4.6 Article

Neurovascular compression findings in hemifacial spasm

Journal

JOURNAL OF NEUROSURGERY
Volume 109, Issue 3, Pages 416-420

Publisher

AMER ASSOC NEUROLOGICAL SURGEONS
DOI: 10.3171/JNS/2008/109/9/0416

Keywords

hemifacial spasm; microvascular decompression surgery; neurovascular compression; root exit zone

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Object. 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. Methods. 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 I 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. Results. 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. Conclusions. 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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