www.nimh.nih.gov
• Substance Abuse and Mental Health Services Administration, part of the US
Department of Health and Human Services
– www.samhsa.gov
• National Institute for Clinical Excellence (for clinical guidelines in UK):
– www.nice.org.uk
NON-GOVERNMENTAL
Advocacy/support sites
• Bazelon Center for Mental Health Law:
– www.bazelon.org
• National Alliance for the Mentally Ill (NAMI):
– www.nami.org
334 PSYCHIATRY AND THE INTERNET
Other sites
• American Psychiatric Association:
– www.psych.org
• Expert Consensus Guidelines Series:
– www.psychguides.com
• Internet Mental Health:
– www.mentalhealth.com
• Mental Health InfoSource:
– www.mhsource.com
• Mental-Health-Matters.com:
– www.mental-health-matters.com
• Mental Help Net:
– www.mentalhelp.net
• Mental Wellness.com:
– www.mentalwellness.com
• Pharmacology Algorithm Project (Harvard):
– http://mhc.com/Algorithms
• PlanetPsych.com:
– www.planetpsych.com
• PSYweb.com:
– www.psyweb.com
• Refdesk.com Mental Health:
– www.refdesk.com/mental.html
• Royal College of Psychiatrists:
– www.rcpsych.ac.uk
Baker L, Wagner TH, Singer S, Bundorf MK (2003) Use of the Internet and e-mail for health care
information: results from a national survey. JAMA 289, 2400.
REFERENCES AND FURTHER READING 335