Facial paralysis, whether partial or complete, causes significant morbidity, impairing the ability to smile, blink, eat, and even taste. Moreover, the alteration of one’s physical appearance can have significant psychosocial implications, leading to social isolation and depression.¹

The facial nerve is primarily responsible for motor innervation of the muscles of facial expression but also carries special sensory fibers supplying taste and parasympathetic fibers controlling salivary function and lacrimation. It can be injured anywhere along its complex course from the brainstem, through the temporal bone and into the face.

The central portion of the facial nerve includes the supranuclear tracts, facial nucleus (lower pons) and brainstem components. Importantly, the superior portion of the motor nucleus, which innervates the upper face, receives bilateral central innervation from the corticobulbar tracts. This anatomy explains why a patient with a stroke or acute central pathology will have forehead-sparing paralysis.²

The intracranial segment of the facial nerve enters the skull base at the internal acoustic meatus, transverses the internal auditory canal, then exits the meatal foramen to form the labyrinthine segment on its way to the geniculate ganglion. The nerve is commonly injured in this perigeniculate location owing to localized inflammation and swelling within a narrow bony channel (Figure 9.1). At the geniculate ganglion, it joins the greater superficial petrosal nerve to supply parasympathetic innervation for the lacrimal, salivary, nasal, palatine, and pharyngeal mucous glands. The tympanic and mastoid segments of the nerve then travel through the middle ear and mastoid to exit at the stylomastoid foramen. The extratemporal segment courses through the parotid gland and ultimately give rise to the five nerves that are responsible for facial motor function—the temporal, zygomatic, buccal, mandibular, and cervical branches.³

Common complaints of facial neuropathy include facial droop, eye irritation, taste changes, and lacrimal dysfunction. Patients should be questioned about constitutional symptoms, ear pain, otorrhea, hearing loss, tinnitus, dizziness, hyperacusis, and rashes. In addition, a history of recent trauma, surgery, travel, tick bites, and cutaneous or parotid malignancies should be obtained. It is also critical to ask about recurrent episodes.⁴

On physical exam, facial motor function is assessed by asking the patient to close the eyes, elevate the brows, smile, and puff cheeks (Figure 9.2). The degree of paralysis should be noted with a detailed description or using the House-Brackmann Scale (see Table 9.1). Additionally, any evidence of synkinesis should be noted. The presence of vesicles or crusted lesions in the external auditory canal, palate, and face may indicate Ramsey-Hunt syndrome. The parotid gland should be palpated carefully to evaluate for masses. The ear should be examined for evidence of otitis media and externa.

A complete neurologic exam should be performed to distinguish an upper motor neuron facial nerve palsy from a lower motor neuron palsy. Central lesions are more likely to spare the forehead, present as a spastic paralysis, and have focal extremity weakness or numbness. Paralysis caused by
peripheral lesions will typically include the forehead and present with flaccid paralysis. Central causes of facial palsies are commonly vascular in etiology but may also be neoplastic, infectious, or autoimmune.