The facial nerve (Cranial Nerve VII or CN VII) is a mixed nerve responsible for controlling nearly all movement and expression in the face. It carries motor, sensory, and parasympathetic fibers, allowing it to manage functions like facial movement, tear production, and the sense of taste. Its intricate course through the skull makes it vulnerable to injury or inflammation, which can lead to various clinical conditions.
Tracing the Anatomical Route
The facial nerve begins deep within the brainstem, emerging from the junction between the pons and the medulla oblongata. It travels alongside the vestibulocochlear nerve (CN VIII) and enters the dense petrous part of the temporal bone through the internal auditory meatus. Because this path is entirely enclosed within hard bone, the nerve is susceptible to damage if swelling occurs.
Inside the temporal bone, the nerve follows the facial canal, where it forms the geniculate ganglion, a cluster of sensory nerve cell bodies. It gives off a branch to the stapedius muscle, which helps dampen loud sounds, before exiting the skull at the stylomastoid foramen, located behind the ear.
Once outside the bone, the nerve trunk travels forward and passes through the parotid gland, a large salivary gland. The nerve does not innervate the parotid gland itself. Within the gland, the main trunk divides into five terminal branches that radiate outward to supply the muscles of facial expression. These branches are named based on the regions they target: temporal, zygomatic, buccal, marginal mandibular, and cervical.
The Three Primary Functions
Motor Control
The primary role of the facial nerve is providing motor control to the muscles of facial expression. This allows individuals to convey emotion through actions like raising the eyebrows, wrinkling the forehead, closing the eyes, and moving the lips.
Special Sensory Input
The facial nerve provides special sensory input for taste. A branch called the chorda tympani carries taste sensations from the anterior two-thirds of the tongue back to the brain. Disruption in the nerve pathway can lead to an altered or complete loss of taste on the affected side.
Parasympathetic Control
The third function involves parasympathetic control, regulating the secretion of glands in the head and neck. The facial nerve controls the lacrimal gland (tears) and the submandibular and sublingual glands (saliva). A lesion high up in the nerve’s course can result in symptoms such as dry eye or reduced salivation on the affected side.
Understanding Facial Nerve Disorders
Disorders of the facial nerve are known as facial palsies, resulting in weakness or paralysis of the muscles it supplies. The most common condition is Bell’s Palsy, a form of acute peripheral facial paralysis. While typically idiopathic, it is often linked to inflammation or swelling of the nerve, possibly due to a viral infection like the Herpes Simplex Virus.
Symptoms develop rapidly, usually reaching maximum weakness within 48 to 72 hours, involving the entire side of the face. Patients experience difficulty closing the eye, drooping of the mouth, and inability to wrinkle the forehead. Due to the nerve’s other functions, patients may also report increased sensitivity to sound (hyperacusis) or a change in taste.
The prognosis for Bell’s Palsy is generally favorable, with 70% to 80% of patients experiencing full spontaneous recovery within six months. Early intervention with corticosteroids is recommended to reduce nerve swelling. Protecting the affected eye is also necessary, as the inability to fully close the eyelid can lead to dryness and corneal damage.
Bell’s Palsy is classified as a peripheral lesion because the damage occurs after the nerve leaves the brainstem, affecting all branches. Other peripheral causes include Ramsay Hunt Syndrome, caused by a varicella-zoster virus infection, and trauma, such as a skull fracture or injury during parotid gland surgery.
A key distinction in diagnosis is differentiating between a peripheral lesion and a central lesion, such as a stroke. Central lesions involve damage to the brain’s control centers and typically spare the muscles of the upper face, allowing the patient to still wrinkle their forehead. This sparing occurs because the upper facial muscles receive input from both sides of the brain, while a peripheral lesion causes weakness in both the upper and lower face on the affected side.