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COMMENTARY
Year : 2018  |  Volume : 66  |  Issue : 4  |  Page : 1043-1044

Treatment of hemifacial spasm: Botulinum toxin versus microvascular decompression


Department of Neurosurgery, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, Telangana, India

Date of Web Publication18-Jul-2018

Correspondence Address:
Dr. Suchanda Bhattacharjee
Department of Neurosurgery, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.237005

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How to cite this article:
Bhattacharjee S. Treatment of hemifacial spasm: Botulinum toxin versus microvascular decompression. Neurol India 2018;66:1043-4

How to cite this URL:
Bhattacharjee S. Treatment of hemifacial spasm: Botulinum toxin versus microvascular decompression. Neurol India [serial online] 2018 [cited 2018 Aug 17];66:1043-4. Available from: http://www.neurologyindia.com/text.asp?2018/66/4/1043/237005




In this issue of the journal, an excellent article on the medical management of hemifacial spasm (HFS) with botulinium toxin has been published.[1] I understand from this article that the medical management of HFS yields symptomatic relief for a period of 30-240 days in the primary variety, and for a period of 90-180 days in the secondary variety of HFS. The authors have elaborately described the clinical features of this condition and have also found that an ipsilateral ear click was a significant clinical finding in their series and should be looked for. However, there is no mention of whether or not the 'browlift sign' or the 'other Babinski's sign', which are considered as being pathognomonic and clinically diagnostic signs for HFS were also present. HFS is often either underdiagnosed or misdiagnosed. There is also lack of population-based data regarding this entity.[2] A study of 203 family physicians in 2004 found that 90.6% were unable to diagnose HFS correctly and that 46.3% did not know how to manage HFS.[3] The worldwide estimates for the prevalence of HFS are 14.5 per 100,000 women and 7.4 per 100,000 men.

In this series in focus,[1] magnetic resonance imaging (MRI) was carried out in 22 cases. Of the 15 primary HFS cases, only 4 had positive MRI findings with the vascular conflict being clearly detectable on the subarachnoid part of the facial nerve, whereas only 1 out of 6 cases in the secondary group had a defined pathology of a schwannoma. The authors, however, have not defined the sequences of MRI that needed to be carried out to demonstrate the etiopathogenetic agent responsible for HFS in their series; it is also not apparent whether or not the MRI sequences which were routinely done were sufficient to pick up all the causative pathologies that were responsible for the HFS.[1]

The authors have mentioned the details of the procedure for the administration of botulinium toxin and have stated that for HFS, botulinium toxin is the treatment of choice. It has definitely been established over the years that botulinium toxin is a low- risk procedure that provides symptomatic relief in patients suffering from this condition. However, the article does not mention anything about other modalities of treatment that are available, especially the surgical option, which is very effective as a treatment modality for HFS.

Microvascular decompression (MVD) provides curative treatment and a long-term relief of symptoms to the tune of 83% to 97% in most of the series.[4] The frequent use of the tremendously improved MRI fast sequences in diagnosing the relationship of the conflicting vessel with the facial nerve helps in defining the etiology of HFS and its management. A surgical separation of this nerve-vessel bonding provides an effective cure. In the cases where the nerve-vessel conflict has not been found, etiologies such as a band of thickened arachnoid, or a crowded posterior fossa resulting in the compression on, or the distortion of the facial nerve, have also been found on surgical exploration. A simple dissection of the vessel, moving it away from the facial nerve in the cerebellopontine angle, and expanding the posterior fossa cavity by performing a suboccipital craniectomy and an occasional duraplasty, provides the necessary solution for the problem. Surgery also helps to provide relief from HFS as well as trigeminal and glossopharyngeal neuralgia, in the small segment of patients, who have associated trigeminal as well as glossopharyngeal nerve conflicts along with HFS concurrently, a condition known as 'painful tic convulsive'. However, surgery does carry a small risk and certain people may not be fit enough to undergo surgery. In these cases, botulinium toxin injection remains the best available option. A meta- analysis of 22 studies studying the safety and effectiveness of MVD for HFS in 5685 patients by Miller et al., has reported that MVD successfully relieves HFS in approximately 9 out of 10 patients with a low rate of symptom recurrence; the complications of this surgery are also uncommon and generally transient. Complete resolution of symptoms following MVD have been reported in 91.1% of the patients over a median follow up period of 2.9-years. Symptoms of HFS recurred in 2.4% of the patients and 1.2% of the patients underwent a repeat MVD during the follow-up period. Transient complications included facial nerve palsy (9.5%), hearing deficit (3.2%) and cerebrospinal fluid leakage (1.4%). Permanent complications included hearing deficit (2.3%), facial palsy (0.9%), stroke (<0.1%) and death (<0.1%). The authors have also stated that microvascular decompression (MVD) is the only treatment option that offers the prospect of a definitive cure for HFS.[5]

Botulinium toxin injections form the most popular treatment options for HFS; however, in the treatment of HFS, there are certain problems associated with this form of management. The injection must be repeated every 3 to 6 months, and in some cases, tolerance can develop. Local complications of these injections include ptosis, blurred vision, and diplopia, which usually improve over days to weeks. Repeated injections also can cause atrophy of target muscles, which may lead to the requirement of botulinum toxin injection of the contralateral (unaffected) side of face for cosmetic reasons.[6]

Botulinium toxin injection remains the most effective, risk-free, temporary-relief strategy for HFS. However, all cases suffering from this condition must be evaluated with a thin-section, steady-state, free precession MRI sequence to detect any offending pathology, besides the routine T1W and T2W MRI. The choice of MVD should be offered to all those patients with HFS who are medically fit to undergo MVD, as the procedure offers the best prospect of a permanent cure, especially if there is any MRI demonstrable pathology that is amenable to surgical removal.[7]



 
  References Top

1.
Pandey S, Jain S. Clinical features and response to botulinum toxin in primary and secondary hemifacial spasm. Neurol India 2018;66:1036-42.  Back to cited text no. 1
  [Full text]  
2.
Kong D-S, Park K. Hemifacial spasm: A neurosurgical perspective. Journal of Korean Neurosurgical Society 2007;42:355-62.   Back to cited text no. 2
    
3.
Tan NC, Tan EK, Khin LW. Diagnosis and misdiagnosis of hemifacial spasm: A clinical and video study. J Clin Neurosci 2004;11:142-44.  Back to cited text no. 3
    
4.
Dannenbaum M, Lega BC, Suki D, Harper RL, Yoshor D. Microvascular decompression for hemifacial spasm: Long-term results from 114 operations performed without neurophysiological monitoring. J Neurosurg 2008;109:410-15.  Back to cited text no. 4
    
5.
Miller LE, Miller VM. Safety and effectiveness of microvascular decompression for treatment of hemifacial spasm: A systematic review. British J Neurosurg 2012;26:438-44.  Back to cited text no. 5
    
6.
Lim EC, Seet RC. Use of botulinum toxin in the neurology clinic. Nature Rev Neurol 2010;6:624-36.  Back to cited text no. 6
    
7.
Sharma R, Garg K, Agarwal S, Agarwal D, Chandra P S, Kale SS, Sharma BS, Mahapatra AK. Microvascular decompression for hemifacial spasm: A systematic review of vascular pathology, long term treatment efficacy and safety. Neurol India 2017;65:493-505.  Back to cited text no. 7
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