Bell’s palsyÂ is a form of facial paralysis resulting from a dysfunction of the cranial nerve VII (theÂ facial nerve) that results in the inability to control facial muscles on the affected side. Several conditions can causeÂ facial paralysis, e.g.,Â brain tumor,Â stroke, andÂ Lyme disease. However, if no specific cause can be identified, the condition is known as Bell’s palsy. Named after Scottish anatomistÂ Charles Bell, who first described it, Bell’s palsy is the most common acuteÂ mononeuropathyÂ (disease involving only oneÂ nerve) and is the most common cause ofÂ acute facial nerve paralysis.
Bell’s palsy is defined as anÂ idiopathicÂ unilateralÂ facial nerve paralysis, usually self-limiting. The hallmark of this condition is a rapid onset of partial or completeÂ palsyÂ that often occurs overnight. In rare cases (1%), it can occurÂ bilaterallyÂ resulting in total facial paralysis.
It is thought that an inflammatory condition leads to swelling of theÂ facial nerve. 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.
CorticosteroidsÂ have been found to improve outcomes while anti-viral drugs have not.Â Early treatment is necessary for steroids to be effective. 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 theÂ corneaÂ may be permanently damaged resulting in impaired vision. In some cases denture wearers experience some discomfort.
Signs and symptoms
Bell’s palsy is characterized by facial drooping on the affected half, due to malfunction of theÂ facial nerveÂ (VIIÂ cranial nerve), which controls the musclesÂ of the face. Facial palsy is typified by inability to control movement in the facial muscles. The paralysis is of the infranuclear/lower motor neuron type.
The facial nerves control a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. They also innervate the stapedial (stapes) muscles of theÂ middle earÂ and carry taste sensations from the anterior two-thirds of the tongue.
Clinicians should determine whether theÂ foreheadÂ muscles are spared. Due to an anatomical peculiarity, forehead muscles receiveÂ innervationÂ from both sides of theÂ 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 on the ipsilateral (same side of the lesion) half side of the face, including to the forehead (contralateral forehead still wrinkles).
One disease that may be difficult to exclude in theÂ differential diagnosisÂ is involvement of the facial nerve in infections with theÂ herpes zosterÂ virus. The major differences in this condition are the presence of small blisters, orÂ vesicles, on the external ear and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existingÂ herpes zosterÂ infection leading to facial paralysis in a Bell’s palsy type pattern is known asÂ Ramsay Hunt syndrome type 2.
Lyme diseaseÂ may produce the typical palsy, and may be easily diagnosed by looking for Lyme-specificÂ antibodiesÂ in the blood orÂ erythema migrans. In endemic areasÂ Lyme diseaseÂ may be the most common cause of facial palsy.
The degree of nerve damage can be assessed using theÂ House-Brackmann score.
Because both theÂ nerve to StapediusÂ and theÂ chorda tympani nerve (taste)Â are branches of the facial nerve, patients with Bell’s palsy may present withÂ hyperacusisÂ or loss of taste sensation in the anterior 2/3 of the tongue.
Although defined as aÂ mononeuritisÂ (involving only one nerve), patients diagnosed with Bellâ€™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”.This is yet an enigmatic facet of this condition.
Some viruses are thought to establish a persistent (or latent) infection without symptoms, e.g., theÂ varicella-zosterÂ virusÂ andÂ Epstein-BarrÂ viruses, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggestedas cause behind the acute Bell’s palsy. StudiesÂ suggest that this new activation could be preceded by trauma, environmental factors, and metabolic or emotional disorders, thus suggesting that stress – emotional stress, environmental stress (e.g., cold), physical stress (e.g., trauma) – in short, a host of different conditions, may trigger reactivation.