20 Facial Nerve Dysfunction Dysfunction of the facial nerve can occur anywhere along the length of the nerve, from the pontomedullary root exit zone to the arborizing branches distal in the parotid gland. In addition to segmental lesions, diffuse facial nerve inflammation may occur. Although hyperkinetic dysfunction in the form of a tic or spasm can occur, the most common dysfunction is weakness. No perfect clinical facial nerve grading scale exists, however, so the House-Brackmann system is widely used as a common language to define dysfunction objectively as best as possible. Facial paralysis may be caused by a wide array of disorders and heterogeneous etiologies, including congenital, traumatic, infectious, neoplastic, and metabolic causes. The clinician must identify a history of diabetes, pregnancy, autoimmune disorders, cancer, prior surgery, or trauma as a potential etiology. Facial nerve dysfunction often occurs in the context of other clinical deficits, such as hearing loss, tinnitus, otorrhea, otalgia, facial mass, and facial hypesthesia, to name a few. Facial nerve dysfunction may certainly result from pathology in the temporal bone, but it may also arise secondary to intracranial and even extratemporal processes. A focused neurologic examination and assessment of the parotid gland are essential components of a clinical evaluation. Radiologic imaging may be helpful in localizing the site of the lesion or injury. If otologic disease is present, then formal audiologic testing is indicated. Less sophisticated clinicians may refer to any facial paralysis as a Bell palsy, when in fact 30% of facial paralyses are due to some definable cause. Bell palsy is defined as idiopathic facial palsy, with some recovery. The etiology of Bell palsy is increasingly understood to result from a herpes simplex virus genicu-late ganglionitis that causes edema and ischemia at the narrow meatal foramen in the labyrinthine segment of the fallopian canal; this nerve edema causes swelling and compression of the nerve with resultant weakness. Bell palsy is a diagnosis of exclusion and usually presents quickly over hours or a few days in the absence of other clinical findings, such as otitis media or a parotid mass. Subtle associated findings can be present, such as periauricular hypesthesia or discomfort. Lyme titers and, if appropriate, evaluation for human immunodeficiency virus (HIV) are part of the diagnostic evaluation. If facial nerve recovery does not begin within 1 month, then magnetic resonance imaging (MRI) with gadolinium of the internal auditory canal and temporal bone is appropriate as well. Bell palsy may be recurrent. Infectious etiologies related to facial nerve dysfunction include:
Facial Paralysis: Site of Origin, Primarily within the Temporal Bone
Bell Palsy
Infectious Etiologies
Acute otitis media
Chronic otitis media
Skull base osteomyelitis
Herpes zoster oticus (Ramsay Hunt syndrome): herpes zoster infection Rare infectious etiologies
Spirochetal infection
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