Jacobs Journal of Clinical Case Reports

Treatment of Benign Essential Blepharospasm and Idiopathic Hemifacial Spasm with Vimpat® (Lacosamide)

*Gary A
Department Of Neurology, United States

*Corresponding Author:
Gary A
Department Of Neurology, United States

Published on: 2015-12-21


Background:Benign essential blepharospasm and hemifacial spasm are currently treated with botulinum toxin therapy, eyelid protractormyectomies, and microvascular decompression of the facial nerve or pharmacologic therapies including anticonvulsants.Because of limited treatment success in some patients, another treatment option is needed.
Methods:Lacosamide (Vimpat®), a novel anticonvulsant released in 2008 for the treatment of partial-onset seizures, was used to treatnine patients. Four patients had hemifacial spasm and four were diagnosed with benign essential blepharospasm. A ninthpatient had both benign essential blepharospasm and hemifacial spasm. Lacosamide selectively enhances the slow inactivation of voltage-gated sodium channels resulting in stabilization of hyperexcitable neuronal membranes and inhibition of repetitiveneuronal firing.
Results:Lacosamide provided rapid and significant relief of hemifacial spasm and benign essential blepharospasm at doses ranging from50 mg bid to 200 mg bid. The symptomatic relief has been sustained in all patients over a period of years.
Conclusions:Lacosamide provided effective symptomatic relief in nine patients with either hemifacial spasm or benign essential blepharospasm. Our experience suggests that lacosamide is a potentially valuable adjunct in the management of these conditions. Nevertheless,the long-term efficacy of lacosamide in hemifacial spasm has yet to be determined.


Hemifacial Spasm; Benign Essential Blepharospasm; Vimpat; Lacosamide; Anticonvulsant


Benign essential blepharospasm (BEB) is a syndrome characterized by excessive or continuous bilateral eyelid closure due to spasm of the orbicularis oculi and adjacent muscles. BEB is considered to be a form of focal dystonia caused by basal ganglia dysfunction. Additionally, brain imaging and electrophysiologic studies suggest pathologic changes in excitability in the anterior cingulate, primary and secondary motor areas [1]. BEB is typically a chronic disorder, but up to about 10% of patients may have a spontaneous remission. Most remissions occur within the first 5 years [2]. BEB is often associated with other oromandibular dystonias. Hemifacial spasm is characterized by a combination of unilateral clonic and tonic spasms of the muscles innervated by the facial nerve. The most common cause of hemifacial spasm (HFS) is now widely recognized as neurovascular contact or compression at the root exit zone of the facial nerve at the lateral pons [3,4]. The movement disorder typically begins in the orbicularis oculi and over the course of years involves the brow, mid and lower face, and neck platysma. The prevalence rate of hemifacial spasm is estimated to be 14.5 per 100,000 in women and 7.4 per 100,000 in men [5,6]. The age of onset is typically between 40 to 50 years of age. Hemifacial spasm, if untreated, is a lifelong condition, and less than 10% of patients experience spontaneous remissions [6]. The medical therapy of choice for HFS is botulinum toxin (BTX).