gms | German Medical Science

Introduction: Hemifacial spasm (HFS) is a cranial nerve rhizopathy with involuntary movement characterized by clonic/tonic contraction of the facial muscles on one side. The most common cause of HFS is focal compression of facial nerve root by an aberrant loop of an artery or arteries; venous compression is less common. Occurrences in childhood or infancy are very rare. Although HFS is not a life-hreatening disease, it often causes distress and psychological disturbances as a consequence of difficulties in conversation, reading and driving. Botulinum toxin injections are minimally invasive but benefits are temporary. Spontaneous disease cure is exceptionally rare.

Objective: Microvascular Decompression (MVD) in Hemifacial spasm (HFS) is widely considered a standard procedure. We discuss our results in a surgical series of 210 pts. treated with MVD from 1980 to 2007.

Methods: We present 210 pts. (52.4% females and 47.6% male patients with a mean age of 53 yrs.). In the last 15 years all the patients were preoperatively studied with Magnetic resonance angiography (MRA) that identified a vascular conflict in 75% of cases. After minimal hair shaving, all the patients underwent a standard retrosigmoid craniectomy. Decompression is achieved by initial artery mobilization and then by tissue implants between the offending vessel/vessels and the seventh nerve without intraoperative electrophysiological monitoring. A cerebellar self-retaining retractor is not employed.

Results: 80% of patients were found to be spasm-free at discharge. One month after surgery 92% of pts. were spasm-free. The postero-inferior cerebellar artery (PICA) was the most frequent offending vessel (40% of cases), then antero-inferior cerebellar artery (AICA) in 15% of cases; vertebral artery (VA) in 20% of cases and double arterial conflict (VA and PICA) in 25% of cases. Surgical complications included: temporary reduction in auditory acuity (7%); temporary facial nerve palsy (House-Brackmann Grade III or worse) in 3% of cases; gait ataxia (0.5%) and cerebellar swelling (0.5%). We did not find any surgical mortality. At an average follow-up of 10 yrs. the recurrence rate was 4% with a prevalence of recurrences in the VA offending vessel population.

Conclusions: As other authors have demonstrated in the past, MVD in HFS is a safe and well-tolerated procedure with a high rate of success. Postoperative facial nerve palsy is a rare complication even without neurophysiological monitoring. We observed many differences with Trigeminal neuralgia (TN): (1) preoperative neuroradiological findings more frequently demonstrate a vascular compression at the root entry zone (REZ); (3) venous compressions is rare; (4) double arterial compression is implicated in about one fourth of the cases (above all VA and PICA) and it determines difficult surgical dislocation of the offending vessels requiring placement of multiple tissue implants. In our opinion this “small space” does not allow any other manoeuvres. In recurrent HFS, reoperation could be the right choice in some selected patients.