Clinical impact of residual lateral spread response after adequate microvascular decompression for hemifacial spasm: A retrospective analysis

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Abstract

Residual lateral spread response (LSR) after seemingly adequate decompression for hemifacial spasms (HFSs) can provide prognostic information about the outcome of microvascular decompression (MVD). In the present study, the main objective was to evaluate the clinical and prognostic impact of residual LSR after adequate MVD for HFS.

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Most cited references 23

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Neurovascular compression findings in hemifacial spasm.

M Kaufmann, Mauricio Campos-Mora (2008)

It is generally accepted that hemifacial spasm (HFS) is caused by pulsatile vascular compression upon the facial nerve root exit zone. This 2-3 mm area, considered synonymous with the Obersteiner-Redlich zone, is a transition zone (TZ) between central and peripheral axonal myelination that is situated at the nerve's detachment from the pons. Further proximally, however, the facial nerve is exposed on the pontine surface and emerges from the pontomedullary sulcus. The incidence and significance of neurovascular compression upon these different segments of the facial nerve in patients with HFS has not been previously reported. The nature of neurovascular compression was determined in 115 consecutive patients undergoing their first microvascular decompression (MVD) for HFS. The location of neurovascular compression was categorized to 1 of 4 anatomical portions of the facial nerve: RExP = root exit point; AS = attached segment; RDP = root detachment point that corresponds to the TZ; and CP = distal cisternal portion. The severity of compression was defined as follows: mild = contact without indentation of nerve; moderate = indentation; and severe = deviation of the nerve course. Success in alleviating HFS was documented by telephone interview conducted at least 24 months following MVD surgery. Neurovascular compression was found in all patients, and the main culprit was the anterior inferior cerebellar artery (in 43%), posterior inferior cerebellar artery (in 31%), vertebral artery (in 23%), or a large vein (in 3%). Multiple compressing vessels were found in 38% of cases. The primary culprit location was at RExP in 10%, AS in 64%, RDP in 22%, and CP in 3%. The severity of compression was mild in 27%, moderate in 61%, and severe in 12%. Failure to alleviate HFS occurred in 9 cases, and was not related to compression location, severity, or vessel type. The authors observed that culprit neurovascular compression was present in all cases of HFS, but situated at the RDP or Obersteiner-Redlich zone in only one-quarter of cases and rarely on the more distal facial nerve root. Since the majority of culprit compression was found more proximally on the pontine surface or even pontomedullary sulcus origin of the facial nerve, these areas must be effectively visualized to achieve consistent success in performing MVD for HFS.

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Pathophysiology of hemifacial spasm: I. Ephaptic transmission and ectopic excitation.

Sofie V Nielsen (1984)

We studied 62 patients with hemifacial spasm to test the presence of ephaptic transmission and ectopic excitation. The zygomatic and mandibular branches of the facial nerve were stimulated separately, recording simultaneously from the orbicularis oculi and mental muscles. Antidromic impulses were transmitted bidirectionally between the two branches. Transmission took place in a fraction of slow conducting motor nerve fibers. After-activity and late-activity were recorded as single potentials or trains, suggesting autoexcitation of fibers. The interspike frequency was 250 to 350 Hz. Hyperventilation produced synchronous clonic-tonic activity, suggesting ectopic excitation caused by hypocalcemia. Ectopic excitation and ephaptic transmission are important pathophysiologic factors in hemifacial spasm.

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Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations.

Peter J. Jannetta, David R. Moller (1985)

Facial muscle responses in patients with hemifacial spasm undergoing microvascular decompression operations were recorded. Two peripheral branches of the facial nerve were stimulated and the electrical responses of muscles innervated by these branches were studied to see how the lateral spread of activity that is known to be present in these patients was affected by decompressing the facial nerve. In some of the patients the hemifacial spasm ceased when the dura mater was opened, in some it ceased when the arachnoid was opened, and in others the spasm persisted until the offending vessel was dissected away from the nerve. The lateral spread of activity elicited by antidromic stimulation of a branch of the facial nerve was less affected by opening of the dura mater or arachnoid: it usually persisted until the blood vessel that had been compressing the facial nerve was removed and reappeared when the vessel that had been compressing the facial nerve was allowed to slip back onto the nerve. This seems to indicate that microvascular decompression of the facial nerve is effective in alleviating hemifacial spasm because it removes the actual cause of the disorder rather than simply causing local injury to the nerve as a result of the procedure.

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Journal

Title: British Journal of Neurosurgery

Abbreviated Title: British Journal of Neurosurgery

Publisher: Informa UK Limited

ISSN (Print): 0268-8697

ISSN (Electronic): 1360-046X

Publication date Created: September 07 2015

Publication date Created: November 02 2015

Publication date (Electronic): June 22 2015

Publication date (Print): November 02 2015

Volume: 29

Issue: 6

Pages: 818-822

Article

DOI: 10.3109/02688697.2015.1054351

PubMed ID: 26098605

SO-VID: 6ceeeadf-d5b9-46ea-8710-08ee27b5834e

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Clinical impact of residual lateral spread response after adequate microvascular decompression for hemifacial spasm: A retrospective analysis

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Core Readings in Statistical Mediation Analysis

Most cited references 23

Neurovascular compression findings in hemifacial spasm.

Pathophysiology of hemifacial spasm: I. Ephaptic transmission and ectopic excitation.

Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations.

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