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.
The effects of acid mucopolysaccharides (1, chondroitin sulfates; 2. sulfated chondroitin sulfate; 3. chondroitin sulfate B and heparan sulfate) on thrombus formation by using a Chandler's technique in connection with the thrombogenic theory of arteriosclerosis were studied. The results using these compounds were as follows. 1) A single intravenous injection of chondroitin sulfates A and C (CS-A and CS-C, 120mg/kg of body weight, each) into 11 and 12 rabbits respectively, prolonged thrombus formation time (TFT), increased the concentrations of hexosamine and galactosamine in plasma, and reduced plasma triglycerides at 60min, after the injection. When CS-A and CS-C were added to human citrated platelet rich plasma in vitro, TFT was more prolonged with CS-C than that with CS-A. When CS-C of low and high molecular weights was added to platelet rich plasma in vitro, CS-C of high molecular weight showed prolonged TFT than that of low molecular weight. 2) A single intravenous injection of chondroitin polysulfate (CPS), 30mg/kg of body weight (sulfur: 15.6%), in 18 rabbits resulted in significant differences (P<0.01) between the values of the pre- and 30 and 60min. after the injection, namely prolongation of TFT and reduction in thrombus weight and plasma tri glycerides. These effects were observed somewhat less but still significantly at a dose of 10mg/kg of body weight of CPS, whereas a dose of 5mg/kg did not inhibit thrombus formation. When chondroitin polysulfates, 15.6% and 9.2% of sulfur-content, were added to plasma in vitro, TFT was strikingly prolonged by CPS (S: 15.6%) than by CPS (S: 9.2%). A prolonged TFT and a reduced thrombus weight were observed by peroral administrations of CPS (S: 14.1%) 400mg/kg of body weight to rabbits. 3) When chondroitin sulfate B and heparan sulfate were added to plasma in vitro, prolongation of the TFT was proved. 4) In the clinical study, TFT showed a slight acceleration in the plasma of the patients with cerebral thrombosis than in the subjects with myocardial infarction or cerebral haemorrhage. But the difference proved not significant.
It has frequently been suggested that in Western Countries, cerebral infarction caused by the occlusive or stenotic lesions of the extracranial cerebral arteries, is more common than that by the intracranial. To investigate the extracranial cerebral arteriosclerosis of Japanese, the atherosclerotic process were assessed in the entire carotid vertebral systems, and compared with the atherosclerosis of circle of Willis, in a series of 84 autopsied cases (23 in cerebral infarcts 61 in controls, unselected in regard to pathological diagnosis), over the 40 years old. Initially, the vessels were cut transversely for the evaluation of stenotic lesions, and when the lumen was occluded or severely narrowed, they were prepared to paraffin sections to facilitate more accurate estimation of the luminal narrowing, and then the degree and severity of atherosclerosis on the entire surface of the vessels were gradded macroscopically by Gore's method, Results obtained are as follows; 1) The degree of atherosclerosis of the common carotid calculated by narrowing index, revealed the highest, and then in order the internal carotid, the vertebral arteries. Atherosclerotic index of the three vessels showed the same trends. 2) The occluded or severely narrowed lesions of the extracranial cerebral arteries were found more frequently in the cases of cerebral infarcts than in controls, but the intracranial cerebral atherosclerosis was more severe in the former than in the latter. 3) Compared the atherosclerosis of the extracranial with that of the intracranial by narrowing index, the prominent lesions were found in the latter. 4) Microscopically, the most frequent findings of the narrowed lesions were the aggregation of amorphous materials in the intimal deep layers at the bifurcation of the vessels, and the calcification at the carotid siphon. It seems attributable that in Japan, the occluded or severely narrowed lesions of the extracranial cerebral arteries may not play any significant roles on the incidence of cerebral infarction, as in Western Countries.
A 77-year-old woman was reported, who showed akinetic mutism after an attack of cerebral thrombosis. The patient was admitted to the hospital complaining anorexia, followed by a development of left facial palsy, left hemiparesis and akinetic mutism, which was characterized by opening eyes to calling, gazing observers, following the movement of objects, escape from the painful stimuli, and forced grasp. Consciousness disturbance was gradually deepened and she died on the 52nd hospital day. Electroencephalograms showed slow α waves (8 to 9 cps) at the parieto-occipital region prior to onset of akinetic mutism, slow δ waves (3 cps) superimposed on the α to θ waves (7 to 8 cps) 3 weeks after the development of mutism, and large slow waves (1 to 2 cps) and irregular α waves (10 cps) on the left hemisphere in the terminal stage. Autopsy showed almost complete obstruction of the siphon of the right internal carotid artery by the organized thrombus, and there were extensive softening at the right precentral gyrus, cingulate gyrus, corpus callosum, hippocampal gyrus and reticular formation of thalamus and hypothalamus. Thus, our case showed extensive lesions encompassing all of 3 main areas of cerebral lesions in the akinetic mutism; that is (1) cerebrum, (2) frontal lobe (cingulate gyrus and corpus callosum) and (3) thalamus and hypothalamus.