Schizophrenia

Overview
• Often a severe and enduring psychiatric
illness
• Comprises a significant proportion of the
consumers of mental health services
• Require long-term treatment using a range
of modalities and services
• Associated with significant psychiatric and
physical morbidity, as well as mortality
 Clinical Presentation
• Presentation may vary from acute to insidious
• A severe psychotic illness characterised by
delusions, hallucinations (usually auditory),
thought disorder and behavioural disturbance
• Often deterioration in social, occupational and
cognitive function
• Clear consciousness – ie to be distinguished from
delirium
 History
• Kraeplin (1855 –1926) – dementia praecox
• Bleuler (1857 – 1959) – schizophrenia
• Kraeplin suggested that aud. Hallucinations,
delusions, thought disorder, affective
falttening and impaired insight were
common to hebephrenia, paranoia, catatonia
and dementia simplex – group of disorders
which he called dementia praecox
 History contd.
• Bleuler – the four As – abnormal thought
association, affective abnormality,
ambivalence, autism
• Schneider (1887 – 1967) – first rank
symptoms
• Current classification – ICD 10/ DSM IV
 First Rank Symptoms
• Thought insertion/broadcast/withdrawal
• Made feelings/impulses/actions/somatic sensations
(a type of delusion)
• Third person auditory hallucinations (running
commentary or arguments)
• Delusional perception
• Thought echo (echo de la pensee or
gendankenlautwerden) – a type of hallucination
 First Rank Symptoms contd.
• 58% of patients with a diagnosis of
schizophrenia show at least one FRS
• 20% never show FRS
• 10% of patients who do not have
schizophrenia show FRS
 Classification
• Crow Type I and II
– Type I – positive symptoms, good response to treatment
– Type II – negative symptoms, poorer response to
treatment
 Classification contd.
• Andreasen – positive and negative symptoms
• Positive symptoms – hallucinations, delusions,
bizarre behaviour, formal thought disorder,
inappropriate affect
• Negative symptoms – affective flattening, poverty
of speech/thought, avolition – apathy, anhedonia,
social withdrawal, inattentiveness
 ICD 10
• Paranoid schizophrenia – prominent
delusions, aud hallucinations. Usually not
much thought disorder or negative
symptoms
• Hebephrenic (disorganised) SCZ – affective
abnormality, thoguht disorder, mannerisms.
May have chronic course
 ICD 10 contd.
• Catatonic schizophrenia – psychomotor symptoms
eg violent excitement, posturing, waxy flexibility,
automatic obedience, perseveration, stupor
• Residual SCZ – “defect state” – positive
symptoms give way to negative symptoms
• Simple schizophrenia – insidious development of
negative symptoms without positive symptoms
 Epidemiology
• Lifetime risk – 1%
• Incidence – 20/100 000 per year
• Low rates in some areas eg Hutterites in US
• High rates in some parts of Sweden, Ireland
• IPSS study (1973) showed that raters
similar in UK/US when used standardised
diagnostic tools
 Epidemiology contd
• Equal prevalence in males and females
• Males diagnosed earlier than women (males
age 15-25 years, females age 25 – 35 years)
• Commoner in urban areas, lower SEGs,
immigrants - Downward drift hypothesis?
• Breeder hypothesis – deprivation, stress of
immigration may increase risk
• Winter birth excess – increase of 7 – 15%
 Aetiological Theories
• Biological, psychological and social
theories proposed
• Biological – biochemical, genetic and
neurodevelopmental
 Biochemical theories
• Main theories are dopamine, serotonin and
excitatory amino acid hypotheses
• DA hypothesis – XS DA activity in mesolimbic
and cortical brain regions
• Amphetamines release DA at synapses and cause + symptoms
(in people who do not have SCZ)
• L-dopa increases central DA concentrations and causes +
symptoms
• All effective anitpsychotics are D2 receptor antagonists;
efficacy correlates with D” occupancy
 Biochemical theories contd.
• However,amphetamines and L-dopa do not
produce negative symptoms
• Antipsychotics are ineffective in 30% of
patients
• Antipsychotics block D2 receptors instantly
but antipsychotic effect not evident for days
 Biochemical Theories contd.
• Serotonin hypothesis – XS serotonin
• LSD and psilocybin are potent 5HT receptor
agonists and cause positive symptoms of SCZ (in
people who do not have SCZ)
• Atypical antipsychotics are potent 5HT receptor
antagonists

• However, LSD produces visual hallucination which

are uncommon in SCZ
 Biochemical theories contd.
• Excitatory amino acid hypothesis –
insufficient EAAs (glutamate and aspartate)
are implicated; phenylcyclidine (PCP),
which antagonises their receptors can
produce + and – symptoms in people
without SCZ.
 Genetics
• Greatest risk factor is having a relative with
SCZ
• 70% of the heritability of schizophrenia is
genetic
• MZ twin – 48% risk; DZ twin 17%
• Child of one parent with SCZ – 13%
• Child of two parents with SCZ – 46%
 Genetics
• Adoption studies indicate that heritability
rates are similar even if adopted away
• Probably polygenic/multifactorial model
• No clear gene responsible although interest
in various genes
 Neurodevelopmental Theories
• Hypothesis states that impaired foetal or
neonatal brain development many sow the
seeds of the onset of psychotic symptoms in
later life
• Patients with SCZ have lower than average
IQ, often subtle psychomotor, behaviourla,
and social abnormalities
 Neurodevelopmental Theories
• Patients with SCZ have more
developmental structural brain
abnormalities
• Soft neurological signs
• Increase in craniofacial and dermatoglyphic
abnormalities
• More obstetric complications recorded
• Exposure to influenza virus?
 Psychological Theories
• Freud – delusions as a way of making sense
of the external world
• Klein – failure to resolve the
paranoid/schizoid position
• Cameron – loss of conceptual boundaries
• Goldstein – concrete thinking
• Difficulties in filtering senory input?
 Familial/Social Theories
• Probably important in precipitating schizophrenia
than causing it
• Lidz – marital schism/marital skew
• Bateson – double bind
• High expressed emotion
• It has been hypothesised that life evetns could
precipitate SCZ – more life events in the 3 weeks
prior to episode than with healthy controls
 Clinical Presentation
• May present with a florid, rapidly evolving
psychosis, or a more insidious onset
• May be preceded by a prodromal period
• Some seem to have had difficulties from
ealry childhood eg preferring solitary play,
anxious and asocial, lack social confidence
 Acute Schizphrenia
• May develop acutely or be preceded by
days/weeks of delusional mood, bizarre
behaviour, social withdrawal, poor self-care
• Anxiety, depression and euphoria may be
seen
• Increased risk of suicide and violence
• May lack insight
• Often need hospitalisation
 Chronic Schizophrenia
• Characterised by avolition, depression,
social withdrawal, and poverty of
thought/speech
• May need encouragement in basic self-care
• Occupational and social activity diminished
• Insight often very poor
• Some will require long-tern residential care
 Diagnosis and Investigation
• Diagnosis – presence of typical symptoms
• Exclusion of other disorder eg organic
causes
» TLE
» CVA
» Drug-induced eg cannabis, speed, steroids
» Alcoholic hallucinosis
» dementia
 Investigations
• No diagnostic test
• Screen for drugs of abuse (urine)
• Bloods for fbc, biochemistry, blood
glucose, TFTs, TPHA and VDRL
• EEG
• ECG
• CT and MRI brain
 Treatment
• May require admission if acutely disturbed
or present a risk to self or others
• Admission may be useful in assessment
• Essential to assess suicide risk as there is a
mortality of about 10% from suicide in SCZ
• May require involuntary detention in some
cases
 Treatment contd.
• Antipsychotic drugs are mainstay of
treatment
• Generally atypicals are first-line treatment
eg olanzapine, respiridone, amisulpiride
• May require depot injection
• Side effects of typicals can be stigmatising
• Side effects of atypicals – screen for DM
 Treatment contd.
• Atypicals have fewer extra-pyramidal side
effects and tend to be better for negative
symptoms that typicals
• Initial management may include use of
sedative medication such as lorazepam
• IM medication may be required in a very
disturbed, involuntary patient
 Treatment contd.
• Maintenance treatment – generally
maintenance on one medication
• Compliance may be a significant problem
because of long-term nature of treatment
and lack of insight
 Treatment contd.
• Psychosocial treatment
» Education of patient and carers
» Reduction of high expressed emotion – shown to
affect relapse rates
» Cognitive behavioural therapy – controversial
» Rehabilitation
» Self –help – Schizophrenia Ireland
 Prognosis
• 22% have one episode and no residual
impairment
• 35% have recurrent episodes and no
residual impairment
• 8% have recurrent epsiodes and develop
significant non-progressive impairment
• 35% have recurrent episodes and develop
significant progressive impairment
 Prognosis contd.
• The majority therefore do not recover fully
• Suicide rate is up to 13%
• Little evidence that anitpsychotic have
altered the course of illness for most
patients
• However, evidence that prolonged
psychosis which is untreated has a bad
prognosis
 Prognosis contd.
• Good outcome is associated with:
– Female
– Older age of onset
– Married
– Higher SEG
– Living in a developing (as opposed to developed) country
– Good premorbid personality
– No previous psych history
– Good education and employment record
– Acute onset, affective symptoms, good compliance with
meds
 Prognosis contd.
• Some of the predictors of outcome are the
consequence of a less severe illness

• Predicting risk of suicide

» Acute exacerbation of psychosis
» Depressive symptoms
» History of attempted suicide