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Various findings suggest auto-immune changes in schizophrenia. We have recently demonstrated that platelets from schizophrenic patients bear auto-antibodies (PAA) which cross-react with brain antigens. Accordingly, treatment of schizophrenia with an immunosuppressant might be of potential benefit. In a recent case study, a chronic schizophrenic patient treated with azathioprine has demonstrated a clear psychiatric improvement preceded by a decrease in PAA level. A phase I study designed for assessing side-effects of short-term azathioprine treatment in a group of schizophrenic patients is described here. From a group of 40 chronic non-responsive patients, 14 patients demonstrating high PAA level have entered the study and 11 have complied all along. Two groups were tested in parallel. In the first (6 patients) 150 mg/day was given for 7 weeks while in the second (5 patients) the same regimen was given for two periods of 7 weeks with an interval of 6 weeks. Blood biochemistry and cell count, as well as determination of PAA were carried out weekly, starting 3 weeks before the trial and continuing up to 7 weeks after the treatment. Two out of 11 patients developed leucopenia in week 4. No other side-effects were recorded in any of the patients. A substantial reduction in PAA was observed in 3 out of 6 patients in group I and 4 out of 5 in group II. Two patients showed improvement of psychiatric symptomatology. Our results demonstrate that short-term azathioprine treatment induces transient leucopenia in 18% of the patients recieving the drug, much alike the percentage reported for other patient populations.

This study evaluates the comorbidity of epilepsy as a variable supporting a viral hypothesis in Autism. Data covering a 30-year period (1960-1989), including general population live births, autistic births, and incidence of viral encephalitis and viral meningitis, were collected for Israel. 290 autistic births were evaluated. The annual birth pattern of subjects with comorbid epilepsy fit the seasonality of viral meningitis. These findings support the role of viral C.N.S. infections in the causality of this disorder.

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