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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 6  |  Page : 1898

Cerebral Venous Sinus Thrombosis: Its Association with Primary Varicella-Zoster Virus Infection

Derince Education and Research Hospital, Pediatric Neurology, Kocaeli, Turkey

Date of Submission08-Feb-2018
Date of Decision09-May-2018
Date of Acceptance08-Nov-2019
Date of Web Publication23-Dec-2021

Correspondence Address:
Betul Kilic
Derince Education and Research Hospital, Pediatric Neurology, Kocaeli
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.333447

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How to cite this article:
Kilic B. Cerebral Venous Sinus Thrombosis: Its Association with Primary Varicella-Zoster Virus Infection. Neurol India 2021;69:1898

How to cite this URL:
Kilic B. Cerebral Venous Sinus Thrombosis: Its Association with Primary Varicella-Zoster Virus Infection. Neurol India [serial online] 2021 [cited 2022 Jan 19];69:1898. Available from:

Varicella-zoster virus (VZV) infection is a frequently seen disease of childhood with a 1% risk of developing complications.[1] A 7-year-old boy who was healthy before presented with cough, fever, continuous holocranial nonthrobbing headache, and nonprojectile vomiting. He had vesicular rash on the trunk, inspiratory crackles throughout all lung fields, and bilateral papilledema.

The count of complete blood, liver function tests, and cerebrospinal fluid (CSF) analysis were in normal limits. CSF pressure was high (400 mm Hg). Polymerase chain reaction (PCR) studies for VZV was positive in the CSF. Magnetic resonance venogram revealed thrombosis of right transverse sinus [Figure 1]a and [Figure 1]b. There was no evidence of thrombosis in terms of biochemical, hematological, genetic, or immunological causes.
Figure 1: (a) Sagittal source image from contrast-enhanced magnetic resonance (MR) venography shows filling defects due to a thrombus of right transverse sinus (b) axial T2-weighted MR images show an area of abnormal increased signal intensity in the right transverse sinus

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The patient was started on intravenous acyclovir, oral diazomide, and subcutaneous low molecular weight heparin (LMWH). He showed good improvement and was asymptomatic within five days. LMWH treatment continued for seven days and oral warfarin was added. Anticoagulation treatment was continued for three months with an significant course of recovery.

VZV infection after venous thrombosis is very uncommon but potentially a severe complication of varicella. Specific pathogenesis of venous thrombosis remains unclear, in a comparable way to VZV arteriopathy, activated varicella can migrate across axons to cause meninges and brain venous sinuses infection. acquired protein C and protein S deficiency secondary to varicella infection can cause thrombosis or cerebral vascular demage.[2],[3]

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  References Top

Padmakumar B, Sun J, Satchithananthan G, Sills JA, Alwaidh MA. Deep venous thrombosis and pulmonary embolism following chickenpox. Ann Trop Pediatr 2004;24:271-4.  Back to cited text no. 1
Nagel MA, Traktinskiy I, Azarkh Y, Kleinschmidt-DeMasters B, Hedley-Whyte T, Russman A, et al. Varicella zoster virüs vasculopathy: Analysis of virus-infected arteries. Neurology 2011;77:364-70.  Back to cited text no. 2
Nguyên P, Reynaud J, Pouzol P, Munzer M, Richard O, François P. Varicella and thrombotic complications associated with transient protein C and protein S deficiencies in children. Eur J Pediatr 1994;153:646-9.  Back to cited text no. 3


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