Based on the work of Elkes and Shore, Sernyl appears to exert its action by the release of adrenaline and noradrenaline in association with the depression of the availability of serotonin in the brain. This is consistent with Brodie's hypothesis(1) that serotonin and noradrenaline are antagonistic chemical mediators regulating the central autonomic system.The importance of kinaesthetic input in preserving the intactness of the body-image is well recognized in studies of the effects of sensory deprivation(2). Nocturnal delusions of the senium due to loss of familiarity with surroundings is also a well recognized phenomenon(3). Hence, disturbance of kinaesthetic input, whether taking place primarily within the brain, due to externally administered agents such as CI 395, or outside the brain as in sensory deprivation, leads to psychotic behaviour with features similar to schizophrenia. "Information input underload" and the disturbance of coding or integration of sensory stimuli at a higher level may be the possible cause of psychotic behaviour.The reversibility of the psychotomimetic effects produced by Sernyl with chlorpromazine, suggests a common mechanism with that seen in temporary psychotic states, such as acute paranoid or schizophrenic reactions. This would support the tentative hypothesis of Luby and associates(4) "that certain primary symptoms of schizophrenia may have their basis in a dys-synchrony or defect in proprioceptive feedback."