Bilateral Thalamic Involvement in West Nile Infection Linked to Anti-CD20 Therapy in a Patient with Multiple Sclerosis
Joyce Jimenez Zambrano1, Daniel Moreno-Zambrano2, Hector Caballero1, Leslie Koltes3, Leighton Mohl3, Scott Belliston3
1Department of Neurology, University of North Dakota School of Medicine and Health Sciences & Sanford Health, 2Larkin Community Hospital, 3Department of Neurology, Sanford Health
Objective:
To highlight the association between neuroinvasive West Nile virus and concurrent ocrelizumab monotherapy in a patient with multiple sclerosis.
Background:

Neuroinvasive West Nile infection occurs in less than 1% of individuals infected by the virus. Affected patients present with meningoencephalitis, flaccid paralysis, and/or encephalopathy, often requiring prolonged intensive care interventions with high risk of premature disability or mortality. We present a case of neuroinvasive West Nile infection resulting in bilateral thalamic injury in a patient with multiple sclerosis on ocrelizumab.

Design/Methods:
N/A
Results:

A 35-year-old female with a history of multiple sclerosis (MS) on ocrelizumab monotherapy presented with bilateral lower extremity weakness and a pressure-like sensation around the abdomen. Initially, high-dose methylprednisolone was administered for suspected MS relapse. The patient subsequently developed fevers with progressive weakness affecting her face, extremities, and bulbar musculature necessitating intubation and transfer to the intensive care unit. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis, elevated protein, and normal glucose, consistent with viral meningoencephalitis. West Nile virus IgM antibodies were detected in serum and CSF, confirming West Nile virus infection. Contrast-enhanced brain magnetic resonance imaging (MRI) exhibited bilateral thalamic T2 hyperintensities with symmetric extension into the cerebral peduncles. Seven sessions of plasmapheresis were given over fourteen days. A follow-up MRI two weeks later demonstrated resolution of previous thalamic findings and minimal residual hyperintense signal in the bilateral cerebral peduncles. Despite these changes, she showed minimal neurologic improvement and remained dependent on mechanical ventilation requiring a tracheostomy. She was later discharged to a long-term care facility.


Conclusions:
Bilateral thalamic involvement is a rare complication of neuroinvasive West Nile virus infection frequently linked to a less favorable prognosis in immunocompromised patients. While plasma exchange therapy demonstrated promising results in terms of resolving radiographic abnormalities in our patient, it has yet to yield substantial clinical improvement. 
10.1212/WNL.0000000000205531