The seventh cranial nerve is predominantly a motor nerve supplying the muscles of facial expression. The sensory component is small, it carries taste sensations from the anterior 2/3rds of the tongue and cutaneous sensations from the anterior wall of the external auditory canal. Disorders of the Facial nerves are usually supranuclear facial palsy,Nuclear or infranuclear facial palsy (LMN) and Bell’s Palsy.
Supranuclear facial palsy
In a supranuclear or upper motor neuron facial palsy, only the lower half of the face is affected. This is because the nuclear center which controls the movements of the upper half of the face has both ipsilateral and contralateral supranuclear center supplying the lower half of the face has mainly or only contralateral supranuclear innervation. Hence a cortical or a subcortical lesion produces paralysis of the lower part of the face on the opposite side. Supranuclear palsy is of two types- Volitional and emotional. In volitional palsy, the involvement is most marked on the voluntary contraction. On automatic involuntary movements such as crying or smiling, there is preservation of function. Here the lesion is in the cortex or in the subcortical pyramindal tracts as they go through the internal capsule, cerebral peduncle or Pons above the facial nucleus. In emotional or mimetic facial paresis, there is no asymmetry or mimetic facial paresis, there is no asymmmetry of the facial muscles on voluntary movements. The patient can close his eye, retract his mouth or blow his cheeks without difficulty. However, the paresis becomes apparent during smiling or crying. Here the lesion is either in the frontal lobes anterior to the precentral cortex or deep seated in the thalamus or basal ganglia.
Nuclear or infranuclear facial palsy (LMN)
The lower motor neuron is the final common pathway. Hence lesions at this site produce weakness of the entire half of the face on the ipsilateral side. The exact site of lesions is determined by the associated signs. In Pontine lesions as in a tumor or vascular occlusion, the facial palsy is associated with ipsilateral sixth nerve paralysis. A cerebellopontine angle lesion, such as acoustic neuroma is associated with ipsilateral eighth and fifth nerve palsies, cerebella signs, and contralateral pyramidal signs. Within the facial canal, the nerve can be affected in many ways. Inflammatory conditions such as herpes Zoster can affect the geniculate ganglion. Other infections like mumps, scarlet fever and malaria, metabolic conditions like diabetes, alcoholism and nutritional deficiency, metastatic neoplasms, neuroleukemia, etc, can affect the facial nerve within the facial canal. Owing to the proximity of the nerve to the middle ear, facial paresis can be a complication of Otitis media, suppuration of temporal bone or mastoiditis. Immediately outside the stylomastoid foramen, the nerve could be involved by tumors of the parotid gland, injuries, obstetrical trauma due to forceps delivery, etc. Involvement of the terminal branches of the nerve is a feature of leprosy, which manifests by involvement of individual muscles. Bilateral facial palsy is usually due to Guillain-Barr’e syndrome or sarcoidosis.
This is the commonest cause of LMN facial palsy. It usually develops spontaneously, often starting with a mild pain in the ear. Sometimes a history of exposure to cold or wind, or a mild systemic infection is obtained. The exact cause is not clear. It is believed to be either compression of the nerve by edma or periosteitis of facial canal, ischemia of the nerve or a viral infection. The disease comes on with abrupt onset of facial palsy which is manifested by deviation of the angle of the mouth to the normal side, and inability to close the eyelids. Food collects in the vestibule of the mouth. The paralysis may be dense involving all muscles or may be partial. In the majority of patients, the facial palsy completely improves. In a few cases the paralysis may be irreversible. In those that recover, signs of recovery start within a week and recovery may be complete in a month. Complications include corneal ulcerations and exposure keratitis, facial contracture and aberrant innervations on recovery. In the acute stage, steroids can be tried. However, physiotherapy is the most important factor to prevent the development of contractures. In those cases which do not recover, plastic surgery procedures to reduce deformity and facial nerve anastomosis to glossopharyngeal nerve have been successfully employed.
These are the disorders of the facial nerve, but this article will not be complete if a very important syndrome is not discussed, the Ramsay-Hunt syndrome. This consists of severe facial palsy associated with vesicles in the pharynx, external auditory canal and sometimes over the mustoid. The 8th cranial nerve may also be involved in many. The lesion is due to herpes zoster affecting the geniculate ganglion.