Facial palsy is a neurological disorder triggered by dysfunction of the seventh cranial nerve, categorized as either central, between the cerebral cortex and brainstem nuclei, or peripheral, between the brainstem nuclei and peripheral organs. Central lesions cause impairment of the contralateral lower facial musculature with associated sparing of the forehead and ocular muscles. Conversely, peripheral lesions produce ipsilateral whole-sided facial hemiplegia including both forehead and ocular muscles. Facial palsy is diagnosed clinically, while imaging studies and additional subsidiary testing (e.g. electromyography, nerve conduction studies), serologies, and rarely biopsy can assist in confirming or refuting the working diagnosis. The differential diagnosis comprises Bell’s palsy (idiopathic), HIV infection, Ramsey Hunt syndrome, Lyme, sarcoidosis, amyloidosis, acoustic neuroma, parotid gland tumor, temporal bone biopsy, otitis media, Guillain-Barre syndrome, and brainstem infarct. Facial palsy is branded as Bell’s palsy if one of the aforementioned etiologies is not identified as the root cause. Herein, we report the case of a 58-year-old male, who presented with left facial weakness involving both the upper and lower face, posterior circulation symptoms in the setting of hypertensive emergency. Initial magnetic resonance imaging (MRI) was unrevealing for any acute process, however given lack of improvement repeat imaging was ordered. The patient was ultimately confirmed to have an acute versus subacute pontine infarct where the seventh and eighth cranial nerve exits at the cerebellopontine angle. Ancillary laboratory studies were non-contributory. Subsequently, the patient’s symptoms continued to improve, blood pressure control was achieved, and was consequently discharged on goal-directed medical therapy. J Neurol Res. 2019;9(1-2):14-17 doi: https://doi.org/10.14740/jnr524
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May 30, 2019
Kazuhiko Sato + 2
Open Access