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Facial Nerve Disorders

The facial nerve is the seventh cranial nerve, or simply CN VII. It emerges from the pons of the brainstem, controls the muscles of facial expression, tear production glands of the eye, saliva production glands of the mouth, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue. The facial nerve can be damaged due to head trauma, surgical procedures or viral infiltration (herpes simplex or Lyme disease). When this occurs, patients have varying degrees of one sided facial palsy or paralysis, which can be temporary or permanent.

Facial Nerve Schwannoma

Facial Nerve Schwannoma (FS) is a benign tumor of the lining or sheath of the facial nerve. It is extremely uncommon, accounting for less than 1% of all intracranial tumors. FS grow at the average rate of 1-2 mm per year. The facial nerve is very resilient and can be fully functional until it is compressed by greater than 50%. This tumor’s slow growth pattern in addition to the nerve’s resilience means that patients are usually non-symptomatic for many years prior to their diagnosis. The trademark of FS is progressive facial palsy and/or spasm. As the tumor grows and compresses the nerve, the symptoms will progress, but in the interim may have episodes of partial or complete resolution. If the tumor is localized to the middle ear, it can cause degradation of bone and result in conductive hearing loss or vertigo. Testing should involve MRI imaging of the temporal bone and internal auditory canal.

Treatment is dependent upon the degree of symptoms or size of the tumor, and patient preferences amongst other factors. Treatment modalities include observation, and surgical micro dissection. Focused radiation is also a possibility, however, because of the infrequent occurrence of the tumor, not much literature on outcomes is available.

Bell’s Palsy (Peripheral Facial Palsy)

Bell’s Palsy is a sudden episode of unilateral facial numbness and paralysis that develops over 48 hours and ranges in severity. There are typically no other symptoms involved in Bell’s Palsy, but audiological testing should be performed to evaluate for concurrent involvement of the nerve of hearing. The cause of Bell’s Palsy has not been concretely identified at this point. However, the most commonly noted association is with a viral invasion, namely herpes simplex, of the facial nerve. Sometimes, after surgery of the ear, Bell’s Palsy can occur due to release of the dormant virus.

Bell’s Palsy should spontaneously resolve within 3-6 months. Although debatable in efficacy, the most noted and beneficial treatments involve oral steroids and antiviral medication. If recurrent episodes occur, or for very severe,, acute paralysis, decompression of the facial nerve may improve facial nerve function. This should only be utilized as a last resort intervention due to its high incidence of risks and/or complications.

Often times, Bell’s Palsy can be confused for a transient ischemic attack (stroke), which causes central facial palsy. Bell’s Palsy causes loss of forehead and brow movement while a patient experiencing a stroke will have preserved forehead and eyebrow movement.

Facial Nerve Decompression for Bell’s Palsy or Trauma:

In situations when Bell’s palsy causes total facial paralysis, surgical intervention within 10-15 days of onset may be considered. Surgery is aimed at alleviating pressure from the facial nerve by drilling out the bone surrounding the nerve. This helps to accommodate for the swelling of the nerve during this event and subsequent events if this recurs. One study showed improvement of symptoms in 91% of patients undergoing decompression within 14 days of onset of acute facial paralysis.

Facial Reanimation Surgery for Facial Paralysis:

Facial reanimation surgery is a procedure that involves moving nerves, muscles, or tendons from different parts of the body to the face. This is done to correct facial paralysis. Dr. Cristobal will decide what nerves, muscles, or tendons to use based on the length of time of the nerve paralysis and the site of injury. Goals of surgery are to achieve either facial symmetry at rest or facial symmetry with voluntary motion.

Herpes Zoster Oticus (Ramsay Hunt Syndrome)

Herpes Zoster Oticus is a shingles outbreak, which occurs in or near the area of the ear. This is more common in those over the age of 60 years. Herpes zoster oticus is the second most common cause of peripheral facial paralysis.

Shingles (herpes zoster) comes from the same virus, which causes chickenpox (varicella zoster). Chickenpox occurs predominately in childhood when the varicella virus localizes in the skin causing multiple itchy and sometimes painful “pox” or vesicles all over the skin. During this viral multiplication, the virus extends to free nerve endings. After the viral infections subsides, the virus remains inside the nerve endings in a non-active (dormant) state. When the virus becomes activated again, it is known as Shingles, or herpes zoster. When this occurs in a nerve ending near or around the ear it is called Herpes Zoster Oticus (Ramsay Hunt Syndrome). Unfortunately, the nerve responsible for moving your face (facial nerve) is within this area. Activation of herpes zoster within the facial nerve causes inflammation, which in turn can cause facial weakness or paralysis of one side of the face.

Commonly symptoms first occur as an upper respiratory infection followed by severe ear pain (otalgia). This then progresses to facial weakness or paralysis on one side, which then may be followed by an eruption of vesicles over the ear canal, around the ear, on the face, or down the neck. Other symptoms may include sensorineural hearing loss on the affected side, ringing in the ear (tinnitus), dizziness or vertigo, or nausea and vomiting. Treatment includes oral steroids and antiviral medication within 3 days of the onset of symptoms. Unfortunately, this does not guarantee complete recovery of symptoms and facial paralysis. About half of cases in adults and 75% in children will experience complete recovery after 3-6 months.

Neoplasms of the parotid gland

The parotid gland is a major salivary gland that is present on either sides of the mouth and in front of each ear. Benign parotid gland neoplasms typically present after the age of 40. Malignant (cancerous) growths predominantly affect women over the age of 60. Often, when neoplasms are found in the parotid, a total or superficial parotidectomy (removal of parotid gland) is necessary. The facial nerve and its branches run through the parotid gland. Dr. Cristobal is specially trained in surgical procedures around and of the facial nerve, with the goal of preserving as much function as possible. There is a 25-50% risk of facial weakness directly after parotidectomy and a 1-2% risk of permanent weakness. With the use of facial nerve neuromonitoring throughout the entire procedure, this risk is kept to a minimum.

The most common form of benign parotid neoplasms are:

1. pleomorphic adenomas (which can later transform into cancer)

2. monomorphic adenomas (Warthin’s tumor)

The most common form of malignant parotid neoplasms are:

1.  mucoepidermoid carcinomas - the exact cause of malignant parotid tumors is still unknown, however they can be caused by metastasis (spread of cancer) from other areas of the body, certain work exposures, reduced immunity, HIV, as well as radiation exposure.

Inflammation of the parotid gland which may also necessitate a parotidectomy:

1. parotid abscesses (collections of pus)

2. deep salivary calculi (mineral deposits)

3. chronic parotitis (long-term inflammation)

4. sialorrhea (excessive salivation)