Review Article
Central Nervous System Vasculopathy In Varicella Zoster Virus Infection
Tapan Mehta*, Ninad Desai and Dimitre MirtchevUniversity of Connecticut Health Center/Hartford Hospital, USA
- *Corresponding Author:
- Tapan Mehta
Chief Resident of Department of Neurology
University of Connecticut Health Center/Hartford Hospital, USA
Tel: +12672370972
E-mail: stapanmehta14@gmail.com
Received date: May 27, 2017; Accepted date: June 15, 2017; Published date: June 17, 2017
Citation: Mehta T, Desai N, Mirtchev D (2017) Central Nervous System Vasculopathy In Varicella Zoster Virus Infection. J Neuroinfect Dis 8:253. doi:10.4172/2314-7326.1000253
Copyright: © 2017 Mehta T, et al. This is an open-access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Abstract
Varicella zoster virus is an exclusively human double-stranded DNA virus that is the causative factor for two ubiquitous conditions: varicella in children and zoster in adults. Both conditions are associated with complications. Centripetal trans-axonal spread via cranial nerve ganglia appears to afford entry into the central nervous system. There is increasing evidence of varicella zoster virus playing a role in the development of giant cell arteritis. First associated with transient ischemic attacks and ischemic strokes, vasculopathy secondary to varicella zoster virus infections has now been associated with aneurysms that may or may not lead to subarachnoid hemorrhage, multifocal vasculitis, arterial dissection, dolicoectasia, cortical venous sinus thrombosis, ischemic cranial neuropathies and spinal cord infarction. Prior knowledge of the myriad clinical manifestations helps in early diagnosis and treatment of the complications.
