OBJECTIVE: Various degenerative cerebral diseases and even depression may cause abnormalities of the cognitive event related potentials (ERPs). We conducted the present study to elucidate the effects of ischemic stroke on the P300 ERP component. MATERIAL AND METHODS: We recorded the P300 wave using an auditory oddball paradigm in 38 consecutive brain infarct patients with mild neurological deficits at 3 and 12 months post-stroke, and in 29 healthy control subjects. RESULTS: Brain infarction slightly prolonged the P300 latency, and the observed delay was related to the presence and degree of post-stroke depression evaluated with the Zung Depression Scale and the DSM-III criteria. Infarction did not affect the P300 amplitude or its distribution on the scalp. The results of the patients with hemispheric brain infarction and those of the patients with brainstem infarction were similar, and also the values of the patients with the left- and right-sided lesions. The normal physiological correlation between subject age and the P300 latency was absent at 3 months post-stroke, but was present at 12 months post-stroke. CONCLUSION: Brain infarction delays the P300 ERP and temporarily distorts its age-related physiology. The increase of the P300 latency seems to be associated with the post-stroke depression.
OBJECTIVE: Various degenerative cerebral diseases and even depression may cause abnormalities of the cognitive event related potentials (ERPs). We conducted the present study to elucidate the effects of ischemic stroke on the P300 ERP component. MATERIAL AND METHODS: We recorded the P300 wave using an auditory oddball paradigm in 38 consecutive brain infarctpatients with mild neurological deficits at 3 and 12 months post-stroke, and in 29 healthy control subjects. RESULTS:Brain infarction slightly prolonged the P300 latency, and the observed delay was related to the presence and degree of post-stroke depression evaluated with the Zung Depression Scale and the DSM-III criteria. Infarction did not affect the P300 amplitude or its distribution on the scalp. The results of the patients with hemispheric brain infarction and those of the patients with brainstem infarction were similar, and also the values of the patients with the left- and right-sided lesions. The normal physiological correlation between subject age and the P300 latency was absent at 3 months post-stroke, but was present at 12 months post-stroke. CONCLUSION:Brain infarction delays the P300 ERP and temporarily distorts its age-related physiology. The increase of the P300 latency seems to be associated with the post-stroke depression.