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|Year : 2021 | Volume
| 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 Submission||08-Feb-2018|
|Date of Decision||09-May-2018|
|Date of Acceptance||08-Nov-2019|
|Date of Web Publication||23-Dec-2021|
Derince Education and Research Hospital, Pediatric Neurology, Kocaeli
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kilic B. Cerebral Venous Sinus Thrombosis: Its Association with Primary Varicella-Zoster Virus Infection. Neurol India 2021;69:1898
Varicella-zoster virus (VZV) infection is a frequently seen disease of childhood with a 1% risk of developing complications. 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.,
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