Schizophrenia

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