THE CROSSMODAL RETARDATION IN REACTION TIME OF PATIENTS WITH CEREBRAL DISEASE

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Abstract
Comparison of the simple reaction times of brain-damaged and control patients to three classes of stimuli under a condition of serial presentation of stimuli gave the following results. Both groups of patients showed slower reaction times to stimuli that had been preceded by a different stimulus than to stimuli that had been preceded by an identical stimulus. The degree of retardation in reaction time to stimuli preceded by a different stimulus in the same sensory modality (ipsi-modal retardation effect) was not different in the two groups of patients. The degree of retardation in reaction time to auditory stimuli preceded by a visual stimulus (crossmodal retardation effect) was also not different in the two groups. The degree of retardation in reaction time to visual stimuli preceded by an auditory stimulus was significantly greater in the brain-damaged than in the control patients, however. Patients with diffuse or bilateral cerebral disease showed a significantly larger crossmodal retardation than control patients; patients with focal lesions did not. Comparison of the results of the present investigation with those of previous studies on schizophrenic patients indicates that both brain-damaged and schizophrenic patients show excessive susceptibility to the crossmodal retardation effect. There is an apparent difference in the "locus" of the effect in the two groups of patients, however, since schizophrenic patients have been found to show particularly marked retardation in reaction to sound stimuli preceded by visual stimuli. Further critical investigation of this apparent difference is indicated. It is concluded that both patients with cerebral disease and schizophrenic patients show excessive susceptibility to the crossmodal retardation effect in simple high-speed performance tasks. The phenomenon cannot be explained in terms of lack of motivation, fatigability or failure to maintain set. It is likely that there is a neurophysiological basis for this behavioral deficit.

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