Primary vs Postparalytic Hemifacial Spasm

We read with interest the recent article by Colosimo and colleagues¹ on hemifacial spasm (HFS), a common movement disorder with a significant impact on quality of life.² The excellent study, which provided a systematic clinical comparison between primary and secondary forms of HFS, highlighted useful clinical information. We were surprised by the high prevalence (23%) of postparalytic HFS among their study cohort. In our prospectively collected series of 200 consecutive HFS patients evaluated at a single tertiary center using similar inclusion criteria, postparalytic HFS accounted for less than 5% of the cases, similar to the 7% observed in another large series in an American cohort.³ This may represent differences in referring patterns among tertiary centers or differential susceptibility among races to HFS following facial nerve damage.

In our limited series of patients with postparalytic HFS, the vast majority presented with orbicularis oculi and orbicularis oris spasm simultaneously at onset; signs of synkinesis were also present in some patients. Separately, in our previous report, most patients with primary HFS had initial symptoms in the periocular muscle.⁴ These independent observations in a different ethnic population corroborate and further support the present findings by the authors.

Because the etiologies of primary and postparalytic HFS have distinct differences, the many clinical similarities (such as female sex and left-sided predominance) between them as highlighted by the authors are intriguing. One hypothesis for the left-sided HFS preponderance in primary HFS is a higher frequency of a larger left vertebral artery compared with the right in humans, which increases the likelihood of neurovascular contact/compression. It would be interesting to determine whether neurovascular contact/compression of the facial nerve coexists with postparalytic HFS, particularly in those who presented with orbicularis oculi twitching only at onset. Because some authors have previously suggested that electromyography could improve the diagnostic rate of postparalytic HFS,³ there is a possibility that some apparent primary HFS cases may have some degree of postparalytic nerve damage.³ This would not be known if electrophysiological studies were not done for all cases.

From the clinical management standpoint, the similar duration of botulinum toxin treatment in both forms of HFS reported by the authors is particularly useful. Other additional information (if available), such as potential differences of the mean botulinum dose and the frequency of treatment adverse effects (such as eyelid weakness, tearing, etc) between primary and postparalytic HFS would be of clinical interest.

Correspondence: Dr Tan, Department of Neurology, Singapore General Hospital, Outram Rd, Singapore 169608 (gnrtek@sgh.com.sg).