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|LETTER TO EDITOR
|Year : 2012 | Volume
| Issue : 6 | Page : 645-646
Cerebral sinus venous thrombosis: A rare complication of primary Varicella zoster virus
Sujay Sada, Anjaneyulu Kammineni, Meena A Kanikannan, Jabeen Afshan
Department of Neurology, Nizams Institute of Medical Sciences, NIMS, Hyderabad, India
|Date of Web Publication||29-Dec-2012|
Department of Neurology, Nizams Institute of Medical Sciences, NIMS, Hyderabad
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sada S, Kammineni A, Kanikannan MA, Afshan J. Cerebral sinus venous thrombosis: A rare complication of primary Varicella zoster virus. Neurol India 2012;60:645-6
|How to cite this URL:|
Sada S, Kammineni A, Kanikannan MA, Afshan J. Cerebral sinus venous thrombosis: A rare complication of primary Varicella zoster virus. Neurol India [serial online] 2012 [cited 2019 Dec 16];60:645-6. Available from: http://www.neurologyindia.com/text.asp?2012/60/6/645/105204
Varicella zoster virus (VZV) cause chicken pox (varicella) after which it establishes latency and can subsequently reactivate to cause herpes zoster. Central nervous system (CNS) complications can follow both primary infection and reactivation of VZV. VZV infection can cause unifocal or multifocal vasculopathy and arterial strokes. Varicella causing venous stroke is very rare, only one case had been reported  and hence this report.
A 30-year-old gentleman with history of chicken pox 15 days back presented with continuous holocranial nonthrobbing headache and nonprojectile vomiting of 2 days duration. Otherwise history was unremarkable. General physical examination revealed healed chicken pox lesions [Figure 1]a and b and normal vital parameters. Neurological examination was normal except for bilateral papilledema. Hemogram and blood biochemistry was normal. Serology for human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg), vasculitis, connective tissue disorders was negative and antistreptolysin O (ASO) titer was not elevated significantly. Antiphospholipid antibodies and sickling were negative. Protein C, protein S, antithrombin III, homocysteine levels were normal. Varicella-specific immunoglobulin G (IgG) was positive in the cerebrospinal fluid (CSF) and blood with reduced serum/CSF ratios of VZV IgG. Chest X-ray and 2D Echo were normal. Computed tomography (CT) brain showed diffuse cerebral edema and hyper dense superior sagittal and right transverse sinuses. Magnetic resonance venogram (MRV) showed thrombosis of superior sagittal and right transverse sinuses [Figure 1]c and d. Patient improved completely with intravenous heparin and oral anticoagulants.
|Figure 1: (a,b) showing healed varicella lesions with scars (c,d) showing MR-venography showing non visualization of superior sagittal and right transverse sinuses|
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Primary VZV infection with delayed-onset hemiparesis typically occurs approximately 6 weeks after primary infection due to vascular thrombosis. Unifocal large-vessel vasculopathy (granulomatous arteritis) usually affects elderly immunocompetent persons, whereas multifocal vasculopathy occurs primarily in persons who are immunocompromised.  Unifocal large-vessel infarcts may follow zoster in a trigeminal distribution and are presumed to result from transaxonal transport of virus from trigeminal afferent fibers that innervate vessels of the anterior circulation.  Similarly, smaller infarcts in deep white and gray matter may reflect transport of VZV from trigeminal or cervical afferent fibers to smaller branches of vessels of the posterior circulation. , Venous thrombosis following chicken pox is very rare  the causal association in this particular case was evidenced by positive varicella antibodies in serum and CSF. VZV vasculopathy patients do not always have VZV DNA in CSF, but diagnosis can be confirmed by anti-VZV antibody in CSF, along with reduced serum/CSF ratios of VZV IgG compared with albumin or total IgG.  The exact pathogenesis of varicella venous thrombosis is not known but similar to VZV arteriopathy, activated varicella may migrate transaxonally to infect meninges and venous sinuses of brain. The mechanisms underlying cerebral vascular events after VZV infection could be vasculitis, thrombosis due to direct endothelial damage, and acquired protein S deficiency. , Our patient developed thrombosis during primary varicella infection and not as a delayed complication. He had no other risk factors for cerebral venous thrombosis. The same pathogenic mechanisms underlying arteriopathy may play a role in the development of cerebral sinus venous thrombosis. The rarity of this entity and the lack of controlled clinical trials in children for the therapy of thromboembolic disease have thus far prevented the development of adequate antithrombotic and anticoagulant therapy protocols for pediatric stroke, VZV-associated stroke inclusive. These patients require antiviral treatment and symptomatic treatment, with IV heparin and oral anticoagulants.
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