Bell's Palsy
Bell's Palsy

Bell’s palsy (Idiopathic Facial Paralysis)

Bell’s palsy is facial weakness affecting the muscles supplied by the seventh cranial nerve.
Clinical Manifestations
The onset of Bell’s palsy is fairly abrupt, maximal weakness being attained by 48 hours as a general rule. Pain behind the ear may precede the paralysis for a day or two. Taste sensation may be lost unilaterally, and hyperacusis may be present. In some cases there is mild cerebrospinal fluid lymphocytosis. MRI may reveal swelling and uniform enhancement of the geniculate ganglion and facial nerve and, in some cases, entrapment of the swollen nerve in the temporal bone. Approximately 85% of patients recover within a few weeks or months. Electromyography may be of some prognostic value; evidence of denervation after 10 - 12 days indicates there has been axonal degeneration, that there will be a long delay (3 - 4 months as a rule) before regeneration occurs, and that it may be incomplete. The presence of incomplete paralysis in the first week is the most favorable prognostic sign.
INCIDENCE: 30 cases / 100,000 persons
GENETICS: A predisposition to cranial neuropathies, especially seventh and third nerve palsies, has been reported.
RISK FACTORS: Diabetes, pregnancy, age >32 years
* Unilateral paralysis of the facial muscles (<1% of the facial palsies are bilateral);
* Ipsilateral loss of taste;
* Possible ipsilateral ear pain;
* Increased or decreased unilateral eye tearing.
* Most cases are idiopathic;
* The cause is often viral (herpes simplex);
* Herpes zoster can cause Bell’s palsy in association with herpetic blisters affecting the outer ear canal or the area behind the ear;
* Bell’s palsy can also be one of the manifestations of Lyme disease.
There are many other causes of acute facial palsy that must be considered in the differential diagnosis of Bell’s palsy. Lyme disease can cause unilateral or bilateral facial palsies; in endemic areas, 12% or more of cases of facial palsy are likely due to infection with Borrelia burgdorferi. The Ramsay Hunt syndrome, caused by reactivation of herpes zoster in the geniculate ganglion, consists of a severe facial palsy associated with a vesicular eruption in the external auditory canal and sometimes in the pharynx and other parts of the cranial integument; often the eighth cranial nerve is affected as well. Facial palsy that is often bilateral occurs in sarcoidosis and in Guillain-Barrй syndrome. Leprosy frequently involves the facial nerve, and facial neuropathy may also occur in diabetes mellitus, connective tissue diseases including Sjogren’s syndrome, and amyloidosis. The rare Melkersson-Rosenthal syndrome consists of recurrent facial paralysis; recurrent-and eventually permanent- facial (particularly labial) edema; and, less constantly, plication of the tongue. Its cause is unknown. Acoustic neuromas frequently involve the facial nerve by local compression. Infarcts, demyelinating lesions of multiple sclerosis, and tumors are the common pontine lesions that interrupt the facial nerve fibers; other signs of brainstem involvement are usually present.
     Tumors that invade the temporal bone (carotid body, cholesteatoma, dermoid) may produce a facial palsy, but the onset is insidious and the course progressive. All these forms of nuclear or peripheral facial palsy must be distinguished from the supranuclear type. In the latter, the frontalis and orbicularis oculi muscles are involved less than those of the lower part of the face, since the upper facial muscles are innervated by corticobulbar pathways from both motor cortices, whereas the lower facial muscles are innervated only by the opposite hemisphere. In supranuclear lesions there may be a dissociation of emotional and voluntary facial movements and often some degree of paralysis of the arm and leg, or an aphasia (in dominant hemisphere lesions) is present.

* Neoplasms affecting the base of the skull or the parotid gland;
* Bacterial infectious process (meningitis, otitis media, osteomyelitis of the base of the skull);
* Brainstem stroke;
* Multiple sclerosis;
* Sarcoidosis;
* Head trauma with fracture of temporal bone;
* Other: Guillain-Barre, carcinomatous or leukemic meningitis, leprosy, Melkersson-Rosenthal syndrome.
Bell’s palsy is a clinical diagnosis. A focused history and neurologic examination will confirm the diagnosis.
* FBS to evaluate for diabetes;
* VDRL in selected patients;
* Lyme titer in endemic areas.
The diagnosis of Bell’s palsy can usually be made clinically in patients with:
(1) a typical presentation,
(2) no risk factors or preexisting symptoms for other causes of facial paralysis,
(3) absence of cutaneous lesions of herpes zoster in the external ear canal,
(4) a normal neurologic examination with the exception of the facial nerve.
     Particular attention to the eighth cranial nerve, which courses near to the facial nerve in the pontomedullary junction and in the temporal bone, and to other cranial nerves is essential. In atypical or uncertain cases, an ESR, testing for diabetes mellitus, a Lyme titer, angiotensin-converting enzyme and chest imaging studies for possible sarcoidosis, a lumbar puncture for possible Guillain-Barre syndrome, or MRI scanning may be indicated. MRI often shows swelling and enhancement of the facial nerve in idiopathic Bell’s palsy.

* Contrast-enhanced MRI to exclude neoplasms is indicated only in patients with atypical features or course.
* Chest x-ray examination may be useful to exclude sarcoidosis or to rule out TB in selected patients before treating with steroids.

* Reassure patient that the disease is most likely a result of a virus attacking the nerve, not a stroke. It is also important to inform the patient that the prognosis is good.
* Avoid corneal drying by applying skin tape to the upper lid to keep the palpebral fissure narrowed. Lacri-Lube ophthalmic ointment at night and artificial tears during the day are also useful to prevent excessive drying.
* The patient should use dark glasses when going outside to minimize sun exposure.
* Although the benefits of corticosteroid therapy remain unproven, most practitioners use a brief course of prednisone therapy.
* If used, prednisone therapy should be started within 4 days of onset of Bell’s palsy.
* Optimal steroid dose is unknown. Prednisone can be given as one 50-mg tablet qd for 7 - 10 days without tapering or can be started at 80 mg and tapered by 5 - 6 mg / day until finished.
* Combination therapy with acyclovir and prednisone has been reported to result in a modest improvement in clinical outcome.
Patients should be monitored for evidence of corneal abrasion and ulceration or hemifacial spasm.
* Of affected individuals, 95% recover satisfactorily within few months.
* Recurrence is experienced in 7% of Bell’s palsy cases.
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