[Spontaneous bursts of high voltage slow wave activities in the EEG of the aged].
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Biomedical subjects
Publications and source records attributed to E Otomo.
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Butoctamide hydrogen succinate (BAHS), which is related to an organic compound naturally occurring in CSF, has been demonstrated to increase REM sleep in cats and yound adults. In the present study, BAHS was confirmed also to increase REM sleep in healthy aged subjects. The subjects were six females (68-77 years of age). The experiment covered 8 consecutive nights. Identical capsules containing either a placebo (linoleic acid) or 600 mg BAHS were administered 1 h prior to recording, which was started at 9 PM. BAHS tended to stabilize sleep. The average number and percentage of REM periods increased significantly during the drug nights compared with the baseline nights (P less than 0.05 and P less than 0.02, respectively). The maximum percentage of BAHS-induced REM sleep was approximately 20%. REM sleep did not exceed the upper limit of the physiological range. A carry-over effect of BAHS occurred during the withdrawal nights. During the drug nights, and the average length of REM periods increased in each sleep cycle. The length especially increased significantly in cycle 3 (P less than 0.05). The interruptions of REM sleep decreased in number. The histogram of REM sleep showed that REM sleep increased in the middle and the latter part of the night with two apparent peaks. Though REM sleep increased, REM density decreased. The mechanisms by which BAHS increases REM density decreased. The mechanisms by which BAHS increases REM sleep suggests that BAHS increases serotonin in the brain, and that serotonin increases REM sleep secondarily. BAHS seems to be a unique drug which increases REM sleep, while other clinically used drugs suppress it.
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The convulsion and electroencephalographic patterns were examined on 2,625 subjects aged 60 and over. Of these, 2000 were consecutive autopsy cases. convulsion was noted in 4% of the 2,625 cases and the incidence of epilepsy was 0.076%. In 26.4% of 72 cases with cerebrovascular disorders who died during the past two years, convulsion was found, and the value indicated a remarkable increase compared with the previous report. Convulsion was noted most frequently in the acute state of cerebral apoplexy and myoclonus was most common. The prognosis of such cases was poor. The incidence of convulsion in 30 consecutive patients with brain tumor was 13.3%. On 20,000 electroencephalograms, the incidence of the typical spike and wave complex was less than 0.005%. No 6 and 14c/sec positive spike was recognized.
The therapeutic efficacy of GABA was compared with pyrithioxine and placebo in 432 patients with cerebrovascular disorders by a multi-center (50 hospitals) double-blind clinical trial. 12 tablets (3 g) of GABA and 3 tablets (600 mg) of pyrithioxine were given daily for 8 weeks. Subjective complaints, neurological and psychiatric findings, activity of daily living were checked at the 4th and 8th weeks after medication. The global improvement rates in GABA-treated groups were 59% and 70% each after 4 and 8 weeks of medication, and were significantly superior to the other two groups. Especially on cerebral arteriosclerosis GABA was more effective than the other two drugs, with statistical significance. As for improvement rates of symptoms there were significant differences between GABA and the other two drugs in subjective complaints and in psychiatric findings. The incidence of side effects was 5%, 20% and 8% in GABA, pyrithioxine and placebo, respectively. The incidence of abnormal laboratory data was 2% (3 cases), 8% (11 cases) and 4% (6 cases), respectively. Those in GABA group were transient and restored to normal values after the trial. It is concluded from these results that GABA is safe and effective in the treatment of cerebrovascular disorders.
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A study was conducted on the electroencephalographical and neuropathological correlations on 96 cases of cerebrovascular disease in order to elucidate the reasons why EEGs are often misleading in the diagnosis of location and size cerebrovascular lesions. The study showed that EEG findings are particularly misleading when the lesions were in the locations as follows: 1) subcortical deep infarctions, 2) cortical infarctions occupying a small proportion of cerebral convexity, or involving an entire hemisphere, or affecting the right hemisphere, 3) basilar thrombosis and infratentorial hemorrhage (primary or secondary to supratentorial lesions). The pathophysiological significance of these results has been discussed.
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