Cerebral venous thrombosis as a complication of chicken pox


Chickenpox is one of the classic childhood disease. It is usually a benign self limiting exanthematous illness. Recently chicken pox has been reported in adults with more severe systemic and neurological complications. Cerebral venous thrombosis (CVT) is a life threatening disorder if not treated in time. We report a patient with post varicella CVT which has not been previously reported.

Keywords: Chickenpox, cerebral venous thrombosis, varicella

How to cite this article:
Menon B, Goyal R. Cerebral venous thrombosis as a complication of chicken pox. Ann Trop Med Public Health 2012;5:520-2
How to cite this URL:
Menon B, Goyal R. Cerebral venous thrombosis as a complication of chicken pox. Ann Trop Med Public Health [serial online] 2012 [cited 2020 Dec 5];5:520-2. Available from: https://www.atmph.org/text.asp?2012/5/5/520/105151

Chickenpox (Varicella) is a benign illness caused by varicella-zoster virus, predominant in childhood. Chicken pox related neurological complications are seen in less than 1% cases of chickenpox. [1] The illness presents with fever and characteristic exanthematous vesicular skin rash. [2] Though it is a self limiting disease, occasionally serious complications can occur. Neurological complications frequently encountered are cerebellar ataxia and encephalitis. Less frequent complications are Guillian-Barré syndrome, menin­goencephalitis, transverse myelitis, aseptic meningitis, ventriculitis, optic neuritis, post-hepatic neuralgia, herpes zoster ophthalmicus and peripheral motor neuropathy. [3] Recent reports have shown similar complications in adults. We report a case of chickenpox with cerebral venous thrombosis previously unreported in an adult with good recovery.

Case Report

33-year-old man was brought to the emergency service with severe headache and irrelevant speech. The illness started with profuse rash predominantly on the trunk and limbs and to a less degree on the face twoweeks back. The lesions were centripetal and were diagnosed to be chicken pox. The lesions were in crusting stage when the patient developed neurological complaints. His symptoms started with sudden onset holocranial headache which was associated with vomiting. Patient gradually developed altered sensorium. There was no history of seizures. Past history was not significant. When patient came to the emergency he was conscious and appeared confused. Skin lesions were in the scab stage. He had nuchal rigidity on neurological examination. Pupils were bilateral equal reacting to light. Fundus was normal. He had fluent aphasia characterized by increased verbal output, word-finding disturbances and phonemic paraphasias in both oral and written language. Right hemianopia and spatial neglect were found on confrontation testing. Motor examination showed minimal right hemiparesis. Patient was diagnosed to have wernickes aphasia in the setting of post varicella infection. His routine investigations including full blood count, blood sugar, renal, liver function tests, electrolytes and blood culture was normal. A plain Computerized tomography scan showed a haemorrhagic infarct in the left temporal lobe with edema and mass effect over the ipsilateral lateral ventricle [Figure 1]. A possibility of venous sinus thrombosis was considered and a Magnetic resonance Venography with gadolinium was done. It showed haemorrhagic infarct with significant perilesionalo edema and adjacent meningeal enhancement in left temporo parietal and occipital lobes with mass effect [Figure 2]. Venography showed loss of normal signal intensity in transverse sinus, sigmoid sinus and straight sinus on left side [Figure 3]. Cerebrospinal fluid examination showed pleocytosis with 40 cells/mm 3 , mildly raised protein 60 mg%, and normal glucose.

Figure 1: Pain CT scan of the head showing a haemorrhagic infarct in the left temporal lobe with edema and mass effect over the ipsilateral lateral ventricle

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Figure 2: MRI of the brain showing haemorrhagic infarct in the left temporo parietal & occipital lobes with significant perilesionaloedema and mass effect

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Figure 3: MRV of the brain showed loss of normal signal intensity in transverse sinus, sigmoid sinus and straight sinus on left side

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Patient was started on antiedema measures consisting of intravenous 20% mannitol and dexamethasone. Low molecular weight heparin was started. Patient started gradually improving. Headache improved and language functions improved gradually over next few days. Patient was discharged on oral anticoagulants with monitoring of coagulation parameters. His thrombophilic and vasculitic workup was negative. His medications were stopped after six months. He is asymptomatic on follow after one year.


Varicella is highly contagious disease of childhood with increasing incidence in adults. [4] As seen in studies, Varicella involves any organ due to the systemic nature of the disease. Disease severity has been shown to be more severe in adults [5] with increase in hospital mortality. [6] Common chicken pox related neurological complications are cerebellar ataxia and encephalitis. [7] However several rare complications related to central nerve system involvement have been reported like aseptic meningitis, Guillian-Barré syndrome, and transverse myelitis. [8] Our patient had post Varicella infective CVT. Several factors predispose to CVT which include infective and non infective causes. In endemic countries infective causes with tuberculosis leading to CVT has been reported. [9] CVT can be caused by a wide range of etiologies. The vasculitic and thrombothilic work was normal which ruled out other etiological possibilities. In our patient, the CSF result suggested an infective etiology. Cerebral venous thrombosis after chicken pox infection has not been reported previously. A mesh data base search with key words, chicken pox, Cerebral venous thrombosis, intracranial sinus thrombosis did not reveal any results. In conclusion, our case demonstrates that a rapid diagnosis of CVT was essential for the proper management of the patient. With this case we wish to add to the literature, CVT as another neurological complication after varicella infection. Being aware of CVT as another neurological complication will assist the emergency physician in proper management.

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3. Gnann JW. Varicella-Zoster virus:Atypical presentations and unusual complications. J Infect Dis 2002;186:91-8.
4. Wilkens EG, Leen CL, Mc Kendrick MW, Carrington D. Management of chickenpox in adults. J Infect 1998;1:49-8.
5. Jones AM, Thomas N, Wilkins EG. Outcome of varicella pneumonitis in immunocompetent adults requiring treatment in a high dependency unit. J Infect 2001;43:135-9.
6. Rawson H, Crampian A, Noah N. Deaths from chickenpox in England and Wales 1995-7: Analysis of routine mortality data. BMJ 2001;323:1091-3.
7. Johnson RT. Viral infections of the nervous system. New York: Raven Press;1982.
8. Caheid Y, Husein C. Severe neurological complications of chickenpox: Report of four cases. Eur J Gen Med 2005;2:177-9.
9. FiorotJúnior JA, Felício AC, Fukujima MM, Rodrigues CA, Morelli VM, Lourenço DM, et al. Tuberculosis: An uncommon cause of cerebral venous thrombosis? Arq Neuropsiquiatr 2005;63:852-4.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.105151


[Figure 1], [Figure 2], [Figure 3]

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