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SCHIZOPHRENIA
Version 2 Final
EBM Schizophrenia
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Document control
Version history
Version
Date
Comments
2 Final
14 October 2011
Signed off by HWWD and CMMS
2e draft
06 October 2011
Re-ordering of intro Section 8 as
suggested by HWWD
Comment from HWWD incorporated
2d draft
15 September 2011
2c draft
29 Aug 2011
External QA comments incorporated
2b draft
03 April 2011
External QA by specialist registrar
2a draft
Int. Q.A.
Changes since last version
Section 1.2
Section 2.3
Section 4 - Medical Conditions and Psychiatric Conditions
Section 6.1.2
Section 6.1.4 - Extrapyramidal (EPS) and Weight Gain and Metabolic Syndrome
Section 6.4
Section 7.1 – Clinical Features
Section 7.2 - Sociodemographic
Section 8.4 – ESA Considerations
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1.
Description
The diagnosis of schizophrenia encompasses a major group of mental disorders of
unknown cause, characterised by a complex set of disturbances of thinking,
perception, affect, cognition and social behaviour.
The typical course of the disease is of acute episodes of hallucinations, delusions
and florid disorganisation of thought; superimposed on a persistent chronic disorder
of initiation and organisation of thought and behaviour.
1.1
Definition
The term schizophrenia was introduced in 1911 by Eugen Bleuler to describe the
chronic psychoses of young and middle life formerly known as dementia praecox.
Bleuler regarded fragmentation of mental processes to be the hallmark of the illness
and chose the name to denote this.
Thus the initial concept of schizophrenia was the fragmentation of mental functions;
delusions and hallucinations were considered to be a transient feature of the illness.
However, as attempts were made to improve the reliability of diagnosis, the
presence of delusions and hallucinations assumed greater importance and the
emphasis shifted from the chronic to the acute phase of the illness.
In 1959, Kurt Schneider attempted to define a set of symptoms that would provide a
reliable basis for the diagnosis of schizophrenia. He identified a set of symptoms
that have become known as first rank symptoms (Appendix B).
Schneider did not
give explicit definitions of these and clinicians have used various definitions that
differ in detail. Mellor (1970) formulated a strict set of definitions (See Glossary of
terms Appendix B).
No biological marker exists for schizophrenia. Diagnosis is made by examination
of the mental state, by clinical interview and observation of the patient’s behaviour.
Historically there have been substantial differences in the diagnostic practices
between the United Kingdom and the United States. In the UK the emphasis is
placed on first rank symptoms, whilst in the USA, a broad concept of schizophrenia
has developed from a tradition influenced by Bleuler. This difference is reflected in
the two major definitions of schizophrenia,
The International Classification of Disease (ICD–10) published by the World
Health Organisation.1
The Diagnostic and Statistical Manual Of the American Psychiatric Association
(DSM–IV ).2
The diagnostic criteria for schizophrenia according to ICD–10 and DSM–IV are given
in Appendix C.
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1.2
Subtypes and Syndromes of Schizophrenia
ICD–10 divides schizophrenia into seven subtypes: paranoid, hebephrenic,
catatonic, undifferentiated, post-schizophrenic depression, residual and simple.
DSM–IV divides schizophrenia into five subtypes: paranoid, disorganised, catatonic,
undifferentiated and residual.
These subtypes are based on presentation and although useful as descriptive
shorthand, do not reliably predict treatment or prognosis.
Schizophrenic symptoms can be seen as:
1. An excess or distortion of normal function =
positive symptoms
or
2. A decrease or loss of normal function =
negative symptoms.
Positive Symptoms
Negative Symptoms
Formal Thought Disorder
Poverty of thought and speech
Disorganised behaviour
Impaired volition
Inappropriate affect
Blunt affect and anhedonia (lack of
ability to experience pleasure)
Delusions
Social withdrawal
Hallucinations
Impaired attention
In chronic schizophrenia, the symptoms appear to segregate into
three core
syndromes.
Negative symptoms appear to cluster together as part of a syndrome termed
psychomotor poverty
Positive symptoms fall into two separate clusters:
reality distortion
disorganisation
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Negative symptoms:
Poverty of speech
Blunted affect
Psychomotor Poverty
Decreased spontaneous
movement
Positive symptoms:
Delusions
Reality Distortion
Hallucinations
Inappropriate affect
Disorganisation
Formal thought disorder
Disorganised behaviour
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2.
Epidemiology
The lack of diagnostic uniformity has been a major problem in the epidemiological
study of schizophrenia, making comparisons between studies almost impossible.
The diagnosis of schizophrenia was more loosely applied in the USA than in the UK.
The US/UK diagnostic project in the 1970s concluded that epidemiological
differences were due to variations in diagnostic practice.
Case finding is a further problem in schizophrenia epidemiological research. Most
studies are based on hospital admissions, which are subject to variations in service
provisions and admission policies. Bias occurs from the inclusion of readmissions,
and over-representation of more severe cases. Case registers that record all first
contacts with the psychiatric services for a specified area, over a specified time
period, are a useful resource in developed countries.
Due to these difficulties, the conclusions reached from epidemiological studies in
schizophrenia are frequently contested.
2.1
Prevalence
The majority of epidemiological studies have estimated the point prevalence of
schizophrenia to be in the range 1.4 to 4.6 per 1000 population3 The lifetime
prevalence (risk) of schizophrenia is estimated at 0.3-0.7% (3 to 7 per 1000
population).4,5
2.2
Incidence
The incidence rate is a better indicator of the morbidity within a population. Its
estimation depends on how reliably the point of onset of the disorder can be
determined and hence is dependent on the diagnostic criteria used.
Studies using restrictive criteria such as ICD–10 , DSM–III and its successors report
incidence rates two to three times lower than those reported by studies which use
broad criteria (ICD–8, ICD–9).
In a recent large systematic review, the median incidence of schizophrenia was
15.2/100,000 persons, and the central 80% of estimates varied over a fivefold range
(7.7-43.0/100,000)
.5
2.3
Epidemiological Variables
Men develop schizophrenia on average 5 years earlier than women. The peak
incidence of onset is between 15-25 years in men and 20 -35 years in women.
The total lifetime risk for the development of schizophrenia is similar in men and
women.6
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There is controversy as to whether the incidence of schizophrenia is showing
variation over time. There have been reports that the incidence in industrial
countries rose in the 19th century and has shown a decline recently. However others
argue that this reflects changing policies in caring for the severely mentally ill.
Diagnostic categories which encompass negative symptoms and long duration of
illness have higher incidence rates for men than for women, whereas those which
include more affective symptoms and brief presentations show similar rates in men
and women. These data suggest that the symptomatic expression of schizophrenia
is more severe in men than in women.7
Schizophrenia occurs in all cultures.
Geographical variation may reflect the effect of environmental and/or genetic
aetiological factors.
In industrialised countries there are more schizophrenic patients in the lower
income groups.6,7 Admission rates for schizophrenia are higher in urban areas than
in rural areas. Within urban settings, admission rates for schizophrenia are higher in
the socially disadvantaged areas.8,9
Two hypotheses have been put forward to explain these findings:
1.
Social Drift Hypothesis postulates that affected individuals drift down to lower
socio-economic classes as a consequence of the social, occupational and
financial disadvantage associated with schizophrenia.
2.
Social Causation Hypothesis suggests that socio-economic deprivation
increases the risk of exposure to possible environmental risk factors, e.g.
obstetric complications and prenatal virus exposure.
Current research suggests that causation (urban environment causes psychosis) is
more important than selection (high-risk individuals move into urban areas) and that
the effect of environmental factors in the urban environment is conditional on genetic
risk (i.e., there may be gene-environment interaction).10,11
There is evidence that some immigrant ethnic groups have a higher risk of
developing psychotic disorders than have native-born individuals, particularly if they
live in a low ethnic density area, or an area where there are fewer people of the
same migrant group.12,13
In the UK, much research has focussed on the high rate of schizophrenia in first and
second generation Afro-Caribbean immigrants.14 The social adversity experienced
by immigrants may explain the high incidence of schizophreni
a.10 The second-
generation effect may have a different aetiology.
Schizophrenic patients are more likely than the general population to be born in
winter or early spring.15 The size of the effect is in the order of 5-10%, although the
explanation is unknown.
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3.
Aetiology
Schizophrenia is a heterogeneous disorder and this may reflect several pathological
processes with different aetiologies. It is currently believed to result from variations
in multiple genes, each contributing a subtle effect, which interact and combine with
each other and with environmental stimuli to impact on both early and late brain
development.
Aetiological factors can be divided into:
1.
Predisposing factors: mainly biological factors, which predispose the individual
to the disorder
2.
Precipitating factors: largely social factors, which precipitate the onset and
relapse of the disorder
Schizophrenia is considered by some as a neurodevelopmental disorder. A possible
environmental insult in a biologically predisposed individual leads to abnormalities in
brain function, which manifest themselves as schizophrenia.16 Abnormalities in brain
structure, brain function, neuronal function and neurotransmitter function have been
reported in schizophrenia.
3.1
Predisposing Factors
A
genetic predisposition to the development of schizophrenia has been shown by
family studies, adoption studies and twin studies.17 It has proved difficult to make an
accurate assessment of the genetic risk.18
Schizophrenia does not follow a Mendelian model of transmission, and both single
gene and polygenic models of inheritance have been postulated. It is unlikely that a
single gene with a large effect will be identified that causes schizophrenia. It is more
probable that it will be found to resemble other non-Mendelian complex disorders
where many different genes make a small, yet significant contribution to disease
vulnerability.
Recently, several susceptibility genes have been identified which may be linked to
schizophrenia.19
Environmental influences are significant; shown by monozygotic twin concordance
rates of <40%.20 Given the heterogeneous nature of schizophrenia, it is likely that
both genetic and non-genetic forms of the disease exist.
People who develop schizophrenia are more likely to have a history of antenatal and
birth complications than the general population.21
As observed above, a 5-10% excess of schizophrenic patients are born in late winter
and early spring. A number of reports have postulated that exposure
in utero to
influenza and other viruses increase the subsequent risk of schizophrenia. This has
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been countered by a similar number of reports that have found no association, and
the theory is controversial.
Older paternal age at conception has been linked to an approximate doubling of the
risk for developing schizophrenia, and while the reason for this observation has not
been advanced, impaired spermatogenesis leading to an increased likelihood of
de
novo mutation has been proposed as a possible explanation.22
3.2
Precipitating Factors
Biological predisposition alone cannot account for the development of
schizophrenia. Interpersonal, social and cultural factors are thought to interact with
genetic vulnerability and environmental factors to influence the development and
course of the disease.
Expressed emotion (EE) is a measure of how families interact based on a
structured interview (The Camberwell Family Interview). Families with high levels of
expressed emotion score highly on critical comments, hostility and over-
involvement. Patients from families with high EE relapse more frequently, regardless
of the severity of symptoms or the behavioural disturbance. However it is likely that
such factors as anxiety may increase the vulnerability of the schizophrenic patient to
critical attitudes on the part of family members and others.23
Abuse of specific drugs can produce a psychosis that mimics schizophrenia,
however drug abuse
per se is thought to precipitate schizophrenia in predisposed
individuals. Systematic reviews of prospective studies have suggested that cannabis
use is associated with increased risk of psychosis and psychotic symptoms.24
3.3
Brain Abnormalities in Schizophrenia
Abnormalities have been reported in brain structure and function in schizophrenia.
Structural abnormalities are seen on computed tomography (CT) and Magnetic
Resonance Imaging (MRI) scans. Brain abnormalities are present at the onset of
schizophrenia. Changes have been noted in the whole brain volume, ventricular
volume, frontal lobes, temporal lobes and limbic structures (Appendix D).
Functional brain abnormalities have been reported in association with the
symptom clusters of psychomotor poverty, disorganisation and reality distortion.
Abnormalities have also been reported with single symptoms and cognitive tasks.
Magnetic Resonance Spectroscopy (MRS) is an in-vivo method that allows
investigation of dynamic processes at the neuronal level, and abnormal neuronal
function has been noted.
There is some evidence of abnormal neuronal membrane metabolism and hence
abnormal synaptic function. The abnormalities appear ongoing, however they
appear to have periodic exacerbations, possibly during the most active phases of
the illness.
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Neurotransmitter abnormalities have been reported in several systems.
Drugs which cause dopamine release (e.g. amphetamines), dopamine agonists (e.g.
bromocriptine) or dopamine precursors (e.g. L- Dopa), produce psychotic symptoms
or worsen schizophrenia, and the clinical potency of neuroleptic drugs correlates
strongly to their binding affinity to dopamine type 2 (D2) receptors. Historically, the
dopamine hypothesis suggested that schizophrenia was due to hyperactivity of the
brain’s dopaminergic system.
However, more recently other neurotransmitter systems have been implicated.
At least 15 receptors have been identified in the
serotonin (5 HT) system. The
atypical antipsychotic drugs are potent 5HT antagonists and have a stronger affinity
for 5HT than for dopaminergic receptors. Their mode of action may reflect
modulation of activity in both systems.
Glutamate and
aspartate are amino acids which act as excitatory
neurotransmitters. Phenylcyclidine binds to amino acid receptors within the brain
and produces a syndrome that mimics both negative and positive symptoms of
schizophrenia.25
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4.
Differential Diagnosis
As the boundaries between schizophrenia and other psychotic disorders are ill
defined, differential diagnosis can be difficult. Diagnosis requires clusters of
symptoms to be recognised over a period of time.
Symptoms suggestive of schizophrenia can be found in several neurological and
psychiatric disorders. Differential diagnosis should consider the following conditions:
Medical Conditions
Delirium
Epilepsy (particularly temporal lobe epilepsy)
Central nervous system neoplasms (especially frontal or limbic)
Central nervous system trauma
Central nervous system infections (especially malaria, other parasitic diseases,
neurosyphilis, herpes encephalitis)
Cerebrovascular accidents
Other central nervous system diseases (leukodystrophy, Huntington’s chorea,
Wilson’s disease, systemic lupus erythematosus etc)
Metabolic and endocrine disorders (e.g. electrolyte imbalance, thyroid disease)
Psychiatric Conditions (Appendix A: Atypical Psychoses)
Schizoaffective disorder
Schizophreniform disorder
Acute and transient psychotic disorders
Persistent delusional disorders
Drug induced psychosis (especially related to the use of amphetamine, LSD and
phencyclidine), both acute intoxication with and withdrawal from
Mania
Psychotic depression
Personality disorder
Schizotypal disorder
Factitious disorder (e.g. Münchausen’s syndrome)
4.1
Comorbidity
Patients with schizophrenia are at greater risk of developing another mental illness
compared with the general population.26 Substance abuse comorbidity is most
common. Anxiety and depressive symptoms are also very common throughout the
course of illness; the estimated prevalence is 15% for panic disorder, 29% for post-
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traumatic stress disorder, and 23% for obsessive-compulsive disorder. It is
estimated that comorbid depression occurs in 50% of patients. These comorbid
conditions adversely affect outcome.
4.1.1 Depression
The prevalence of depressive symptoms among patients with schizophrenia has
been reported to range from 25% to 81%, depending on the treatment setting, phase
of the illness, and the definition of depression.27
Depressive features are often present in the early phases of psychotic episodes,
during acute episodes and after recovery from psychosis (post-psychotic
depression).28
Patients experiencing depressive symptoms when in remission from a psychotic
episode are at a high risk of suicide. This is especially true of young males with good
premorbid functioning and high expectations.
Depression in schizophrenia needs to be differentiated from:
Neuroleptic induced dysphoria
Neuroleptic induced akinesia
Negative symptoms of schizophrenia
Depressive symptoms during an acute episode may improve with antipsychotic
medication regardless of the antipsychotic agent used. Clozapine appears to be
effective in decreasing suicide in schizophrenia.29
Antidepressant treatments do not appear to be more effective than placebo when
used alone to treat depression in schizophrenia.
4.1.2 Substance Abuse
The prevalence of substance misuse in schizophrenia is dependent on demographic
factors.30 It has been reported as almost 50%, with schizophrenic patients three
times more likely to misuse drugs or alcohol than the general population.31
Patients with schizophrenia who misuse drugs have a tendency to use activating
drugs rather than central nervous system depressants such as alcohol, hypnotics
and opiates.32
The preferred drugs mimic the effects of schizophrenia and cause relapse, such as:
PCP (angel dust)
Cocaine/crack
LSD
Amphetamines
Marijuana and other cannabis products
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There is evidence to suggest that schizophrenic patients with better premorbid
functioning are more likely to misuse drugs. Paradoxically, those patients who have
a better prognosis with regard to their schizophrenia are most at risk of descending
into drug misuse and its attendant problems
.32
The complications of drug misuse in schizophrenia are:
Exacerbation of symptoms
Increased relapse and hospitalisation
Homelessness and downward social drift
Violent and criminal behaviour
Poor compliance
Decreased response to medication
Poor prognosis and outcome in established psychotic illness
Substance abuse frequently goes undetected in schizophrenia, and the first rule of
effective management is to maintain a high index of suspicion. Patients with a dual
diagnosis of schizophrenia and substance misuse are often passed between acute
psychiatric services and substance misuse services. This can be minimised by
having an agreed management policy.
4.1.3 Medical Comorbidity
The increased medical comorbidity in schizophrenia is well recognised.33 It is largely
due to chronic conditions, especially cardiovascular disease (because of obesity,
hyperlipidaemia, diabetes, smoking, sedentary life style, the adverse effects of some
antipsychotic medications, and other factors).34
In recent years, HIV infection has been reported with increasing frequency.35
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5.
Clinical Course
The clinical course of schizophrenia shows significant variability in mode of onset,
degree of symptom persistence and long-term outcome. The following phases may
or may not be present in any individual.
5.1
Onset
5.1.1 Premorbid Phase
Social and cognitive defects may appear in childhood
Subtle motor, linguistic and social dysfunction has been reported in children who
later develop schizophrenia
In the prepsychotic stage of illness these children show increasing
developmental deviation with age, with cognitive slippage becoming more
marked in early adolescence36,37
5.1.2 Prodromal Phase
This precedes the acute onset of florid psychotic symptoms and may last several
months
Subtle behavioural changes are followed by preoccupation and social
withdrawal. This is characterised by odd ideas, eccentric interests, changes in
affect, unusual speech and bizarre perceptual experiences
Agitation becomes prominent and arises before overt psychosis appears
There is continuing debate as to whether treatment should be initiated in this
stage, i.e. before overt psychotic symptoms appear
5.1.3 Acute Onset
The onset of schizophrenia may be abrupt
Dysphoria, irritability, obsessional thoughts, poor concentration and sleep
disturbance occur over a few weeks
This is followed by the development of delusions and hallucinations, and a rapid
deterioration in occupational and social functioning
May be precipitated by a stressful experience or drug abuse
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5.2
Acute Phase
The most frequent symptoms of acute schizophrenia found in the International Pilot
Study of Schizophrenia (IPSS)38 were:
Symptom
Frequency (%)
Lack of insight
97
Auditory hallucinations
74
Ideas of reference
70
Suspiciousness
66
Flatness of affect
66
Second person hallucinations
65
Delusional mood
64
Delusions of persecution
64
Thought alienation
52
Thoughts spoken aloud
50
83% achieve a remission within 12 months, however 14% only achieve a partial
remission
Mean time to achieve a remission was 42 weeks, median time was 10 weeks
5.3
Medium and Long-term Course
Schizophrenia is a chronic illness; those who recover may experience relapses
many years after the initial presentation
Historically, the course of schizophrenia was considered to be one of continuous
deterioration. This is now thought to be overly pessimistic; however there is a
wide range of variability
The greatest variability occurs in the initial stages of the disease, with the clinical
course becoming established within the first five years
In most cases, the course follows one of four broad patterns (Table 1)
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5.3.1 Table 1: Initial Course of Schizophrenia (derived from Shepherd)39
Course of Disease 5
Residual
Number of Acute
years after First Episode
Functional/Cognitive
Psychotic Episodes
(% of cases)
Impairment
Complete Remission (22%)
Single
None
Episodic Remittent (35%)
Multiple
None or minimal
Episodic with stable deficit
Multiple
Impairment following first
(8%)
episode, subsequent
episodes return to this level
of impairment
Episodic with progressive
Multiple
Increasing impairment
deficit (35%)
following each acute
exacerbation
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6.
Treatment
Treatment of schizophrenia can be broadly divided into treatment of acute psychotic
episodes, prevention of relapse and minimising functional disability. Treatment
includes drug and psychosocial interventions, the former being used for treatment of
acute episodes and prevention of relapse, and the latter for prevention of relapse
and disability.
Early recognition is important. Recent research has demonstrated that the longer the
time between the emergence of psychotic symptoms and the start of antipsychotic
treatment, the more unfavourable the outcome.40,41
6.1
Drug Treatment
6.1.1 Typical Antipsychotic Drugs
The term ‘neuroleptic’ was introduced in the 1950’s to characterise compounds that
had an antipsychotic effect that was not due to sedation.
These are now called ‘typical’ antipsychotic compounds and include
chlorpromazine, trifluoperazine, flupenthixol, haloperidol and
pimozide.
Typical antipsychotic compounds are more effective in treating the positive
symptoms of schizophrenia than the negative symptoms. No one drug is superior to
another, however they do differ in their side effect profile; as a rule the higher the
potency, the higher the risk of extrapyramidal side effects; the lower the potency, the
greater the risk of sedation, hypotension, anticholinergic effects and seizures.
6.1.2 Atypical Antipsychotic Drugs
Atypical antipsychotic drugs are a new diverse group of compounds that include
amisulpride, clozapine, olanzapine, risperidone, quetiapine, sertindole,
amisulpride, ziprasidone and
zotepine.
Atypical antipsychotics:
Are effective in reducing positive symptoms
May be more effective in reducing negative symptoms than typical antipsychotics
Cause less extrapyramidal side effects than typical antipsychotics
6.1.3
Newer Atypical Antipsychotic drugs
A number of new antipsychotic agents are currently under development and some of
these appear to show promise. Side effects however continue to present a
challenge.42
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6.1.4 Side effects of Antipsychotics
Antipsychotic agents have wide ranging side effects that are distressing to patients
and some are potentially fatal.
CNS Side Effects:
Sedation
Commonly seen on initiation of treatment
Extrapyramidal
Includes dystonia, akathisia and drug-induced Parkinsonism
(EPS)
(tremor, rigidity and bradykinesia).
Can occur with all antipsychotics, but atypical less likely than
typical to produce EPS.
Lowest likelihood with quetiapine and clozapine.
Treated with anticholinergic drugs such as procyclidine or
orphenadrine.
Tardive
About 5% of patients develop TD for each year of treatment
Dyskinesia (TD)
with antipsychotics.
Two types of abnormal movement are commonly seen:
Stereotypies: Commonly involve the mouth and face; chewing,
grimacing; lip smacking/licking pursing; lateral tongue
movements or protrusion, although there may be complex
movements affecting any part of the body.
Dystonic movements: Commonly involve cranial and neck
muscles, e.g. tonic jaw deviation and torticollis. Involvement of
truncal muscles can produce severe scoliosis.
Can occur up to 6 months after the drugs are discontinued.
The elderly are most at risk; the risk of TD increases threefold
after 40 years of age.
TD is seen with typical and atypical antipsychotics, although
clozapine, olanzapine and risperidone are said to have a
lower propensity to cause this problem and have been used to
treat TD.
Discontinuation of the antipsychotic may improve tardive
dyskinesia, or paradoxically, may increase it.
Anticholinergic agents (benzotropine) and GABA receptor
agonists (clonazepam) are useful for dystonia but not for
stereotypies.
Seizures
Antipsychotics lower the seizure threshold; the risk is greatest
in those receiving low potency typical antipsychotics or
clozapine.
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Other Side Effects
Anticholinergic
Dry mouth, blurred vision, urinary hesitancy or retention,
Effects
constipation and flushing are commonly seen early in treatment.
Tolerance often develops and treatment is not needed.
If symptoms persist then relief may be obtained by switching to a
high potency antipsychotic.
Cardiovascular
ECG changes, tachycardia and postural hypotension are
commonly seen.
Risks are greater in those with pre-existing cardiovascular
disease and in the elderly.
All classes of antipsychotic cause prolongation of the QT interval,
and concern has been expressed that this could be associated
with fatal arrhythmia.
Endocrine Effects
Hyperprolactinaemia is common with many antipsychotics.
Results in gynaecomastia and impotence in men, galactorrhoea,
and menstrual irregularities in women.
Skin
Common allergic skin reactions include a maculopapular rash,
peri-orbital swelling and urticaria.
Chlorpromazine is associated with photosensitivity, pigment
changes in exposed skin, and granular deposits within the cornea
and lens.
Haematological
Benign leucopenia occurs in approximately 10% of patients
treated with antipsychotics.
Agranulocytosis is a potentially fatal side effect which occurs in
0.005% of patients treated with typical antipsychotics, and 1% of
patients receiving clozapine. It is usually reversible on
discontinuation of medication. Patients commenced on clozapine
should undergo strict haematological monitoring.43
Hepatic Effects
Abnormal liver function tests are common but of little significance.
Patients taking chlorpromazine sometimes develop jaundice.
Weight Gain and Weight gain is a common side effect of all antipsychotic agents;
Metabolic
on average 10kg is gained. Weight gain occurs early in treatment
Syndrome
and stabilises after 1-2 years. It is an important issue with regard
to compliance.
Related to this is metabolic syndrome (obesity, dyslipidaemia,
glucose intolerance, insulin resistance and hypertension) which
occurs at a higher rate in those with schizophrenia and is thought
to be explained, at least in part, by both typical and atypical
antipsychotic drug use.
Neuroleptic
NMS is a rare idiosyncratic reaction that can occur with any
Malignant
antipsychotic agent, independently of dose or duration of
Syndrome
treatment. Development of NMS constitutes a medical
emergency.
Patients present with worsening of extrapyramidal symptoms,
muscle
rigidity
and
autonomic
instability
(tachycardia,
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hypotension, hypertension or wide swings in blood pressure) and
hyperthermia (commonly >41°C.)
Mortality may be as high as 20%, secondary to multiple organ
failure.
6.2
Acute Treatment of Psychosis
Treatment should begin as soon as the diagnosis is established as:
Delay in the initiation of treatment is associated with a slower resolution of
psychotic symptoms, and the level of remission may be compromised
A long duration of the illness before neuroleptic medication is commenced is a
strong predictor of future relapse
About 30% of schizophrenic patients show poor response to drug treatment, with
persistent psychotic symptoms and functional impairment despite medication. In this
situation it is important to exclude covert non-compliance as a reason for treatment
failure.
6.3
Maintenance Drug Treatment
The aim of maintenance therapy is to maintain maximal well-being and psychosocial
function with the minimum dose of medication, to monitor long-term medication, and
to complete active rehabilitation and social reintegration.
Following the first episode of psychosis,
20-25% of patients will not relapse at all,
or will have a significant period between relapses. Unfortunately, this group cannot
be identified prospectively.
75-80% of patients with schizophrenia will experience one or more relapses;
the risk of relapse is greatest following discontinuation of antipsychotic medication.
For patients who show a poor response to treatment, discontinuation of treatment is
not an option.
Patients who have had several psychotic episodes usually require life-long
maintenance antipsychotic medication. For the majority this is in the form of
continuous drug therapy which may be administrated orally or by intramuscular
depot injection.
Intermittent drug therapy may be an alternative in those who refuse to take
medication but agree to regular psychiatric monitoring. This involves the early
initiation of treatment during the prodromal phase of a relapse.
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6.4
Psychosocial Management of Schizophrenia
Psychological interventions are
useful in helping schizophrenic patients cope with
chronic disability and dealing with the psychological problems common to everyone.
Psychotherapy should aim to resolve the patient’s personal and environmental
problems, and focus on rehabilitation needs. This is incorporated into the framework
of psychosocial rehabilitation.44
Environmental manipulation (providing supportive housing, day activities and ready
access to welfare benefits) is important for the prevention of social disadvantage.
Psychosocial approaches are important in the long-term management of
schizophrenia and other psychoses. Numerous strategies have been used with
varying degrees of success.
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Psychosocial Treatment
Evidence of Benefit
Psychodynamic
Only limited evidence that insight or growth
psychotherapy
orientated treatments are beneficial.45
Cognitive Behavioural
There is limited evidence that suggests CBT may
Therapy
reduce relapse rates.46
There is also preliminary evidence that this
therapy is useful for those patients who continue
to experience psychotic symptoms despite
optimal drug treatment.47,48
Family Intervention
Systematic reviews of randomised controlled
trials (RCTs) has found that family intervention
significantly reduces relapse rates compared with
usual care.49,50
Although thought to work through reducing
expressed emotion, some part may be played by
increased compliance with treatment (both
medication and clinic attendance).
Family therapy has not been found to
significantly affect social functioning.
Psychoeducational Therapy
There is limited evidence that psychoeducation
improves compliance, however one systematic
review has found it to be effective against
relapse.51
Social Skills Training
Interpersonal skills acquired within such a
treatment environment often do not generalise
into behavioural change in the community, and
supportive social environments may be more
valuable than specific treatment sessions.
There is only limited evidence from RCTs that
social skills training may reduce relapse rates
.49
6.5
Compliance with Treatment
Non-adherence to antipsychotic medications is common, with estimates of non-
compliance in the range of 50%, and even higher soon after the onset of the
disorder.52
Non-compliance is associated with high rates of relapse and readmission.
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FACTORS ASSOCIATED WITH NON-COMPLIANCE
Demographic Variables
Young and elderly patients
Males
Members of ethnic minority groups
Illness Related Variables
High levels of positive symptoms
Poor insight
Substance and alcohol abuse
Social and Personal Attitudes
Prejudices against treating mental disorders with
drugs
Stigma associated with mental illness
Iatrogenic
Physician underestimation of non-compliance
Lack of information given to patients and carers
Failure to recognise and treat side effects
Inconsistency in diagnosis and treatment
Drug Related
Side effects, especially extrapyramidal side
effects, akathisia, sexual dysfunction and weight
gain
Feared side effects
Patients perceive little benefit from medication
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7.
Prognosis
The outcome of schizophrenia can be considered as:
a) Symptomatic recovery
b) Recovery of social functioning
Although clinical and social recovery are closely linked, social recovery often occurs
in the presence of persisting symptoms.
The outcome of schizophrenia is worse in developed countries compared to
developing countries.
About 20% to 25% of patients have complete recovery following the first episode.
The remainder have a varied course which may involve relapses and ongoing
cognitive deficit.
7.1
Factors Indicating a Poor Prognosis53
Sociodemographic
Male, Single
Pre-morbid Adjustment
Previous psychiatric history
Premorbid personality problems
Poor social relationships
Poor work/educational record
Clinical Features
Insidious onset
Onset in adolescence
Multiple psychotic episodes, prominent positive
symptoms
Lack of insight
Marked cognitive impairment
Cerebral ventricular enlargement or sulcal
widening
Discontinuation of medication
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7.2
Factors Indicating Good Prognosis
Sociodemographic
Female
Precipitating stressor
Clinical Features
Acute presentation with florid psychotic symptoms
Evidence of schizoaffective features
Marked mood disturbance at onset
Family history of affective illness
7.3
Mortality
Age-standardised mortality rates among people with schizophrenia are
approximately double that of the general population and their lifespan is abbreviated
by approximately 15–20 years.
About 25% of the excess mortality is due to higher rates of suicide and about 10% to
greater risk of accidents. The remainder of the excess mortality is attributable to a
range of medical conditions, with cardiovascular disease contributing to the greatest
number of excess death
s.6
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8.
Main Disabling Effects
The basic
disabilities in schizophrenia are due to:
Positive and negative psychotic symptoms
A range of abnormalities in psychological functioning, such as poor attention and
concentration; and failure to recognise, and act on, social or affective cues
These disabilities cause
Poor interpersonal skills: affects relationships with family, carers and the wider
community. This impacts on participation in leisure and social activities
Inability to carry out tasks: affects
self-care and occupational performance
Persisting moderate to severe disability is present in 40% of males with
schizophrenia and 25% of females.
Disability may also arise as a side effect of the treatment of schizophrenia, such as
the abnormalities of motor function secondary to antipsychotic medication.
8.1
Schizophrenia, Work and Vocational Rehabilitation
Most people with severe mental illness identify paid employment as one of their
goals, with 53-61% of patients with schizophrenia expressing a desire to work.
54
Competitive employment (holding a regular community job as opposed to being
employed in a program overseen by a rehabilitation agency) has been estimated at
less than 20% for severely mentally ill patients.
A prospective study in the 1970s by the Tavistock Institute of Human Relations,55
investigated the employment outcome of a cohort of patients discharged following
admission for acute schizophrenia. This showed that the outcome was best for those
patients who returned to their own occupation.
Following an admission for an acute psychotic episode, perceived obstacles to
returning to their own occupations were:
A lack of liaison between health professionals and employers
A patient’s belief that work might have caused their illness
A perceived lack of support for patients, their colleagues and supervisors
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Patients with schizophrenia were more likely to remain in jobs that were
characterised by:
A high objective quality (good opportunities for learning and advancement,
freedom to organise work and time, and feedback on performance)
Good supervision
Good social climate within the work group
Work organised so that they were working with at least one other person, in a
small (<10) group
Interesting work, and a feeling that the quality of work mattered more than the
amount they did
This is in contrast to the sorts of jobs that patients with schizophrenia are often
directed towards by well-meaning professionals.
The study also showed that loss of employment due to dismissal was a rare
occurrence. However following an admission, patients appeared to stay in jobs for
shorter periods of time, and voluntarily left employment more often.
Loss of employment may be a symptom of schizophrenia, rather than its
consequence. By leaving a job perceived as stressful, patients are consciously or
subconsciously reducing their stress levels. Late arrival at work and a failure to
return to work after lunch can also be regarded as manifestations of ‘withdrawal’
behaviour. One of the consequences of this is a poor employment record, which is
often regarded by employers as a more serious handicap than a psychiatric history.
Concealment of their illness or employment history in order to obtain employment
may be a long-standing source of anxiety.
Clinicians are often concerned about encouraging patients to seek employment,
fearing that the stress of employment may adversely affect them. However studies
do not report adverse clinical outcomes following the change to supported
employment programmes, and indeed there have been improvements in non-
vocational outcomes reported.56
The costs to the individual with schizophrenia resulting from the low employment
rate include financial limitations, social stigma and poor self esteem.57
The estimated total societal cost of schizophrenia in England was £6.7 billion in
2004/05. Of this, the burden of indirect costs to society was huge, amounting to
nearly £4.7 billion.58
There is a long history of
vocational rehabilitation in schizophrenia, which was
traditionally provided by hospital or clinic based workshops and subsequently by
sheltered employment programmes. The value of vocational rehabilitation
programmes has been questioned, based on the negative data concerning patients’
employment following discharge.
Recent developments include
Supported Employment Programmes which have
been shown to be more effective in increasing the rates of competitive
employment.59
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Given the strong and consistent evidence base for the effectiveness of supported
employment in helping individuals with schizophrenia achieve competitive
employment, access to such facilities should be offered wherever possible.60,61,62
Research-based principles of vocational rehabilitation for psychiatric disabilities
include:63
Use of situational assessment in the evaluation of vocational skills and potential
Offering clients competitive or supported employment rather than sheltered or
unpaid work
Rapid placement into paid community employment rather than lengthy
prevocational training
Ongoing vocational support
Tailoring of job support and development to the client’s individual preferences
Avoidance of economic disincentives to work
8.2
Disability Discrimination Act
22% of patients with schizophrenia will have a single episode from which they will
make a complete recovery and these patients are able to return to the work place. A
further 35% will have an episodic remitting course and may be able to return to work
between psychotic episodes.
Schizophrenia and the atypical psychoses are covered by the Disability
Discrimination Act under ‘Mental Impairment’. The activities most likely to be
affected by schizophrenia are:
Perception of risk of physical danger
The ability to concentrate, learn and understand
Memory
Manual dexterity and physical co-ordination may be affected by the side effects
of medication
“Long-term” means that the impairment must have lasted for, or is likely to last for,
twelve months or longer. As those who have a single episode cannot be identified
prospectively, then this will apply to all new cases of schizophrenia.
8.3
Assessing the Claimant
Schizophrenia causes social disability; side effects of psychotropic medication may
cause motor disturbances and physical disabilities.
Whilst it may appear that claimants are functioning relatively well in the community,
this may reflect the level of support being provided. Without support some people
might neglect to take care of their personal needs and omit to take medication. As a
consequence, without such support some could return to a severely disturbed
mental state.
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The examining doctor should bear in mind that claimants with schizophrenia may
have little insight into their disorder and may underestimate their level of disability,
while claimants with delusional disorders may actively deny that they have a mental
illness.
On greeting the claimant and on initial observation, extra-pyramidal side effects,
stereotypies or dystonias of tardive dyskinesia may be apparent. The appearance of
the claimant may be unkempt, pointing to poor self-care, and they may appear
distracted, suggestive of active hallucinations. Prominent negative symptoms such
as flat affect or poverty of speech may be apparent and indicate probable severe
restriction of social functioning.
The typical day history may show the patient to be living independently, or in a
hostel or group home. These vary in structure and support, from high dependency,
that can provide 24-hour care, to semi-independence of a supported flat with
someone visiting daily or less often.
8.4
ESA Considerations
People with schizophrenia may not be able to express adequately their disabilities
on the ESA50 form, and there may be inadequate documentary evidence from
general practitioners, hence the level of disability may not be apparent from the
evidence available to the medical adviser scrutinising the file before assessment.
Appropriate consideration must be given to the history of the course of the illness
(as detalled in 5.3.1. Table 1).
Claimants attending with a carer, community psychiatric nurse (CPN) or community
psychiatric social worker are likely to have a high level of social disability as may
those living in supported housing or attending at a day unit.
The HCP will find that the functional limitations caused by schizophrenia may affect
Understanding and Focus (hazards, personal action) and Social Interaction (coping
with social engagement). Other descriptor groups may fall to be considered if other
co-morbid mental health conditions are present. These effects will be detected by
the mental health assessment using the clinical history, the typical day history, and
the mental state examination.
Hallucinations and reduced perceptions of risk may suggest that consideration be
given to the non-functional descriptor of “substantial risk to any person”. The
significantly increased suicide risk should also be considered.
In general, the review period will depend on the history. The mean time to achieve a
remission from a
first episode of psychosis is 42 weeks1364, hence cases which
satisfy LCW
do not merit review in less than 12 months.
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Cases in which there has been a recent relapse should also have prognosis advice
of 12-18 months.
Following the first episode of psychosis, cases in which there is a
residual
cognitive deficit (episodic with stable deficit), or cases which show a
progressive
cognitive deficit with time (episodic with stable deficit), should be reviewed less
frequently.
Review advice of “not less than 2 years” or “in the longer term” is
appropriate.
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Appendix A - Atypical Psychoses
Introduction
Atypical non-organic psychoses are a group of disorders that do not belong to the
two major groups of psychoses: schizophrenia or the affective psychoses (bipolar
illness).
There is confusion surrounding the definition of these disorders, with different names
being given to the same disorder and the same name being given to dissimilar
clinical conditions. However the disorders can be broadly divided into two groups:
1.
Schizoaffective disorders in which symptoms of schizophrenia and affective
psychosis occur in the same illness.
2.
Paranoid disorders characterised by delusions in the absence of other features
of psychosis.
The atypical psychoses are listed in table 1, together with the authority responsible
for defining them. Where dissimilar conditions have the same name they are listed
separately.
Table 1: Atypical Psychoses
Schizoaffective Group
Schizoaffective disorder
ICD–10
Schizoaffective disorder
DSM–IV
Schizophreniform
DSM–IV
Brief Psychotic disorder
DSM–IV
Acute Polymorphic Psychotic disorder
ICD–10
Paranoid (delusional) Disorders
Acute Delusional Psychotic disorder
ICD–10
Persistent Delusional disorder
ICD–10
Delusional disorder
DSM–IV
Erotomanic
Grandiose
Jealous
Persecutory
Somatic
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Schizoaffective Disorder
The definitions of schizoaffective disorder provided by ICD–10 and DSM–IV are
generally used and these are compared in table 2.
Table 2: Comparison of Diagnostic Criteria for Schizoaffective Disorder
(derived from Mellor)
ICD–10
DSM–IV
Symptoms Schizophrenic and affective
Major depressive or manic
symptoms simultaneously present,
concurrent with Type A
both prominent.
schizophrenic symptoms.
At least one, preferably two
At least 2 weeks of delusions
schizophrenic symptoms
and hallucinations without
prominent mood disorder.
Course
Recurrent
Not included in criteria but in
Manic defect unusual
preamble, better than
schizophrenia, worse than
Depressive defect sometimes
mood disorder.
Tends to be chronic
Types
Manic, mixed, depressive
Bipolar, depressive
Includes affective type of
schizophreniform psychosis
Exclude
Patients with separate episodes of
Organic disorders,
schizophrenia and affective
schizophrenia, psychotic mood
disorder
disorders
The definition of schizoaffective disorder has varied so much that epidemiological
data is of limited value. Best estimates give an
incidence of 2 cases per 100,000
per year which is similar to that of mania. Schizoaffective disorders are estimated to
occur at 50-85% of the rate of schizophrenia, and so comprise a clinically significant
population. There are no epidemiological studies of prevalence for schizoaffective
disorders.
The
clinical features of schizoaffective disorder are:
Relatively high levels of premorbid function
Median age of onset 29 years (>schizophrenia, <affective disorders)
More common in females
60% have a precipitating event, nature of event variable, may be physical (e.g.
childbirth) or interpersonal (e.g. change in a relationship)
Periodic, rapid onset of symptoms, degree of remission after weeks or months
Symptom clusters that are primarily affective or primarily schizophrenic may
predominate at different times in the same patient
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Some cases mainly resemble schizophrenia = schizophrenic type schizoaffective
disorder, whilst others resemble mainly affective disorder = affective type
schizoaffective disorder
Generally better course than schizophrenia, poorer course than affective
disorder. However there are subgroups that resemble schizophrenia or affective
disorders more closely
Levels of impairment intermediate between schizophrenia and affective disorder
The management of the schizoaffective disorders is best considered by dividing
them into two broad subtypes, according to symptom predominance:
Affective type schizoaffective disorder
Antipsychotic medication e.g. clozapine, risperidone, olanzapine
Antidepressants, mood stabilisers (e.g. lithium) or anticonvulsants (e.g. valproate
or carbamazepine)
Schizophrenic type schizoaffective disorder
Antipsychotic medication alone often enough to treat affective symptoms
Treatment may be augmented with lithium or antidepressant medication
Electro-convulsive therapy may reduce mortality rates
Poor prognostic features of schizoaffective disorder include:
Poor inter-episode recoveries
Persistent psychotic symptoms in the absence of affective features
Poor premorbid social adjustment
Chronicity
Higher number of schizophrenia like symptoms
Considerable controversy now surrounds the diagnosis of schizoaffective disorder,
and although it is used in both DSM-IV and ICD-10 it encroaches on both
schizophrenia and bipolar disorder. It is often held that schizoaffective disorder is
best regarded either as a comorbid set of symptoms that occur as a by-product of
schizophrenia and bipolar disorder or that it should be regarded as a mid-point on a
continuum between them.65,66
Schizophreniform Psychosis
The term schizophreniform was first used in 1937 to identify those patients with
schizophrenic symptoms who had a good prognosis.
Schizophreniform psychosis is a DSM–IV diagnosis with the same diagnostic criteria
for schizophrenia, however the total duration of the illness (prodrome, active phase
and recovery) is of less than 6 months duration.
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The ICD–10 equivalent diagnosis is acute schizophrenia-like psychotic disorder
(F23.2). Schizophreniform psychosis is included in ICD–10 as a subtype of
Schizophrenia.
The
epidemiology of schizophreniform disorder has not been studied.
Clinically it is characterised by:
Acute onset of psychotic symptoms
Confusion, disorientation and perplexity at the height of the psychosis
The
treatment of schizophreniform psychosis is as for schizophrenia. Large doses
of antipsychotic medication may be needed initially. If symptoms return on reduction
of antipsychotic medication, then the diagnosis is of schizophrenia.
For a
good prognosis, the patient should have 2 of the following prognostic factors:
The psychotic symptoms appear within 4 weeks of the onset of the illness
Confusion, disorientation and perplexity
Good premorbid social and occupational functioning
The absence of blunted or flat affects
Acute and Transient Psychotic Disorders
The heterogeneous group of acute and transient psychotic disorders are
characterised by:
Sudden onset (within 2 weeks or less)
Presence of typical syndromes with polymorphic (changing and variable) or
schizophrenic symptoms
Presence of associated acute stress (e.g. bereavement, job loss, psychological
trauma etc)
Six categories of acute psychoses are presented in ICD–10; only two are discussed
here.
1. Acute polymorphic psychotic disorder without symptoms of schizophrenia
Onset over a period of hours or days, no previous psychiatric disorder
(except other similar episodes)
Often affects young adults, especially women in their thirties
Active stages disappear completely in a few weeks or months, relapses
can occur but there is no psychiatric disturbance between successive
episodes
Specific symptoms change from day to day and even from hour to hour and may
include:
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Polymorphic psychotic symptoms:
Varied delusional themes including grandeur, persecution, influence,
possession, body transformation (depersonalisation), derealisation or world
alteration. These themes change with time.
Other symptoms include hallucinations, illusions, interpretations and intuitions.
Mood changes:
As a consequence of the delusions, the patient experiences mood changes and
emotional turmoil, manifesting as depression or euphoria (without reaching
diagnostic criteria for affective disorders).
Confusion:
Consciousness fluctuates and there is a specific disorientation with respect to
time and place and a ‘dreamlike state’.
ICD–10 criterion of duration of less than 1 month distinguishes it from
schizophrenia and manic or depressive episodes. If resolution of symptoms has
not occurred after 3 months, the diagnosis should be changed to persistent
delusional disorder or non-organic psychotic disorder.
2. Acute polymorphic disorder with symptoms of schizophrenia (F23.1)
This diagnostic category combines the symptoms of acute polymorphic psychotic
disorder (above) with some typical symptoms of schizophrenia. F23.1 can be a
provisional diagnosis which is changed to schizophrenia if the criteria persist for
more than a month.
Historically, this has also been described as cycloid psychosis (an episode with
clouding of consciousness and a marked alteration in thinking).
The symptoms listed above are associated with some schizophrenic symptoms
that are present most of the time:
Passivity phenomena: thought insertion, thought withdrawal, thought
broadcast, made will, made actions, somatic passivity
Hallucinations with commentary
Catatonic behaviour
Negative symptoms
Cycloid psychoses have been reported to have a better prognosis than
schizophrenia and schizoaffective disorders, and as the diagnostic criteria are
the same, one can tentatively extrapolate this to the whole group.
Treatment of acute and transient psychotic disorders
Both typical and atypical antipsychotic drugs are used. Benzodiazepines may be
used to produce rapid sedation. If mood disorders or cyclic episodes occur,
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treatment with antidepressants, mood stabilisers (lithium or valproate) or
anticonvulsants (carbamazepine) may be indicated.
Psychological therapies, social, and family therapies may all be used.
Persistent Delusional Disorders
A delusion may be loosely defined as a mistaken idea that is held unshakeably by
the patient, and which cannot be corrected.
Delusional disorder (ICD–10 -F22 and DSM–IV 297.1) is a psychotic disorder in
which a stable and well-defined delusional system co-exists with a personality that
retains many normal aspects. This is in contrast to schizophrenia where there is
widespread disorganisation of personality in addition to psychotic features.
Delusional disorder is the name now applied to the illness previously known as
paranoia.
Definition of delusional disorders (ICD–10 F22.0)
a) A delusion or set of related delusions, other than those described as typically
schizophrenic, must be present; the most common are persecutory, grandiose,
hypochondriacal, jealous or erotic.
b) The delusion(s) must be present for at least 3 months.
c) The general criteria for schizophrenia are not fulfilled.
d) There are no persistent hallucinations, but there may be transitory or occasional
auditory hallucinations that are not speaking in the third person or making a
running commentary.
e) Depressive symptoms or episodes may be intermittently present, but the
delusional symptoms must persist at times when there is no disturbance of
mood.
f)
There must be no evidence of primary or secondary organic mental disorder or
of a psychotic disorder due to psychoactive substance use.
Subtypes: persecutory, litigious, self-referential, grandiose, hypochondriacal,
jealous, erotomanic.
There have been no detailed epidemiological studies, and as only markedly
abnormal behaviour brings the patients to psychiatric attention, it is probably
underestimated. The prevalence is thought to be about 0.03% and the lifetime risk
0.05-0.1% (i.e. one tenth that of schizophrenia).
The age of onset is commonly 40-55 years, however cases have been described
from late adolescence. The sex ratio appears to be equal. Male patients appear to
have a younger age of onset and the condition can be compatible with marriage and
continued employment.
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Patients with delusional disorder rarely complain directly of their delusions and are
often presented to psychiatric services by their families, or as a result of some legal
process. An independent account of the illness from someone who knows the
patient well is a necessity, especially if the delusional content is ‘culturally
acceptable’.
The premorbid personality is often asocial and there may be an excess of schizoid
and paranoid personality disorders. However in some cases the ‘personality
disorder’ may be a prodrome of the il ness and resolves when the patient recovers.
The onset may be gradual or acute.
All cases of delusional disorder occur in clear consciousness and have a stable and
persistent delusional system. Within the delusional context, the patient has a
heightened sense of self-reference, and ordinary events take on extraordinary
significance. Patients’ delusional beliefs are unshakeable, and they deny any mental
illness. The patient is able to move from normal to delusional modes of thinking with
ease.
Delusional disorder is usually categorised according to the delusional content as
follows:
Erotomania (de Clerambault’s syndrome): the patient believes that a particular
person is in love with them. When the ‘lover’ rejects approaches, further delusional
elaborations occur. This is more common in women, however male sufferers present
major forensic problems. Legal remedies have little effect on the patients’ beliefs
and do not alter behaviour.
Grandiose: patients have erroneous and extravagant delusional beliefs about
themselves that may include social status, wealth, intellectual powers and spiritual
gifts.
Jealous (Othello syndrome): This is characterised by the delusion that a partner
(usually a spouse) has been unfaithful. Morbid jealousy is a general term for
pathological jealousy that may be a symptom of psychiatric conditions other than
delusional disorder (commonly alcoholism). Morbid jealousy is not always
delusional. Patients will consistently question their partner as they seek evidence to
support the delusion. The condition is difficult to treat and tends to recur with a new
partner. It should be suspected in cases of domestic violence.
Persecutory: The patients are usually the subject of the persecution, but
occasionally it is someone close to them. The delusional system is very well
organised. Frustrated that the proper authorities take no action, patients may
attempt to expose their ‘persecutors’ in a public forum such as the law courts or
‘letters to the editor’.
Somatic: delusions of physical abnormality or of a physical disorder characterise
this subtype. The delusional content may be of size or form (delusional
dysmorphophobia), illness, infestation, and leaking smells and secretions from
bodily orifices (monosymptomatic hypochondriacal psychosis).
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The first aim in the management of delusional disorders is to achieve a therapeutic
relationship with a patient who does not want to participate in psychiatric treatment.
Patients are often angry and hostile to those responsible for their entry into
treatment, and these feelings may be extended to psychiatric staff.
Although the current evidence supports the use of pimozide as the antipsychotic of
choice for delusional disorders, concerns have been raised regarding its cardiotoxic
side effects, and some psychiatrists prefer to use the atypical antipsychotics,
risperidone or olanzapine.
As it is a chronic condition, long-term maintenance treatment is required. It is
estimated that a third of patients will be able to discontinue their medication.
Unfortunately, this group cannot be identified prospectively.
Psychotherapy and counselling have a limited role in therapy and there is no
evidence that psychological methods by themselves can eliminate delusions.
Persistent delusional disorders are
chronic, probably lifelong conditions. They
have previously had a reputation for being untreatable, as many patients are
unwilling to accept that they have a mental disorder or that they require psychiatric
treatment. However if they can be persuaded to co-operate and accept treatment,
the conditions respond in a large proportion of cases.
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Appendix B - Glossary
Schneider’s First Rank Symptoms
1. Voices commenting on the patient’s actions
2. Voices arguing or discussing the patient
3. Audible thoughts
4. Diffusion or broadcasting of thoughts. The patient, during the process of
thinking, has the experience that his thoughts are not contained within his own
mind
5. Thought withdrawal. The patient describes his thoughts being taken from his
mind
6. Thought insertion. Thoughts ascribed to others. The patient experiences
thoughts which have not the quality of being his own
7. 'Made' volitional acts. The patient experiences his actions as being completely
under the control of an external influence
8. 'Made' impulses (drives). A powerful impulse overcomes the patient to which he
almost invariably gives way. The impulse to carry out this action is not felt to be
his own, but the actual performance of the act is
9. 'Made' feelings. The patient experiences feelings which do not seem to be his
own
10. Somatic passivity. The patient is a passive and invariably a reluctant recipient of
bodily sensations imposed upon him by some external agency
11. Delusional perception The delusion arises from a perception which to the patient
possesses all the properties of a normal perception, and which he
acknowledges would be regarded as such by anyone else. This perception
however has a private meaning for him, and the second stage, which is the
development of the delusion, follows almost immediately
Symptomatology: Glossary
Abnormal Perceptions
Hallucinations are sensory perceptions in the absence of external stimuli and are
commonly auditory.
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a)
Second person voices address the patient directly.
b)
Third person voices address the patient in the third person.
c)
Running commentary voices describe his/her actions as they occur, referring
to him/her in the third person.
d)
Thought Echo (Audible Thoughts) voice repeats patient’s thoughts either
simultaneously or after a brief delay.
Olfactory and visual hallucinations may occur, but are not diagnostic..
Abnormal Thoughts
Delusions are false beliefs, based on incorrect inference about reality, that are
inconsistent with the patient’s educational and cultural background and are not
amenable to reasoning
a)
Persecutory delusions: the belief that one is harassed or persecuted.
b)
Delusions of reference: the belief that events, objects or the behaviour of
others, refer to oneself.
c)
Delusions of control:
the belief that external forces control one’s thoughts,
emotions or movements.
d)
Delusional Perception: the attribution of abnormal significance, usually with
self-reference, to a genuine perception, without any understandable rational or
emotional justification.
Delusions of persecution and of reference have little diagnostic specificity but are
common in schizophrenia.
Thought Disorder
Disorders of thought process are inferred from abnormalities observed in the spoken
and written language of the patient.
a)
Loosening of associations: the logical associations between the ideas
expressed are loose or incomprehensible; when severe, speech becomes
incoherent.
b)
Poverty of content of speech: speech is sufficient in amount, but conveys little
information due to vagueness, stereotypy or repetition.
c)
Thought block: a sudden interruption in the train of thinking.
Passivity Phenomena
a)
Thought Insertion: the experience of thoughts that are not one’s own, being
inserted into one’s mind.
b)
Thought Withdrawal: the experience that thoughts are removed from one’s
mind.
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c)
Thought Broadcasting: the experience that one’s thoughts are broadcast so
that others might share them.
d)
Made Will: the patient is impelled by an impulse to act, which is experienced as
arising from an alien source.
e)
Made Actions: the patient experiences his actions as being executed by an
external influence, such that he is a passive observer of his own actions.
f)
Made Affect (Made Feelings): feelings are experienced as being imposed by
an external agency.
g)
Somatic Passivity: the experience of external influence over bodily functions.
Abnormal Affect
a)
Blunted Affect: a failure to express feelings verbally or non-verbally even when
talking about issues which would normally engage the emotions.
b)
Incongruous affect: a qualitative abnormality in which the affective response is
incompatible with the ideas or thoughts expressed.
Disorders of Volition
a)
Weakened volition: manifests as a lack of spontaneous motor activity, often
accompanied by a lack of spontaneity in speech and affect.
b)
Disjointed volition: characterised by over-activity in an ill-directed manner,
resulting in a reduced ability to resist impulses to act.
c)
Catatonic Stupor: immobility and apparent unawareness of surroundings.
d)
Catatonic Excitement: intense, purposeless and disorganised activity.
e)
Stereotypy: repeated purposeless patterns of actions.
f)
Waxy flexibility: sustaining for a prolonged period of time the position in which
the body or limbs are placed.
g)
Echopraxia: pathological automatic imitation of another person’s movements.
h)
Negativism: automatic resistance to instructions or attempts at movements.
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Appendix C - Diagnostic Criteria
ICD–10 Diagnostic Criteria for Schizophrenia
A minimum of
one very clear symptom belonging to groups (a) to (d) below or
symptoms from at least two of the groups (e) to (i) below.
For most of the time, during a period of
one month or more:
a) Thought echo, thought insertion or withdrawal, and thought broadcasting;
b) Delusions of control, influence or passivity, clearly referred to body or limb
movements or specific thoughts, actions or sensations; delusional perception;
c) Hallucinatory voices giving a running commentary on the patient’s behaviour, or
discussing the patient among themselves, or other types of hallucinatory voices
coming from some part of the body;
d) Persistent delusions of other kinds that are culturally inappropriate and
completely impossible, such as religious or political identity, or superhuman
powers and abilities (e.g. being able to control the weather, or being in
communication with aliens from another world);
e) Persistent hallucinations in any modality, when accompanied either by fleeting
or half-formed delusions without clear affective content, or by persistent
overvalued ideas, or when occurring every day or for weeks or months on end;
f)
Breaks or interpolations in the train of thought, resulting in incoherence or
irrelevant speech or neologisms;
g) Catatonic behaviour, such as excitement, posturing or waxy flexibility,
negativism, mutism, and stupor;
h) “Negative” symptoms such as marked apathy, paucity of speech, and blunting or
incongruity of emotional responses, usually resulting in social withdrawal and
lowering of social performance; it must be clear that these are not due to
depression or antipsychotic medication;
The diagnosis of schizophrenia should not be made in the presence of extensive
depressive or manic symptoms unless it is clear that the schizophrenic and affective
symptoms antedated the affective disturbance.
If both schizophrenic and affective symptoms develop together and are evenly
balanced, the diagnosis of schizoaffective disorder should be made, even if the
schizophrenic symptoms alone would have justified the diagnosis of schizophrenia.
DSM–IV Diagnostic Criteria for Schizophrenia
A.
Characteristic symptoms: Two (or more) of the following, each present for a
significant portion of time during a 1-month period (or less if successfully
treated):
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1) Delusions
2) Hallucinations
3) Disorganised speech (e.g. frequent derailment or incoherence)
4) Grossly disorganised or catatonic behaviour
5) Negative symptoms, i.e. affective flattening, alogia or avolition.
Note: Only one criterion A symptom is required if delusions are bizarre or
hallucinations consist of a voice keeping up a running commentary on the
person’s behaviour or thoughts, or two or more voices conversing with each
other.
B.
Social/Occupational dysfunction: For a significant portion of time since the onset
of the disturbance, one or more major areas of functioning such as work,
interpersonal relations, or self-care are markedly below the level achieved prior
to the onset (or when the onset is in childhood or adolescence, failure to achieve
the expected level of interpersonal, academic or occupational achievement).
C.
Duration: Continuous signs of the disturbance persist for at least 6 months. This
6 month period must include at least 1 month of symptoms (or less if
successfully treated) that meet criterion A (i.e. active phase symptoms) and may
include periods of prodromal or residual symptoms. During these prodromal or
residual periods, the signs of the disturbance may be manifested by only
negative symptoms, or two or more symptoms listed in Criterion A, presented in
an 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 because either (1) no major
depressive, manic or mixed episodes have occurred concurrently with the active-
phase symptoms; or (2) if mood episodes have occurred during active-phase
symptoms, their total duration has been brief relative to the duration of the active
and residual periods.
E. Substance/general medical condition exclusion: The disturbance is not due to
the direct physiological effects of a substance (e.g. a drug of abuse, a
medication) or a general medical condition.
F. Relationship to a pervasive developmental disorder: If there is a history of
autistic disorder or another pervasive developmental disorder, the additional
diagnosis of schizophrenia is made only if prominent delusions or hallucinations
are also present for at least a month (or less if successfully treated).
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Appendix D - Aetiological Factors
Neuropathological changes in schizophrenia
Whole Brain Changes
MRI studies have shown significant reduction in cerebral volume in
schizophrenia, more marked in the temporal lobes.
This decrease in cerebral volume is not necessarily accompanied by decreases
in other brain regions (e.g. midbrain and pontine areas may show increases).
Ventricular System
Enlargement of lateral and third ventricles;
Ventricular volume increased by approximately 40%; increases may be more
pronounced on the left side;
Changes may be more prominent in male patients;
Possible association with impaired performance on neuropsychological tests and
negative symptoms;
A poor prognostic factor.
Frontal and Temporal Lobes
Show a consistent reduction in volume and cortical thickness67
Temporal lobe abnormalities more pronounced in males and in those with
familial schizophrenia.
Limbic Structures
The volume of the hippocampus and the amygdala is reduced bilaterally by 4.5-
10%;
Reductions in the parahippocampal gyrus in the region of 9-14% have been
reported. These volume reductions are the largest reported of any brain area.
Basal Ganglia
Contradictory results from studies, probably due to the effect of neuroleptics, which
increase basal ganglia volume.
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9.
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Hunsley J, Mash EJ, editors. A guide to assessments that work. Oxford: Oxford
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Gitlow S. Substance use disorders: a practical guide, 2nd ed. Philadelphia:
Lippincott Williams & Wilkins; 2007.
Andreasen N, Black DW. Introductory textbook of psychiatry, 4th ed. Washington,
D.C: American Psychiatric Publishing; 2006.
Rumsey JM, Ernst M. Neuroimaging in developmental clinical neuroscience.
Cambridge, UK: Cambridge University Press; 2009.
McKenna PJ. Schizophrenia and related syndromes, 2nd ed. London: Routledge;
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National Collaborating Centre for Mental Health [Online]. Core interventions in the
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