Bilateral sixth nerve palsy in West Nile meningoencephalitis.

Abstract

Editor’s note:The Journal of Neuro-Opthalmology welcomes letters as written or e-mail correspondence. Send e-mail to:[email protected]. To the Editor: We report a novel case of bilateral sixth nerve palsy associated with West Nile meningoencephalitis. A 73-year-old previously healthy man presented with vertigo, vomiting, headache, and fever. On examination, he was lethargic, confused, and febrile to 39.1°C (102.4° F). He was oriented to self, but not place or date. He was inattentive, followed simple commands only after repeated requests, and could not perform calculations. Although the patient had difficulty naming objects, he could recall the names of the president of the United States and the quarterback of the New England Patriots. General physical examination was notable for mild meningismus. On neurologic examination, bilateral sixth nerve palsies, with inability to abduct either eye past the midline, were present. A mild left facial nerve palsy was observed, with flattening of the nasolabial fold. The other cranial nerves were normal. Motor strength was normal, and without involuntary movements. Deep tendon reflexes were slightly diminished throughout, and the plantar responses were flexor. No release signs were observed. Cerebrospinal fluid (CSF) examination revealed a leukocyte count of 56/mm3 (84% polymorphonuclear, 14% lymphocytic) and red blood cell count of 2/mm3. CSF glucose was normal, and CSF protein slightly elevated at 120 mg/dl. Ampicillin, ceftriaxone, and acyclovir were administered. CSF cultures were negative for bacterial and fungal pathogens. CSF VDRL, Lyme antibody, cryptococcal antigen, and PCR for herpes simplex virus were also negative. CSF immunoglobulin M (IgM) for West Nile virus, sent to the Massachusetts State Laboratory, was positive at 4.15 (normal, <2.0). Magnetic resonance imaging of the brain without contrast was unremarkable. The patient defervesced over the next 3 days, and all antibiotics were discontinued. He was discharged to rehabilitation 9 days after admission with significant improvement in his mental status and cranial neuropathies. No residual neurologic deficits were present 6 months after hospital discharge. Neurologic syndromes associated with West Nile infection include meningoencephalitis, encephalitis, aseptic meningitis, cerebellar ataxia, flaccid paralysis, and a poliomyelitis-like syndrome. Autopsy studies have shown most severe inflammation in the medulla and cranial nerve roots (1–3). No specific data are available on the prevalence and outcome of sixth nerve palsies in West Nile infection. In one study, cranial neuropathies were reported in two (11%) hospitalized patients with West Nile infection in New York and New Jersey in 2000, but neither had an ocular motor palsy (1). In the original New York City outbreak in 1999 (2), 13 of 59 (22%) hospitalized patients had cranial neuropathies, but ocular motor involvement was not specified. There is at least one previous report of sixth nerve palsy associated with West Nile infection. Vaispapir et al. (4) reported a patient with bilateral optic neuritis, right lateral rectus palsy, right facial nerve palsy, and cerebellitis. West Nile encephalitis also has been associated recently with anterior uveitis, vitritis, and chorioretinitis (5,6). Reports on the long-term outcomes of patients with West Nile meningoencephalitis are conflicting. In one study of hospitalized older patients with West Nile infection (7), 88% of survivors had regained baseline function 3 months after discharge. However, only 19% of patients had focal neurologic findings at presentation. By contrast, most survivors of the 1999 New York outbreak (8) had persistent manifestations 1 year later, including fatigue (67%), memory loss (50%), difficulty walking (49%), and muscle weakness (44%). West Nile virus infection reached epidemic proportions in the United States in 2002, with 3389 confirmed human cases (9). Physicians should suspect West Nile infection when patients present in the summer and fall months with fever and neurologic or ophthalmologic manifestations.