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OBJECTIVES—(1) To test the hypothesis that minor physical anomalies are increased in patients with schizophrenia and (2) to investigate differences in the prevalence of minor physical anomalies in patients with familial and sporadic schizophrenia and their first degree relatives. METHODS—A weighted Waldrop assessment was carried out on 214 subjects in five groups: schizophrenic patients from multiply affected families; first degree relatives of these familial schizophrenic patients; sporadic schizophrenic patients; first degree relatives of these sporadic schizophrenic patients, and normal controls. Broad and narrow criteria for abnormality were defined based on the distribution of minor physical anomalies in the control group. RESULTS—(1) The total schizophrenic group did not have a significant increase in minor physical anomalies using a narrow criterion of abnormality, but did when a broader criterion was used. (2) A significant increase in the proportion of subjects with an abnormally high number of minor physical abnormalities was shown in the group of sporadic schizophrenic patients (uncorrected p

BackgroundIt has been suggested that the increased rate of psychotic illness among African–Caribbeans living in Britain is due to an excess of pregnancy and birth complications (PBCs).MethodWe therefore compared the frequency of PBCs in a group of White psychotic patients (n=103) and a comparable group of patients of African–Caribbean origin (n=61); the latter consisted of 30 first-generation (born in the Caribbean) and 31 second-generation (born in Britain) individuals.ResultsWhite psychotic patients were more than twice as likely to have a history of PBCs as their African–Caribbean counterparts (odds ratio=2.34, 95% confidence interval (CI) 0.88–6.47, P=0.062). The same trend was observed among patients with a DSM–III diagnosis of schizophrenia (odds ratio=l.65, 95% CI 0.56–4.97, P=0.32). The rate of PBCs was similar among the first- and second-generation Caribbean psychotic patients.ConclusionsThe increased rate of psychotic illness that has been reported among the African–Caribbean population in Britain is not due to an increased prevalence of PBCs.

BackgroundWe investigated the hypothesis that prenatal exposure to the 1957 A2 influenza increases the risk of schizophrenia in adulthood.MethodWe traced a cohort of individuals known to have been exposed to the 1957 influenza epidemic during gestation and an unexposed cohort matched for period of gestation and hospital of birth. Follow-up information on psychiatric illness in subjects was sought from two sources: maternal interview and psychiatric hospital admission data.ResultsFollow-up information was obtained on 54% of the sample: 238 subjects from the influenza-exposed group and 287 subjects from the unexposed group. There was no increased risk of schizophrenia among the exposed cohort compared to the unexposed cohort (relative risk 1.1; 95% CI 0.41–2.95), although there was an increase in depressive illness (relative risk 1.59; 95% CI 1.15–2.19).ConclusionsThe association between prenatal influenza and an increased risk of schizophrenia in adulthood has thus far been found only in population-based data and is not supported by the present observational study which has information about exposure and outcome in individuals.

SynopsisAge and sex-adjusted first admission rates for operationally-defined schizophrenia and other non-affective psychosis in different ethnic groups were calculated over the period 1988–1992 in a defined catchment area in South London. Standardized rates for schizophrenia, corrected for age- and gender-related under-reporting in the 1991 census and a 20% underestimate of the size of the ethnic minority populations in the area, were not only higher in the Afro-Caribbean group (SMR: 3·1; 95% Cl: 2·0–4·7), but also in the African group (SMR: 4·2; 95% Cl: 2·8–6·2). It was further found that higher rates were not specific to schizophrenia. These findings suggest that some common factor associated with ethnic minority membership is important in producing an excess of psychotic illness.

Objective: Studies in Finland, England, and Denmark have reported that individuals exposed to the 1 957 A2 influenza pandemic during their second trimester in utero are at greater risk for later schizophrenia. However, other studies in England, the United States, and Holland reported no such association. The authors’ goal was to shed light on these conflicts. Method: They compared the number of individuals who later developed schizophrenia who were born in the 5 months after the peak prevalence ofthree distinct 1 957 influenza epidemics in Japan with the mean number of individuals who later developed schizophrenia who were born in the corresponding months ofthe 4 years surrounding the epidemics. Results: A significantly greater number offemales but not males who later developed schizophrenia were born during the risk exposure months than in the non-risk-exposure months. Conclusions: These f indings, although weak, lend support to the claim that in utero exposure to influenza epidemics is a risk factor for adult schizophrenia. (AmJ Psychiatry 1995; 152:450-452)

Background Axon-guidance proteins play a crucial role in brain development. As the dysfunction of axon-guidance signaling is thought to underlie the microstructural abnormalities of the brain in people with autism, we examined the postmortem brains of people with autism to identify any changes in the expression of axon-guidance proteins. Results The mRNA and protein expression of axon-guidance proteins, including ephrin (EFN)A4, eEFNB3, plexin (PLXN)A4, roundabout 2 (ROBO)2 and ROBO3, were examined in the anterior cingulate cortex and primary motor cortex of autistic brains (n = 8 and n = 7, respectively) and control brains (n = 13 and n = 8, respectively) using real-time reverse-transcriptase PCR (RT-PCR) and western blotting. Real-time RT-PCR revealed that the relative expression levels of EFNB3, PLXNA4A and ROBO2 were significantly lower in the autistic group than in the control group. The protein levels of these three genes were further analyzed by western blotting, which showed that the immunoreactive values for PLXNA4 and ROBO2, but not for EFNB3, were significantly reduced in the ACC of the autistic brains compared with control brains. Conclusions In this study, we found decreased expression of axon-guidance proteins such as PLXNA4 and ROBO2 in the brains of people with autism, and suggest that dysfunctional axon-guidance protein expression may play an important role in the pathophysiology of autism.