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Hemifacial Spasm Following a Blow to the Mandible Causing Blunt Injury to the Peripheral Facial Nerve —Case Report—

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Hemifacial Spasm Following a Blow to the Mandible Causing Blunt Injury to the Peripheral Facial Nerve —Case Report— Neurol Med Chir (Tokyo) 45, 192¿195, 2005 Hemifacial Spasm Following a Blow to the Mandible Causing Blunt Injury to the Peripheral Facial Nerve —Case Report— Satoru SHIMIZU,RyusuiTANAKA, Sumito SATO, and Kiyotaka FUJII Department of Neurosurgery, Kitasato University School of Medicine, Sagamihara, Kanagawa Abstract A 40-year-old male presented with hemifacial spasm manifesting as paroxysmal spontaneous twitches in the left peribuccal region persisting for 3 months. The symptoms began 7 days after an accident, when a signboard hit his left mandibular angle. Physical examination showed no trauma-related change in his face, and no neurological abnormality except for the twitches. Magnetic resonance imaging also showed no abnormalities of the facial nerve and adjacent regions. Electrophysiological studies showed synkinesis, so hemifacial spasm caused by peripheral facial nerve injury was suspect- ed. The symptoms subsided 4 months after the injury. Blunt injury to the facial nerve branches might cause hemifacial spasm. Key words: hemifacial spasm, peripheral facial nerve, injury Introduction Hemifacial spasm (HFS) is a well-known condition resulting from compression of the facial nerve in the root exit zone by blood vessels or rarely by other lesions.2) HFScausedbyperipheralinjuryofthe nerve accounted for only 0.12% of 1688 cases of HFS.2) This clinical entity was established in the 1930s,1,4,10) but later case reports are very rare.5,6) We describe a case of traumatic HFS resulting from blunt injury to the facial nerve. Case Report A 40-year-old male was hit on the left mandible and Fig. 1 T2-weighted magnetic resonance image neck by a wooden signboard, weighing about 10 kg, showing no abnormal findings in the facial during a storm on April 4, 2002. He felt swelling and nerve and adjacent regions. pain in the impact site, but no other symptoms. He noted spontaneous twitches in the left peribuccal region 7 days after the accident, which occurred Physical examination showed no trauma-related several times a minute and were enhanced when change in his face or neck. Neurological examina- he spoke or ate. The sensation of contracture of the tion demonstrated no abnormality except for the whole left side of the face continued. He was twitches in his left peribuccal region. Magnetic referred to our department on July 23, over 3 months resonance imaging showed no abnormalities of the after the accident. His medical history was noncon- facial nerve and adjacent regions (Fig. 1). Elec- tributory. tromyography of the left three facial muscles, frontalis, orbicularis oculi, and orbicularis oris, also Received June 1, 2004; Accepted November 9, 2004 revealed no abnormalities. The strength duration 192 Traumatic HFS 193 lesions near the facial nuclei are considered to be the cause of both facial myokymia and spastic paretic facial contracture. Focal seizure of the face without limb movement may be interpreted as HFS. Such involuntary contractures show similar aspects to HFS, but the present case was considered to be HFS, based on the combination of the symptoms of intermittent spontaneous contracture limited to the peribuccal muscle, and the electrophysiological findings of normal latency in blink reflex and presence of synkinesis. HFS associated with facial nerve compression by Fig. 2 Simultaneous electromyography recordings the intracranial vasculature may result from three from the bilateral orbicularis oculi (upper) pathophysiologies: aberrant regeneration,2) ephaptic and orbicularis oris muscles (lower) show- transmission (artificial synapse or cross-talk),3) and ing synkinesis on the left after stimulation kindling.8) The former two mechanisms require that of the left frontalis muscle. the nerve fibers innervating the facial muscles associated with spasm lie in close apposition. There- fore, these mechanisms are unlikely to be relevant to HFScausedbyinjuryofregionalperipheralfacial curve and chronaxy, motor nerve conduction, and nerve branches. The kindling mechanism involves blink reflex were also normal. However, synkinesis damage to the facial nerve (focal demyelination) was induced in the left orbicularis oris muscle by leading to ectopic excitation in the regeneration stimulation of the left frontalis muscle (Fig. 2), process, resulting in reorganization of the facial compatible with the HFS findings. The frequency motor nucleus and co-contraction in the affected of twitches could be reduced by administration of facial muscles, although the exact mechanism is clonazepam and then gradually decreased without uncertain.7,8) This central mechanism does not treatment, only becoming marked on one occasion require close anatomical relationships between the on August 8. nerve branches innervating the facial muscles Follow-up electrophysiological studies, performed associated with spasm and thus is the most likely 9 months after the injury, revealed persistent explanation of HFS following peripheral facial synkinesis, but no other remarkable findings. No nerve injury (post-paralytic HFS).5,6) Although recurrence of the symptoms has been detected for specification of the exact causative lesion in the 1 year after the final episode. present case is difficult, subcutaneous hematoma and swelling of the soft tissue surrounding the Discussion affected peripheral branch of the facial nerve may have caused reorganization of the facial motor The present case of involuntary contracture must be nucleus by compression of the nerve, analogous to differentiated from other pathologies associated the physical compression by a vessel in typical HFS. with hemifacial contracture in adults, such as Cases of peripheral facial nerve injury associated facial synkinesis, hemifacial contracture, facial with HFS, including the present case, are summa- myokymia, spastic paretic facial contracture, and rized in Table 1.5,6) Previous cases occurred after focal seizure of the face.2) Both facial synkinesis and cuts (dueling sword, glass, razor, or sheet steel) or hemifacial contracture are associated with peripher- grazing with a bullet,4–6) and any of the temporal, al facial nerve palsy, commonly Bell's palsy, and zygomatic, buccal, or marginal mandibular manifest as contracture of the hemifacial muscles. branches might have contributed.5,6) Slight weak- The contracture is evoked when a purposeful ness in the facial muscles innervated by the injured motion is attempted in facial synkinesis, whereas nerve branches was occasionally found. Spontane- the contracture is continuous in hemifacial contrac- ous twitches at the site of initial damage continued ture. Facial myokymia consists of rapid undulation for 2 to 12 months after the injury, followed by co- and flickering of the facial muscles from the contraction of all ipsilateral hemifacial muscles, frontalis muscle to the platysma, usually unilateral- rarely including the platysma, with diffusion on ly. Spastic paretic facial contracture involves paretic blinking. Electrophysiological studies showed syn- and contracted states on the affected side, with or chronous spontaneous activity, diffusion on blink- without association of myokymia. Intramedullary ing, and pathological synkinesis involving co-con- Neurol Med Chir (Tokyo) 45,April,2005 194 S. Shimizu et al. Table 1 Summary of cases of traumatic hemifacial spasm Injury to the face Site of contraction Case Author (Year) Age/ Weakened Period injury Symptomatic No. Sex Site Type Spontaneous Diffusion* muscle to onset period 1Martinellietal.65/M jaw (rt) cut peribuccal hemiface orbicularis 12 mos 5 yrs** (1983)5) oris 2 52/M periocular (rt) cut periocular hemiface orbicularis 10 mos 5 yrs** oculi 3Martinellietal.24/F peribuccal (lt) cut peribuccal hemiface none 2 mos 1 yr** (1992)6) 4 48/F zygomatic ＋ cut periocular hemiface none 3 mos 1 mo** frontal (lt) 5 43/M nasogenienus cut peribuccal hemiface ＋ none 6 mos not sulcus (lt) platysma described 6 74/M zygomatic (rt) graze zygomatic ＋ hemiface zygomatic 6 mos 51 yrs** periocular 7 Present case 40/M mandibular hit peribuccal none none 7 days 4 mos angle (lt) *Evoked by voluntary movement. **Final course not described. months. The zygomatic branch, buccal branch, or marginal mandibular branch of the facial nerve innervating the peribuccal muscles and adjacent to the injured mandibular angle may have been damaged, resulting in the HFS, judging from the anatomical relationships (Fig. 3).9) The short period between the injury and onset observed in this case might be due to the absence of regeneration of the damaged nerve. The reasons for such differences in clinical features are unclear, but suggest that blunt injury may have different effects from sharp injury to the nerves. HFScausedbyperipheralfacialnerveinjuryis very rare, but blunt injury to the face should be considered as a possible cause. Acknowledgments Fig. 3 Photograph of a cadaver specimen showing We thank Ms. Emi Kawashima and Mr. Yuya the anatomical relationships between the Onozawa, Clinical Laboratory, Kitasato University impact site of the present case (dashed Hospital for their technical assistance in elec- circle) and the peripheral facial nerves, the trophysiological studies. temporal (1), zygomatic (2), buccal (3), and marginal mandibular branches (4). References 1) Bittorf A:Uber Ä Mitbewegungen im Facialisgebiet. traction of antagonist muscles. Information on the Dtsch Ztschr Nervenh 121: 221, 1931 (Ger) prognosis of traumatic HFS is limited, but the 2) Digre K, Corbett JJ: Hemifacial spasm: differential longest symptomatic period was about 50 years,
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