A devastating disorder Occurs in about 1% of the population No major sex differences in prevalence rates Costs of care >30 Billion Dollars annually Many homeless are untreated or stop medications.
In general, schizophrenia.. Is a disorder of thought and emotion Is not a “split-personality” disorder
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
Kraepelin (1855 –1926) – dementia praecox Bleuler (1857 – 1959) – schizophrenia Kraepelin suggested that auditory hallucinations, delusions, thought disorder, affective flattening and impaired insight were common to hebephrenia, paranoia, catatonia and dementia simplex – group of disorders which he called dementia praecox
Bleuler – the four As – abnormal thought association, affective abnormality, ambivalence, autism Schneider (1887 – 1967) – first rank symptoms Current classification – 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
Crow Type I and II
I – positive symptoms, good response to treatment Type II – negative symptoms, poorer response to treatment
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
Many Subtypes of Schizophrenia
Based on the symptoms that are presented. Paranoid Catatonic Disorganized Others
Paranoid schizophrenia – prominent delusions (grandeur or persecution), auditory hallucinations. Usually not much thought disorder or negative symptoms. Age of onset (late twenties and thirties)
Disorganised speech and behavior, flat affect, marked regression to primitive, disinhibited behavior, severe thought disorder and poor contact with reality. Patients tend to be younger than 25
Mutism Negativism Psychomotor retardation or excitation posturing
Meets criteria for schizophrenia but does not meet the criteria for paranoid, catatonic or disorganised
An absence of prominent delusions, disorganised speech/behavior or catatonic behavior. Absence of overt positive symptoms but tend to have negative symptoms.
Brief psychotic disorder
Hallucinations Delusions Disorganised or catatonic behavior Symptoms more than 1 day but less than 30 days.
Symptoms (delusions/hallucinations/disorganised speech/negative symptoms) lasting for 1 month but less than 6 months. Patients have affective symptoms – depressive episode after the psychosis resolves Return to their premorbid level of functioning
Schizophrenia symptoms Major depressive episode/manic or mixed episode Delusions or hallucinations for at least 2 weeks in the absence of mood symptoms Better prognosis than SCZ but worse than patients with affective disorders
Nonbizarre delusion for at least 1 month No impairment in level of functioning The patients are usually reliable except if its in relationship to their functioning Erotomanic, Jealous, grandiose, somatic, Mixed Mean age of onset - 40 years
Lifetime risk – 1% Incidence – 20/100 000 per year IPSS study (1973) showed that rates similar in UK/US when used standardised diagnostic tools
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%
Biological, psychological and social theories proposed Biological – biochemical, genetic and neurodevelopmental
Main theories are dopamine, serotonin and excitatory amino acid hypotheses DA hypothesis –excess of 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 – excess of serotonin
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; phencyclidine (PCP), which antagonises their receptors can produce + and – symptoms in people without SCZ.
Greatest risk factor is having a relative with SCZ MZ twin – 47-48% ; DZ twin 12-17% Child of one parent with SCZ – 12% Child of two parents with SCZ – 40% First degree relative -12 % Second degree relative-5-6 %
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
Hypothesis states that impaired foetal or neonatal brain development may sow the seeds of the onset of psychotic symptoms in later life Patients with SCZ have lower than average IQ, often subtle psychomotor, behavioral, and social abnormalities
Patients with SCZ have more developmental structural brain abnormalities Soft neurological signs Increase in craniofacial abnormalities More obstetric complications recorded Exposure to influenza virus?
Brain Abnormality Hypothesis
Identified by CT and Cerebral Blood Flow Studies
Some Patients have one or more of the following. Reduction of blood flow to the left Globus Pallidus Problems in the frontal lobes Medial temporal lobe is thinner Anterior Hypothalamus is smaller (especially left side) Lateral and third ventricles are enlarged
Sulci are also enlarged (especially in the temporal and frontal lobes Indicated reduced numbers of neurons
Freud – delusions as a way of making sense of the external world Cameron – loss of conceptual boundaries Goldstein – concrete thinking Difficulties in filtering sensory input?
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 events could precipitate SCZ – more life events in the 3 weeks prior to episode than with healthy controls
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 early childhood e.g. preferring solitary play, anxious and asocial, lack social confidence
May develop acutely or be preceded by days/weeks of delusional mood, bizarre behaviour, social withdrawal, poor selfcare Anxiety, depression and euphoria may be seen Increased risk of suicide and violence May lack insight Often need hospitalisation
Characterised by avolition, depression, social withdrawal, and poverty of thought/speech May need encouragement in basic selfcare 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 e.g. organic causes
TLE CVA Drug-induced
steroids Alcoholic hallucinosis dementia
e.g. cannabis, LSD,
No diagnostic test Screen for drugs of abuse (urine) Bloods for FBS, biochemistry, blood glucose, TFTs, TPHA and VDRL EEG ECG CT and MRI brain
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
Antipsychotic drugs are mainstay of treatment Generally atypicals are first-line treatment e.g. olanzapine, respiridone. May require depot injection Side effects of typicals can be stigmatising Side effects of atypicals – screen for DM
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
Maintenance treatment – generally maintenance on one medication Compliance may be a significant problem because of long-term nature of treatment and lack of insight
of patient and carers Reduction of high expressed emotion – shown to affect relapse rates Cognitive behavioural therapy Rehabilitation
22% have one episode and no residual impairment 35% have recurrent episodes and no residual impairment 8% have recurrent episodes and develop significant non-progressive impairment 35% have recurrent episodes and develop significant progressive impairment
The majority therefore do not recover fully Suicide rate is up to 13% Little evidence that antipsychotic have altered the course of illness for most patients However, evidence that prolonged psychosis which is untreated has a bad prognosis
Good outcome is associated with:
age of onset Married Higher SEG
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 medicines
Predicting risk of suicide
exacerbation of psychosis Depressive symptoms History of attempted suicide