Hemifacial spasm is a chronic condition affecting aged people with female predominance. Among our patients, mean of age was 51.8 years, where females are affected more than twice as males similar to what was reported in literature (mean age was 49.2 years, the ratio of females to males was 3.6:1). Hypertension and diabetes prevailed among our patients, similar observation noted by Chaudhry et al., who stated that hemifacial spasm and hypertension were coexistent in 40% of cases and hypertension can cause vessel ectasia which is the underlying etiology in most of the patients [1]
Although we believe that the best treatment option in cases suffering from hemifacial spasm is MVD, which may in certain cases be assisted by endoscopy, yet in patients where no definite vascular conflict identified in the MRI, or in those patients who were unfit for any surgical maneuver we had to seek other treatment modalities.
The current pharmacological management of hemifacial spasm included baclofen, carbamazepine, clonazepam, local doxorubicin, and other antiepileptic drugs (AEDs). Both baclofen and AEDs produced intolerable adverse effects, and new effective drugs are needed. Levetiracetam is an anticonvulsant drug with anti-kindling effect which is considered the pathogenesis of hemifacial spasm. There were few reports describing the efficacy of levetiracetam in the treatment of hemifacial spasm. We used a dose ranging from 1500 to 2000 mg that was higher than the dose in literatures (500–1500 mg) and yet showed non-increase in side effect because of the safety profile of the drug. All patients showed good compliance with maintained efficacy similar to Kurado et al., who showed a maintained response. One patient in our study showed poor response with levetiracetam that may be attributed to the compressive nature of the condition [2].
Gabapentin (GBP) is an antiepileptic drug with a safety profile and a mechanism of action involving GABAergic activities. It exerts its effect by reduction in either ephaptic transmission or hyperexcitability of the motor nucleus of the seventh nerve by increasing GABA levels. It showed efficacy in reducing hemifacial spasm in a dose ranging from 800 to 1200 mg which was lower than the dose prescribed in other series (900–1600 mg). All side effects were temporary except for one patient who suffered from confusion that necessitated reduction of the dose. An open-label pilot study with this drug showed an overall success rate of 69.5% which was comparable to our results [3].
The mean of Botox dose was 36.7 U that was similar to the mean reported by Sorgun et al. (34.5 U with range 19.5–85 U). Among our patients, there was a mean of 7 days of delay similar to what was found by Sorgun et al. An average of 8 days lapsed since the first improvement (range 1–40). According to Kollewe et al., Rudzinska, and Poonyathalang et al., the latency was between 2 and 14 days. In our study, Botox effect lasted from 15 to 24 weeks (mean 20.5 weeks) similar to what was found by Kollewe et al. and Poonyathalang et al., where the mean duration of improvement was 15.7 weeks (range 6.5–24.3 weeks). Overall success rate was 83.3% among our patients. Similar result was reported by Sorgun et al., where the degree of improvement was 73.7%. According to literature, 86.7% of patients treated with botulinum toxin injections (range 73–96.9%) reported an improvement [4,5,6,7,8,9,10].
Nearly one third of our patients suffered from side effect that was temporary (resolved within a maximum of two months). According to literature, side effects were usually mild and transient and improved within a month. Ptosis was our most frequent side effect similar to what was reported by Sorgun et al. (range 2.5–72.2%) followed by facial weakness (range 4.5–76.9%). The side effect duration and degree were related to several factors like age. Price et al. found that orbital injections near the inner canthus were related to a higher incidence of ptosis. Defazio et al. found that the percentage of side effects was be related to dosage. Cakmur et al. reported higher success rates, longer durations of improvement, and fewer side effects with pretarsal injections [4, 9, 11, 12].
Among the surgical group, AICA was the main compressing vessel. Similarly, Li et al., Dannenbaum et al., Hyun et al., and Fukuda et al. found that AICA was the responsible vessels. Badr-El-Dine et al., Cheng et al., and Mooij et al. found that PICA was the main offending vessel [13–19].
We had one patient who showed delayed cure (14%) for only 4 days. According to Sindou et al., delayed effect ranged from 5% to 50% in literature. Jo et al. who studied a delayed cure among surgically treated patients stated that not all of the patients are cured immediately after surgery. Ishikawa et al. found a delay in cure in 50% of patients that last for a week in 25%, one month in 50%, and eight months in 90% of delayed cured patients [20,21,22].
All our patients enjoyed either excellent or good cure rate with no recurrence during follow up. Huh et al. found that the surgical outcome of MVD was excellent or good in 94.6% (n = 1442). According to Miller et al., cure of spasm occur in 91.1% of the patients, delayed in 11.2%, and recurrence rate was 2.4%. Surgery was repeated in 1.2%. Excellent result occurred in 84% with recurrence rate 1.5%. Sindou et al. reviewed 5.935 patients and found that excellent results obtained in a range from 68% to 94.1%, recurrence rate was low 1%, incomplete resolution (more than or equal to 50% relief) ranged from 4.6% to 19% and failure (effect less than 50%) from 3.6% to 15.5% [20, 23,24,25].
We had one case with CSF leak that required repeated lumbar puncture with antibiotic coverage. Two cases showed temporary decrease in hearing that returned to preoperative status within one month. According to Sindou et al., CSF leakage was reported as a frequent complication ranging from 2.5% to 10% which was presented as pseudomeningeocele, rhinorrhea, or CSF fistula with secondary meningitis. Huh et al. stated in his review of literature that 35.8% of patients suffered from complication where facial palsy, hearing deficit, and lower cranial nerve dysfunction were the most common ones. The mean time to recovery from transient hearing impairment was longer than that of facial palsy that could be explained by the fact that motor nerves (facial nerves) are less susceptible than the cochlear nerve to traction and/or ischemic trauma. The time to improve in hearing deficit was within 12 months that was longer than with our patients (within 1 month) that could be due to milder hearing affection with our patients. Sindou et at. reported that not all postoperative hearing dysfunctions are not from internal ear or cochlear nerve damages, some are related to middle ear alterations. Opening of large mastoid cells may generate an impression of otophonia. Middle ear effusion of fluid (blood or CSF in first postoperative days) through opened mastoid cells may alter auditory conduction [20, 23].
The study aims at highlighting that hemifacial spasm although being not so frequent in the neurosurgical practice, but those patients suffer a lot, and should be offered a treatment plan in spite of any co-morbid medical condition. We hereby illustrate our experience in dealing with such cases, according to their general condition and imaging. Microvascular decompression of the facial nerve is the treatment of choice whenever possible. Introducing an endoscope for better visualization of the root entry zone adds up to the effectiveness and precision of the procedure and thus offering our patient the best available treatment modality. Neurophysiological monitoring of the facial nerve and brain stem-evoked potentials were used to add more safety to the operative procedure.
