West Nile myelitis, a known cause of acute flaccid paralysis, usually manifests with findings of asymmetric limb weakness and hyporeflexia. Electrodiagnostic studies suggest a process involving anterior horn cells, hypothesized to be either direct virally mediated injury or an autoimmune response. Therefore it is rare to see such a case with symmetric weakness and preserved reflexes. 

We present a 70 year old female who initially began experiencing fevers, nausea, vomiting and generalized fatigue for several days. This was soon joined by acute bilateral lower extremity weakness and urinary retention. She was admitted for presumed focal spinal infection leading to spinal cord compression. Initial physical examination was notable for 0/5 bilateral lower extremity strength, preserved sensation, and preserved lower reflexes. MRI of whole spine revealed severe multilevel stenosis but no clear signs of abscess or osteomyelitis. EMG showed severely reduced CMAPs in tibial, median and ulnar distributions; there was normal distal latency and conduction velocity. This did not suggest critical illness neuropathy or a demyelinating process but rather an acute motor neuronopathy given the lack of prolonged CMAP durations. A lumbar puncture returned positive for West Nile IgM. During hospitalization her weakness persisted and she eventually became areflexic. She was treated symptomatically and was eventually accepted to an acute rehabilitation facility.

This case illustrates the unique nature of patients with West Nile centrally neuroinvasive disease who rarely may present with symptoms commonly associated with compressive myelopathy or critical illness neuropathy, such as initially preserved reflexes and symmetric leg weakness. It is important to recognize this variation in order to avoid misdiagnosis or misdirected treatments.