HSC Section 3 - Trauma, Critical Care and Sleep Medicine

Sun et al

Other causes of acute facial palsy for which the efficacy of surgical decompression has not been shown, such as Ramsay-Hunt syndrome, are beyond the scope of this article. Ramsay-Hunt syndrome is differentiated from Bell palsy by the presence of otalgia, periauricular vesicles, hearing loss, or vestibular symptoms. Causes of sub- acute or recurrent facial palsy, including facial nerve neuromas and facial nerve vascular malformations, are also beyond the scope of this article.

SURGICAL APPROACH Rationale for Middle Cranial Fossa Approach for Bell Palsy

The surgical approach for Bell palsy has evolved as the understanding of its patho- physiology has changed. Historically, the stylomastoid foramen and chorda-facial junction have both been proposed as the sites of disorder in Bell palsy. 7–10 Conse- quently, transmastoid decompression was initially advocated, but later found to be ineffective when performed alone. 11,12 Increased knowledge regarding the site of nerve compression and conduction blockade in Bell palsy became available following the description of the middle cranial fossa (MCF) approach by William House in 1961. 13 The MCF approach provides ac- cess to the facial nerve from the cisternal to the proximal tympanic segments, while allowing for preservation of auditory and vestibular function. Using the MCF approach, Fisch and Esslen 14 performed facial nerve decompression on a series of patients with Bell palsy and found pronounced edema and vascular injection of nerve proximal to the geniculate ganglion in 11 out of 12 patients. In a separate part of this study, 3 pa- tients were treated with total intratemporal exposure of the facial nerve via a combined MCF and transmastoid approach, and intraoperative evoked electromyography (EEMG) of the facial nerve from the stylomastoid foramen to the internal auditory canal (IAC) was performed. The conduction abnormality was located within the IAC, prox- imal to the geniculate ganglion (GG) in all 3 patients. Subsequently, this finding was corroborated in a larger series of patients. 15,16 Eighteen patients with 90% to 98% degeneration on electroneurography (ENoG) underwent decompression. Intraopera- tive EEMG was attempted for all patients and successfully performed for 16 patients. Of these 16 patients, 15 (94%) had a conduction block proximal to the GG and 1 had a conduction block at the origin of the chorda tympani. These data suggest that, for almost all patients with Bell palsy, the conduction block occurs proximal to the GG and decompression should therefore include the fallopian canal proximal to the GG. Anatomic studies corroborate these intraoperative conduction findings. The labyrin- thine segment of the fallopian canal is the narrowest segment along the entire course of the facial nerve, measuring 0.69 mm in diameter on average. 17 In addition, a tight arachnoid band is present at the proximal extent of the labyrinthine segment of the fal- lopian canal and acts as a chokepoint of constriction in the setting of edema. 17,18 Several studies have shown herpes simplex virus-1 19–22 or varicella zoster virus– associated inflammatory infiltration 23 in clinically diagnosed Bell palsy. Thus, the cur- rent understanding of the pathophysiology of Bell palsy is that viral reactivation in the GG leads to lymphocytic infiltration and perineural edema that spreads along the course of the facial nerve. 24,25 Edema in the labyrinthine segment may lead to cessa- tion of axoplasmic flow caused by compressive pressure in the fallopian canal. Further neural edema may cause cessation of vascular flow and the onset of ischemia, and wallerian degeneration distal to the point of constriction. Surgical decompression via an MCF approach therefore offers an opportunity to restore blood flow across the point of constriction by decompression of bone and lysis of the arachnoid band while preserving inner ear function.

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