Abnormal autonomic activity in patients with schizophrenia has been reported, but how psychotic states influence the autonomic nervous system (ANS) has remained unclear due to methodological limitations. The influence of psychotic states on ANS activity in patients with schizophrenia was investigated using a recently developed method of analysis based on heart rate variability which assesses cardiac sympathetic and parasympathetic function separately. Cardiac autonomic function (CAF), together with psychotic states, was assessed at the beginning and the end of an 8-week study period in 53 patients with chronic schizophrenia. The CAF in age- and sex-matched control subjects was also examined. There were no significant differences between the patients and the control subjects in the mean R-R interval (RRI) or in the indices of the sympathetic and the parasympathetic function. In the patients who changed in psychotic states, the parasympathetic index was significantly decreased without significant changes in the sympathetic index when their psychotic states were more pronounced, suggesting psychotic states suppressed the parasympathetic function without affecting the sympathetic function. In these patients, the mean RRI was smaller when their psychotic states were more pronounced. Our results demonstrate that psychotic states affect the ANS, suggesting a relationship between cerebral cognitive and peripheral ANS activities, and that this is presumably mediated through the parasympathetic nervous system. These findings are discussed in comparison with previous reports on the CAF in schizophrenia.

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The authors report a patient carrying a missense mutation in exon 10 of tau that causes a substitution at codon 301 (P301S). Although the patient shares the rapidly progressive frontotemporal dementia of the other reported pedigrees with P301S, the clinical phenotype is unique in that parkinsonism was a major symptom in the early stage and because behavioral symptoms with dementia became prominent 2 years after the onset of the disease. This study substantiates the notion that tau mutations at codon 301 can show various phenotypes.

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