Vascular compression of cranial nerves: II: pathophysiology.
The pathophysiology of trigeminal neuralgia, hemifacial spasm and other disorders that can be cured by microvascular decompression of cranial nerves, is reviewed and different hypotheses about its pathophysiology are discussed. It is found that the pathophysiology of these disorders is complex and other factors than vascular compression are necessary to cause symptoms. While the efficacy of the microvascular decompression (MVD) operation is indisputable, it is questionable if the symptoms and signs of these disorders are caused by abnormal neural activity in the respective cranial nerves that result from the compression from a blood vessel. Instead, studies point to hyperactivity and hyperexcitability of the respective nuclei as a cause of the symptoms and signs of these disorders. Results of several studies indicate that irritation of the cranial nerve in question from close contact with a blood vessel may promote such development, and it seems necessary that other factors in addition to the vascular contact must be present in order that such a condition develops.
Møller
A R
AR
University of Texas at Dallas, Callier Center for Communication Disorders 75235-7298, USA.
D002530:Cerebellopontine Angle / Q000098:blood supply; D002536:Cerebral Arteries / Q000473:pathology*; D003391:Cranial Nerves / Q000503:physiopathology* / Q000601:surgery; D019299:Decompression, Surgical; D005152:Facial Muscles / Q000294:innervation; D019569:Hemifacial Spasm / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D008866:Microsurgery / Q000379:methods; D009408:Nerve Compression Syndromes / Q000503:physiopathology* / Q000601:surgery; D013478:Superior Mesenteric Artery Syndrome; D009435:Synaptic Transmission