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Takao Soda

Publications and source records attributed to Takao Soda.

3 recordsLinked to original sources

Stroke recurrence within the first year following cerebral infarction--Tottori University Lacunar Infarction Prognosis Study (TULIPS).

OBJECTIVES: To identify determinants of recurrence after ischemic stroke in the Japanese population. MATERIALS AND METHODS: We enrolled 885 patients with acute ischemic stroke that had been admitted to our community hospitals. A total of 831 cases were followed for 1 year after the index stroke. Patients were assigned to one of the ischemic stroke subtype groups based on the NINDS Stroke Data Bank criteria. RESULTS: Rates of stroke recurrence were significantly different among stroke subtype groups: 14.4% in cardioembolic infarction, 7.3% in atherothrombotic infarction (ATI), 6.2% in lacunar infarction (LI) and 7.8% in infarction of uncertain cause. Previous history of stroke was the predictor of stroke recurrence for the groups of ATI and LI patients, and diabetes mellitus was the predictor of recurrence for the group of LI patients. CONCLUSION: The rate of recurrence and risk factors for stroke recurrence are different by stroke subtypes.

Aged↗

The antiplatelet aggregation effects of aspirin suppositories.

To confirm that aspirin suppositories are an effective treatment for acute ischemic stroke, we examined the suppressive effects of 200-mg aspirin suppositories on platelet aggregation. Aspirin suppositories suppressed platelet aggregation induced by ADP or collagen, and the suppression continued for 24 h. There was no significant difference in suppression of platelet aggregation between aspirin administered by suppository and orally given aspirin. These results suggest that aspirin suppositories are a useful treatment for acute ischemic stroke.

Adenosine Diphosphate↗

Brainstem infarction presenting with neurogenic stuttering.

We reported a sixty-year-old man who developed acquired stuttering after a brainstem infarction. Infarctions were detected in the midbrain and upper pons. Neurogenic stuttering of this patients indicated that the midbrain and upper pons could be lesion sites responsible for acquired stuttering. We speculated that the reticular network extending from the brainstem to the frontal cortices, and the periaqueductal gray matter could be closely related regions generating neurogenic stuttering.

Brain Stem Infarctions↗