Facial palsy – Facial nerve or seventh cranial nerve is largely a motor nerve supplying muscles of face. It arises from its nucleus located in the pons. The nerve follows a long course within the skull and leaves it through the stylomastoid foramen. While passing through the facial canal, it gives off a nerve to the stapedius muscle and ehorda tympani. In its course a small number of sensory fibers going to external auditory meatus carry fibers which excite salivary secretions as well as convey taste impulses from the anterior two thirds of tongue.
Facial palsy may result due to:
1. A supra nuclear lesion involving the pyramidal fibers Upper motor neurone (UMN).
2. Infra nuclear or nuclear lesion involving lower motor neurone.
Upper motor neuron lesion (UMN)
Commonest cause is internal capsule lesion due to cerebral thrombosis or infarction. Characteristically the lower half of face is involved more severely than the upper half. This is because the nuclear center which controls the movements of the upper half of the face has both ipsilateral and contra lateral connections. Thus upper part of face has got bilateral nerve supply.
Patient is able to raise furrows on forehead, close his eyes though lower half of face is involved. Emotional movements such as laughing, smiling are preserved, since these are not dependent on the same supra nuclear pathway from the pyramidal tract as voluntary movements.
Lesions in the region of cortical or sub cortical produce paralysis of lower part of face on opposite side. This is because of association of facial neurons with pyramidal tracts as they pass through the internal capsule, cerebral peduncle or pons above the level of facial nucleus.
Lower motor neurone (LMN)
It may be nuclear or infranuclear type. The facial nerve neurons may be involved within the pons, in the posterior fossa (cerebellopontine angle)within the temporal bone and after leaving the skull. The lesion is lower motor neuron type and the whole half of face on the involved side is paralyzed. The clinical features in each group shall vary per the site of lesion.
1. Pontine lesion – Massive lesions at this site involve adjacent structure especially 6th nerve resulting in paralysis of external rectus muscle. If there is involvement of spinal tracts, nucleus of trigeminal nerve and of spinothalamic tracts there is sensory loss along with pyramidal lesion of the limbs on opposite side.
Causes include syringobulbia. Tumours (glioma) vascular lesios, polio, infective polyneuritis and disseminated sclerosis.
2. Cerebellopontine angle – Because of proximity of facial nerve at this place to 5th, 6th and 8th cranial nerves, the lesion involves all three. There is facial paralysis, deafness and loss of taste in anterior two thirds of tongue. Causes include cerebellopontine angle tumor, acoustic neuroma and syphilitic meningitis.
3. Within the temporal bone involvement of facial nerve is due to fracture of skull, infections of the middle ear and mastoid. Because of proximity of the nerve to temporal bone middle ear infections suppuration of temporal bone and mastoiditis involve it as a result of direct spread to nerve.
Facial palsy paralysis caused by a lesion within the middle ear is associated with loss of taste in the anterior two thirds of tongue and when the nerve is involved in the facial canal between branching of nerve to stapedius and ganglion of facial nerve, in addition to facial paralysis, loss of taste in anterior two thirds of tongue, impairment of salivary secretions and hyperacusis occurs.
Ramsay hunt syndrome is another entity when herpes zoster involves the geniculate ganglion causing facial paralysis through secondary involvement of the motor fibers of the nerve and deafness due to herpetic involvement in the external auditory meatus. Involvement of facial nerve within the stylomastoid foramen occurring generally as a result of exposure to cold or idiopathic produces facial paralysis known as Bell’s palsy.
After leaving the skull the nerve may be involved by inflammation from glands behind the angle of jaw, parotid gland tumors, trauma, surgical operations, poly neuritis and sarcoidosis.
Bell’s palsy
It is a common manifestation of isolated facial nerve involvement and is quite frequently seen. It may occur at any age. It comes acutely and is considered to be due to acute inflammation of the nerve probably due to viral aetiology. The involvement of nerve occurs in its course within the stylomastoid foramen. Other causes include interstitial neuritis middle ear disease and periostitis of temporal bone. The nerve is swollen oedematous resulting in compression of nerve fibers. In a great majority of cases no predisposing cause is seen and often the lesion is ascribed as ‘exposure to cold’.
Symptoms
There is unilateral involvement of face on the paralyzed side. Often the onset is acute. There may be pain behind the ear in the mastoid region or around the angle of jaw.
Both upper and lower half of face are equally effected. Patient is unable to raise furrows on forehead, frowning is not possible. Palpebral fissure is widened and patient is unable to close eye on paralysed side. Eversion of lower eye lid, leads to impairment of absorption of tears which overflow. Nasolabial fold is flattened and the mouth is drawn to opposite normal side. Patient is unable to blow his cheeks or whistle. Since mouth is displaced, tongue is deviated to the normal side. There is inability to show teeth.
Food may accumulate between teeth and cheeks. When the involvement of nerve is at the point when chorda tympani leaves it there is loss of taste on the anterior two thirds of tongue and when branch to stapedius is involved there is hyperacusis (increased acuity of hearing with undue sensitivity to low tones).
Diagnosis of bell’s palsy is made on clinical grounds especially when it is isolated facial nerve involvement and there is no evidence of any other cranial nerve involvement. Onset is acute and generally comes in an apparently healthy individual.
Treatment
1. Since the eyes are exposed because of aversion of lower eye lid there is danger of developing exposure keratitis. Patient must wear dark glasses to protect the eyes from damage. An antibiotic eye cream may be used two times a day.
2. Steroids (prednisolone 60 mg/day in divided doses) along with course of amoxycillin (250 mg 8 hourly) are started at the earliest. Their use is indicated to reduce edema round about the nerve.
3. Heavy doses of vitamin B12 (1000 ugm per day I/M) have non-specific role but have been found beneficial.
Electro-physiological tests are of help in predicting the outcome. Galvanic current is used to stimulate the facial muscles. As soon as some power returns patient is encouraged to practice closing his eyes as well as retracting the angle of the mouth by gentle finger massage three to four times a day. If no recovery takes place within 6 to eight weeks, cosmetic surgery including renervation of nerve may be considered. In cases where bell’s palsy is due to middle ear disease treatment should be directed towards it but when it has followed an operation in that region or trauma or suigery, recovery is poor.
Course and prognosis
Most cases of bell’s palsy recover though complete recovery may not take place and the person is left with residual facial paralysis. Certain sequlae may develop in a number of cases where recovery is not complete. These include:
1. Crocodile tears: Because of aversion of lower eye lid patient is shedding tears constantly.
2. Contracture on the side of facial palsy in paralyzed muscles, and this is evident when patient smiles.
3. Facial tics
4. Clonic facial spasm.
