Clinical History

Many aspects of the patient's history help the clinician determine the anatomical site of lesion for a facial nerve disorder, as well as lead to the proper diagnosis. Some basic historical information to gather includes the following:

Temporal presentation: Sudden onset suggests an inflammatory or vascular etiology (e.g., Bell's palsy or stroke), whereas a slowly progressive palsy suggests a neoplastic process, especially if there are episodes of facial twitching (e.g., facial nerve neuroma). The length of time with the paralysis and any spontaneous improvement should be noted, because Bell's palsy should improve within 6 months, whereas palsy caused by a tumor does not. In patients with a history of trauma or surgery, a palsy occurring immediately afterward suggests transection of the nerve (which requires prompt surgical evaluation), whereas a delayed onset usually implies edema of the nerve (which usually improves with time). If there are recurrent episodes of palsy on the same side, one should consider tumor as the etiology; however, if the recurrence is contralateral, one should consider Bell's palsy.

Extent of involvement: It is important to assess the amount of facial palsy present initially, so that changes

over time can be documented. The exact areas of weakness should be noted, because sparing of forehead motion or emotional facial expression suggests a central etiology, whereas palsy of both the upper and lower face suggests a peripheral lesion. If only one or two distal branches of the facial nerve are affected, possible etiologies include parotid gland tumors, facial surgery, or facial trauma. Bilateral involvement, which are called facial diplegia, can be found in Lyme disease, Mobius' syndrome, Bell's palsy, and Guillain-Barre(c) syndrome. y , y

Precipitating elements: Alcoholism, diabetes mellitus, autoimmune diseases, malignancy, hypertension, sarcoidosis, acute porphyria, hyperthyroidism, and pregnancy have been associated with facial palsy. In addition, many infectious diseases can cause CN VII palsy, such as tuberculosis, mononucleosis, poliomyelitis, syphilis, and human immunodeficiency virus. A recent ear infection, with or without otorrhea, is suspicious for an otological infection or cholesteatoma as the possible etiology. An upper respiratory infection commonly precedes Bell's palsy. Facial palsy has been seen after immunizations for polio and rabies and after exposure to toxins like arsenic, carbon monoxide, and ethylene glycol. A family history of facial nerve palsy is seen with Melkersson-Rosenthal syndrome and occasionally with Bell's palsy. Maternal infections (e.g., rubella), drugs used during pregnancy (e.g., thalidomide), and a difficult delivery, especially if forceps were used, have been associated with facial palsy at birth. y

Associated features: A history of other neurological disorders or any evidence of neurological symptoms (e.g., headache, hemiplegia, loss of sensation, cranial nerve dysfunction, changes in balance or tendency to veer toward the same side) should be elicited, while seeking evidence of central pathology. In addition, it is imperative to check for signs and symptoms referable to the ear (e.g., otalgia, otorrhea, hypersensitivity to sound, hearing loss, tinnitus, or vertigo). To help localize the site of lesion, one should note whether other functions of CN VII are involved in patients with facial weakness (e.g., change in tearing, change in taste, reduced salivation). A history of vesicles in the ear, especially if there are CN VIII symptoms, suggests Ramsay Hunt syndrome. A history of tick bites and rash (erythema chronicum migrans) suggests Lyme disease. Facial swelling and fissuring of the tongue is seen with Melkersson-Rosenthal syndrome.


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