A 71-year-old man presented initially with one month of progressive weakness and areflexia in the bilateral lower extremities. Initial cerebrospinal fluid (CSF) analysis demonstrated albuminocytological dissociation, confirming the clinical suspicion of AIDP.  Serum WNV IgM and IgG were elevated.  Patient improved with empiric intravenous immunoglobulin (IVIg) treatment and inpatient rehabilitation.  

The patient then presented seven months later with recurrent bilateral leg weakness, upper motor neuron signs, and a T3 sensory level.  Initial magnetic resonance imaging (MRI) of the spinal cord was unremarkable and CSF studies continued to show elevated protein and positive WNV IgG. He was treated with IVIg again, but symptoms continued to progress. Repeat MRI of thoracic spine showed T2 hyperintensity at the T1-T2 level with enhancement.  He was subsequently treated with IV steroids for transverse myelitis and he improved clinically.

Neurologic manifestations of WNV include encephalopathy, polyneuropathy, myelitis, ataxia, and extrapyramidal symptoms. These syndromes do not typically recur, and any post-infectious inflammatory manifestation occurs soon after exposure. Our patient not only first developed AIDP due to WNV but additionally re-presented seven months after this initial diagnosis with post-WNV transverse myelitis. This case emphasizes the importance of a thorough neurological examination, as well as the necessity to maintain a systematic approach when evaluating patients with repeated neurological complaints.  This was evident in our patient who experienced a unique combination of neurological sequelae of WNV.