2015
DOI: 10.1093/tropej/fmv036
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A Combination of Moyamoya Pattern and Cerebral Venous Sinus Thrombosis: A Case of Tubercular Vasculopathy

Abstract: Early vascular involvement affecting both arterial and venous structures has not hitherto been reported in CNS tuberculosis. Early recognition of secondary complications of CNS tuberculosis is crucial to prevent the morbidity and mortality associated with TBM.

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Cited by 11 publications
(7 citation statements)
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“…Moyamoya vasculopathy has been described with basal meningitis due to tubercular meningitis and suprasellar tuberculomas. [ 8 9 ] The extensive vascular network in the circle of Willis makes these arteries susceptible to infection and inflammation. Acute moyamoya phenomenon has been described after acute vascular narrowing due to subarachnoid hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…Moyamoya vasculopathy has been described with basal meningitis due to tubercular meningitis and suprasellar tuberculomas. [ 8 9 ] The extensive vascular network in the circle of Willis makes these arteries susceptible to infection and inflammation. Acute moyamoya phenomenon has been described after acute vascular narrowing due to subarachnoid hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…Moyamoya vasculopathy usually occurs as a late complication in a known case of CNS TB. The presence of multi-territorial ischaemic infarcts, ivy sign (FLAIR hyperintensity and contrast enhancement due to prominence of leptomeningeal collateral vessels) and attenuation of supraclinoid ICA with prominent collateral vessels on angiography point to the diagnosis of moyamoya disease [8]. Vasculitis due to CNS TB, in contrast, affects small-and medium-sized vessels (thalamo-perforating and lenticulostriate arteries) causing lacunar infarcts in ganglio-thalamic regions [9].…”
Section: Tuberculosis With Secondary Moyamoya Vasculopathymentioning
confidence: 99%
“…VWM may be useful for the diagnosis of TBM-related vascular complication and monitoring of the treatment. CSVT in children is treated by anticoagulation with heparin (conventional or low molecular weight) or oral warfarin for 3 months 3. Infarcts in TBM are usually considered secondary to arteriopathy; however venous infarcts, though rare, should be kept in the differentials.…”
Section: Descriptionmentioning
confidence: 99%