1.

Conception-historical development
2. Epidemiology
3. Etiology-main findings in studies of schizophrenia
4. Clinical manifestations and subtypes Conception
z The acute syndrome
z The chronic syndrome - historical development of
z Subtypes of schizophrenia idea about schizophrenia
5. Diagnosis and classification
z Diagnostic criteria
z Differential diagnosis
6. Treatment
7. Course and prognosis

Conception and history Conception and history

‹ The key points in the historical development of the idea of
schizophrenia mainly include:
z In 1893, Emil Kraepelin proposed a group of psychiatric
syndrome named as ‘dementia praecox’.
¾ The common characteristic of which was a peculiar
destruction of the internal connections of the psychic
personality.
¾ It developed relatively early in life, and its course is likely
deteriorating and chronic; but was not followed by any
organic changes of the brain, detectable at that time.
¾ He also divided dementia praecox into four subtypes:
① Catatonic
② Hebephrenic
③ Paranoid
④ Simple
z In 1911, Eugen Bleuler, renamed Kraepelin’s dementia praecox
as ‘schizophrenia’ .
¾ He used the concept of ‘schizophrenia’ to denote a
‘splitting’ of psychic functions, which he thought to be of
central importance for this syndrome.
¾ He also proposed that four kind of fundamental symptoms
were central to the disorder, called ‘4A’ because of the
initial letters, and were ‘primary’ for the diagnosis:
① Affective blunting
② Disturbance of association (fragmented thinking)
③ Autism
④ Ambivalence (fragmented emotional response)

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Conception and history
z Kurt Schneider(1887-1967): He identified a group of psychotic
symptoms as some characteristic hallucinations, delusions
and gave them the privilege of ‘the first rank symptoms’ of
schizophrenia, which is even now important in the diagnosis of
schizophrenia, e.g.
¾ Hearing own thoughts being spoken aloud
¾ Third-person (arguing) hallucinations
¾ Second-person (commentary) hallucinations
¾ Somatic hallucinations
¾ Thought withdrawal or insertion
¾ Thought broadcasting
¾ Delusional perception
¾ Feelings or actions experienced as made by external
agents.
Conception and history
In summary, schizophrenia can be defined as:
‹ Schizophrenia is a severe and complex psychiatric syndrome,
z with its etiology being uncertain yet,
z phenomenologically being characterized in general by
profound and characteristic disturbances of perception,
thought, emotions, and behavior.
z Clear consciousness and intellectual capacity are usually
maintained although certain cognitive deficits may evolve in
the course of time.
z The first onset occurs typically during and after early
adulthood, and the illness course is likely deteriorating and
chronic and prolong until the late life.

Epidemiology
‹ Schizophrenia is a disorder with low incidence but a relatively high
prevalence and cost, reflecting its chronicity in most patients.
z The annual incidence is about 0.16-0.54 per 1000 population.
z The annual prevalence is about 1.4-4.6 per 1000 population.

Epidemiology z The lifetime risk of developing schizophrenia is about 7-10 per

1000 population, i.e., 1%.
‹ Patients with schizophrenia have a reduction in life expectancy of
about 20% compared with the general population.
‹ The excess mortality partly (28%) resources from suicide:
z About 9.8% of male and 6.8% of female patients with
schizophrenia committed suicide, being equal to or even higher
than the suicide rate in psychotic depression.
z The actual mortality due to suicide is likely to be even higher,
since a proportion of the death classified as accidental or of
undetermined cause are probably suicide.

Epidemiology
z Several risk factors have been suggested as relatively specific
to schizophrenic suicide:
¾ being young and male

Etiology
¾ experiencing a chronic disabling illness with multiple
relapses and remissions
¾ realistic awareness of the deteriorating course of the
condition
¾ comorbid substance abuse
¾ loss of faith in treatment. -main findings in studies
‹ The onset of schizophrenia characteristically occurs between the
ages of 15 and 45; the mean age of onset is about five years earlier of schizophrenia
in men than in women.

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Etiology-Overview Etiology-Overview
‹ Schizophrenia exemplifies the whole range of biological,
psychological and social factors considered important in
psychiatric causation, and the methods which have been applied to
try and identify them.
1. The most important influence is genetic, with about 80% of the
risk of schizophrenia being inherited.
2. A number of environmental factor contribute too, and which
interact with the genetic predisposition.
3. These together lead to a neurodevelopmental disturbance which
either causes, or renders the vulnerability to schizophrenia.
4. Schizophrenic brain is slightly smaller than normal, and there
are localized alterations in brain structures and function, leading
to the view that the syndrome is a disorder of dysconnectivity
within and between brain regions.

Etiology-Overview Etiology-Genetics
5. Acute schizophrenia syndrome is associated with excess ‹ Family, twin, adoption and gene studies have been used by genetic
dopamine neurotransmission, while the persistent cognitive studies of schizophrenia, illustrating that this disorder is likely
impairments may result from deficient dopamine function the inheritable.
prefrontal cortex. Both may be secondary to abnormalities of the
1. Family studies
glutamate system.
z The lifetime risk is several times higher than that of general
6. Psychosocial factors as trigger, can significantly influence the
population in the biological relatives of schizophrenia
onset and course of illness.
patients
‹ Finally, it is emphasized that there are few certainties about the
z The closer the relationship, the higher the lifetime risk:
etiology of schizophrenia, and even where facts are robust, their
interpretation (mechanisms) often remain unclear. Thus, • Nephews and nieces 2.2%
schizophrenia at present is still a disorder without certain etiology.
• Patient’s half siblings 3.2%
• Patient’s parents 4.4%
• Patient’s siblings 8.5%
• Patient’s children 12.3%
• Patient’s children (both parents schizophrenic) 36.6%
Data adapted from Shields(1980)

Etiology-Genetics Etiology-Genetics
2. Twin studies 3. Adoption studies
z The concordance rate (where both twins have the same z Strong evidence that the familial clustering of schizophrenia
disorder) is several-fold higher in monozygotic (MZ) twins are mainly caused by genetic factors.
than dizygotic (DZ) twins.
¾ Luxenberger (1928): Adopted by other families
Averagely after 36 years
since 3 days of birth
• 11/19 in MZ twins 0/13 in DZ twins.
¾ Birth Registration Center of Norway, data 1901-1930: Cases: Cases:

• 25-38% in MZ twins 4-10% in DZ twins. 47 adoptees who had 5 adoptees developed

been born to mothers schizophrenia
¾ Maudsley Twin Series in London (1999): with schizophrenia Matched for
environment of
• 42% in MZ twins 1.7% in DZ twins. Controls: upbringing
¾ Cardno and Gottesman’s literature review (2000) Controls:
50 adoptees who had
been born to mentally None developed
• 50% in MZ twins 10% in DZ twins.
normal mothers schizophrenia
Representative figures
Heston, 1966

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Etiology-Genetics
4. Gene studies
z Some susceptibility genes of schizophrenia have been found,
but none of them alone can cause schizophrenia.
¾ Some chromosomal loci like 2p, 8p, 13q and 22q are
linked to schizophrenia, with high or very high
probability.
• p and q refer to the short and long arm of the
chromosome respectively.
¾ Several specific genes are associated with schizophrenia,
especially neuregulin-1 (8p) and dysbindin-1 (6p).
• Neuregulin is involved in many aspects of neuronal
and glial growth and synaptic plasticity.
• Dysbindin is also involved in synaptic functioning
and signaling.
Etiology-Pre/perinatal risk factors
1. Obstetric complications
z Retrospective studies: schizophrenia patients have reported
more obstetric complications than their unaffected siblings
or normal controls.
z Meta-analyses: odds ratio≈2 (Geddes et al, 1999)
z However, it is unclear which specific complications are
relevant. (premature rupture of membranes, birth before 37
weeks, anoxia, and low birth weight were suggest to have
significant effects) .
z Possible explanations:
¾ Being directly causal ?
¾ Reflection of pre-existing fetal abnormality ?
¾ Reflection of fetus’ genetic background ?
Etiology-Pre/perinatal risk factors
3. Winter birth
z Excess winter birth: schizophrenia is slightly more frequent
among people born in the winter than those in the summer.
¾ Being more prominent at areas of higher latitudes.
¾ Being more common in patients without a family history.
z Possible explanations:
¾ Higher prevalence of influenza earlier in the winter ?
¾ Shortness of sunshine thus insufficient of vitamin D?
Etiology-Genetics
5. The model of inheritance
z The ratios of the frequency of schizophrenia reported by
family, twin, and adoption studies, and the weak effects of
susceptibility genes, do not fit any simple Mendelian pattern,
thus the disorder seems not caused by a single major
dominant or recessive gene.
z At present, the predominant concept concerning the model
of inheritance is ‘Polygenic theory’:
Schizophrenia arises from the cumulative effect of several genes, as a
so-called complex or non-Mendelian genetic disorder. The liability to
schizophrenia lies on a continuum in the general population, and is
expressed when a certain threshold of genetic susceptibility is
exceeded. None of the genes are either necessary nor sufficient, and
they act as risk factors but not determinants of the disease. That is, the
variants are polymorphisms but not mutations.
Etiology-Pre-/perenatal risk factors
2. Maternal influenza and other infections
z Retrospective studies: fetuses exposed to influenza during
the second trimester have an increase risk of schizophrenia.
z Animal studies: prenatal influenza affects brain development.
z However, many studies are negative, so the association
between influenza and schizophrenia has been hard to
established.
z Other possibly relevant maternal infections:
¾ Toxoplasmosis
¾ Poliomyelitis
¾ Measles
¾ Varicella
Etiology-Social and psychosocial risk factors
1. Social class: higher prevalence in lower social class.
2. Place of residence: large cities have higher risk.
3. Migration: Migrants have higher risk.
4. Stressful life events:
z Experiencing a life event doubles the risk of developing
schizophrenia over the subsequent 6 month (Paykel, 1978).
z Life events may also increase the risk of relapse of
schizophrenia (Bebbington et al., 1993).
z The severity of schizophrenic symptoms over time
correlated with life events (Norman and Malla, 1993).
z However, there is no evidence that patients with
schizophrenia suffered more life events than the general
population.
5. Culture: incidence being similar in widely different cultures,
suggesting culture is not an important factor.
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Etiology-Personality factors Etiology-Structural brain changes
‹ Current view: Summary of structural brain changes in schizophrenia
z Schizophrenia is the most severe end of a continuum called MRI brain imaging findings Post-mortem findings
‘schizophrenia spectrum’.
zDecrease brain volume z Decrease brain weight
¾ The mild form of the spectrum, ‘schizotypal personality
disorder (STD)’, being characterized by peculiarities of zEnlarged lateral ventricle z Absence of neurodegenerative
thinking, odd beliefs, and eccentricities of appearance, changes
zEnlarged third ventricle
behavior, interpersonal style, and thought, but rarely z Absence of gliosis
presenting intense and persistent overt psychotic zSmaller medial temporal lobes
symptoms (e.g., delusions and hallucinations) is thought z Decreased pre-synaptic markers
zDecreased cortical grey matter
to be ‘a prototype of schizophrenia’ z Decreased markers of dendrites
zReduced cerebral asymmetry
¾ Another form is schizoid personality disorder, primarily z Smaller pyramidal neurons in some
characterized by a very limited range of emotion, both in areas
expression of and experiencing, and indifferent to social
relationships, also related to schizphrenia. z Fewer thalamic neurons

z However, many schizophrenia patients have no obvious

personality disorder before the onset, and only a minority of
people with schizotypal or schizoid personalities develop Sc.

Etiology-Functional brain changes Etiology-Functional brain changes

‹ Purpose: ‹ Universally accepted finding:
z Assess cerebral blood flow (CBF) and metabolic activity. z Hypofrontality-decreased activity in the frontal lobe of
schizophrenia.
‹ Techniques:
z Correlations with three clinical syndromes of Sc (Liddle, 1987):
z Positron emission tomography (PET).
Syndrome symptoms Regional CBF correlates
z Single-photon emission tomography (SPET).
z Functional magnetic resonance imaging (fMRI). Reality Delusions, Overactivity of left
disturbance hallucinations medial temporal lobe
‹ Designs: Cingulated cortex
z Measurement of regional CBF at rest. Disorganization Formal thought Anterior cingulated,
disorder, right ventral frontal
z Patterns of cerebral activation and deactivation associated inappropriate affect, cortex, bilateral parietal
with specific neuropsychological tasks. bizarre behavior regions
z Correlation of patterns of regional cerebral CBF with the Psychomotor Flat affect, poverty of Underactivity of
presence of specific symptoms. poverty speech, decreased prefrontal cortex
spontaneous
movement

Etiology-Neurochemical findings Etiology-Neurochemical findings

1. Hyperdopaminergia-excessive dopamine release in acute Sc. 2. Serotonin (5-HT)
z Evidence z Evidence
¾ Repeated use of amphetamine, which may increase the ¾ The hallucinogen, lysergic acid diethylamide (LSD), is an
release of dopamine at central synapses, can induce a agonist at 5-HT2 receptors.
disorder similar to acute schizophrenia.
¾ Atypical antipsychotic drugs possess 5-HT2 antagonist
¾ All antipsychotic drugs are dopamine antagonists, and properties.
their affinity at D2 receptors is the property which
¾ Allelic variation in the 5-HT2A gene may be a minor risk
correlates best with their clinical potency.
factor for schizophrenia.
¾ Further studies have shown an excessive dopamine
¾ Decreased expression of 5-HT receptors in the frontal
release in acute schizophrenia without using amphetamine.
cortex of schizophrenia patients seen both in post-mortem
¾ In patients in remission, dopamine release returns to and functional imaging studies.
normal, suggesting that excess dopamine release is
directly related to acute schizophrenic syndrome.

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Etiology-Neurochemical findings Etiology-Neurochemical findings
3. Glutamate – NMDA receptor hypofunction 4. Others
z Evidence z γ- aminobutyric acid (GABA)
¾ Antagonists of NMDA type of glutamate receptor (e.g. z Neuropeptides
phencyclidine and ketamine) can induce a schizophrenia-
z adrenoreceptors
like syndrome.
¾ NMDA receptor modulators such as glycine have some
antipsychotic effects.
¾ Alterations in pre and post-synaptic indices of glutamate
signalling, especially in the medial temporal lobe, wherein
glutamate receptors are reduced.
¾ Much research indicated that the dopaminergic
dysfunction is secondary to aberrant regulation by
glutamatergic neurons.
¾ Most of the identified susceptibility genes are involved in
glutamate transmission
NMDA: N-methyl-D-aspartate

Manifestations
SYMPTOMS OF SCHIZOPHRENIA
Positive symptoms: excesses or distortion of normal function
Symptom Function disturbed

Clinical
Hallucinations Perception
Delusions Cognitive and inferential thinking
Positive formal thought disorder Language

manifestations
Bizarre behavior Behavioral organization and control

Negative symptoms: decreases in or loss of normal function

Symptom Function lost
Alogia Fluency of thought and speech
Affective blunting Fluency of emotional expressiveness
Avolition Volition and drive
Anhedonia Emotional attachment and hedonic capacity
Attention impairment attention
Andreasen NC. Schizophrenia-From Mind to Molecule. 1994.

Manifestations-Acute syndrome Manifestations-Acute syndrome

Thus, the predominant clinical features in acute schizophrenia are
The most frequent symptoms of acute schizophrenia positive symptoms.

Symptoms Frequency (%) ‹ Hallucinations:

Lack of insight 97 z May occur in any modality, but auditory ~ are the most prevalent.

Auditory hallucination 74 z The third-person (arguing) and second-person (commentary and

command) auditory ~, and, audible thought or thought-echoing
Delusion of reference 70 are relatively specific.

Suspiciousness 66 z Visual hallucinations are less common and usually occur

together with other kinds of ~.
Voice speaking to the patient 65
z Tactile, olfactory, gustatory, and somatic ~ sometimes occur,
Delusional mood 64 being often interpreted by the patients in delusional ways.

Delusions of persecution 64

Thought spoken aloud 50

Shorter Oxford Textbook of Psychiatry, 5th edit.

6
Manifestations-Acute syndrome Manifestations-Acute syndrome
‹ Delusions: ‹ Disorders of the form and flow of thought:
z Primary delusions are characteristic but difficult to identify with z Loosening of associations (e.g., talking past the point, derailment:
certainty. verbigeration or word salad) are common in server patients.
• Appears suddenly and with full conviction but without any mental z Thought blocking is a strong suggestive of schizophrenia,
events leading up to it. especially when the patient interpret the experience in a
z Persecutory delusions are common but less specific. delusional way.

z Delusion of control, and of thought insertion, withdrawal and z Poverty of thought and perseveration can also occur, but less
broadcasting are less common but of greater diagnostic value--- specific.
passivity phenomena.

Manifestations-Acute syndrome Manifestations-Acute syndrome

‹ Abnormalities of mood: ‹ Impaired insight:
z Sustained alterations in nature such as anxiety, depression, z Insight is almost always impaired.
irritability and euphoria.
¾ Most patients do not accept that their experiences result from
z Sustained alterations in fluctuation mainly include emotional illness, but usually ascribe them to the malevolent actions of
blunting or flattening, and anhedonia. other people.
z Incongruity of the affect, such as inappropriate affect and ¾ This lack of insight is often accompanied by unwillingness to
ambivalence. accept treatment.

Finally, we emphasize the variability of the clinical picture.

Few patients experience all the symptoms introduced above,
Whilst others already have features of ‘chronic’ syndrome at first
presentation.

Manifestations-Chronic syndrome Manifestations-Chronic syndrome

The most frequent symptoms of chronic schizophrenia Thus, the chronic syndrome is characterized by the negative symptoms,
sometimes called defect state, showing as:
Characteristic Frequency (%)
Social withdrawal 74 ‹ Poverty of speech or alogia
Underactivity 56 z Reduced amount of speech
Lack of conversation 54 z Little information in speech, vague, repetitive
Few leisure interest 50
‹ Blunted emotion or flat affect
Slowness 48
z No stimulus can elicit emotional response.
Depression 34
Odd behavior 34 z Patients may stare vacantly, with lifeless eyes and expressionless
face
Neglect of appearance 30
Odd posture or movements 25 ‹ Lack of drive or avolition
Threats or violence 25 z Lack of drive and initiative to any goal-directed activities (e.g.,
Socially embarrassing behavior 8 work, school), even everyday life (e.g., self-care, personal hygiene)
Sexually unusual behavior 8 z May engage in aimless and repeated activities, e.g., stereotypies,
Suicidal attempts 4 posturing, negativism (catatonic symptoms).
Shorter Oxford Textbook of Psychiatry, 5th edit.

7
Manifestations-Chronic syndrome
‹ Social withdrawal and anhedonia
z Lack of interest or enjoyment in activities and relationships.
z Withdrawal from social encounters and the social behavior may
deteriorate in ways that embarrass others.
z Lack of the ability to feel pleasure.
As with acute schizophrenia, the symptoms and signs of the chronic
stage are variable.
Some patients still have delusions or hallucinations, but they tend to
be held with little emotional response.
At any stage, positive symptoms may recur or become exacerbated,
they may be in response to life events, or discontinuation of
medications.
Manifestations-Subtypes
3. Catatonic schizophrenia
z Characterized by striking motor symptoms, and by changes in
activity varying between excitement and stupor.
z The other symptoms are not prominent.
z Relatively better prognosis.
4. Simple schizophrenia
z Characterized by the insidious development of negative
symptoms, without evident delusion and hallucinations.
z Difficult to identify reliably, and the category is now infrequently
used.
z Poor prognosis
Diagnosis
Manifestations-Subtypes
1. Paranoid schizophrenia
z The commonest type.
z Characterized by persecutory delusions, often systematized, and
by persecutory auditory hallucinations.
z The other symptoms are not prominent.
z Later age of onset, better prognosis, than other types.
2. Hebephrenic schizophrenia or disorganized schizophrenia
z Characterized by prominent formal thought disorder and
affective symptoms.
z Moods are variable, with behavior often appearing silly and
unpredictable.
z Delusions and hallucinations are fleeting and not so
systematized.
z Negative symptoms occur early, contributing to poor prognosis.
Manifestations-Subtypes
5. Undifferentiated schizophrenia
z The term for cases which do not fit readily into any of the above
subtypes, or where there are equally prominent features of more
than one subtypes.
6. Other terms
z Residual schizophrenia refers to a stage of chronic
schizophrenia when, for at least 1 year, there have been
persistent negative symptoms but no reoccurrence of positive
symptoms.
z Deficit syndrome describes a subtype of schizophrenia with early,
severe and persistent negative symptoms.
Criteria for schizophrenia in ICD-10
‹ The normal requirement for a diagnosis of schizophrenia is that a
minimum of one very clear symptom (and usually two or more if
less clear-cut) belonging to any one of the groups listed as (a) - (d)
below, or symptoms from at least two of the groups referred to as
(e) - (h), should have been clearly present for most of the time
during a period of 1 month or more.
(a) Thought echo, thought insertion or withdrawal, and thought
broad casting
(b) Delusion of control, inference, or passivity, clearly referred to
body or limb movements or specific thoughts, actions, or
sensations; delusional perception
(c) Commentary or arguing auditory hallucinations, 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.
Continue
8
Criteria for schizophrenia in ICD-10
Continued
(e) Persistent hallucinations in any modality, when accompanied
either by fleeting or half formed delusions without clear
affective content
(f) Breaks or interpolations in the train of thought, resulting in
incoherence or irrelevant speech or neologisms.
(g) Catatonic behavior, such as excitement, posturing, waxy
flexibility, negativism, mutism, and stupor.
(h) Negative symptoms such as 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 there are not due to
depression or neuroleptic medication.
(i) A significant and consistent change in the overall quality of
some aspects of personal behavior, manifest as loss interest,
aimlessness, idleness, a self-absorbed attitude, and social
withdrawal.
Criteria for schizophrenia in DSM-IV
Continued
B. Social/occupational dysfunction
For a significant portion of the 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.
C. Duration
Continuous sings 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 and may conclude:
Periods of prodromal or residual symptoms, the signs of the
disturbance may be manifested by only negative symptoms or two
symptoms listed in criterion A present in an attenuated form (e.g., odd
beliefs, unusual perceptional experiences)
Continue
Treatment
and Prognosis
Criteria for schizophrenia in DSM-IV
A. Characteristic symptoms of the active phase
Two or more of the following, each present for a significant
portion of time during a 1-month period (or less if successfully
treated).
1. Delusions
2. Hallucinations
3. Disorganized speech (e.g., frequent derailment or
incoherence)
4. Grossly disorganized or catatonic behavior
5. Negative symptoms, i.e., affective flattening, alogia, or
avolitions
Continue
Criteria for schizophrenia in DSM-IV
Continued
D. Schizoaffective and mood disorder exclusion
Schizoaffective disorder ad 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 episode 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 or a general medical condition.
F. Relationship to a pervasive developmental disorder
If there is a history of autistic disorder or another pervasive
development disorder, the additional diagnosis of schizophrenia is
made only if prominent delusions or hallucinations are also present
for at least 1 month (or less if successfully treated).
Treatment and prognosis
‹ Antipsychotic medication is the most effective treatment for
schizophrenia, especially for acute psychotic phase.
‹ According to the mechanisms, typical (classical) and atypical
(unclassical) antipsychotics are included:
¾ Typical antipsychotics:
• Block D2 receptors
• Effective for positive symptoms, but almost ineffective for
negative symptoms
• More and severe side effects, especially extrapyramidal side
effects, e.g., involuntary movements, severe shaking, twisting
of the body, extreme restlessness
• E.g., chlorpromazine, chlorprotixene, clopenthixole…
¾ Atypical antipsychotics
• Act on both D2 and 5-HT2 receptors
• Work with both positive and negative symptoms
• Fewer and lighter side effects.
• E.g., clozapine, olanzapine, quetiapine, risperidone…
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Treatment and prognosis Treatment and prognosis

Lehman AF, Liberman JA, et al.: Practice guideline for the treatment of patients with schizophrenia. 2004 Lehman AF, Liberman JA, et al.: Practice guideline for the treatment of patients with schizophrenia. 2004

Treatment and prognosis

Treatment and prognosis

Lehman AF, Liberman JA, et al.: Practice guideline for the treatment of patients with schizophrenia. 2004 Lehman AF, Liberman JA, et al.: Practice guideline for the treatment of patients with schizophrenia. 2004

Treatment and prognosis Treatment and prognosis

‹ The development of community-based services has led to increasing Factors predicting the outcome of schizophrenia
emphasis on psychological interventions in the treatment of
schizophrenia. Good prognosis Poor prognosis
‹ The purposes are: Sudden onset Insidious onset
¾ Enhancement of interpersonal and social functioning Short episode Long episode

¾ Promotion of independent living in the community No previous psychiatric history Previous psychiatric history

¾ Attenuation of symptoms severity and associated co-morbidity Prominent affective symptoms Negative symptoms
(e.g., substance misuse) Paranoid type Simple and hebephrenic type

¾ Improvement in personal illness management. Older age at onset Younger age at onset

‹ Methods, e.g.,: Married Single, separated, widowed, divorced

¾ Family therapy Good psychosexual adjustment Poor psychosexual adjustment

¾ Cognitive behavior therapy Good previous personality Abnormal previous personality

¾ Social skill training Good work record Poor work record

¾ Supported employment Good social relationships Social isolation
¾ Illness management skills Compliance with treatment Poor compliance with treatment
¾ Integrated treatment for co-morbid substance misuse Shorter Oxford Textbook of Psychiatry, 5th edit.

10
 Main reference
Gelder M, Harrison P, Cowen Phillip: Shorter Oxford
Textbook of Psychiatry. 5th Edti. Oxford, Oxford
University Press, 2005.
Lehman AF, Liberman JA, et al.: Practice guideline for the
treatment of patients with schizophrenia. 2nd edit. 2004.

Homework
1. Read the textbook through the pages 96-133
2. Read through this courseware.
3. Read the book Practice guideline for the treatment of
patients with schizophrenia, 2nd edit. APA. 2004.

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