The Prolongation of Inhibition in Brain-Damaged Patients

Abstract

The present study is an extension of an earlier investigation concerned with the time course of altered responsiveness in cerebrally damaged and normal patients to successively presented auditory stimuli. When presented with two stimuli which were separated by one, three and five seconds, the intact individuals tended to judge them as equal or to overestimate the intensity of the second tone. In contrast, the neurologically damaged patients tended to underestimate the intensity of the second tone, a tendency which diminished as the time interval between tones increased. These findings were interpreted as suggesting that an alteration in the recovery course of excitability occurs as a consequence of brain damage, and is reflected in the slow return towards baseline responsiveness shown by the cerebrally damaged patients. One hypothesis which was advanced to account for this alteration in excitability pattern, and which was tested in the present study, was that the basic mechanisms of arousal and inhibition are the same in both the normal and brain-damaged subjects, but that the latency period for recovery is increased following cerebral damage. This interpretation was suggested by the fact that the braindamaged subjects' total time curve for restored responsiveness was parallel to but significantly lower than that shown in the one to three second curve of the control group. Extrapolation of the brain-damaged subjects' recovery curve suggested that when nine seconds separated the two stimuli, the brain-damaged patients should perform as did the control subjects when three seconds separated the stimuli. The time intervals between successive stimuli, therefore, were extended to seven, eight and nine seconds in order to determine whether the cerebrally damaged patients would in fact come to perform as predicted. Twenty left hemiplegic and twenty age and sex matched control patients were utilized to test the hypothesis. The results confirmed the hypothesis and are consistent with the conclusion that the persistent underestimation of the intensity of the second of two successively presented auditory stimuli by cerebrally damaged patients was the product of a marked increase in the latency period required for a return to normal levels of responsiveness after stimulation in such patients. It was suggested that the prolongation of inhibition shown by the brain-damaged patients may be caused by alterations in the recovery properties of the reticulo-cortical system, or by changes in the decay rate or spread of inhibition of a local excitation-inhibition system, or by changes in the chain of chemical reactions which are required for the recovery of normal excitability patterns. Thus, there may be multiple mechanisms which are differentially disturbed by damage to different parts of the nervous system but which contribute to the occurrence of the same behavioral defect. The findings point strongly to the conclusion that a reduction in the elasticity of the neural response system is one major consequence of cerebral injury.