Bell's palsy is a paralysis of the facial nerve resulting in inability to control facial muscles on the affected side. Several conditions can cause a facial paralysis, e.g., brain tumor, stroke, and Lyme disease. However, if no specific cause can be identified, the condition is known as Bell's Palsy. Named after Scottish anatomist Charles Bell, who first described it, Bell's palsy is the most common acute mononeuropathy (disease involving only one nerve), and is the most common cause of acute facial nerve paralysis.
It is thought that an inflammatory condition leads to swelling of the facial nerve (nervus facialis). The nerve travels through the skull in a narrow bone canal beneath the ear. Nerve swelling and compression in the narrow bone canal are thought to lead to nerve inhibition, damage or death. No readily identifiable cause for Bell's palsy has been found, but clinical and experimental evidence suggests herpes simplex type 1 infection may play a role.
Doctors may prescribe anti-inflammatory and anti-viral drugs. Early treatment is necessary for the drug therapy to have effect. The effect of treatment is still controversial. Most people recover spontaneously and achieve near-normal to normal functions. Many show signs of improvement as early as 10 days after the onset, even without treatment.
Often the eye in the affected side cannot be closed. The eye must be protected from drying up, or the cornea may be permanently damaged resulting in impaired vision.
The facial nerves control a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, and salivation. They also innervate the stapedial (stapes) muscles of the middle ear and carry taste sensations from the anterior two thirds of the tongue.
Clinicians should determine whether the forehead muscles are spared. Due to an anatomical peculiarity, forehead muscles receive innervation from both sides of the brain. The forehead can therefore still be wrinkled by a patient whose facial palsy is caused by a problem in one of the hemispheres of the brain (central facial palsy). If the problem resides in the facial nerve itself (peripheral palsy) all nerve signals are lost, including to the forehead.
One disease that may be difficult to exclude in the differential diagnosis is involvement of the facial nerve in infections with the herpes zoster virus. The major differences in this condition are the presence of small blisters, or vesicles, of the external ear and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete).
Lyme disease may produce the typical palsy, and may be easily diagnosed by looking for Lyme-specific antibodies in the blood. In endemic areas Lyme disease may be the most common cause of facial palsy.
The degree of nerve damage can be assessed using the House-Brackman Score.
In some research the herpes simplex virus type 1 (HSV-1) was identified in a majority of cases diagnosed as Bell's palsy. 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. 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 oedema, 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. The quote below captures this hypothesis and the implication for other types of treatment:
It is also possible that HSV-1 replication itself is not responsible for the damage to the facial nerves and that inhibition of HSV-1 replication by acyclovir does not prevent the progression of nerve dysfunction. Because the demyelination of facial nerves caused by HSV-1 reactivation, via an unknown immune response, is implicated in the pathogenesis of HSV-1-induced facial palsy, a new strategy of treatment to inhibit such an immune reaction may be effective.
A range of annual incidence rates have been reported in the literature: 15, 24, and 25-53 (all rates per 100,000 population per year). Bell’s palsy is not a reportable disease, and there are no established registries for patients with this diagnosis, which complicates precise estimation.
Prednisolone, a corticosteroid, if used early in treatment of Bell's palsy, significantly improves the chances of complete recovery at 3 and 9 months when compared to treatment with the anti-viral drug acyclovir or no treatment at all.
The possible link between Bell's palsy and the herpes simplex and varicella zoster virus has led to the prescription of anti-viral medications (such as acyclovir or valaciclovir) to patients with unexplained facial palsy. Recently (2007), a large randomized clinical trial reported no additional benefit from acyclovir beyond that from prednisolone alone.
The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). Surgical procedures to decompress the facial nerve have been attempted, but have not been proven beneficial.
A 2005 practice parameter from the American Academy of Neurology states that "corticosteroids are safe and probably effective, and that acyclovir is safe and possibly effective".
Physiotherapy is also a vital part of Bell's palsy since it is a nerologic condition. Facial kabat techniques and criostimulation along with exercises based on facial mimicry have shown good results in clinical practice.
Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections which branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination - but some nerves may sidetrack leading to a condition known as synkinesis. For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily.
In addition, around 6% of patients exhibit crocodile tear syndrome on recovery, where they will shed tears while eating. This is thought to be due to faulty regeneration of the facial nerve, a branch of which controls the lacrimal and salivary glands.