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Bell's Palsy and Other Causes of Facial Nerve Paralysis 

Facial Paralysis

The differential diagnosis of facial palsy is divided into several large categories: birth, trauma, neurologic, infection, metabolic, neoplastic, toxic, iatrogenic, and idiopathic. Several areas of interest over the past several years have been the association of facial paralysis with Lyme disease, human immunodeficiency virus (HIV), human T-lymphotropic virus type I (HTLV-1), and HSV. A careful history at the time of presentation includes questioning regarding exposure to tick bites and risk factors for HIV. With regards to HSV, perhaps no other topic has elicited more controversy within the otologic community regarding the Bell's palsy, bells palsy, bells palsey, bell's palsey, bell palsy, bell palsey

Infectious Causes

Bell's Palsy

Bell's palsy is a lower motor neuron, ipsilateral facial paresis, which is acute in onset, is frequently preceded by a viral prodrome, and is generally regarded as polyneuropathic. Affecting roughly 20 people per 100,000 per year, it is equally distributed between the sexes and sides of the face. The risk to pregnant women is 3.3 times greater than that for nonpregnant women. The risk of recurrence is 10%, and 

Both Adour and May and Klein describe a prodromal illness before the onset of Bell's palsy (60% of patients), with frequent associated facial numbness, epiphora, pain, dysgeusia, hyperacusis, and 

Adour and May and Klein disagree on calling Bell's palsy a diagnosis of exclusion. Adour et al advocate making the diagnosis based on the history and clinical symptoms and the presence of dysgeusia and hyperacusis. May and Klein recommend excluding other diagnostic entities

The treatment of Bell's palsy has become less controversial and involves both medical and surgical options. In 2001, a large controlled study was published on the treatment of Bell's palsy with corticosteroids, showing an 89% complete functional recovery in 194 patients treated with steroids compared with a 64% complete recovery in control patients. Despite some criticism of the study and other studies that corroborated Adour's findings, steroid use for Bell's palsy is

Because a viral cause has long been postulated, a study reviewed the use of antiviral agents [5] in the treatment of Bell's palsy. In a randomized, double-blinded, controlled study, patients treated with prednisone and acyclovir were found to have a statistically significant faster time to recovery and more complete recovery than patients treated with prednisone alone. The treatment group received 60 mg prednisone per day for 4 days, tapering over a total of 10 days, with 400 mg acyclovir taken five times per day for 10 days. With the advent of new antivirals with 


Surgical decompression for Bell's palsy is advocated only in patients who have had an ENOG that demonstrates a CAP amplitude decrease of greater than 90% and who are in a

Expected time of recovery of function ranges from weeks to 12 months. In patients who have partial paralysis (neurapraxia), approximately 94% recover full function within months. The absence of recovery by 4 months indicates a likely poor outcome with either no return of

Esslen, in data generated by natural history ENOG and that correlate well with the clinical landmark study of Peitersen, determined that in

Herpes Zoster Oticus (Ramsay Hunt Syndrome)

In 1907, Ramsay Hunt generated his classic description of a syndrome characterized by facial paralysis, herpetiform vesicular eruptions, and vestibulocochlear dysfunction. In contrast to Bell's palsy, the viral cause of Ramsay Hunt syndrome is not disputed. Vesicular eruptions may

Lyme Disease

Lyme disease is a tick-borne spirochete ( Borrelia burgdorferi) infection known to cause erythema chronicum migrans, meningopolyneuritis, myocardial conduction abnormalities, and Lyme arthritis. Initially associated with tick bites in the northeastern United States, the disease is

Facial Paralysis from Bacterial Infection

Facial paralysis may occur from an acute bacterial infection of the middle ear or mastoid, chronic otitis media, or necrotizing otitis externa. In 1982, Pollock and Brown  reported the incidence of facial paralysis in 1250 patients with otitis media at 0.16% compared with 2% in the preantibiotic era. The route of infection is thought to be via the bony dehiscences of the fallopian canal, with resultant edema and vascular

In cases of acute paralysis with otitis media, treatment consists of intravenous antibiotics and surgical myringotomy. If paralysis persists more than 2 weeks or if fever persists more than 48 hours, a mastoidectomy with facial nerve decompression is advocated. For chronic otitis

Noninfectious Causes

Trauma

Intratemporal facial paralysis may be of a catastrophic origin (head trauma) or may be iatrogenic in nature. In head trauma, the facial nerve is the most commonly injured cranial nerve, with temporal bone fractures as the likely cause. One study reports 70 documented temporal bone

Temporal bone fractures are typically described in terms of the relationship of the fracture line to the long axis of the petrous pyramid. Longitudinal fractures are most common and constitute 90% of fractures. Injury commonly occurs to the facial nerve in the region of the

Neoplasm

Intuitively, it would seem that a facial nerve palsy secondary to a tumor would be relatively slow in onset. Characteristic is a paralytic course that is progressive beyond 3 weeks. A sudden onset, however, does not rule out the possibility of a neoplasm. Jackson et al have noted the incidence of sudden facial palsy in 27% of patients who have neoplastic involvement of the nerve. This has been substantiated by Neely and

Melkersson-Rosenthal Syndrome

Characterized by facial paralysis, episodic facial swelling, and a fissured tongue (scrotal tongue or lingua plicata), Melkersson-Rosenthal syndrome-associated paralysis typically begins in adolescence and has been described as both sporadic and familial. The cause is unknown.

REHABILITATION

With facial paralysis, either temporary or permanent, great attention is paid to protection of the eye. Major factors affecting the eye are lagophthalmos, paralytic ectropion of the lower lid, concomitant trigeminal nerve loss, and decreased tear production. After paralysis, it is

Long-term treatment for paralysis may include tarsorrhaphy, lateral canthoplasty, and gold weight implant to the upper lid. Ophthalmologic consultation is indicated. Priorities of rehabilitation are corneal protection, comfort, preservation of vision, improved function, and esthetic

Restoration of function to the face is possible with several techniques. After a traumatic injury to the nerve, a microsurgical reanastomosis or nerve grafting is possible. Grafting donor sites include the sural, great auricular, and median antebrachial cutaneous nerves. For Bell's palsy, a wait of 12 months is advocated to monitor for spontaneous return of function before surgical intervention. Electromyography may be