Anatomy and pathology of the facial nerve.

Abstract

Clinical Presentation Symptoms of facial nerve palsy depend on the location of injury. The motor nucleus of CN VII has dorsal and ventral divisions that supply the upper and lower face, respectively. There is bilateral innervation of the dorsal division but only contralateral innervation of the ventral division. Supranuclear lesions affect upper motor neurons proximal to the motor nucleus in such locations as the cerebral cortex, internal capsule, and cerebral peduncle. This results in central facial palsy that affects the contralateral lower face but spares the forehead and brow muscles. Infranuclear lesions occur distal to the facial nerve nucleus and produce peripheral facial palsy affecting the ipsilateral upper and lower face. Within the infranuclear pathway, the presence of additional symptoms can help further localize lesions. Involvement of CN VI presents with lateral rectus palsy, or inability to abduct the eye. This suggests a lesion of the facial colliculus in the pons, in which efferent CN VII fibers encircle the CN VI motor nucleus. Involvement of CN VIII causes auditory or vestibular symptoms. This suggests a cisternal or canalicular lesion in which CN VII and VIII nerve roots course together after emerging from the cerebellopontine angle. Finally, certain branches of the facial nerve control specialized functions. The greater superficial petrosal nerve controls lacrimation, the stapedius dampens sound transmission in the inner ear, and the chorda tympani is responsible for taste. Lesions proximal to the geniculate ganglion lose all three functions, lesions between the geniculate ganglion and stylomastoid foramen have preserved lacrimation, and extracranial lesions spare all three functions. Anatomy and Pathology of the Facial Nerve