Neuromuscular Dysfunction in Schizophrenia*

During the last 7 years, there have been a number of investigations of the incidence of various types of neuromuscular dysfunction in patients with schizophrenic and affective illnesses and their first-degree relatives in comparison with appropriate controls, including nonpsychotic psychiatric patients. Before reviewing these studies, it may be of value to discuss why neuromuscular dysfunction might be expected in virtually any disease of the nervous system—a category in which, thanks to recent genetic studies, we may now confidently include schizophrenia and the primary affective illnesses. The evidence for central nervous system involvement in a variety of diseases with apparently primary skeletal muscle involvement will also be presented. There are numerous instances of known disease of the brain in which pathologic changes in lower motor neurons, with consequent effects on skeletal muscle fiber morphology and function, are found. "Central atrophy" is the name given to the atrophy of skeletal muscle fibers, which frequently develops after various chronic brain diseases, particularly tumors of the parietal lobe (Fenichel, Daroff, and Glaser 1964, Koinov and Markov 1971, and Van Crevel 1969). Depth electrode studies in chronic schizophrenics have demonstrated abnormal electrical discharges in various parts of the cerebral cortex, including the parietal lobe (see Mirsky 1969). The mechanism of central atrophy is believed to be loss of the trophic (nutrient) influence of the upper