WNV is a neurotropic virus with predilection to brainstem, cerebellum and the anterior horn cells of the spinal cord. The mechanisms of neuroinvasion include entry into the central nervous system by direct infection of vascular endothelium. 

This is a case series of five patients admitted to our inpatient neurology service.

Case 1: 45-year-old woman presented with sudden onset fever and left (L) lower extremity (LLE) weakness. The strength of her LLE was 2/5 in all muscle groups and was areflexic.

Case 2: 68-year-old man presented with altered mental status and flaccid quadriplegic. His initial motor exam showed 0/5 strength in all 4 extremities and was areflexia.

Case 3: 56-year-old woman with history of pancreatic and renal transplant presented with altered mental status and lower extremity weakness severe in L >right (R).

On exam, distal strength in LLE was 1/5 and RLE was 3/5 with hyporeflexia.

Case 4: 36-year-old man presented with personality and behavioral changes with neuropsychiatric symptoms.

Case 5: 34-year-old woman with history renal transplant and presented with acute mental status changes. On examination, nystagmus and opsoclonus and bilateral lower extremity weakness with hyporeflexia.

CSF sample of three patients was positive for WNV IgM antibody, one patient was positive on Polymerase Chain Reaction and one patient was positive for IgG antibody.

Neuroinvasive variants in WNV is seen in less than 1% of those infected but the mortality can be up to 10%. Our case series highlights neuroinvasive spectrum of WNV disease ranging from acute segmental motor paresis, flaccid paralysis, acute rhombencephalitis and neuropsychiatric complications. These presentations should be considered during differential diagnosis and the presence of WNV IgM antibody in the CSF which is suggestive of acute infection.