Bell’s palsy is an acute peripheral nerve palsy of cranial nerve VII. This nerve innervates the muscles that allow facial expression. It also carries parasympathetic fibers to the lacrimal and salivary glands, as well as sensory fibers that contribute to taste on the anterior 2/3 of the tongue.
The annual incidence of Bell’s palsy is 15 to 30 persons per 100,000 per year with equivalent numbers of men and women affected. It affects people of all ages with peak prevalence in the 40s.
Bell’s palsy occurs more commonly in people with diabetes and pregnancy, and in those who have had Bell’s palsy in the past, there is an 8% risk of recurrence.
Bell’s Palsy Signs and Symptoms
People with an acute case of Bell’s palsy complain of weakness or complete inability to move one side of the face. When examining the patient, the facial creases and nasolabial folds on the affected side disappear. In addition, the forehead unfurrows, and the corner of the mouth droops.
On the affected side, the eyelid will not completely close, and lower eyelid will sag. When the patient tries to close the eye, it may roll upwards, which is known as Bell’s phenomenon.
Patient’s will often complain of eye irritation which can occur from lack of lubrication. Production of tears decreases, but on examination, the eye may appear to tear excessively because of the loss of control of the eyelid.
Food and saliva may gather on the affected side of the mouth and may spill out from the corner of the mouth. Patients may complain of numbness, but facial sensation overall is retained.
These symptoms can progress from onset over three days to one week. If symptoms progress over more than two weeks, this should prompt consideration of other differential diagnoses.
Bell’s Palsy Etiology
Bell’s palsy is thought to be provoked by inflammation of cranial nerve VII (facial nerve), which leads to compression, with possible ischemia and demyelination. This diagnosis has been believed to be idiopathic, where the cause of the inflammation is unknown.
There is current research being performed to assess if HSV-1 could be a possible etiology. It has been seen in patients affected by Bell’s palsy that their HSV-1 titers have been elevated by PCR testing. However, these studies have failed to isolate HSV viral DNA in biopsies.
Herpes zoster, EBV, CMV, adenovirus, rubella virus, influenza B, mumps, and coxsackievirus are other pathogens that are believed to contribute to Bell’s palsy cases potentially.
Other medical conditions can cause an isolated peripheral facial nerve palsy that is difficult to differentiate from Bell’s palsy. Lesions in the ear or parotid gland, such as a cholesteatoma or salivary gland tumors, can cause cranial nerve VII compression and paralysis.
Guillain-Barré syndrome, Lyme disease, otitis media, Ramsay Hunt syndrome, Sjögren syndrome, Melkersson-Rosenthal syndrome, and sarcoidosis are causes of peripheral nerve palsies that are similar to Bell’s palsy.
Even though these diagnoses can cause an isolated facial nerve palsy, they typically will have additional findings that will point to their etiology. Those with Lyme disease often have a history of tick exposure, joint pain, or rash.
The facial nerve palsy with acute or chronic otitis media is often more gradual in onset, and have associated ear pain and fever.
People with Ramsay Hunt syndrome have prodromal ear pain and often develop a vesicular rash in the ear canal.
Guillain-Barré syndrome and sarcoidosis more often will affect both facial nerves as opposed to unilateral presentation. Tumors present with symptoms over weeks to months.
Central nervous system lesions, such as multiple sclerosis, cerebrovascular accident, or tumor, can also lead to cranial nerve VII palsy. However, specific motor neurons that innervate the forehead cross at the brainstem. In this case, the fibers of the facial nerve innervating the forehead come from both hemispheres of the brain.
Supranuclear lesions (central) that affect the facial nerve will not cause paralysis of the forehead on the affected side, which will cause unilateral facial paralysis with forehead sparing. In these cases, performing a brain MRI should be considered.
In the past, influenza vaccines were known to have an association with Bell’s palsy, but currently, all available vaccines in the United States have not been associated with causing facial nerve palsy.
Performing The History And Physical Exam
When evaluating these patient’s, a full detailed history and physical should be gathered. This includes the onset and progression of symptoms. Medical history, such as if there are any rashes, joint pain, fever, recent tick exposure, or history of nerve palsy should be included.
Physical examination should consist of careful inspection of the tympanic membranes, ear canals, oropharynx, peripheral nerves in the extremities, palpation of the salivary glands, and evaluation of the cranial nerves.
Workup For Bell’s Palsy
Laboratory testing is typically not indicated for these individuals in an outpatient setting. If a patient has significant findings in their history of tick exposure, Lyme antibody titers should be performed.
Other laboratory testing that could be done includes an ACE level, HIV, VDRL, ESR, and hemoglobin A1c.
Diagnostic studies including EMG/NCS can be done in patients with complete lesions for prognosis evaluation.
If there are symptoms that are atypical of Bell’s palsy present, including involvement of more than just cranial nerve VII deficits, further evaluation is needed. Those with insidious onset or forehead sparing should undergo imaging of the head.
Those with bilateral palsy or who do not improve within 2-3 weeks after symptoms present should be considered for neuroimaging, if not done prior, and referral to neurology.
Treating Bell’s Palsy
Oral prednisone is used for treatment to reduce inflammation in Bell’s palsy. It is typically prescribed in a 10-day tapering course (such as 60 mg for five days, followed by 40 mg for five days or 60-80 mg daily for seven days).
Due to the believed role of HSV-1 in cases of Bell’s palsy, antivirals such as Acyclovir and Valacyclovir are often given. Acyclovir is dosed at 400 mg five times daily for seven days. Valacyclovir is dosed as 1 g three times daily for seven days.
Studies have shown there is a high rate of spontaneous recovery of Bell’s palsy without steroid or antiviral therapy. The Copenhagen Facial Nerve Study found that in 2,570 persons, 85 percent of patients returned to baseline without medication.
Due to this, some have questioned whether medication is needed for Bell’s palsy routinely. The problem is for the 15 percent of patients who do not fully recover; they will likely have cosmetic changes that they will not be pleased with.
Due to acyclovir, valacyclovir, and short courses of oral steroids being relatively safe medications, those who present within three days of onset of symptoms should be offered antiviral and corticosteroid therapy.
In the past, surgical decompression of the facial nerve was recommended within three weeks of onset of symptoms if a patient had a persistent functional deficit. However, the most common complication of this procedure is hearing loss, which occurs in 3 to 15 percent of cases. Based on the risk of this complication, the American Academy of Neurology does not recommend surgical decompression for Bell’s palsy.
Complications of Bell’s palsy include ocular irritation leading to corneal ulceration. In patients that are unable to close their eye entirely, artificial tears should be used.
If there is permanent eyelid weakness, tarsorrhaphy or implantation of weights in the upper eyelid can be performed. Referral to ophthalmology would be indicated in this instance.
Facial asymmetry or muscle contractures may be treated with surgery or Botox injections. Referral to plastic surgery would be indicated in this instance.
Am Fam Physician. Bell’s Palsy: Diagnosis and Management. 2007 Oct 1;76(7):997-1002.
Ferri’s Clinical Advisor, Bell’s Palsy. 2017.
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