Møller A R
Department of Neurological Surgery, University Pittsburgh School of Medicine, Pennsylvania.
Acta Neurochir (Wien). 1991;113(1-2):24-30. doi: 10.1007/BF01402110.
The various hypotheses regarding the pathophysiologies of trigeminal neuralgia and hemifacial spasm are reviewed, and the results of recent physiological studies on the pathogenesis of hemifacial spasm are discussed. Evidence is presented that strongly supports the hypothesis that the symptoms and signs of hemifacial spasm are caused by hyperactivity in the facial motonucleus. Some of the contradictions regarding the prevalence of vascular conflicts in the cerebellopontine angle and the symptoms of vascular compression are discussed, and a hypothesis is presented that assumes that a suitable substrate must be present, in addition to vascular compression of the respective cranial nerve root, for the symptoms and signs of a cranial nerve vascular compression disorder to develop. Finally, it is discussed how this hypothesis can explain some of the differences between the disorders that can be cured by microvascular decompression of respective cranial nerves.
本文回顾了关于三叉神经痛和半面痉挛病理生理学的各种假说，并讨论了近期关于半面痉挛发病机制的生理学研究结果。有证据强烈支持半面痉挛的症状和体征是由面神经运动核的活动亢进引起的这一假说。文中讨论了关于小脑脑桥角血管冲突发生率和血管压迫症状的一些矛盾之处，并提出了一种假说，即除了相应颅神经根的血管压迫外，还必须存在合适的底物，才能引发颅神经血管压迫性疾病的症状和体征。最后，探讨了这一假说如何解释通过相应颅神经微血管减压可治愈的疾病之间的一些差异。
