Common, serious psychiatric disorder, characterized by psychotic symptoms (see PSYCHOSIS), with recurrent acute episodes of illness occurring against a background of progressive, chronic disability. The aetiology of schizophrenia is at present incompletely understood: diagnosis is based on clinical examination, and rests on the recognition of clusters of SIGNS AND SYMPTOMS.
The modern concept of schizophrenia has evolved over the last century. It has its roots in the classification of mental disorders by Emil Kraepelin (1856–1926) into two broad groups based on long-term outcome. He distinguished between manic depressive insanity (see MANIC DEPRESSION), which he considered to resolve completely between episodes, and DEMENTIA PRAECOX which he believed led to either progressive impairment or only partial recovery. This latter condition is the forerunner of contemporary classifications. The term SCHIZOPHRENIA itself (it comes from Greek, schizein: to cleave) was coined by Paul E. Bleuler (1857–1939) who emphasized a psychological view of dementia praecox, and considered core aspects of the illness to relate to a splitting or ‘loosening of associations’ between such mental activities as cognition and AFFECT. (Schizophrenia does not involve a splitting of personality, but a loss of these associations.) As the concept developed, it became clear that the term schizophrenia was being used in a vague and imprecise way. Lack of agreed diagnostic criteria hampered the study of the disorder and led to wide variations in diagnostic practice. The description by Kurt Schneider (1887–1967) of proposed FIRST-RANK SYMPTOMS of schizophrenia represented a preliminary step in the development of operationalized diagnostic criteria, though Schneider himself recognized that this symptom profile was not specific to schizophrenia, and many of the symptoms occurred in other psychotic disorders.
Older classification systems used the terms HEBEPHRENIA, PARANOIA and CATATONIA to describe different types of schizophrenia. Contemporary classification systems have devel oped from these and use a number of subtypes of schizophrenia: DSM-IV recognizes paranoid, catatonic, undifferentiated and residual types. Alternatively, the signs and symptoms were differentiated by Tim Crow into TYPE I SCHIZOPHRENIA and TYPE II SCHIZOPHRENIA. Characteristic of type I were the so-called ‘positive’ symptoms (signs and symptoms abnormal by their presence) including DELUSION, HALLUCINATION, disorganized speech and thinking, and disorganized or catatonic behaviour. Type II included the so-called ‘negative’ symptoms of schizophrenia (features abnormal by their absence) include WITHDRAWAL, APATHY, and flat or inappropriate MOOD.
Schizophrenia affects men and women equally, though men tend to have an earlier onset, with half of male sufferers being hospitalized before the age of 25. Life-time prevalence is estimated at between 1 and 1.5%. Though the aetiology of schizophrenia is poorly understood, there is little doubt that the disorder is a brain disease. Enlargement of the lateral and third ventricles (see VENTRICULAR ENLARGEMENT) with a reduction in cortical volume is a consistent finding in COMPUTERIZED AXIAL TOMOGRAPHY. FUNCTIONAL NEUROIMAGING techniques reveal reduced frontal activity (HYPOFRONTALITY), and neuropsychological investigations confirm frontal dysfunction in many cases. The ANTIPSYCHOTIC efficacy of DOPAMINE receptor blocking drugs (see DOPAMINE HYPOTHESIS OF SCHIZOPHRENIA) suggests dysfunction of dopaminergic systems. Cellular architecture abnormalities have been reported in limbic areas such as the HIPPOCAMPUS. Recent findings suggest that EXCITATORY AMINO ACID systems may be dysfunctional. Genetic factors appear to play an important role with a 10-fold increase in the prevalence of schizophrenia amongst the children of a schizophrenic parent over the general population rate. The concordance rates of MONOZYGOTIC TWINS are estimated at 47% (for DIZYGOTIC TWINS the rate is 12%). Psychosocial factors also play an important role, and families with high levels of hostility, criticism or over involvement (so-called high EXPRESSED EMOTION) may lead to high relapse rates in the condition.
The mainstay of treatment in schizophrenia is drug therapy. Traditional antipsychotics such as CHLORPROMAZINE and HALOPERIDOL have been used effectively for many years, but are increasingly being replaced by newer, so-called ATYPICAL ANTIPSYCHOTICS, which appear to have a better side effect profile, particularly with regard to EXTRAPYRAMIDAL SIDE-EFFECTS. CLOZAPINE appears to be more effective than other antipsychotics, and may have activity against negative as well as positive symptoms. This drug’s propensity to cause haematological side-effects in 1–2% of patients (which may be fatal if undetected) necessitates regular blood monitoring, and restricts its use to treatmentresistant cases at present. Specific psychotherapeutic strategies (see PSYCHOTHERAPY) have met with limited success, though preliminary reports of the use of COGNITIVE THERAPY are encouraging. Novel theoretical approaches to schizophrenia based on the premise of dysfunctional METAREPRESENTATION are also generating cognitive approaches to the disorder (see Frith, 1993). Family work directed to reducing expressed emotion may reduce relapse rates. A key factor in psychosocial management is the development of a flexible therapeutic alliance with patients directed at maintaining drug COMPLIANCE and anticipating and responding to crises.
Prognosis is good for only 20–30% of sufferers—half of the patients diagnosed with schizophrenia will experience repeated relapse and hospitalization. The remaining 20–30% will experience moderate symptoms, and a significant degree of disability. It is estimated that 10–15% of patients with schizophrenia will die by SUICIDE.
References
Crow T.J. (1980) Molecular pathology of schizophrenia: more than one disease process? British Medical Journal 280:66–68.
