The cranial nerve vascular compression syndrome: II. A review of pathophysiology.
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.
Møller
A R
AR
Department of Neurological Surgery, University Pittsburgh School of Medicine, Pennsylvania.
D003389:Cranial Nerve Diseases / Q000503:physiopathology* / Q000601:surgery; D003391:Cranial Nerves / Q000098:blood supply / Q000503:physiopathology; D005156:Facial Neuralgia / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D008866:Microsurgery / Q000379:methods; D009408:Nerve Compression Syndromes / Q000503:physiopathology* / Q000601:surgery; D009460:Neurologic Examination; D013035:Spasm / Q000503:physiopathology / Q000601:surgery; D014277:Trigeminal Neuralgia / Q000503:physiopathology / Q000601:surgery