Abstract
Visual evoked responses (VERs) were recorded in 73 patients with apoplexy at range from 36 to 71 years and in 75 patients without apoplexy at range from 11 to 75 years as control. The photic stimulus was presented at a frequency of 1/3sec. and a lamp was placed 20cm distant in front of the subject's closed eyes. The electrical activities were recorded from the scalp electrodes placed at both the occipital regions with reference electrode on each ipsilateral ear lobe. The activities were averaged by the digital computer (ATAC 501-20 Nihon koden) after 50 flashes were practiced. The name of each peak given by Cigánek was adopted for analysis in the present study. The peak latency appeared to be satisfactorily reproduced but the amplitude was not.
The each peak latency was inclined to be delayed gradually, with the increase of age in both the groups of cotrol and patients with apoplexy. Moreover, the mean value of the peak latency in the apoplexy group was greater than that of control group at each age group. As far as the age group sof forty and fifty, the differences in W2, W3, W4 and W5 between control apoplexy were of statistical significance (P<0.01).
Abnormal VERs were found in 18 (5, in control and 13, in apoplexy) of 148 subjects and those could be devided into 3 types as follows;
1) Latency asymmetry only. 2) Latency and wave form asymmetry. 3) Wave form asymmetry only.
It was characteristic that the latency delay was chiefly found in W2 and W3 and that the wave form asymmetry was found in W4 and W5
Two of 5 patients with visual field defect had normal findings in the VERs and the remaining 3 had abnormal findings. However, their abnormalities were observed not in the primary response but in the secondary one.
It seemed that there is not any characteristic correlation between the abnormal VERs and the lesion in patients with apoplexy; They were discussed in detail in the text.
Of 13 abnormal VERs in the patients with apoplexy, 10 were recorded in acute stage, within one month after the onset. Therefore, it appeated tha this abnormal findings in the VERs resulted from the hypofunction and the impediment for the conduction at the synapsis, both of which were due to hemispherical diffuse brain edema in acute stage. However, it seemed that the abnormal VERs were also caused by extensive damage of the brain in the patients at chronic stage; the patients with occlusion of internal cerebral artery or middle cerebral one.
