Facial Nerve Paralysis
Facial Nerve Paralysis (Bell’s Palsy)
Bell’s Palsy is a sudden paralysis of the facial nerve. It is characterized by sudden onset (<48 hours) of weakness in facial movement on one side of the face, that progresses to its most severe stage within 7 days. The individual often will initially notice symptoms such as a mild asymmetry of the smile and dryness of the eye due to a slower blink response. These symptoms can quickly progress in severity, even resulting in complete paralysis of the affected side of the face. Associated symptoms of numbness/pain of the head and neck, or headache may precede or accompany the facial nerve weakness.
Bell’s Palsy was previously characterized as an idiopathic disorder that is, a disorder for which there was no identifiable cause. However, in recent years research has shown strong evidence that Bell’s Palsy may be caused by a virus. Herpes Simplex Virus (HSV) has been identified in patients affected by Bell’s Palsy, and is seen as a likely candidate. Current thinking is that HSV, or another similar virus carried by the host, is activated in the facial nerve and causes the paralysis. This understanding has altered our treatment of Bell’s Palsy in recent years (see treatment below).
Other diseases that cause facial weakness can be misdiagnosed as Bell’s Palsy, so care must be taken to differentiate the symptoms of those diseases before diagnosing Bell’s Palsy. Classic Bell’s Palsy should have a rapid onset of weakness and, when treated appropriately, return to normal or near normal function within weeks to months after onset. Factors that may suggest a different diagnosis include the following: 1) symptoms that progress over a slower course of time, 2) severe pain localized to the ear, 3) hearing loss, 4) facial tics, 5) unresolved facial nerve weakness several weeks after onset 6) recurrent facial nerve weakness and7) facial nerve paralysis on both sides of the face. Many causes of facial paralysis or weakness exist and include, among others:
Infections, including Otitis media, mastoiditis, cholesteatoma, Ramsay Hunt syndrome (herpes zoster oticus), cytomegalovirus, Epstein Barr virus, HIV, tuberculosis, Lyme disease, cat scratch disease, and fungal infections Benign tumors including facial nerve schwannomas, parotid tumors, facial nerve hemangioma, vestibular schwannoma, and glomus tumors Malignant Tumors including primary sarcoma, carcinoma, parotid cancers, and metastatic cancers Other causes including stroke, myasthenia gravis, multiple sclerosis, Melkersson-Rosenthal syndrome and temporal arteritis.
All patients with sudden facial nerve weakness should be evaluated, if possible, within 72 hours of onset by a physician specializing in Bell’s Palsy. Evaluation includes examinations of the ear, a thorough head and neck exam, hearing testing, and assessment of the degree of facial nerve weakness. Patients with a complete weakness require specialized electrical testing of the nerve using Electroneuronography (EnoG). In most cases, the hearing is not affected. An Audiogram will identify whether the hearing system is affected.
Treatment is usually initiated immediately for patients with suspected Bell’s Palsy using steroids and antiviral therapy unless a contra-indication to their use exists (such as the use of steroids in a diabetic patient). While a significant percentage of patients with Bell’s Palsy may have full recovery of function without any treatment, both steroids and antiviral therapy have been proven to increase the likelihood of complete success. Because it is impossible to identify at the onset of the symptoms, those patients who are likely to fully recover without medical therapy, treatment is usually recommended for everyone for whom it is medically appropriate. Individuals with grade VI weakness need to be carefully monitored by a neurotologist using ENoG testing. For these patients, a surgical intervention called Facial Nerve Decompression may be necessary to improve likelihood of return of facial nerve function, especially if the ENoG results fall below a predetermined level. Management of the eyelid weakness and eye care are critical at the initial stage of treatment, as severe weakness will leave the eye unprotected and at risk for corneal scratches and infections.
Patients who do not have classic Bell’s Palsy symptoms may require further evaluation including MRI scanning and laboratory tests. Persistent paralysis may be treated, restoring motion and tone to the affected side of the face, with a nerve transfer surgery called Facial – Hypoglossal Nerve Reconstructive Surgery.