Bell’s palsy is a type of facial paralysis that results in an inability to control the facial muscles on the affected side.[1] Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or rarely both sides of the face. Other symptoms include drooping of the eyelid, a change in taste, pain around the ear, and increased sensitivity to sound. Typically symptoms come on over 48 hours.
The cause of Bell’s palsy is unknown. Risk factors include diabetes and a recent upper respiratory tract infection. It results from a dysfunction of cranial nerve VII (the facial nerve). Many believe that this is due to a viral infection that results in swelling. Diagnosis is based on a person’s appearance and ruling out other possible causes.[1] Other conditions that can cause facial weakness include brain tumor, stroke, Ramsay Hunt syndrome, and Lyme disease.[2]
The condition normally gets better by itself with most achieving normal or near-normal function.[1] Corticosteroids have been found to improve outcomes, while antiviral medications may be of a small additional benefit.[3][4] The eye should be protected from drying up with the use of eye drops or an eyepatch. Surgery is generally not recommended. Often signs of improvement begin within 14 days, with complete recovery within six months. A few may not recover completely or have a recurrence of symptoms.[1]
Bell’s palsy is the most common cause of one sided facial nerve paralysis (70%).[2][5] It occurs in 1 to 4 per 10,000 people per year.[2] About 1.5% of people are affected at some point in their life.[6] It most commonly occurs in people between ages 15 and 60. Males and females are affected equally. It is named after Scottish surgeon Charles Bell (1774–1842), who first described the connection of the facial nerve to the condition.[1]
Facial nerve: the facial nerve’s nuclei are in the brainstem (they are represented in the diagram as a „θ“). Orange: nerves coming from the left hemisphere of the brain. Yellow: nerves coming from the right hemisphere of the brain. Note that the forehead muscles receive innervation from both hemispheres of the brain (represented in yellow and orange).
Bell’s palsy is characterized by a one-sided facial droop that comes on within 72 hours.[7] In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.[8][9]
The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, via the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bell’s palsy may present with loss of taste sensation in the anterior 2/3 of the tongue on the affected side.[10]
Although the facial nerve innervates the stapedial muscles of the middle ear (via the tympanic branch), sound sensitivity and dysacusis are hardly ever clinically evident.[10]
Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bell’s palsy may have “myriad neurological symptoms” including “facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness” that are “unexplained by facial nerve dysfunction”.[11]
Cause
Some viruses are thought to establish a persistent (or latent) infection without symptoms, e.g., the varicella-zoster virus[12] and Epstein-Barr viruses, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggested[13] as a cause of acute Bell’s palsy. Studies suggest that this new activation could be preceded by trauma, environmental factors, and metabolic or emotional disorders, thus suggesting that a host of different conditions may trigger reactivation.[14]
Familial inheritance has been found in 4–14% of cases.[15] Bell’s palsy is three times more likely to occur in pregnant women than non-pregnant women.[16] It is also considered to be four times more likely to occur in diabetics than the general population.[17]
Pathophysiology
Anatomy of the face.
Bell’s palsy occurs due to a malfunction of the facial nerve (VII cranial nerve), which controls the muscles of the face. Facial palsy is typified by inability to control movement in the muscles of facial expression. The paralysis is of the infranuclear/lower motor neuron type.
It is thought that as a result of inflammation of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal (the stylomastoid foramen), blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bell’s palsy per se. Possible causes include tumor, meningitis, stroke, diabetes mellitus, head trauma and inflammatory diseases of the cranial nerves (sarcoidosis, brucellosis, etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy.[18] In a few cases, bilateral facial palsy has been associated with acute HIV infection.
In some research the herpes simplex virus type 1 (HSV-1) has been identified in a majority of cases diagnosed as Bell’s palsy.[19] This has given hope for anti-inflammatory and anti-viral drug therapy (prednisone and acyclovir). Other research, however, identifies HSV-1 in only 31 cases (18 percent), herpes zoster (zoster sine herpete) in 45 cases (26 percent) in a total of 176 cases clinically diagnosed as Bell’s Palsy.[13] That infection with herpes simplex virus should play a major role in cases diagnosed as Bell’s palsy therefore remains a hypothesis that requires further research.
In addition, the herpes simplex virus type 1 (HSV-1) infection is associated with demyelination of nerves. This nerve damage mechanism is different from the above-mentioned – that edema, swelling and compression of the nerve in the narrow bone canal is responsible for nerve damage. Demyelination may not even be directly caused by the virus, but by an unknown immune system response.
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