I. What every physician needs to know.

Bell’s palsy, also known as idiopathic facial paralysis, is a common condition, which may have permanent sequelae. Key to management is pattern recognition, which is largely dependent on the physical exam and differentiation from acute stroke. Treatment within a short period of time from onset has a significant but modest effect.

II. Diagnostic Confirmation: Are you sure your patient has Bell's palsy?

The diagnosis of Bell’s palsy has several main components. The first is a careful history, paying attention to the nature of onset, which is typically rapid and painless. A thorough neurological exam follows looking for evidence of other cranial nerve involvement or clues to alternate diagnoses. Subsequently, neuroimaging or laboratory testing may be performed if the diagnosis is uncertain, to assist in ruling out other etiologies.

A. History Part I: Pattern Recognition:

The initial key to recognizing Bell’s palsy lies in differentiating a central from a peripheral facial nerve (cranial nerve VII) palsy. Because movement of the upper forehead has bilateral central innervation, a stroke will typically leave a patient with some degree of sparing of forehead weakness. However, as the nerves have decussated prior to forming the facial nerve, a patient with a Bell’s palsy will not have sparing of the forehead. The entire half of the face therefore is classically weak. Patients may of course present with incomplete paralysis or mild weakness.

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At times, patients will note eyelid twitching, tinnitus, pain around the ear and jaw, and dry eyes. Alterations in taste are also common but may not be a spontaneous complaint.

B. History Part 2: Prevalence:

Bell’s palsy is said to affect 40,000 people annually in the United States. It is more common in diabetics, those with concurrent infections and pregnant patients.

C. History Part 3: Competing diagnoses that can mimic Bell's palsy.

The fairly acute onset of Bell’s palsy and typical accompanying features and physical exam are fairly specific. However, other etiologies are of course possible. Vascular diseases (atherosclerotic or vasculitic) may mimic Bell’s palsy. The most commonly confused process would be a stroke resulting in a cranial neuropathy. Typically strokes would affect more than just one cranial nerve and present as a pattern of dysfunction.

One should consider malignancies as well, particularly in cases that do not resolve or improve in the typical 6-8 weeks after onset. Infectious etiologies such as syphilis, tuberculosis, lyme disease or extension of otitis are possible, but again, uncommon.

D. Physical Examination Findings.

A careful general neurological exam is critical to the diagnosis of Bell’s palsy and exclusion of other diagnoses. Much of the examination occurs as one takes a history from the patient. One can easily see facial movements during conversation and note lid closure during blinking. Other cranial nerve disorders are usually apparent, as is hemiparesis.

Beyond a careful examination of motor and sensory function, reflexes and the general physical exam, a deliberate examination of the cranial nerves is of paramount importance. One needs to recognize the nature of a peripheral seventh nerve palsy, which will affect both the upper and lower face. This distinguishes a Bell’s palsy from a central process which primarily affects the lower face.

A thorough head and neck exam is also important. Evidence of cellulitis, otitis, lymphadenopathy, and vesicles (zoster) all may be clues to an alternate etiology.

Likewise, a general physical examination may disclose evidence of systemic disease manifesting in an unusual way as facial nerve palsy.

E. What diagnostic tests should be performed?

A thorough history and physical examination are typically the only “tests” that need to be performed. In cases that do not appear to be entirely consistent, imaging and other testing may well be appropriate.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Laboratory studies are not typically necessary.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

While not usually necessary, atypical presentations may warrant imaging. The most common study ordered would be a magnetic resonance image (MRI) to evaluate for evidence of malignancy (cerebellopontine angle tumors, facial nerve schwannoma, etc.), evidence of infarction and infection. In cases of suspected cerebrovascular disease, magnetic resonance angiography (MRA) may be appropriate as well.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Cerebral imaging is commonly performed and infrequently necessary or revealing.

III. Default Management.

Historically, the management of Bell’s palsy has been somewhat controversial. However, the preponderance of the evidence has demonstrated little role for anti-virals and a significant benefit for corticosteroids. Anti-virals have been shown to result in less recovery at 1 year than corticosteroids. In a Cochrane analysis, corticosteroids were found to decrease rates of incomplete recovery of nerve function and motor synkinesis. There was not, however, a significant difference in cosmetic outcomes at 6 months.

A. Immediate management.

Therapy should include administration of oral corticosteroids. Typical doses are 1mg/kg/day or 60mg/day for a total of 7-10days with or without a taper. Common practice is to start steroids immediately and as per most studies, within 72 hours of symptom onset. In addition, patients with significant lid weakness should be counseled about the need to keep their eye moist. Over the counter ointments and patching at night are adequate for this purpose.

B. Physical Examination Tips to Guide Management.


C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

No laboratory tests are recommended.

D. Long-term management.


E. Common Pitfalls and Side-Effects of Management


IV. Management with Co-Morbidities

No change in standard management.

A. Renal Insufficiency.

No change in standard management.

B. Liver Insufficiency.

No change in standard management.

C. Systolic and Diastolic Heart Failure

No change in standard management, beyond the potential use of short-term steroids.

D. Coronary Artery Disease or Peripheral Vascular Disease

No change in standard management.

E. Diabetes or other Endocrine issues

Given that patients are treated with relatively high dose corticosteroids, diabetic patients are at risk for transient hyperglycemia.

F. Malignancy

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

No change in standard management.

I. Gastrointestinal or Nutrition Issues

No change in standard management.

J. Hematologic or Coagulation Issues

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment

No change in standard management.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

These patients are not typically admitted to hospital.

B. Anticipated Length of Stay.


C. When is the Patient Ready for Discharge.


D. Arranging for Clinic Follow-up

Follow-up with the patient’s primary care physician is appropriate. In severe or atypical cases, follow-up with a neurologist is recommended.

1. When should clinic follow up be arranged and with whom.

Follow-up with the patient’s primary care physician within 1 week is prudent. If symptoms do not improve, referral to a neurologist is appropriate in order to consider other potential diagnoses.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Patients are not typically admitted.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

No tests commonly need to be followed as an outpatient.

E. Placement Considerations.

Patients are not typically placed for this disease.

F. Prognosis and Patient Counseling.

Patients should be aware of the long-term sequelae of dry eyes, including corneal damage and blindness. While frequently short-lived, lid weakness may persist and require ophthalmology follow-up.

Patients may develop synkinesis, or misdirection of the repairing facial nerve fibers. In this situation, when a patient smiles, their eye may close on the side of the prior palsy.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.

There are no core indicators for this diagnosis.

VII. What's the evidence?

Gilchrist, JM. ” Seventh cranial neuropathy.”. Semin Neurol. vol. 29. 2009. pp. 5-13.

Gilden, DH. “Clinical practice. Bell's Palsy”. 23:. vol. 351. 2004. pp. 1323-31.

Lockhart, P, Daly, F, Pitkethly, M, Comerford, N, Sullivan, F. ” Antiviral treatment for Bell's palsy (idiopathic facial paralysis).”. Cochrane Database of Systematic Reviews. 2009.

Salinas, RA, Alvarez, G, Daly, F, Ferreira, J. “Corticosteroids for Bell's palsy (idiopathic facial paralysis).”. Cochrane Database of Systematic Reviews. 2010.

Numthval, P, Thakkinstian, A, Dejthevaporn, C, Attia, J. “Corticosteroid and antiviral therapy for Bell's palsy: a network meta-analysis”. 5:. vol. 11. 2011. pp. 1