Facial nerve paralysis

Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, and so there are a number of causes that may result in facial nerve paralysis. The most common is Bell's palsy, an idiopathic disease that may only be diagnosed by exclusion.

A thorough medical history and physical examination are the first steps in making a diagnosis.

During the physical examination, a distinction must first be made between paralysis and paresis (incomplete paralysis). Not surprisingly, paralysis is far more serious and requires immediate treatment.It must also be determined whether the forehead is involved in the motor defect or not. This is usually accomplished by assessing how well a patient can raise his or her eyebrows. The question is an important one because it helps determine if the lesion is in the upper motor neuron component of the facial nerve, or in its lower motor neuron component. If the mimetic muscles do not contract anymore, facial nerve surgery is indicated, for example smile surgery.

Laboratory investigations include an audiogram, nerve conduction studies (ENoG), computed tomography (CT) or magnetic resonance imaging (MRI).

Supranuclear and nuclear lesions
Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus.

The facial nucleus itself can be affected by infarcts of the pontine arteries.

Bell's palsy
Bell's palsy is the most common cause of acute facial nerve paralysis (>80%). Previously considered idiopathic, it has been recently linked to herpes simplex infection. Another more severe form of facial palsy, called Ramsay-Hunt syndrome, is linked to herpes zoster infection of the facial nerve. Other, less common, etiologies are Lyme disease polio, TB.

Bell's palsy is an exclusion diagnosis. Some factors that tend to rule out Bell's palsy include: Bell's palsy is believed in the most recent studies to be due to herpes virus. Other proposed etiologies include vascular problems in the inner ear. Treatment includes steroids and antivirals. {The sequel of cerebrovascular disease(CVA)could be one cause of the facial nerve disease.}H.H.Li 4/27 2011
 * 1) Recurrent paralysis
 * 2) Slowly progressive paralysis (The onset of Bell's palsy is very sudden, usually within 24 hours all the symptoms have been manifested)
 * 3) Twitching
 * 4) Associated symptoms (either cochlear or neurologic)

Trauma
Physical trauma, especially fractures of the temporal bone, may also cause acute facial nerve paralysis. Understandably, the likelihood of facial paralysis after trauma depends on the location of the trauma. Most commonly, facial paralysis follows temporal bone fractures, though the likelihood depends on the type of fracture.

Transverse fractures in the horizontal plane present the highest likelihood of facial paralysis (40-50%). Patients may also present with hemotympanum (blood behind the tympanic membrane), sensory deafness, and vertigo – the latter two symptoms due to damage to vestibulocochlear nerve (cranial nerve VIII) and the inner ear. Longitudinal fracture in the vertical plane present a lower likelihood of paralysis (20%). Patients may present with hematorrhea (blood coming out of the external auditory meatus), tympanic membrane tear, fracture of external auditory canal, and conductive hearing loss.

Traumatic injuries can be assessed by computed tomography (CT) and nerve conduction studies (ENoG). In patients with mild injury, management is the same as with Bell's palsy – protect the eyes and wait. In patients with severe injury, progress is followed with nerve conduction studies. If nerve conduction studies show a large (>90%) change in nerve conduction, the nerve should be decompressed. The facial paralysis can follow immediately the trauma due to direct damage to the facial nerve, in such cases a surgical treatment may be attempted. In other cases the facial paralysis can occur a long time after the trauma due to oedema and inflammation. In those cases steroids can be a good help.

Herpes zoster oticus
Herpes zoster oticus is essentially a herpes zoster infection that affects cranial nerves VII (facial nerve) and VIII (vestibulocochlear nerve). Patients present with facial paralysis, ear pain, vesicles, sensorineural hearing loss, and vertigo. Management includes Antiviral drugs and oral steroids.

Acute and chronic otitis media
Otitis media is an infection in the middle ear, which can spread to the facial nerve and inflame it, causing compression of the nerve in its canal. Antibiotics are used to control the otitis media, and other options include a wide myringotomy (an incision in the tympanic membrane) or decompression if the patient does not improve.

Chronic otitis media usually presents in an ear with chronic discharge (otorrhea), or hearing loss, with or without ear pain (otalgia). Once suspected, there should be immediate surgical exploration to determine if a cholesteatoma has formed as this must be removed if present. Inflammation from the middle ear can spread to the canalis facialis of the temporal bone - through this canal travels the facial nerve together with the steatoacoustisus nerve. In the case of inflammation the nerve is exposed to edema and subsequent high pressure, resulting in a periferic type palsy.

Neurosarcoidosis
Facial nerve paralysis, sometimes bilateral, is a common manifestation of neurosarcoidosis (sarcoidosis of the nervous system), itself a rare condition.

Moebius syndrome
Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Tumors
A tumor compressing the facial nerve anywhere along its complex pathway can result in facial paralysis. Common culprits are facial neuromas, congenital cholesteatomas, hemangiomas, acoustic neuromas, parotid gland neoplasms, or metastases of other tumours.

Patients with facial nerve paralysis resulting from tumours usually present with a progressive, twitching paralysis, other neurological signs, or a recurrent Bell's palsy-type presentation. The latter should always be suspicious, as Bell's palsy should not recur. A chronically discharging ear must be treated as a cholesteatoma until proven otherwise; hence, there must be immediate surgical exploration.

Computed tomography (CT) or magnetic resonance (MR) imaging should be used to identify the location of the tumour, and it should be managed accordingly.

Often, since facial neoplasms have such an intimate relationship with the facial nerve, removing tumors in the this region becomes perplexing as the physician is unsure how to manage the tumor without causing even more palsy. Typically, benign tumors should be removed in a fashion that preserves the facial nerve, while malignant tumors should always be resected along with large areas of tissue around them, including the facial nerve. While this will inevitably lead to heightened paralysis, safe removal of a malignant neoplasm is worth the often treatable palsy that follows. In the best case scenario, paralysis can be corrected with techniques including hypoglossal-facial nerve anastomosis, end-to-end nerve repair, cross facial nerve grafting, or muscle transfer/transposition techniques, such as the gracilis free muscle transfer.