Facial Palsy

This is weakness of the facial muscles as a result of damage to, or inflammation of, the facial nerve. The condition is usually temporary and affects only one side of the face.

Causes

Facial palsy is most often due to Bell's palsy, which occurs for no known reason. Less commonly, the condition is associated with herpes zoster (shingles) affecting the ear and facial nerve. Facial palsy may also result from surgical damage to this nerve, or compression of the nerve by a tumour.

Symptoms

Facial palsy usually develops suddenly. The eyelid and the corner of the mouth on one side of the face droop, and there may be pain in the ear on that side. The ability to wrinkle the brow or to close the eye may be lost, and smiling is distorted. Depending on which nerve branches are affected, the sense of taste may be impaired or sounds may seem to be unnaturally loud.

Treatment

In many cases, facial palsy clears up without treatment. Pain can be relieved by taking analgesics (painkillers), and exercising the facial muscles may aid recovery. It may be necessary to tape the eyelid shut at bedtime in order to avoid the risk of corneal abrasion. Bell’ s palsy may be treated with corticosteroid drugs to reduce inflammation and speed recovery. Re-routing or grafting of nerve tissue may help people suffering from palsy caused by an injury or a tumour.

Disorders of the facial nerve

Summary

Facial nerve—in upper (but not lower) motor neuron lesions there is relative preservation of power in the upper facial muscles. In Bell’s palsy, onset is rapid and frequently heralded or accompanied by aching pain in or around the ear: treatment with prednisolone improves the prognosis. Hemifacial spasm is characterized by irregular clonic or simultaneous twitching movements of the facial muscles, usually of insidious onset; injections of botulinum toxin may be helpful. Glossopharyngeal nerve—rarely affected in isolation, when it is very difficult to detect any neurological deficit; usually affected in combination with the vagus nerve.

Facial nerve disorders

The seventh cranial nerve (facial nerve) is largely motor. The nerve traverses the facial canal in the petrous temporal bone in close relationship to the middle ear and emerges at the stylomastoid foramen. Its branches pass forward through the parotid gland to be distributed to the muscles of the face and the platysma. Within the petrous bone, a branch is given to the stapedius muscle. The chorda tympani, carrying the taste fibres from the anterior two-thirds of the tongue, joins the nerve within the facial canal and a small branch supplies cutaneous sensation to the external auditory meatus. The nerve also carries preganglionic parasympathetic fibres destined for the lachrymal gland.

The distinction between upper and lower motor neuron lesions of the facial muscles is usually easy. In general, with upper motor neuron lesions there is relative preservation of power in the upper facial muscles, because these have a representation in both cerebral hemispheres. There is no loss of tone with upper motor neuron lesions, so that the sagging of the face that is an unsightly feature of lower motor neuron palsy does not occur.

In common with the trigeminal nerve, the facial nerve may be affected by tumours in the cerebellopontine angle. In the past, it was often involved in middle ear infections. It may be involved in meningeal carcinomatosis, fractures, and tumours of the skull base, in a variety of cranial neuropathies, and cephalic herpes zoster, but the most common lesion by far is Bell’s palsy. More peripherally, the nerve may be compromised in tumours of the parotid gland.

Bell’s palsy

This term describes idiopathic facial palsy and is usually unilateral facial paralysis of relatively rapid onset due to a lesion of the nerve within the facial canal. Taste may also be affected. It has an annual incidence of 20 to 32 per 100 000 and may develop at any age, most commonly between 20 and 50 years, and affects both sexes equally. There is some, but inconclusive, evidence that it is a manifestation of herpes simplex infection. In the acute stage, the nerve is swollen and compression within the facial canal may contribute to the damage to the nerve fibres.

The onset is rapid and is frequently heralded or accompanied by aching pain below the ear or in the mastoid region. This clears within a few days and is not present in every case. The paralysis usually reaches its maximum severity after 1 or sometimes 2 days. Complete paralysis may occur. This may cause a mild dysarthria and some difficulty in eating because of food collecting between the gums and the inner sides of the cheek and the escape of fluid when drinking. The face sags, and on smiling is drawn across to the unaffected side. Paralysis of orbicularis oculi renders voluntary eye closure impossible and, particularly in the older subject, ectropion develops. This can result in conjunctival injury from foreign bodies or conjunctivitis. If the paralysis is partial, the lower face is usually affected to a greater extent than the upper.

In the more severe cases, loss of taste over the anterior two-thirds of the tongue is often present, and paralysis of the stapedius muscle may result in a lack of tolerance for high-pitched or loud sounds, called hyperacousis.

Bell’s palsy has to be distinguished from selective lesions of the facial nerve within the brainstem, in which instance taste will not be affected. Lesions in the brainstem almost always cause fifth or sixth nerves palsies and long tract symptoms or signs as well. With respect to peripheral lesions, middle ear disease requires exclusion. Facial paralysis may also be caused by herpes zoster as described below. A lesion of the facial nerve may be part of a more generalized disorder of which diabetes, Lyme borreliosis, and sarcoidosis are the most important. Bell’s palsy is rarely bilateral and bilateral facial paralysis would raise the possibility of another disorder, such as sarcoidosis, Guillain–Barré syndrome, or Lyme borreliosis.

In approximately 85% of patients with Bell’s palsy, especially those with mild weakness, the paralysis is the result of a local conduction block within the facial canal without axonal degeneration. The conduction block is presumably the consequence of segmental demyelination. Provided that such cases do not progress to more severe weakness, remyelination is rapid and all recover fully within a few weeks. In cases where there is total paralysis, axonal degeneration is likely to have occurred so that recovery has to take place by axonal regeneration, which is slow. Evidence of reinnervation does not appear in under 3 months and the ultimate recovery is often incomplete or may fail to occur altogether. After reinnervation the regenerated axons may form inappropriate connections, causing synkinesis and crocodile tears. In synkinesis, blinking results in a simultaneous twitch of the angle of the mouth. Crocodile tears are caused by aberrant parasympathetic reinnervation so that food elicits weeping instead of salivation.

Axons remain excitable distal to the lesion for 3 or 4 days after interruption. It is therefore not possible to be certain from electrodiagnostic tests whether axonal degeneration has taken place until later. After that stage, electrical stimulation of the facial nerve at the stylomastoid foramen will still elicit a muscle contraction if the paralysis is due to conduction block, whereas none will be obtained if axonal degeneration has taken place.

Because most patients with Bell’s palsy recover completely, it was difficult to discover from observational studies whether different treatments helped. However, in a large high-quality trial the percentage of patients with complete recovery after 9 months was significantly increased from 81.6% without to 94.4% with prednisolone, 25 mg twice daily for 10 days. Another trial obtained similar results with prednisolone 60 mg daily for 5 days and then a reducing dose for the next 5 days. In the same trials oral aciclovir made no difference. There is no evidence of efficacy from antiviral agents alone although it is still possible that they might have a small effect when used in conjunction with corticosteroids. In patients with severe palsy causing ectropion, stitching the lateral parts of the eyelids, lateral tarsorrhaphy, may be performed to protect the eye. Electrical stimulation of the paralysed facial muscles has not been shown to have a significant effect on the ultimate prognosis.

In those cases in which regeneration is inadequate, cosmetic operations may be considered to counteract the facial deformity. The angle of the mouth may be elevated by a fascial sling attached to the temporalis fascia, but the result is never highly satisfactory. Restoration of facial tone may be achieved by anastomosis of the hypoglossal to the facial nerve, but at the expense of denervation of the tongue on that side. Any operation should not be contemplated before an adequate length of time has been allowed for regeneration. This should be of the order of one year.

Read more: Bell's palsy diagnosis and treatment - technical

Facial paralysis related to ‘geniculate’ herpes zoster (Ramsay–Hunt syndrome)

Facial paralysis of rapid onset accompanied by severe pain in and around the external auditory meatus and in the throat may accompany ‘cephalic zoster’. Vesicles may be detectable in the ear and ulceration in the fauces, or anywhere on the head. Occasionally there is concomitant vertigo, tinnitus, and some deafness due to involvement of the eighth nerve (‘otic herpes zoster’). Prognosis for recovery of the facial paralysis is stated to be less good than in Bell’s palsy. It is not known whether antiviral agents or corticosteroids are helpful.

Hemifacial spasm

This consists of a unilateral disturbance affecting the facial muscles, producing irregular clonic or simultaneous twitching movements of the facial muscles, usually of insidious onset. It most commonly occurs in middle-aged women. There may be a mild degree of facial weakness, but not severe paralysis. Usually no underlying cause is demonstrable. The condition selectively affects the facial nerve, within the brainstem or in the posterior fossa. Hemifacial spasm is painless. If it is associated with pain, there may be a lesion in the cerebellopontine angle compressing both the trigeminal and facial nerves.

It begins with intermittent twitching of the facial muscles such as around the eye or at the angle of the mouth. These movements gradually become more frequent and extend to involve the rest of the facial muscles, often gradually advancing over the course of some years. If they become severe, the face is contorted by irregular clonic spasms which may keep the eye closed for prolonged periods. The facial distortion is often a considerable embarrassment to the patient, who finds that the spasms tend to be aggravated by emotional stress.

In severe cases, injections of botulinum toxin may be helpful, but these have to be repeated. If exaggeration by emotional factors is evident, the administration of diazepam or a similar preparation may produce a marginal improvement. Neurosurgical intervention to relieve compression of the facial nerve by aberrant vessels in the posterior fossa may be helpful in selected cases.

The condition must be distinguished from benign fasciculation of the face, which usually occurs around the eyes, related to fatigue or emotional tension, and from facial myokymia that is occasionally encountered as a manifestation of multiple sclerosis. The latter consists of a persisting irregular rippling movement of the facial muscles that usually subsides after a week or two. These conditions can be distinguished by electromyography.

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