There is significant and independent variation of incidence of schizophrenia and other psychoses in terms of sex, age, ethnicity, and place. This confirms that environmental effects at the individual, and perhaps neighborhood level, may interact together and with genetic factors in the etiology of psychosis.

Background. The incidence of schizophrenia in the African-Caribbean population in England is reported to be raised. We sought to clarify whether (a) the rates of other psychotic disorders are increased, (b) whether psychosis is increased in other ethnic minority groups, and (c) whether particular age or gender groups are especially at risk.

An increasing number of studies are demonstrating an association between childhood abuse and psychosis. However, the majority of these rely on retrospective self-reports in adulthood that may be unduly influenced by current psychopathology. We therefore set out to explore the reliability and comparability of first-presentation psychosis patients' reports of childhood abuse. Psychosis case subjects were drawn from the Aetiology and Ethnicity of Schizophrenia and Other Psychoses (ÆSOP) epidemiological study and completed the Childhood Experience of Care and Abuse Questionnaire to elicit abusive experiences that occurred prior to 16 years of age. High levels of concurrent validity were demonstrated with the Parental Bonding Instrument (antipathy: r(s)=0.350-0.737, P<.001; neglect: r(s)=0.688-0.715, P<.001), and good convergent validity was shown with clinical case notes (sexual abuse: κ=0.526, P<.001; physical abuse: κ=0.394, P<.001). Psychosis patients' reports were also reasonably stable over a 7-year period (sexual abuse: κ=0.590, P<.01; physical abuse: κ=0.634, P<.001; antipathy: κ=0.492, P<.01; neglect: κ=0.432, P<.05). Additionally, their reports of childhood abuse were not associated with current severity of psychotic symptoms (sexual abuse: U=1768.5, P=.998; physical abuse: U=2167.5, P=.815; antipathy: U=2216.5, P=.988; neglect: U=1906.0, P=.835) or depressed mood (sexual abuse: χ(2)=0.634, P=.277; physical abuse: χ(2)=0.159, P=.419; antipathy: χ(2)=0.868, P=.229; neglect: χ(2)=0.639, P=.274). These findings provide justification for the use in future studies of retrospective reports of childhood abuse obtained from individuals with psychotic disorders.

These findings suggest that DUP is influenced both by aspects of the early clinical course and by the social context.

Patients with schizophrenia and related psychoses have an excess of minor neurological abnormalities (neurological soft signs) of unclear neuropathological origin. These include poor motor coordination, sensory perceptual difficulties and difficulties in sequencing complex motor tasks. Neurological soft signs seem not to reflect primary tract or nuclear pathology. It still has to be established whether neurological soft signs result from specific or diffuse brain structural abnormalities. Studying their anatomical correlates can provide not only a better understanding of the aetiopathogenesis of soft signs, but also of the pathophysiology of schizophrenia. Surprisingly few studies have investigated the brain correlates of neurological soft signs. In the present study, we investigated the relationship between brain structure and neurological soft signs in an epidemiologically based sample of 77 first-episode psychosis patients. We used the Neurological Evaluation Scale for neurological assessment and high-resolution MRI and voxel-based methods of image analysis to investigate brain structure. Higher rates of soft neurological signs (both motor and sensory) were associated with a reduction of grey matter volume of subcortical structures (putamen, globus pallidus and thalamus). Signs of sensory integration deficits were additionally associated with volume reduction in the cerebral cortex, including the precentral, superior and middle temporal, and lingual gyri. Neurological soft signs and their associated brain changes were independent of antipsychotic exposure. We conclude that neurological soft signs are associated with regional grey matter volume changes and that they may represent a clinical sign of the perturbed cortical-subcortical connectivity that putatively underlies psychotic disorders.

Neuropsychological dysfunction, specifically impairment of set-shifting and error monitoring, contributes to poor insight in psychosis. Specific relations with different dimensions of insight and the putative role of metacognitive functions require further study.

Typical antipsychotic drugs act on the dopaminergic system, blocking the dopamine type 2 (D2) receptors. Atypical antipsychotics have lower affinity and occupancy for the dopaminergic receptors, and a high degree of occupancy of the serotoninergic receptors 5-HT2A. Whether these different pharmacological actions produce different effects on brain structure remains unclear. We explored the effects of different types of antipsychotic treatment on brain structure in an epidemiologically based, nonrandomized sample of patients at the first psychotic episode. Subjects were recruited as part of a large epidemiological study (AESOP: aetiology and ethnicity in schizophrenia and other psychoses). We evaluated 22 drug-free patients, 32 on treatment with typical antipsychotics and 30 with atypical antipsychotics. We used high-resolution MRI and voxel-based methods of image analysis. The MRI analysis suggested that both typical and atypical antipsychotics are associated with brain changes. However, typicals seem to affect more extensively the basal ganglia (enlargement of the putamen) and cortical areas (reductions of lobulus paracentralis, anterior cingulate gyrus, superior and medial frontal gyri, superior and middle temporal gyri, insula, and precuneus), while atypical antipsychotics seem particularly associated with enlargement of the thalami. These changes are likely to reflect the effect of antipsychotics on the brain, as there were no differences in duration of illness, total symptoms scores, and length of treatment among the groups. In conclusion, we would like to suggest that even after short-term treatment, typical and atypical antipsychotics may affect brain structure differently.

BackgroundMany studies have found high levels of compulsory admission to psychiatric hospital in the UK among African–Caribbean and Black African patients with a psychotic illness.AimsTo establish whether African–Caribbean and Black African ethnicity is associated with compulsory admission in an epidemiological sample of patients with a first episode of psychosis drawn from two UK centres.MethodAll patients with a first episode of psychosis who made contact with psychiatric services over a 2-year period and were living in defined areas were included in the (ÆSOP) study. For this analysis we included all White British, other White, African–Caribbean and Black African patients from the ÆSOP sampling frame. Clinical, socio-demographic and pathways to care data were collected from patients, relatives and case notes.ResultsAfrican–Caribbean patients were significantly more likely to be compulsorily admitted than White British patients, as were Black African patients. African–Caribbean men were the most likely to be compulsorily admitted.ConclusionsThese findings suggest that factors are operating at or prior to first presentation to increase the risk of compulsory admission among African–Caribbean and Black African patients.