Facial paralysis

Facial paralysis

Facial 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.

Causes

Facial paralysis is almost always caused by:

Damage or swelling of the facial nerve, which carries signals from the brain to the muscles of the face

Damage to the area of the brain that sends signals to the muscles of the face

In people who are otherwise healthy, facial paralysis is often due to Bell's palsy. This is a condition in which the facial nerve becomes inflamed.

Stroke may cause facial paralysis. With a stroke, other muscles on one side of the body may also be involved.

Facial paralysis that is due to a brain tumor usually develops slowly. Symptoms can include headaches, seizures, or hearing loss.

In newborns, facial paralysis may be caused by trauma during birth.

Other causes include:

Infection of the brain or surrounding tissues

Lyme disease

Sarcoidosis

Tumor that presses on the facial nerve

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.

Infranuclear lesions

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 toherpes 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:

Recurrent paralysis

Slowly progressive paralysis (The onset of Bell's palsy is very sudden, usually within 24 hours all the symptoms have been manifested)

Twitching

Associated symptoms (either cochlear or neurologic)

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.

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 theotitis 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

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