Summary
It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve.
In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Apfelbaum RI (1988) Surgical management of disorders of the lower cranial nerves. In: Schmidek HH, Sweet WH (eds) Operative neurosurgical techniques. Indications, methods, and results, Vol 2. Grune and Stratton, Orlando, Florida, pp 1097–1109
Esslen E (1957) Der Spasmus facialis eine Parabiosserscheinung: Elektrophysiologische Untersuchungen zum Entstehungsmechanismus des Facialisspasmus. Dtsch Z Nervenheil 176: 149–172
Ferguson JH (1978) Hemifacial spasm and the facial nucleus. Ann Neurol 4: 97–103
Gardner WJ (1962) Concerning the mechanism of trigeminal neuralgia and hemifacial spasm. J Neurosurg 19: 947–958
Gardner WJ (1966) Crosstalk — the paradoxical transmission of a nerve impulse. Arch Neurol 14: 149–156
Haines SJ, Torres F (1991) Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm. J Neurosurg 74: 254–257
Howe JF, Loeser JD, Calvin WH (1977) Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pains of root compression. Pain 3: 25–41
Itagaki S, Saito S, Nakai O (1988) Intraoperative recording of evoked EMG in patients with hemifacial spasm-possible physiological mechanism. Facial N Res Jpn 8: 143–146
Itagaki S, Saito S, Nakai O (1989) Electrophysiological study onhemifacial spasm-usefulness in etiological diagnosis and pathophysiological mechanism. Brain Nerve (Tokyo) 41: 1005–1011
Jannetta PJ (1977) Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction, and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Acta Neurochir (Wien) 20: 145–154
Jannetta PJ (1980) Neurovascular compression in cranial nerve and systemic disease. Ann Surg 192: 518–525
Jannetta PJ, Hackett E, Ruby JR (1970) Electromyographic and electronmicroscopic correlates in hemifacial spasm treated by microsurgical relief of neurovascular compression. Surg Forum 21: 449–451
Kugelberg E (1952) Facial reflexes. Brain (Lond) 75: 385–396
Lehman HJ, Ule G (1964) Electrophysiological findings and structural changes in circumscript inflammation of peripheral nerves. Prog Brain Res 6: 169–173
Martinelli P, Gabellini AS, Lugaresi E (1983) Facial nucleus involvement in postparalytic hemifacial spasm. J Neurol Neurosurg Psychiatry 46: 586–587
Martinelli P, Giuliani S, Ippoliti M (1992) Hemifacial spasm due to peripheral injury of facial nerve: a nuclear syndrome? Mov Disord 7: 181–184
MØller AR (1987) Hemifacial spasm: ephaptic transmission or hyperexcitability of the facial motor nucleus? Exp Neurol 98: 110–119
MØller AR (1991) The cranial nerve vascular compression syndrome: I. A review of treatment. Acta Neurochir (Wien) 113: 18–23
MØller AR (1991) The cranial nerve vascular compression syndrome: II. A review of pathophysiology. Acta Neurochir (Wien) 113: 24–30
MØller AR (1991) Interaction between the blink reflex and the abnormal muscle response in patients with hemifacial spasm: results of intraoperative recordings. J Neurol Sci 101: 114–123
MØller AR, Jannetta PJ (1984) On the origin of synkinesis in hemifacial spasm: results of intracranial recordings. J Neurosurg 61: 569–576
MØller AR, Jannetta PJ (1985) Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations. Neurology 35: 969–974
MØller AR, Jannetta PJ (1985) Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations. Neurosurgery 16: 612–618
MØller AR, Jannetta PJ (1986) Blink reflex in patients with hemifacial spasm: observations during microvascular decompression operations. J Neurol Sci 72: 171–182
MØller AR, Jannetta PJ (1986) Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations. Exp Neurol 93: 584–600
MØller AR, Jannetta PJ (1987) Monitoring facial EMG responses during microvascular decompression operations for hemifacial spasm. J Neurosurg 66: 681–685
MØller AR, Sen CN (1990) Recordings from the facial nucleus in the rat: signs of abnormal facial muscle response. Exp Brain Res 91: 18–24
Nielsen VK (1984) Pathophysiological aspects of hemifacial spasm. Part I. Evidence of ectopic excitation and ephaptic transmission. Neurology 34: 418–426
Ruby JR, Jannetta PJ (1975) Hemifacial spasm: ultrastructural changes in the facial nerve induced by neurovascular compression. Surg Neurol 4: 369–370
Saito S, MØller AR (1993) Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity. Neurol Res 5: 225–231
Saito S, Itagaki S, Nakai O (1990) Neurophysiological study on hemifacial spasm - - the abnormality and origin of the electromyographic response to stimulation of the facial nerve. Brain Nerve (Tokyo) 42: 621–627
Sen CN, MØller AR (1987) Signs of hemifacial spasm created by chronic periodic stimulation of the facial nerve in the rat. Exp Neurol 98: 336–349
Sunderland S (1951) The function of nerve fibers whose structure has been disorganized. Anat Rec 109: 503–509
Author information
Authors and Affiliations
Additional information
All work of the above manuscript was done at the University of Pittsburgh School of Medicine.
Rights and permissions
About this article
Cite this article
Kuroki, A., Møller, A.R. Facial nerve demyelination and vascular compression are both needed to induce facial hyperactivity: A study in rats. Acta neurochir 126, 149–157 (1994). https://doi.org/10.1007/BF01476426
Issue Date:
DOI: https://doi.org/10.1007/BF01476426