42-year-old female with multiple sclerosis (MS) since 2014, previously on glatiramer, presents with 2-day onset bilateral arm weakness and altered mentation. Admitted to the intensive care unit due to worsening encephalopathy and aspiration pneumonia requiring intubation for airway protection.

Neurological examination revealed flaccid tone and areflexia in bilateral upper extremities, intact sensation, and neck/shoulder pain. She failed multiple extubation attempts due to diaphragm weakness and inability to initiate spontaneous respiration.

MRI brain revealed no acutely enhancing demyelinating plaques suggestive of MS flare, acute infarction, or meningeal enhancement; however, showed increased number of demyelinating plaque burden compared to prior imaging. MRI cervical spine revealed stable spinal lesions without abnormal post-contrast enhancement. Lumbar puncture revealed mixed pleocytosis (128 cells), elevated protein (57), normal glucose, elevated IgG (9.1), negative PCR panel. Infectious serology was obtained and West Nile virus IgM and IgG eventually returned positive.

West Nile virus (WNV) meningoencephalitis causes a clinical picture of fever, encephalopathy, and meningeal irritation with acute flaccid paralysis, intact sensation, and areflexia on clinical exam due to lesion of anterior horn cells. This virus should especially be considered during mosquito season in late summer and early fall, in the time frame this patient presented.

Less than 1% of WNV cases are neuroinvasive, mainly affecting high-risk patients such as elderly and immunocompromised. Diagnosis can be delayed or obscured due to many factors such as mimicking other anterior horn pathologies (such as poliomyelitis), patients on immunomodulator treatments (which may blunt serologic immunoglobulin response), and baseline neurological deficits (demyelinating conditions, spinal stenosis, prior stroke, etc.).