2020
DOI: 10.1016/j.radcr.2020.05.009
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Cerebral venous thrombosis: report of 2 cases of hemorrhagic venous infarction

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Cited by 5 publications
(6 citation statements)
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“…22 Guidelines in human medicine for diagnosing venous infarction include: infarction not conforming to a major arterial vascular territory, crossing the typical arterial boundaries, or extending over more than one arterial distribution; presence of multiple isolated lesions; involvement of subcortical regions with sparing of the cortex, or cortical-subcortical topography; often hemorrhagic component; proximity to a venous sinus. [24][25][26][27][28] The retrograde venous pressure caused by thrombosis severely reduces the cerebral blood flow through a vicious cycle of increased intracranial pressure, blood-brain barrier disruption with edema and hemorrhage, and reduced CSF drainage, leading to neuroparenchymal ischemia and necrosis. 23,26,29,30 The restricted diffusion in acute venous thrombosis suggests that cytotoxic edema is mainly responsible for the MRI changes, and that vasogenic edema follows but is not the primary pathological event.…”
Section: Discussionmentioning
confidence: 99%
“…22 Guidelines in human medicine for diagnosing venous infarction include: infarction not conforming to a major arterial vascular territory, crossing the typical arterial boundaries, or extending over more than one arterial distribution; presence of multiple isolated lesions; involvement of subcortical regions with sparing of the cortex, or cortical-subcortical topography; often hemorrhagic component; proximity to a venous sinus. [24][25][26][27][28] The retrograde venous pressure caused by thrombosis severely reduces the cerebral blood flow through a vicious cycle of increased intracranial pressure, blood-brain barrier disruption with edema and hemorrhage, and reduced CSF drainage, leading to neuroparenchymal ischemia and necrosis. 23,26,29,30 The restricted diffusion in acute venous thrombosis suggests that cytotoxic edema is mainly responsible for the MRI changes, and that vasogenic edema follows but is not the primary pathological event.…”
Section: Discussionmentioning
confidence: 99%
“…Neck pain and stiffness was reported in CVTinduced hemorrhagic venous infarction and acute subarachnoid hemorrhage. [30][31][32] In the CVT severity scale, neck discomfort was added as item 18.…”
Section: Discussionmentioning
confidence: 99%
“…CVST results in venous hypertension and the resultant cerebral edema can cause a range of symptoms such as nausea, vomiting, headache, seizures, and focal neurologic deficits [4,5,9]. These symptoms are highly non-specific and are usually attributed to the underlying brain tumor; this is the reason why many reports estimated an approximate 7-day delay between the onset of symptoms and the diagnosis [9]. CVST can potentially lead to serious complications.…”
Section: Discussionmentioning
confidence: 99%
“…CVST can potentially lead to serious complications. About 50% of patients with CVST develop infarction and/or hemorrhage [9]. The underlying venous hypertension was thought to be the main driver causing reduced effective drainage of affected brain tissue resulting in venous congestion with subsequent oxygen debt and eventual infarction.…”
Section: Discussionmentioning
confidence: 99%