MANAGEMENT OF RAMSAY±HUNT SYNDROME. S. Gupta 1 , O. Melamed 2 ; 1 UCLA School of Medicine, Los Angeles, CA; 2 Olive View±UCLA Medical Center, Sylmar, CA (Tracking ID #75744) LEARNING OBJECTIVES: 1. Clinical presentation and pathophysiology of Ramsay±Hunt Syndrome 2. Lack of outcome benefit from head imaging, IV therapy, and surgery for RHS 3. Improved outcome with early treatment. CASE INFORMATION: A 30-year-old female presented to the urgent care clinic for evaluation of left ear pain, vertigo, left facial paralysis and small vesicles over the left pinna. The patient's past medical history was significant for chickenpox at the age of eight. On physical examination the patient had left ear swelling and erythema with multiple 0.5±1.0 mm vesicles around the pinna and marked erythema involving the external auditory canal. There was a positive Bell's phenomenon (the eyeball rolling up and outward on attempting to close the affected eye). A facial paralysis involved the left levator labii and left frontalis muscles. A left sensorineural deficit was observed with Weber test lateralizing to the right and a positive (normal) Rinne test bilaterally. The diagnosis of Ramsay±Hunt Syndrome was made. The patient was discharged from the clinic on a regimen of Acyclovir and Prednisone. She was instructed to avoid pregnancy, contact with pregnant women or neonates. IMPLICATIONS/DISCUSSION: Clinical presentation of unilateral facial paralysis and a vesicular rash on the ear (zoster oticus), often accompanied with hearing loss, tinnitus, nausea, vomiting, vertigo and nystagmus was first described by J Ramsay Hunt in 1907. Vestibulocochlear symptoms were explained by the anatomical proximity of the eighth nerve and the geniculate ganglion within the temporal bone. The pathophysiology of RHS involves the reactivation of varicella-zoster virus (VZV) within the geniculate ganglion and secondary edema in the facial nerve resulting in facial nerve palsy. VZV is considered a major etiologic agent of Bell's palsy. Use of contrast enhanced MRI in diagnosis of RHS does not appear to provide much information as enhancement of the geniculate ganglion, meatal fundus, and facial nerve is observed independent of etiology. Most patients with Bell's palsy tend to recover to complete or near normal function even without treatment. One prospective study found that 85% of patients showed signs of remission within the first 3 weeks, with 71% recovering complete function, 13% left with insignificant sequelae, and 16% left with permanently diminished function. Although most patients with RHS improve, many patients are left with functional and cosmetic deficits. Treatment of RHS with oral acyclovir and prednisone (AS therapy) may improve outcome. Two separate studies showed complete recovery in 75% of patients with RHS treated with AS. There has been no evidence of improvement in outcome with intravenous administration of either acyclovir or prednisone, though many patients are still admitted to the hospital for IV therapy. There is also insufficient evidence for efficacy of surgical facial nerve decompression. Evidence for improved outcomes with earlier administration of therapy have been observed. In one study 75% of patients beginning AS treatment within 3 days of onset of facial paralysis had complete recovery, compared with 30% of patients beginning therapy after 7 days. Earlier therapy decreased nerve degeneration and improved recovery of hearing.