The most common form of facial paralysis is idiopathic i.e. bells palsy. The incidence rate of this disorder is about 23 per 100000 annually or about 1 in 60 or 70 persons in a lifetime. It is a paralysis of the 7th cranial nerve resulting in loss of control over the facial muscles on the affected side. Several conditions can cause a facial paralysis e.g. stroke, brain tumor and Lyme disease. The sign appears as rapid onset of partial or complete palsy usually in a single day. Cranial nerve 7 control most facial muscles including those needed to smile, blink and wrinkle the forehead.
The pathogenesis of the paralysis is unknown.
The few autopsied cases of this disease have shown only non descript changes in the facial nerve and not inflammatory changes as is commonly presumed.
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The exact cause of bells palsy is unknown. Sometimes exposure to cold wind is also cited as a cause for e.g. sleeping with an open window in a chilly night, exposure to wind etc.
Also evidence shows that even viral infection can be a cause of the disease. The virus causes inflammation and puts pressure on the nerve. The herpes simplex virus and lyme disease is found to trigger the disease. Herpes simplex virus type 1 is found to play role in causing the disease. While in case of a lyme disease, the facial nerves are damaged and it is found to trigger the disease.
Also people with diabetes and hypertension are at a greater risk for bells palsy.
The onset of bells palsy is fairly abrupt maximal weakness attained by 48 hours as a general rule. Pain behind the ear may precede the paralysis for a day or two. Taste sensation may be lost unilaterally and hyperacusis may be present. In some cases there is mild CSF lymphocytosis. Fully 80 percent of patients recover within a few weeks or months.
The common symptoms of bells palsy include a rapid onset of weakness, numbness, heaviness, or paralysis of one side of the face. Other symptoms include pain behind the ear, inability to close one eye completely, drooling, taste impairment, hypersensitivity to sound by the ear on the affected side, watering of the eye on the side affected, speech difficulties etc. both complete and partial paralysis results in drooping of both the corner of the mouth and the eyelids.
Some patients also suffer from neurological symptoms such as severe headache, pain in the neck, facial tingling, loss of memory, imbalance, ipsilateral limb weakness, ipsilateral parasthesias etc.
Electromyography may be of value in distinguishing a temporary conduction defect from a pathologic interruption in the continuity of nerve fibers. Evidence of denervation after 10 days indicates that there has been axonal degeneration and that there will be a long delay before regeneration occurs and that it may be incomplete. The presence of incomplete paralysis in the first week is the most favorable prognostic sign.
Protection of the eye during sleep, massage of the weakened muscles, and a splint to prevent drooping of the lower part of the face are the measures generally employed in the management of such cases. Eyes should be specially cared for in case of a bells palsy. The inability to close one eye may lead to corneal abrasions and other injuries, especially during sleep. Whatever may be the treatment the patient is taking, one should wear goggles during day and use eye drops to prevent drying and a bland eye ointment should be applied before retiring to the bed.
For inducing artificial tear one can use polyvinyl alcohol, hydroxypropyl methylcellulose and carboxy methylcellulose. Skin tape or eye patch can be used to keep the eyes closed and lubricated.
A course of Prednisone beginning with 60 to 80 mg daily during the first 5 days and then tapered over the next 5 days may be beneficial. The prednisone is of steroid. The scientific basis of this treatment is that it helps in reducing the inflammation of the nerve and shortens the recovery period. However sometimes it shows little benefit. Steroid therapy was found to be useful in a group of patients with Diabetes. The drugs usually recommended are prednisone, methylprednisolone and prednisolone.
Surgery is not recommended immediately because the purpose of surgery is to relieve the pressure on the nerve and prevent permanent nerve damage. But in case of this disease the nerve is already damaged approximately in the first two weeks and there is no use in surgery in such a case. Therefore in the second week of the illness the surgery is to be considered. Also permanent hearing loss may occur as a result of surgery.
Sometimes the patient shows improvement completely or with minimal defects even without treatment.
Usually patients presenting with complete paralysis, usually marked by an inability to close eyes and mouth are treated. Early treatment within 3 days of the onset is more effective.
Some practitioners prescribe acyclovir to treat herpes simplex virus or varicella zoster virus as anti-viral medication. But later it has been found that it does not show any additional benefits other than prednisone.
Unroofing of the nerve in the facial canal has been practiced, but there is no evidence that this measure is helpful and it may be harmful.
It is difficult to prevent the disease. However by having a strong immune system one can prevent the disease.
There are many other causes of facial palsy. Tumors that invade the temporal bone (carotid body, cholesteatoma, dermoid) may produce a facial palsy, but the onset is insidious and the course progressive.
The Ramsay Hunt Syndrome, presumably due to herpes zoster of the geniculate ganglion, consists of a severe facial palsy associated with a vesicular eruption in the pharynx, external auditory canal, and other parts of the cranial integument; often the eight cranial nerve is affected as well.
Acoustic neuromas frequently involve the facial nerve by local compression. Infarcts and tumors are the common pontine lesions that interrupt the facial nerve fibers. Bilateral facial paralysis occurs in acute inflammatory polyradiculoneuritis (Guillain Barres syndrome) and in a variety of sarcoidosis known as uveoparotid fever (Heerfordt syndrome). The Melkersson - Rosenthal syndrome consists of a rarely encountered triad of recurrent facial paralysis, recurrent and eventually permanent - facial edema, and less constantly, placation of the tongue; many causes of this rare syndrome have been suggested, but none has been established. Leprosy frequently involves the facial nerve.
A puzzling disorder is the facial hemiatrophy of Romberg. It occurs mainly in females and is characterized by a disappearance of fat in the dermal and subcutaneous tissues on one side of the face. It usually begins in adolescence or early adult years and is slowly progressive. In its advanced form, the affected side of the face is gaunt, and the skin is thin, wrinkled and rather brown. The facial hair may turn white and fall out, and the sebaceous glands become atrophic. The muscles and bones are not involved as a rule. Sometimes the atrophy becomes bilateral. The condition is a form of lipodystrophy, and the localization within a dermatome suggests a disorder of some neural trophic factor of unknown nature. There is no treatment other than transplantation of skin and subcutaneous fat by a plastic surgeon.
Facial myokymia refers to a fine rippling activity of the facial muscles; it may be caused by a plaque of multiple sclerosis. Blepharospasm is an involuntary recurrent spasm of both eyelids that occurs in elderly persons as an isolated phenomenon or with varying degrees of spasm of other facial muscles. Relaxant and sedative drugs are of little help, although in many patients this disorder subsides spontaneously. Severe persistent cases of blepharospasm or hemifacial spasm are now successfully treated by local injection of botulinus toxin into the orbicualris oculi; the spasms are relieved for 3 to 4 months, and the injections can be repeated without morbidity.
All these forms of nuclear or peripheral facial palsy must be distinguished from the supranuclear type. In the latter, the frontalis and orbicularis oculi muscles are involved less than those of the lower part of the face, since the upper facial muscles are innervated by corticobulbar pathways from both motor cortices, whereas the lower facial muscles are innervated only by the opposite hemisphere. In supranuclear lesions there may be a dissociation of emotional and voluntary facial movements, and often some degree of paralysis of the arm and leg or aphasia (in dominant hemisphere lesions) is conjoined.