脳神経被刺激症状(顔面痙攣等)の発生機序について

―椎骨脳底動脈系血管構築についての考察―

抄録

Pathogenesis of hemifacial spasms is still obscure. To elucidate the etiology, 61 patients with this clinical syndrome were closely examined. Surgical findings of all patients and vertebral arteriograms of 51 patients disclosed characteristic changes of the vertebro-basilar artery system and its branches. The vertebral artery was invariably larger in diameter ipsilaterally to the affected side of the face, made a sharp or hair-pin like angulation at the origin of the third segment of the vertebral artery and gave off branches almost rectangularly from the top of this angulated part toward the internal auditory meatus. On the other hand, the S-shaped basilar artery with the abovementioned asymmetrical changes in diameter of the vertebral arteries gave off the anterior inferior cerebellar artery toward the internal auditory canal of the affected side with an absent or hypoplastic posterior inferior cerebellar artery. Operative procedures demonstrated that the facial nerve was invariably compressed by an ectated or radundant artery which showed right turn and local “arteriosclerotic” changes at its cross-compressing site. The peculiar vasculature changes of the vertebro-basilar artery and the compressing artery may be congenitally present, and subsequently, an exaggerated intraluminal blood stream or pressure of the larger sized vertebral artery is likely to apply a stronger hemodynamic force to the wall of the angulated part of the vertebral artery, resulting in ectasia or redundancy of the peripheral branches originating from this point and also wall thickening of the right-angled part of the compressing artery which just happens to lie close enough to the exit zone of the facial nerve from the brain-stem. These vasculature findings appear to provide an important key to solve the problem of why a certain artery can cross-compress the facial nerve and why the vast majority of hemifacial spasms develop on one side of the face.