Abstract Details

WNV is a common cause of viral encephalitis in the United States. It can be associated with a variety of neurological manifestations including meningitis, encephalitis and flaccid myelitis. Typically, an inflammatory response is seen in the cerebrospinal fluid (CSF). Typical neuroimaging abnormalities include hyperintense T2/fluid-attenuated inversion recovery  (FLAIR) images. Hyperintensities on unenhanced T1 images are not associated with neuroinvasive WNV.

To present and discuss possible mechanisms of a combination of typical and atypical clinical, radiographic, and serological features in a case of neuroinvasive West Nile virus (WNV)

Case Report

A 53 year-old male with non-alcoholic steatohepatitis underwent orthotopic liver transplant three weeks prior to presentation and developed fever and diarrhea. On day 4, multifocal myoclonus and torticollisdeveloped. His standing tacrolimus was stopped. Brain MRI was unremarkable. CSF studies were non-inflammatory with no elevation in protein; two leukocytes noted (100% neutrophilic). WNV IgM was equivocal. By day 6, his level of consciousness declined and he developedflaccid paralysis resulting in quadriplegia necessitating intubation. Liver and renal function mildly elevated.  Repeat imaging demonstrated T2/FLAIR hyperintensities along the corticospinal tract and T1 non-enhancing hyperintensity in bilateral globus pallidus. Repeat CSF was inflammatory (one leukocyte, elevated protein); however, WNV IgM levels were now positive, as was a repeat PCR, confirming the diagnosis of neuroinvasive WNV. 

Neuroinvasive WNV is common in the immunocompromised population. This case demonstrates two atypical findings: the complete lack of an inflammatory CSF on initial testing likely in the setting of immunocompromise, as well as basal ganglia T1 hyperintensities that have not been previously described. Mechanisms for the imaging findings are unknown but may include microvascular inflammation including microhemorrhages.  A high level of clinical suspicion including repeat testing is warranted in these patients. Additionally, this case expands the differential diagnosis of T1 hyperintensities and the growing protean manifestations of neuroinvasive WNV.