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Vii Nerve Palsy — Evaluation and Management VII NERVE PALSY VII NERVE PALSY — EVALUATION AND MANAGEMENT The eye cannot close and constantly weeps. The mouth dribbles, the speech is interfered with and mastication impaired. The delicate shades of continence are lost. Joy, happiness, sorrow, shock, surprise, all conditions have for their common expression the same blank stare. (Brunnell, 19279.) Facial nerve palsy is a devastating and readily visible nerve injury. Loss of tone and movement is disfiguring and causes a functional disability to eye closure, chewing, speech and facial expression. The prevalence of facial palsy in the general population is about 1:5 000, mak- ing it a common-enough clinical entity for all general practitioners to be familiar with.1,2 In most cases no definite aetiology is identified (idiopathic/Bell’s palsy). The diagnosis of an idiopathic palsy however can only be made by excluding all SHAMLAN K NAIDOO other potential causes of facial palsy. The routine assumption that all facial MB BCh, FCORL (SA) palsies are idiopathic means that many correctable causes, e.g. of otological ori- Consultant Otorhinolaryngologist gin, might be left too late to achieve any favourable outcome. Department of Otorhinolaryngology and ANATOMY Head and Neck Surgery The facial nerve leaves the brainstem and enters the internal auditory canal with Nelson Mandela School of Medicine the auditory nerve. Within the temporal bone it has three branches: University of KwaZulu-Natal •greater superficial petrosal nerve — to lacrimal glands and glands within Durban nasal and palatal mucosa • chorda tympani — to taste buds and anterior two-thirds of the tongue Shamlan Naidoo is a consultant otorhino- • stapedial nerve — stapedius muscle in middle ear. laryngologist in the Department of As it exits the skull, it divides into branches within the parotid gland to supply the Otorhinolaryngology and Head and Neck muscles of facial expression. Surgery at the Nelson Mandela School of Medicine, King Edward VIII and Inkosi AETIOLOGY Albert Luthuli Central hospitals. His Facial paralysis is a diagnostic challenge, with a wide differential diagnosis interests are head and neck surgery and (Table I). Nevertheless, every effort must be made to determine a treatable cause. otology. Idiopathic/Bell’s palsy Between 50% and 80% of all facial paralysis is idiopathic.2,3 There is no sex predilection but the incidence rises in pregnant women. Bell’s occurs at any age, with a slight preponderance in patients over 65 years. Ten per cent may be bilat- eral.3,4 Although idiopathic, compelling research supports an infectious cause, namely herpes simplex virus.5 Typically, sudden-onset unilateral facial paresis progresses to paralysis over 1 - 5 days.3 The prognosis for Bell’s is generally good, with most patients (85 - 90%) recovering completely within 1 month.2,3 The remaining 15% will not usually show signs of recovery for 3 - 6 months.2,3 A protracted recovery over a period of months increases the likelihood of sequelae such as facial weakness, tics, spasms and synkinesis. The palsy is not Bell’s if there is/are: • signs of trauma • vesicles on the head and neck • multiple cranial nerve involvement 254 CME May 2004 Vol.22 No.5 VII NERVE PALSY Table I. Differential diagnosis of facial nerve palsy Idiopathic Tumours Systemic/metabolic Bell’s palsy Parotid Diabetes mellitus Melkerson-Rosenthal Cholesteatoma Pregnancy CP angle tumour Sarcoidosis Glomus Autoimmune disorders Carcinoma (1°/2°) Porphyria Facial nerve neuroma Leukaemia Trauma Congenital Infection Temporal bone fractures Compression injury Herpes zoster oticus Iatrogenic injury Mobius syndrome Otitis media Birth trauma Dystrophia myotonica Mastoiditis Facial injuries Diabetic otitis externa Penetrating wounds to the ear TB Barotrauma Lyme disease HIV Infectious mononucleosis • otological infection Facial paralysis as a complication of cholesteatoma, facial nerve neuroma, • other CNS lesions HIV infection has been reported, par- ear and cerebellopontine angle (CPA) • facial palsy at birth. ticularly in the early stages of HIV and tumours.2,4 Suspicious symptoms occasionally as the first manifestation include slowly developing paresis over Trauma of the infection.6 a period of more than 3 weeks, facial Trauma is the second most common twitching, other cranial nerve deficits, cause of facial nerve paralysis. These Acute otitis media with a dehiscent recurrent ipsilateral paresis and a patients may present with bloody otor- facial canal in the middle ear can parotid mass. rhoea, haemotympanum, dizziness lead to inflammation along the nerve, and deafness. Longitudinal fractures of causing paralysis. Chronic otitis media The most common malignant tumours the temporal bone comprise 80% of may also cause facial paralysis sec- causing facial paralysis are mucoepi- all temporal bone fractures and facial ondary to cholesteatoma or inflamma- dermoid and adenoid cystic carcino- nerve injuries occur in 10 - 20% of tion of the nerve. mas of the parotid. these. Transverse fractures comprise only 20% of fractures, yet the inci- Facial palsy in children is TB otitis CLINICAL EVALUATION dence of facial nerve injuries is 50%.4 media until proven otherwise. By no History Other causes of traumatic paralysis means does this infer that TB treatment include iatrogenic, birth canal should be commenced without an ENT A thorough history is paramount to trauma/forceps delivery, penetrating assessment to exclude life-threatening narrowing the differential diagnosis: parotid or middle ear trauma and causes like cholesteatoma or • onset of palsy (sudden/delayed) facial fractures. leukaemia. • duration and rate of progression • complete or incomplete palsy Infections Malignant/diabetic otitis externa is a • associated symptoms (hearing loss, The most common cause is herpes life-threatening osteitis of the temporal otorrhoea, otalgia, vertigo, vesi- zoster oticus (Ramsay-Hunt syndrome). bone, causing facial palsy and otal- cles, CNS symptoms) Reactivation of the varicella zoster gia, usually due to Pseudomonas • medical history (diabetes, pregnan- virus causes severe otalgia, deafness, aeruginosa. The diagnosis is made on cy, CVA, previous ear/parotid dis- facial paralysis and a vesicular erup- clinical suspicion in susceptible orders) tion on the ear, face, neck or oral cav- patients (diabetics, immunosuppressed, • history of trauma or previous sur- ity. Patients may also have varying patients on chemotherapy, etc.), and is gery (e.g. ear, parotid). degrees of deafness and vestibular confirmed by a positive bone scan. Examination symptoms. Only about 50% of patients regain normal facial function. Other Tumours A complete head and neck examina- infections include TB, otitis media, oti- About 5% of facial nerve palsies are tion, including assessment of the ears, tis externa, syphilis, Lyme disease, etc. due to tumours — parotid tumours, parotids, eyes (keratitis), upper aerodi- May 2004 Vol.22 No.5 CME 255 VII NERVE PALSY nerve excitability (NET), maximal provides excellent bony assessment stimulation test (MST), electroneu- of temporal bone fractures, the mid- rography (ENOG) and electromyo- dle ear and mastoid. graphy (EMG) are useful in patients • Other tests to exclude specific ill- who have complete paralysis to nesses, e.g. diabetes, sarcoidosis, determine the prognosis for return autoimmune disease, etc. of facial function. • The once popular topognostic tests MANAGEMENT (Schirmer’s, stapedial reflex, sali- Treatment of facial paralysis depends vary flow assessment) are based on on its cause. The role of the emer- the principle that lesions distal to a gency physician is to: branch of the facial nerve will •provide adequate eye protection spare the function of that branch. • exclude obvious causes These are now considered to be of • initiate appropriate therapy historical interest only and of little • seek timeous ENT referral. use in determining site of lesion, or in predicting outcome. Eye protection Fig. 1. Lower motor neuron lesion. • Radiological evaluation — per- Poor upper eyelid closure and dimin- formed in patients with a history of ished lacrimation may lead to corneal gestive tract and neurology (cranial recurrent paralysis, CNS symptoms, dryness, punctate keratopathy, ulcera- nerves) is mandatory. The next step is suspected CPA lesions, otological tion and ultimately decreased vision. to assess whether the nerve injury is findings, history of trauma and in Patients should use artificial tears liber- complete or incomplete, upper motor patients with delayed nerve recov- ally during the day, and close the eye neuron (UMN) or lower motor neuron ery. Gadolinium-enhanced MRI is with a patch after application of an (LMN): the procedure of choice to exclude eye ointment at night. They should • UMN lesions (e.g. CVA) — upper CPA lesions or brain lesions. CT avoid dust, and wear eye protection 3rd of the face is spared • LMN lesion — weakness or paraly- sis of the entire face (Fig. 1). FACIAL PALSY Typical findings in peripheral nerve palsy: • ONSET • At rest — less prominent wrinkles • DURATION on the affected side, eyebrow •RATE OF droop, flattened nasolabial folds, PROGRESSION and corner of the mouth turned HISTORY • RECURRENCE down. • ASSOC. • Inability to wrinkle forehead, raise SYMPTOMS eyebrows, purse lips, show teeth, • MEDICAL or whistle. Eye closure may be HISTORY incomplete. As a rule all LMN facial palsies will require an ENT referral to complete HEAD & NECK the more specialised aspects of exami- • ENT nation and investigation. • CRANIAL NERVE •PAROTID
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