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Biomedical subjects

G Araki

Publications and source records attributed to G Araki.

At least 37 records · Page 2Linked to original sources

[Dynamic pathophysiology of cerebral infarction and revascularization. I. Ischemic cerebral edema].

A natural history of ischemic cerebral edema was analyzed in 100 patients with occlusive cerebrovascular diseases admitted within one week of onset, with serial computed tomography (CT) and angiograms. Cerebral edema was defined as a low-density area with mass sign on CT. A total of 446 studies of CT were performed. In 40 patients with major completed stroke admitted 24 hours of onset, a total of 73 studies of CT were taken within 48 hours of onset, and a timing of appearance of cerebral edema was analyzed. Patients were allocated to two groups according to the findings on angiograms; 68 patients who showed occlusive lesions on sequential angiograms (the group of no-recanalization), and 32 patients who showed reopening of occluded vessels on the first or sequential angiograms (the group of no-recanalization). In the group of no-recanalization a low-density area gradually appeared between 6 and 24 hours of onset A. mass sign reached its peak on the 3rd day with a peak incidence of 56%, and midline shift was present in 30% of the cases. It was resolved within 2 weeks in most cases. In the group of recanalization, a low density area appeared after 4 hours and rapidly increase after 6 hours. All patients had a low-density area at 12 hours of onset. A mass sign progressed until the 6th day with a peak incidence of 82%, and midline shift was present in 50% of the cases. The duration of mass sign was longer than that in the group of no-recanalization. These results suggest that the permissible duration of ischemia is considered to be within 6 hours of onset in profound ischemia. After 6 hours, ischemic tissue damage may not be reversible by the revascularization, even if CT shows no change during ischemia. An abrupt revascularization may not contribute to the recovery of brain damage, but accelerate the ischemic cerebral edema.

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Clinical evaluation of GABA in the treatment of cerebrovascular disorders. Multi-center double-blind study in comparison with pyrithioxine and placebo.

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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[Arterial occlusion following cerebral vasospasm (author's transl)].

1. The present study analysed the clinical course, the serial angiograms and the CT scans of the patients with angiographic arterial occlusion following vasospasm after subarachnoid hemorrhage. The occlusion was observed in 6 out of 84 patients with vasospasm. 2. The angiograms which showed this phenomenon were obtained between the 11th and the 30th day of the illness. The affected vessels were the branches of middle cerebral artery. 3. Thrombus formed on the intima which had been injured by vasospasm is suspected to be a genesis of this arterial occlusion. The pathological findings of a case in this series support this concept. 4. The surgical procedure during the direct aneurysmal operation performed in the period of "smooth narrowing" seems to be a contributing factor to the arterial occlusion. There was no correlation between antifibrinolytic therapy and this phenomenon except in one case. 5. Fibrinolytic therapy after clipping of aneurysm may be a treatment of choice for this arterial occlusion following vasospasm.

Cerebral Angiography↗