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Causes of facial nerve problems can include:
Bell's palsy is a rapid onset paralysis of the facial musculature on one side of the face, without an apparent cause. It ordinarily affects all branches of the nerve, from the forehead to the neck. A viral illness preceding the paralysis, ear pain, changes in taste, facial numbness, and tongue numbness are commonly associated symptoms.
The cause of Bell's palsy is uncertain, as its other name, idiopathic facial paralysis, reflects. There is evidence to suggest a viral cause, with most data pointing to infection with herpes simplex virus (HSV). While it is difficult to prove this cause and effect relationship conclusively, the fact that Bell's palsy appears to respond to antiviral and anti-inflammatory medications further supports the relationship between HSV and Bell's palsy.
Most cases of Bell's palsy resolve spontaneously, with no noticeable change in facial expression seen after recovery. However, it has been shown that treatment with steroids can either improve or speed up complete recovery, and it is very frequently prescribed for this condition. It has also been shown to cause a decrease in Bell's palsy associated pain. Steroids do have some potential side effects. Therefore, in patients with other health problems, steroid use may not be indicated. Among the potential problems are altered blood sugar levels, stomach ulcers, and mood and personality changes.
A large study examining whether the antiviral agent, acyclovir, would improve recovery in Bell's palsy, showed that if the medication is begun within three days of the onset of the paralysis, it appears to improve recovery. However, the beneficial effect does not appear to be dramatic. There is much controversy surrounding the role for antiviral medication in the treatment of Bell's palsy.
Since the evidence points to an inflammatory process causing destruction within the nerve, and since the facial nerve travels in a tight bony canal from where it exits the brain to where it enters the face, attempts have been made to open up the bony canal during the acute inflammatory phase of Bell's palsy. The rationale for this approach is that if the nerve gets inflamed, it swells, and swelling inside a tight canal will then choke off the blood vessels to the nerve, and cause additional damage by depriving the nerve of its blood supply. The surgical procedure to open the bony canal is called total facial nerve decompression.
A multi-institution study using this treatment showed that a subset of patients with severe Bell's palsy did benefit from decompression surgery, if it was performed soon enough after the onset of the paralysis.However, to perform total facial nerve decompression is a serious undertaking, and is not without risks and complications, one of which is inadvertent damage to the facial nerve. Therefore, the decision to proceed with decompressive surgery is one that needs to be made jointly between patient and surgeon, with a full understanding of potential risks and benefits.
For recurrent Bell's palsy, or unsatisfactory / prolonged recovery, see other options in the Facial Nerve Disorders Treatment Options section.
The recovery from Bell's palsy tends to follow one of two pathways. The majority of patients begin recovery within three weeks of the onset of paralysis. These patients tend to recover fully and represent approximately 85% of all Bell's palsy patients. This is known as the "rapid recovery" group. A smaller set of patients experiences delayed or incomplete recovery, and requires additional therapy to improve outcome. This "delayed / partial recovery" group represents roughly 15% of patients.
Generally, those patients with return of some facial nerve function by the third week, or who don't experience complete paralysis, tend to follow the rapid recovery pattern, while those who have complete paralysis extending beyond three weeks tend to follow the delayed recovery pattern.
Sometimes removal of an acoustic neuroma, or other skull base tumor in a similar location, results in postoperative facial palsy. This is related to manipulation of the facial nerve during tumor removal. Nerves are extremely sensitive to any manipulation, and can be either temporarily or permanently altered by any surgical procedure around them.
Tumors are sometimes closely associated with the facial nerve, and may even be adherent to it. The removal of larger tumors has a higher probability of causing facial nerve dysfunction than the removal of smaller tumors. Occasionally, tumors distort the anatomy so that key structures are difficult or impossible to identify. Sometimes the degree of function of the facial nerve or recovery ability cannot be determined.
The recovery phases that follow different degrees of neural injury are outlined below. These can be followed when the status of the nerve is known, though occasionally the status of the nerve is not known at the conclusion of surgery, making management of the resulting facial palsy difficult.
There are three recognized phases of recovery.
When facial weakness develops in the presence of a parotid gland tumor, it suggests that the tumor is affecting the function of the nerve. Tumors tumors that affect function are more likely to be malignant cancers rather than benign growths.
For complete malignant tumor removal with preoperative facial nerve weakness, a portion of the facial nerve may need to be removed. If this is the case, the nerve is usually reconstructed to permit regeneration if possible.
When facial nerve function is abnormal following parotid surgery, it is important to distinguish the cause of the weakness. The most common cause is nerve stretching that occurs during tumor removal. In that situation, complete recovery is likely. The degree of nerve weakness appears at the time of recovery. Complete facial paralysis takes longer to recover from than mild facial weakness.
Occasionally, and more frequently with malignant parotid tumors, the facial nerve must be cut to adequately remove the entire tumor. Sometimes it is possible to perform a neural graft at the time of surgery, in order to promote regeneration from the native facial nerve stump. In situations where the tumor extends deeply along the nerve or extensively into the facial musculature, grafting is not feasible, and delayed facial paralysis management is employed.
Melkersson Rosenthal syndrome is characterized by a triad of symptoms, including relapsing facial
paralysis, facial edema, and a fissured tongue. It appears to have
a familial inheritance pattern, though the specific mode of
inheritance has not been established. With repeated episodes of
facial palsy,recovery can diminish. For this reason, some doctors
feel that facial nerve decompression is indicated since it appers
to decrease the severity of the facial palsy in subsequent
episodes. This approach is generally reserved for severe cases with
impending long term facial dysfunction, rather than for routine
cases.
Recovery phases from bouts of facial palsy caused by Melkersson Rosenthal syndrome follow a similar time course to recovery from Bell's palsy. Later bouts may recover more slowly and less completely.
Facial paralysis that occurs following head trauma can be due to several different injuries. Most commonly, fractures of the temporal bone through which the facial nerve travels (These are also called Skull Base Fractures.), lead to either temporary or permanent damage to the nerve. Less commonly, direct brainstem injury or a stroke related to the trauma can lead to central nervous system malfunction, so that the facial muscles do not work properly, even if the nerve itself is intact.
Temporal bone fractures are classified into either
longitudinal or
transverse fractures,
depending on their position through the
bone.
Longitudinal fractures are the more common of the two, and account for 80% of all temporal bone fractures. These are usually sustained from a blow to the side of the head. It may rupture the tympanic membrane (ear drum), and can result in bleeding from the ear. In about 20% of these, the facial nerve is injured in the temporal bone.More commonly the cause of the facial paralysis is from swelling within the bony canal through which the nerve runs. Since there is no room for swelling to occur, the nerve gets "squeezed" within the facial canal. The blood supply gets choked, and the nerve malfunctions as a result.
If this is the case, the facial muscles are
sometimes seen to be working normally immediately after the injury,
but become weak in the ensuing several hours to days, as swelling
sets in. When a patient is badly injured with head trauma, the
health care providers are often occupied in managing the life
threatening injuries in the first hours after any serious accident,
and facial nerve function is not noted until the patient is
conscious.
Measures to decrease swelling, such as administration of steroids, can hasten recovery. Another approach to relieve the squeezing phenomenon on the nerve is to perform a facial nerve decompression, though some feel this is a large operation for a problem likely to resolve on its own. It is important to emphasize that in cases of delayed facial nerve weakness, standard management is eye protection and patience. Regeneration falls along a spectrum, and facial nerve recovery can take months to a year.
Transverse fractures comprise 20% of temporal bone fractures, and usually result from a blow to the front or back of the head. These tend to be more severe injuries, since the force required to fracture the temporal bone in its transverse dimension is greater than that required for a longitudinal fracture. The pathway for these fractures may be directly through the inner ear (containing the hearing and balance organs), so hearing loss and vertigo are common. The facial nerve canal is also more commonly disrupted, and there is a 50% incidence of facial paralysis.
The immediate occurrence of facial paralysis with a transverse temporal bone fracture, suggests disruption of the nerve, and may be repaired when the patient is medically stable. The complicating factor is that often other life threatening issues exist, and require attention before the temporal bone fracture is addressed. Moreover, the best assessment of facial function requires a cooperative patient, and many patients are comatose following head trauma, making this impossible.
Patient with transverse temporal bone fracture, attempting to smile. |
Patient with transverse temporal bone fracture, attempting to grimace. |
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Many infectious and inflammatory processes can change facial nerve function. This occurs either through direct effects on the nerve, or because generalized inflammation causes swelling in the tight bony canal through which the facial nerve runs. This chokes the nerve of its blood supply, and causes it to malfunction from lack of nutrition. Some diseases affect the facial nerve in well understood ways, and others are poorly understood. Below some of the diseases whose pathophysiologic effects on the facial nerve are understood.
Lyme disease is a spirochetal infection caused by the organism Borrelia Burgdorferi.
It is ordinarily transmitted through a deer
tick vector, and is recognized by a characteristic "Bull's Eye"
lesion at the site of the tick bite. In the acute phase of the
disease, this round red mark with a pale center can appear, though
in up to 50% of infected individuals the lesion goes unrecognized
or does not develop at all. The second phase of the disease,
presenting 3-6 weeks after infection, is characterized by migrating
joint pains, fatigue, generalized weakness, and cranial
neuropathies. It is during this phase that facial palsy may occur.
It can be an isolated symptom, or occur in conjunction with
dysfunction of the other cranial nerves. A blood test for the
detection of Lyme disease is available, and it is treated with
antibiotics.
Multiple Sclerosis (MS) is a demyelinating disease in which the sheaths surrounding myelinated motor nerves are broken down, preventing them from conducting signals appropriately. It can affect any motor nerve, including the facial nerve. It may wax and wane substantially, so that nerve function fluctuates according to the activity of the disease. During periods of disease remission, neural function often returns to normal.
Diabetes Mellitus (DM) is a lack of internal control over blood sugar levels, based on failure of the islet cells in the pancreas to produce insulin. Blood sugar levels are critical for maintaining proper homeostasis,* and lack of proper control over these levels causes many organ systems to develop disease prematurely. Among these is the nervous system. Neuropathies are common in later stages of DM. The facial nerve, like any other nerve, is susceptible to malfunction on the basis of this DM-associated neuropathy.
There are several causes of congenital facial paralysis. These include genetic problems, in utero problems that develop during pregnancy, or paralysis resulting from trauma at delivery. It is important to try and identify the cause of the paralysis, since management differs according to etiology.
Certain genetically determined syndromes have facial paralysis as a phenotypic features. The best known of these is Mobiius Syndrome, in which there is a congenital absence of the facial nerve on both sides. This results in a dense bilateral facial paralysis with no possibility of spontaneous function of the facial musculature.
These represent the typical features of Mobiius Syndrome.
Goldenhar's Syndrome is a maldevelopment of
the first and second branchial arches, leading to hemifacial microsomia and facial nerve abnormalities. In some cases, there is
evidence pointing to an early in utero problem that contributes to the development of hemifacial microsomia.
When a newborn has completely normal anatomic development, but a facial palsy is present at birth, the possibility of birth trauma to the nerve must be considered. Cases of facial nerve damage from skull base fractures, from forceps delivery, and from shoulder dystocia have been reported. Injuries are virtually always crush injuries rather than transection injuries, and the prognosis for spontaneous recovery is good.
Facial nerve dysfunction can be seen in patients suffering from acute and/or chronic otitis media. There are a number of ways that the nerve can be affected. Usually the state of nerve function and the likelihood of full recovery are dependent on the time of onset of facial nerve symptoms during the course of the ear disease, and the facial nerve paralysis.
Facial paralysis of sudden onset during an acute ear infection is indicative of an acute inflammation leading to malfunction. This tends to occur in infants and young children, because infection spreads through small gaps in the bony canal surrounding the nerve. Ordinarily, prompt treatment of the infection, including removal of infected material in the middle ear via a temporary hole in the ear drum, will lead to resolution of the reversible nerve dysfunction.
Facial paralysis or paresis (partial paralysis) immediately following ear surgery can be related to one of several things.
Sudden facial paralysis in the setting of chronic ear disease suggests compression on the nerve. Pressure on the nerve can occur if the disease involves erosion of bone, as is seen with cholesteatoma. Prompt surgical intervention, with the removal of diseased tissue, and nerve decompression may result in full recovery of function.
Synkinesis and facial spasms refer to hyperkinetic facial syndromes, and both involve involuntary muscle contraction.
Synkinesis refers to the phenomenon whereby deliberate movement of one segment of the face results in movement in another segment of the face. The classic example of this is when intended eye closure results in a turning up of the corner of the mouth, and when a spontaneous smile results in unintentional eye closure. This occurs following facial nerve damage, when the fibers that are regenerating are misdirected, ultimately reaching target muscles for which they were not intended.
Facial spasms refer to involuntary, intermittent or persistent contractions of the facial musculature. It can involve selected muscles (orbicularis oculi in essential blepharospasm, for example), or the entire hemiface (hemifacial spasm).
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