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Facial Nerve Palsy
ALTERNATIVE NAMES: Bell's palsy, facial paralysis.
DEFINITION: Dysfunction of the facial nerve leading to variable degrees of facial paralysis.
WHAT IS GOING ON IN MY BODY? The facial nerve exits the brain stem and enters the temporal bone through an opening that houses both the two nerves for balance and the nerve for hearing. It then enters a tight, bony canal, which has approximately a 90° bend in it. At this bend where the geniculate ganglion exists, it is 0.6 mm in diameter. The facial nerve then horizontally crosses through the middle ear space and descends vertically through the mastoid to exit the mastoid, go through the parotid gland, and then divide into five separate branches which innervate the main facial muscle groups in the forehead, around the eye, mid-face; around the lip, and in the superficial muscles in the skin of the neck. The facial nerve also has a branch that helps transmit taste information from the front part of the tongue, lacrimal gland, and stimulates the submandibular glands, which generate saliva and another branch to the lacrimal gland for tearing. Facial paralysis occurs whenever there is a disruption of the transmission of the electrical signal through the facial nerve to the muscles of the face. In the case of Bell's palsy, the best evidence to date is that this is a result of a member of the herpes virus family that causes an infection in the nerve. Because the nerve is tightly bound in the bony canal, especially at the geniculate ganglion, any swelling in the nerve disrupts its blood supply, which can then affect nerve function. There is another form of herpes virus infection (Ramsay Hunt syndrome) which affects not only the facial nerve's ability to stimulate the facial musculature but can also affect a small branch of the facial nerve which helps deliver sensation from the ear canal. There are other forms of facial nerve injury that can occur. Certainly trauma where the facial nerve is cut can lead to a facial paralysis. Certain tumors within the cranial cavity, temporal bone, or parotid gland that invade and damage the nerve can also lead to facial paralysis.
WHAT ARE THE SIGNS AND SYMPTOMS? With Bell's palsy there is usually facial weakness of variable speed of onset and completeness. An individual will usually notice that there is weak or absent movement of either the entirety or portions of the face. With Bell's palsy it is not uncommon to have complaints of pain, dry mouth, dry eye, and disturbance of taste in the front two-thirds of the side of the tongue where the facial weakness is occurring. In a Bell's palsy, upon examination there may be facial weakness or paralysis. Typically the entire face is affected. When the individual attempts to forcefully close their eyes, the eye on the side of the weakness moves upward and outward (Bell's phenomenon). The nerve for taste and saliva stimulation (chorda tympani) courses through the middle ear space and can usually be seen in the upper posterior aspect of the eardrum. Because there is inflammation involving this nerve, it may appear to be red and swollen. There might be no saliva seen coming from the submandibular gland opening which is under the front of the tongue.
If the paralysis is a result of trauma, there will be obvious soft tissue injury on that side of the face. It can also occur because of fractures that go through the temporal bone usually seen in high-speed motor vehicle accidents or other high-velocity trauma to the head. With individuals who have a slowly progressive facial paralysis, especially affecting only certain parts of the face, there has to be great concern that there may in fact be a tumor. In that case, there may be a mass that can be felt in the parotid gland or visualized through the eardrum. Patients with facial paralysis that spares the forehead have an intracranial process (e.g., stroke, tumor) that affects the brain signals coming to the origin of the nerve in the brain stem.
WHAT ARE THE CAUSES AND RISKS? The main causes are mentioned above. The major risk factor in Bell's palsy is the degree of nerve injury. In individuals having less than 90% injury to the nerve, full recovery of facial function with only minimal residual deformity is the norm. However, in those individuals with Bell's palsy with a greater than 90% degree of nerve injury, even though the facial tone recovers, there may be loss of selective facial zone movement (synkinesis). For example, if there has been over 90% nerve injury, when the face recovers and an individual goes to close the eye, not only will the eye close, but there may be forehead, mid-face, or mouth contraction. There is often loss of the ability to move only an isolated section of the face. The risks of tumor or trauma where there is complete disruption of the integrity of the nerve, if the nerve is not reconnected in some fashion, is total facial paralysis, with the resultant sagging of the face and its significant deformity. The main long-term consequences of facial paralysis are excessive drying of the-cornea of the eye, which could lead to blindness, and drooping of the mouth, which leads to drooling problems. One other cause worth mentioning would be chronic otitis media with cholesteatoma. A cholesteatoma is an expanding mass of skin in the middle ear space that can erode the bony covering over the facial nerve, inflame it, and result in facial paralysis. These individuals usually have a history of diminished hearing and chronically draining ear.
HOW TO PREVENT THE DISEASE: There is no known way to prevent Bell's palsy or the specific kind of tumors that could cause a facial nerve injury. However, if a tumor is discovered in the parotid or there is chronic ear disease, then early diagnosis and treatment can arrest the disease process before it affects the nerve. Ramsay Hunt syndrome, which is a viral infection of the facial nerve, is the equivalent of shingles. Shingles can occur when an individual is exposed to someone who has an active chicken pox infection. Therefore, it is possible that Ramsay Hunt syndrome may be prevented by avoiding contact with those during the active phase of their chicken pox infection (when blisters are present).
HOW IS IT DIAGNOSED? The main means of diagnosis of Bell's palsy is based upon the historical rapidity of the facial nerve paralysis and the physical examination. In some respects it is a diagnosis of exclusion. If there are no tumors, trauma, middle ear infections, or intracranial tumors damaging the nerve, then it is presumed to be Bell's palsy. It has a very typical recovery course. If an individual has incomplete facial paralysis, then there is almost 100% certainty that complete normal facial function will recover in three to four weeks. In fact, 85% of patients with Bell's palsy will have completely normal facial nerve function return within a month of onset. In those, however, who have complete facial paralysis occurring within the first seven to 10 days of a Bell's palsy, it is very important to try to determine the degree of injury. This is vital in not only being able to counsel the patient as to the rapidity of their recovery but also to determine how aggressive the management of the facial paralysis must be. In individuals undergoing electroneurography, which is a means by which the integrity of the facial nerve function is measured, should there be less than 90% facial nerve injury, then aggressive treatment with oral steroids and anti-herpes virus medications is the mainstay of therapy. In patients who have greater than 90% facial nerve injury, they are at significant risk for developing a permanent facial motor nerve dysfunction. These usually take three months to recover facial function, and what function returns is usually abnormal. Should an individual suffer more than 90% injury, then not only is there aggressive steroid and anti-viral medications employed, but operative removal of the bony wall around the facial nerve, particularly around the area of the geniculate ganglion, may allow normal recovery of facial function. This procedure, facial nerve decompression, is relatively controversial, but a very recent report suggests that it can be beneficial. Older forms of facial nerve testing whereby the site of injury is determined are not as useful as electroneurography in determining prognosis. These older forms of diagnosis involve identifying whether or not the stapedius reflex is intact, measuring salivary flow from the submandibular gland, rates of tear production, or maximal threshold stimulation.
Those individuals who continue to have a complete facial nerve paralysis after three months of observation do not have Bell's palsy and a very high suspicion of malignancy needs to be considered. If the malignancy exists in the middle ear and parotid, these are often visible or can be determined by touch. If the middle ear or parotid area are entirely normal, then a CT scan or MRI of the brain and skull base are performed. For patients having central facial paralysis (forehead works normally but the middle and lower portions of the face are paralyzed), an MRI of the brain is the main mode of diagnosis. These patients also need neurologist consultation.
WHAT ARE THE LONG-TERM EFFECTS? For the individual with a Bell's palsy that completely recovers normal facial function, there are no long-term effects. For someone who has some degree of facial weakness, particularly affecting the muscles around the eye, then excessive dryness of the cornea is a concern, which can lead to excessive eye dryness and potential corneal injury, with resultant pain and blindness. One of the major long-term effects in a facial nerve which is imperfectly recovered is cosmetic deformity during facial contraction (synkinesis). For traumatic transection in the temporal bone, surgical or traumatic injury to the facial nerve in the ear or face, or tumor involvement of the facial nerve, total facial paralysis may result. There are a variety of treatments for complete paralysis involving static methods of eyelid closure and corner of mouth suspension. There are attempts to create some dynamic function by use of muscle slings from the masseter or temporalis muscles, nerve grafts from the normal side to the abnormal side, or transposing the nerve to the tongue to the portion of nerve beyond the injury.
AM I PUTTING OTHERS AT RISK? No.
WHAT ARE THE TREATMENTS? For acute Bell's palsy, as mentioned above, steroids and anti-herpes virus medications are the mainstay of therapy. If eye irritation occurs, then lubrication is important. For the individual whose Bell's palsy takes three months to recover, the main concern has to do with eyelid closure. In most of these, eye health can be maintained with ointments and drops, but some individuals need to have surgical attachment of the lateral parts of the upper and lower eyelids to prevent excessive eye dryness. If there is soft tissue injury with transection of the facial nerve, microscopic repair with or without nerve graft is imperative. Obviously, the greater the segment of nerve that is injured, the less the chance of any facial function recovery. For those who have a cancer affecting facial nerve function, the cancer plus any involved surrounding tissue must be removed. At the time of the operation, nerve grafts are placed in between the tumor-free portions of the facial nerve.
WHAT ARE THE SIDE EFFECTS TO THE TREATMENTS? The side effects are related to the various medications that are employed. The side effects of the surgical therapies involve mostly scarring and failure of restoration of normal facial nerve function.
WHAT HAPPENS AFTER TREATMENT? Hopefully, in Bell's palsy, facial paralysis will completely recover. Once again, if recovery is incomplete, then there may be some abnormal facial functioning. In those with a more complex facial nerve injury either from trauma or surgery, if the immediate repair does not work, then other forms of dynamic facial nerve re-animation or static face suspension may be employed.
HOW DO I MONITOR THE DISEASE? Monitoring is best done in concert with a specialist in facial nerve function and diseases, particularly an otolaryngologist. The more complex cases are sent to neurotologists, who have additional training which can help should the nerve need to be decompressed.
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