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The facial nerve (seventh cranial nerve) allows for the movement of the muscles of facial expression, such as smiling and closure of the eye. It exits the brainstem alongside the hearing and balance nerve (eighth cranial nerve). Both structures then enter the hearing bone (temporal bone) through the internal auditory canal. The facial nerve then enters its own canal within the hearing bone and passes through the middle ear behind the eardrum and then the mastoid behind the ear. The nerve then leaves the temporal bone beneath the external ear and branches out to supply function to the muscles of facial expression. Along its course through the temporal bone, the facial nerve gives off branches that supply tearing function to the eye, salivary gland function, taste to a portion of the tongue and to a small muscle that attenuates movement of the stapes (middle ear hearing bone).
Loss of function of the facial nerve most often occurs between its exit from the brainstem and its exit from the temporal bone. It is important to differentiate between complete loss of function (paralysis) and weakness (paresis) of the facial muscles. Diagnosis of facial nerve disorders requires assessment of the entire course of the facial nerve.
An audiogram (hearing test) is often obtained in order to assess any associated involvement of the hearing apparatus. Radiographic imaging such as MRI (magnetic resonance imaging) and CT (computerzed tomography) may be performed to further assess the course of the facial nerve.
When the loss of facial function is complete, tests may be obtained to assess prognosis for return of function. Electroneuronography (ENOG), is a study that is performed within the first two weeks of onset of the paralysis in order to determine the prognosis for return of function. Electromyography (EMG) is a study that may be utilized to assess long standing facial paralysis to determine whether the nerve and facial muscles are recovering.
The most common complication arising from facial paralysis is loss of the ability to close the upper eyelid. Initial treatment of all acute facial palsies includes the use of ocular lubricants to prevent excessive drying of the eye and ulceration of the cornea. If the loss of facial function is expected to be long term, a minor surgical procedure may be performed to aid in eye closure. This most typically involves placement of a gold weight under the skin of the upper eyelid to aid in closure of the eye.
Causes Of Facial Paralysis
Bell's palsy is the most common cause of facial paralysis. This disorder has historically been referred to as facial paralysis of unknown cause. Therefore it is always important to rule out all potential known causes before making this diagnosis. Current thinking is that Bell's palsy is secondary to an inflammatory process caused by the Herpes Simplex virus. It is know that this virus resides dormant in portion of the facial nerve in the vast majority of individuals. Some sort of stressful event triggers activation of the virus. This then results in swelling of the nerve within its bony canal within the temporal bone and subsequent loss of function.
The goals of early medical treatment involve efforts to reduce swelling of the nerve, as well as fighting the viral cause. Steroids, such as prednisone, are often prescribed to reduce swelling of the facial nerve within its bony canal. Antiviral drugs, such as Valtrex, are frequently utilized to treat the herpes simplex virus. When the paralysis is complete, ENOG may be obtained in an effort to determine prognosis for return of function. When the prognosis is poor and identification of the problem is early in its course, surgery may be offered. The goal of surgical intervention is to open the facial nerve canal to decompress the nerve in order to prevent the complications of persistent swelling and compression. This procedure may involve opening a portion or the entire course of the facial nerve within the temporal bone. In order to avoid injury to the inner ear, this approach may involve an incision above the ear with exposure of the facial nerve through a middle cranial fossa craniotomy.
Herpes Zoster Oticus or Ramsay Hunt Syndrome is facial paralysis secondary to the Varicella Zoster virus. This is the same virus that causes "shingles" and in fact this disorder is often referred to as "shingles of the ear" or "shingles of the facial nerve." Individuals with this syndrome will often present with similar symptoms to Bell's Palsy. Additionally however, these individuals will also have rash around the opening of the external ear (the shingles) and severe pain around the ear. Treatment is similar to Bell's Palsy, although surgery is rarely, if ever recommended.
Trauma to the head may result in a fracture of the temporal bone. This may result in an immediate or delayed loss of function of the facial nerve. The cause may be either due to a severing of the nerve (causing immediate paralysis), swelling of the nerve or impingement of bone fragments into the nerve (causing delayed paralysis). If the loss of function is delayed and partial, treatment typically involves use of steroids to reduce swelling. When the paralysis is immediate, one must be concerned regarding a transection of the nerve. Treatment is then surgical and requires exposure of the course of the involved portion of the nerve and repair as indicated. Additionally, a delayed complete loss of function of the facial nerve with a poor prognosis for recovery suggested by ENOG may occur. Surgical exploration of the facial nerve may be offered with decompression and repair performed as indicated.
The facial nerve may be injured by either penetrating trauma to the ear or as a result of a related surgical procedure. In these situations the nerve should be surgically explored as soon as possible. In these situations, the nerve is most often severed. The nerve may then be repaired primarily or with a graft.
Infections of the middle ear or mastoid bone may result in facial nerve paresis or palsy. The initial treatment typically requires management of the underlying infection. This may be with antibiotics, but may also require surgery to control the infection and treat any direct involvement of the facial nerve.
A tumor of the facial nerve (facial nerve neuroma) may cause a progressive loss of function. These tumors are benign and slow growing. When the loss of function is significant the tumor may be removed and the involved portion of the facial nerve is repaired with a nerve graft.
Tumors arising from the hearing and balance nerve (acoustic neuroma) may be associated with loss of facial function. It is rare to see this before treatment, but when it occurs, the involved portion of the nerve is repaired with a graft. If a graft is not possible, a portion of the nerve to the tongue may be utilized to restore function to the facial muscles (facial - hypoglossal anastamosis).
It should be noted that recovery of a surgically repaired facial nerve will be very slow. It may be as long as six months before any return of function is seen and as long as twelve to eighteen months before recovery is complete. While nerve grafting will result in improved function, complete return of normal function is rare.
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