Case 9
Contributors
Dr.Ambika Sunil Gayad,
Dr.Arpita
Diagnosis
Cerebral venous sinus thrombosis with hemorrhagic infarct
Radiological Findings, Disease course and Management
MRI Brain
T1W
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T2W
DWI GRE
FLAIR
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Findings
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Areas of diffusion restriction noted in the right temporal region – suggestive of acute infarct.
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There is evidence of T2 heterogenously hyperintense,T1 iso to hypointense areas which show blooming on gradient sequence suggestive of hemorrhage within the infarct.
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Hemorrhage approximately measures 4.8 x 3.2 x 3.4cm (AP X TR X CC)
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Perihemorrhagic edema is seen causing mass effect on the surrounding brain parenchyma and temporal horn of right lateral ventricle. However, no significant midline shift
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Venous sinuses : Loss of flow voids noted in the sigmoid sinus, transverse sinus and jugular bulb on the right side – suggestive of thrombosis
Diagnosis
Hemorrhagic infarct in the right temporal region, with cerebral venous sinus thrombosis as described above.
Disease course management
Patient was managed conservatively
Follow-up after 2 weeks: Patient improved
​Discussion
Cerebral venous thromboses and infarcts are rare but associated with serious consequences prompt diagnosis and treatment.
Venous thrombosis may be
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spontaneous or
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secondary to trauma, infection or as a complication of surgery.
Risk factors
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Transient states of hypercoagulability from dehydration, oral contraceptives, and pregnancy or
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Permanent hypercoagulability from genetic causes
Cerebral veins are thin, valveless structures that do not contain smooth muscle.
Venous infarcts occur due to obstruction of the venous system by
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thrombus or
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external compression
Rise in venous pressure results in cortical edema and the appearance of vasogenic edema on imaging. As the venous pressure continues to rise, it ultimately leads to cytotoxic edema.
When there is a rapid rise in venous pressure, the friable valveless venous vasculature is unable to withstand the pressure, leading to parenchymal hemorrhage.
Imaging Findings
Hyperdense sinus or T1-hyperintense sinus
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Noncontrast CT: A hyperdense sinus may be the only sign of a thrombosed dural sinus in the absence of venous infarction
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CT or MR venogram: filling defect within the sinus
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MRI of the brain: T1 hyperintense thrombus or
loss of T2 flow void effect within the dural sinus
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Gradient echo sequence: may demonstrate susceptibility hypointensity within the thrombosed venous sinus
Cerebral edema
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Gyral swelling: effacement of the adjacent sulci
Gray-white differentiation relatively preserved frequently accentuated with the presence of vasogenic edema
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Vasogenic edema: T2 hyperintensity of the subcortical and periventricular white matter with sparing of the cerebral cortex.
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Arterial infarct: cytotoxic edema with blurring of the gray and white matter interface from edema
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Diffusion-weighted sequence (DWI):Differentiation of vasogenic and cytotoxic edema in a venous infarction Cytotoxic edema:restricted diffusion
Vasogenic edema:T2 shine through
Hemorrhage
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Location: typically cortical or paramedian not confined to a typical arterial vascular territory
References
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Lu, A., Shen, P. Y., Dahin, B. C., Nidecker, A. E., Nundkumar, A., & Lee, P. S. (n.d.). Cerebral venous thrombosis and infarct: Review of imaging manifestations. Retrieved September 16, 2016, from http://appliedradiology.com/articles/cerebral-venous-thrombosis-and-infarct-review-of-imaging-manifestations