JCPSLP Vol 20 No 2 July 2018

Entrepreneurship in speech-language pathology

Facial nerve palsy and speech-language pathology intervention using sEMG Terri Herne and Anne Whitworth

This study evaluated the outcomes of an intensive speech-language pathology early discharge service for facial nerve palsy. Twelve participants diagnosed with facial nerve palsy underwent an intensive, individualised treatment program based on mime and neuromuscular re-education with both surface electromyography (sEMG) and mirror biofeedback. Significant group level gains in facial symmetry and quality of life were seen, with a concomitant significant reduction in facial nerve weakness. At an individual level, significant gains were seen in 9 of the 12 participants. The addition of the sEMG was reported to provide crucial feedback in the early stages of intervention when mirror feedback was not visible. These results provide promising evidence of the combined benefits of neuromuscular re- education with biofeedback during the early discharge phase of rehabilitation and impetus to support a larger trial. Introduction Facial nerve palsy (FNP) is a debilitating disorder arising from damage to the facial nerve (cranial nerve VII) and results in weakness of the muscles of facial expression, dysarthria and dysphagia due to poor lip seal, reduced control of saliva and general reduced oral control (Van Gelder, Philippart, & Hopkins, 1990). The socio-emotional consequences of altered facial expression for communication and quality of life (Dalla Toffola et al., 2012; Van Swearingen, 2008; Devriese, Schumacher, Scheide, DeJongh, & Houtkooper, 1990) compound the impact for the individual and yet, despite the severe consequences, evidence of effective treatments have been relatively sparsely reported and usually from outside a speech- language pathology perspective. Aetiology, symptomatology and course of FNP Due to the unique pathways of the facial nerve, FNP may arise from a central lesion of the upper motor neuron (UMN) or from a lower motor neuron lesion (LMN) of the facial

nerve. The UMN fibres of the facial nerve run via the cortico–bulbar pathway from the motor cortex to the facial nucleus and while the majority of fibres cross over to the contralateral side of the face, there are significant ipsilateral connections (Barr, 1975; Yildiz, et al., 2005). A central facial palsy involving the UMN fibres will frequently arise from a stroke and, while it results in paralysis of the opposite side of the face, it is likely to present with only weakness of eye closure and retained movement of the forehead. Weakness of eye closure frequently impairs winking but slower total eye closure can usually be achieved as the upperface has bilateral (ipsilateral and contralateral) corticonuclear innervation which preserves activation of these muscles. Facial asymmetry can also occur with the lower face, at rest and on movement of the affected side, along with frequent problems of drooling and soft tissue biting when eating (Van Gelder et al., 1990). While damage to the LMN fibres can arise from a number of pathologies (e.g., varicella-zoster, herpes simplex, mononucleosis, stroke, traumatic brain injury, head and neck cancer, tumours), the most common cause of LMN facial palsy is Bell’s palsy, with overall incidence of LMN FNP reported as 23–35 cases per 100,000 people (Pereira et al., 2011). With LMN damage, there is weakness on the same side of the lesion, causing inability to move the forehead on the ipsilateral side and smoothness of that side of the forehead, weakness of the muscles of facial expression, poor or nil eye closure, visible flattening of the nasolabial fold and sagging of the affected side due to compensatory contralateral contraction of the muscles (Sardesai & Moe, 2010). There is often, as a consequence, pulling of the affected side of the face towards the unaffected side on attempts at movement. Baricich, Cabrio, Paggio, Cisari, and Aluffi (2012) report that prognosis of FNP depends on the aetiology of the nerve damage where traumatic and surgical lesions can have poorer prognoses, related to the type/degree of damage to the nerve. Regardless of neurological origin, a common sequela of FNP is synkinesis, the simultaneous, involuntary activation of different facial muscles during attempted facial expression, usually winking of the eye or hyper contraction of the unaffected side of the face during an activity such as smiling (Baricich et al., 2012). This may arise from hyper excitability of the facial nuclei or disorganised regeneration of the nerve (Dalla Toffola et al., 2005) and occurs in anywhere between 1.7–42% of cases of FNP (Shafshak, 2006). Often occurring after prolonged facial palsy, this causes a mass action of all facial muscles and alters facial expression. The impact of FNP is therefore seen to extend

KEYWORDS BIOFEEDBACK EARLY DISCHARGE FACIAL NERVE PALSY INTENSIVE sEMG THIS ARTICLE HAS BEEN PEER- REVIEWED

Terri Herne (top) and Anne Whitworth

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JCPSLP Volume 20, Number 2 2018

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