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West Nile Virus Encephalomyelitis with Polio-like Paralysis & Nigral Degeneration

Published online by Cambridge University Press:  02 December 2014

Kristian T. Schafernak
Affiliation:
Division of Neuropathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
Eileen H. Bigio*
Affiliation:
Division of Neuropathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
*
Division of Neuropathology, Northwestern University Feinberg School of Medicine, 710 N. Fairbanks Court., Olson 3-459, Chicago, Illinois, 60611, USA
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Abstract

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Background:

Patients infected with West Nile virus (WNV) may develop acute neurologic disease, which can be severe or even fatal, including WNV meningitis, encephalitis, and an irreversible acute flaccid paralysis or poliomyelitis-like syndrome. Movement disorders have also been described.

Report:

We report combined neuronal loss, gliosis, and neurofibrillary tangle formation in the substantia nigra of a 41-year-old man with a history of WNV encephalomyelitis and poliomyelitis-like paralysis.

Conclusion:

Clinically our patient did not display parkinsonism, however, it is interesting to speculate whether, in the absence of the residual subacute poliomyelitis-like syndrome, the neuropathologic findings could have eventually evolved clinically into WNV-associated postencephalitic parkinsonism.

Résumé:

RÉSUMÉ:Contexte:

On peut observer une atteinte neurologique aiguë, parfois sévère et même fatale, chez les patients infectés par le virus du Nil occidental. Il peut s’agir d’une méningite ou d’une encéphalite avec paralysie flasque aiguë ou syndrome ressemblant à une poliomyélite irréversible. Des troubles du movement ont également été rapportés.

Observation:

Nous décrivons le cas d’un patient de 41 ans ayant une histoire d’encéphalomyélite et de paralysie ressemblant à une poliomyélite chez qui nous avons observé une perte neuronale combinée, une gliose et des amas neurofibrillaires dans la substance noire.

Conclusions:

Ce patient n’avait pas de manifestations cliniques de parkinsonisme. Cependant, on peut se demander si, en l’absence du syndrome résiduel subaigu ressemblant à une poliomyélite, cette atteinte neuropathologique aurait pu causer éventuellement un parkinsonisme post-encéphalitique associé au VNO chez ce patient.

Type
Original Articles
Copyright
Copyright © The Canadian Journal of Neurological 2006

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