A case of cerebellar infarction induced by repeated neck rotation ("bow-hunter's stroke") is reported. The most likely mechanism is that repeated rotational neck movement brings about thickening of the atlanto-occipital membrane, fixing the vertebral artery in the vascular groove of the atlas. The vertebral artery is thus pinched at the time of neck rotation, leading to thrombus formation. Embolization results in cerebellar infarction. Surgical decompression of the vertebral artery at the level of the atlas in this case relieved the symptoms, and postoperative angiography demonstrated good flow within the vertebral artery even when the neck was rotated. It was not necessary to restrict the patient's neck movement postoperatively.

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The effects of hemoglobin and cerebrospinal fluid from patients with subarachnoid hemorrhage (CSF-SAH) on endothelium-dependent relaxation were studied. At 10" 6 M, hemoglobin somewhat inhibited the endothelium-dependent relaxation induced by A23187 in rings of canine basilar artery. At 3 x 10~6 M, it almost completely inhibited the same response. At 3 x 10~6 M, hemoglobin did not significantly inhibit smooth muscle relaxation mechanisms as papaverine-induced relaxation was not inhibited by hemoglobin. It was also demonstrated that pretreatment of arterial rings with CSF-SAH resulted in a dose-dependent inhibition of relaxation induced by A23187. The inhibitory effect of CSF-SAH was prominent in the case in which a high oxyhemoglobin concentration was measured by spectrophotometry. Normal CSF from patients without SAH did not affect endothelium-dependent relaxation. These results suggest that hemoglobin released from lysed erythrocytes inhibits endothelium-dependent relaxation of canine basilar arteries and may also play an important role in the pathogenesis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. (Stroke 1987;18:938-943)

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