Treatment of hemifacial spasm

Introduction Hemifacial spasm (HFS) is characterized as involuntary irregular clonic or tonic movements of the facial muscles innervated by cranial nerve VII on one side of the face and is most often a result of vascular compression of the facial nerve at the root exit zone (Wang and Jankovic, 1998). Facial muscle twitches usually begin in the periocular region and can progress to involve the cheek and perioral muscles. Hemifacial spasm is almost always unilateral; however, when bilateral, the two sides are always asynchronous. Atypical cases have been reported to initiate in the orbicularis oris and buccinator muscles and gradually spread upward to involve the orbicularis oculi (Ryu et al ., 1998). At times, with involvement of the platysma muscle, a tremor-like appearance of the head can develop (Frei and Truong, 2008). Muscles involved in HFS include the orbicularis oculi, frontalis (rarely), corrugator, nasalis, zygomaticus, risorius, orbicularis oris and sometimes the platysma (Fig. 13.1). Hemifacial spasm is more prevalent in females, commonly begins in the fifth decade and tends to have a fluctuating course. In contrast to essential blepharospasm, symptoms often continue during sleep and can provoke insomnia. Emotion and stress tend to exacerbate facial twitching. Ear clicks can occur which resolve with treatment of the HFS (Rudzinska et al ., 2010). Although benign, HFS can be disabling because of social embarrassment and excessive closure of the affected eye, interfering with vision. Symptoms can progress over time and facial weakness may develop independent from botulinum neurotoxin (BoNT) therapy. Hypertension is thought to be a risk factor for the development of HFS (Oliveira et al ., 1999).