The effect of TRH on cerebral blood flow in patients with spinocerebellar degeneration and cerebrovascular disease was investigated. Cerebral blood flow was measured by the 133Xenon arterial injection method before, and 30 min after, the intravenous administration of 1000 micrograms of TRH. TRH had no effect on mean arterial blood pressure in either group. In the spinocerebellar degeneration group, cerebral blood flow increased slightly after the injection of TRH, from 52.7 +/- 10.5 to 56.7 +/- 16.0 ml/100 g brain/min. In two patients with spinocerebellar degeneration, whose autonomic function was normal and whose brainstem structure appeared normal in the CT scan, cerebral blood flow increased from 54.8 to 66.4 ml (21.2%), and from 68.6 to 79.9 ml (16.5%), respectively. In the patients with cerebrovascular disease, cerebral blood flow did not change (49.7 +/- 10.8 ml before and 49.4 +/- 12.6 ml after TRH). Cerebral blood flow reportedly increases following an intravenous injection of TRH in animals, supposedly due to the activation of intrinsic cerebral vasodilative fibers situated in the submesencephalic brainstem region. Our results are consistent with this hypothesis and with the clinical finding that TRH especially improves ataxia in spinocerebellar degeneration where there is no pyramidal involvement or disorder of deep sensation.

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