Hyperacute Transcapillary Stroke - MR T1-w sequences
Hyperacute Transcapillary Stroke - MR T1-w sequences
Search Pattern Assist ?History
Exam
Purpose
2 Assess the noncontrast T1-w MR for hyper or isointense thrombus in one or more intracranial (stem, trunk, division, perforator, pial, choroidal, or subcortical penetrating) arteries.
3 Assess the noncontrast T1-w MR for hyperintense thrombus in one or more dural sinuses (sagittal, torcula, transverse, sigmoid, straight "delta sign").
4 Assess the noncontrast T1-w MR for hyper or isointense thrombus in one or more pial, deep central, or deep medullary veins (cord sign).
5 Assess the noncontrast T1-w MR for sequestered infarction, especially laminar necrosis.
6 Assess the noncontrast T1-w MR for centronuclear hyperdensity (usually bilateral) indicating chronic post ischemic injury.
7 Assess noncontrast T1 MR for venous congestion within the expanded medullary veins due to distal venous egress block.
8 Assess the post contrast T1-w MR for for reduced parenchymal contrast intensity in any oligemic site.
9 Assess the post contrast T1 for intraluminal thrombus in one or more major arteries, or of one or more pial veins or dural sinuses to confirm either an arterial or venous stroke.
10 Assess the post-contrast T1 for evidence of re-routed pial venous collateral and larger vein egress re-routing. (i.e. filling into measial or lateral tentorial confluences, the vertex venous confluence, the superior sylvian vein to sphenoparietal sinus to the cavernous sinus pathway, the orbital veins, the posterior fossa egress veins).
11 Assess the post contrast T1 for evidence of inflammatory enhancement along small distal arteries, especially subcortical or deep central terminal arteries within the Virchow-Robin spaces, or along the perforating arteries within Virchow-Robin spaces. These are features of an inflammatory CNS angiitis.
12 Assess the post-contrast T1 for post ischemic contrast leak, indicating dysautoregulation (post oligemic loss of blood brain barrier including PRES).
13 Assess for evidence of raised intracranial pressure, which includes evidence of brain swelling from venous congestion, optic hydrops/retroglobal edema, early hydrocephalus, effaced sulci, pseudotumor cerebri, or possibly PRES with early mass effects with herniation.
14 Assess for nasopharyngeal/retropharyngeal infection/tumor with skull base extension and possible dural or cavernous sinus thrombosis.
15 Assess for evidence of raised intracranial pressure, which includes evidence of brain swelling from venous congestion, optic hydrops/retroglobal edema, early hydrocephalus, effaced sulci, pseudotumor cerebri, or possibly PRES with early mass effects with herniation.
Prior Study
Findings
MR T1-w sequence noncontrast
There is evidence of acute parenchymal cytogenic edema or post ischemic leukomalacia matching any arterial afferent perfusion zone, any watershed zone, nor any efferent venous egress zone. [Yes/No]
There is evidence of hyperintense, acute, intraluminal arterial thrombosis in a major stem, trunk, division or pial artery perfusion zone. [Yes/No]
There is evidence of hyperintense, acute, intraluminal arterial thrombosis in a recognizable perforator, choroidal, or deep subcortical penetrating artery/arteries. [Yes/No]
There is evidence of hypo or hyperintensity within the deep medullary veins, or the deep venous system to suggest congestion, stasis, thrombosis, or increased (high flow) medullary venous hyperemia. [Yes/No]
There is hyperintensity within the cortical ribbon consistent with sequestered infarction (laminar necrosis). [Yes/No]
There is hyperintensity within the centronuclear structures consistent with chronic low grade ischemic changes. [Yes/No]
There is enlargment of the Virchow-Robin spaces surrounding either the perforating arteries or the penetrating arteries. [Yes/No]
There is luminal abnormal isointensity (lack of flow void) or hyperintensity within one or more dural sinuses (delta sign) indicative of acute thrombus on the noncontrast T1. [Yes/No]
There is evidence of hyper or isointensity within one or more cortical or central veins on noncontrast T1. [Yes/No]
There is evidence of dilatation of the intraorbital veins, and optic hydrops (dilated CSF space around the optic nerves) on pre or post contrast T1 MR. [Yes/No]
There is evidence of abnormal ventriculomegaly consistent with early hydrocephalus, pseudotumor, or PRES. [Yes/No]
MR T1-w sequence post contrast
There is reduced or absent post contrast signal intensity within brain parenchyma (cortical ribbon and/or subcortcial white matter) consistent with low or absent transcapillary perfusion. [Yes/No]
There is hyperemic pial circulation without contrast leak consistent with collateral pial drainage. [Yes/No]
There is hyperemic perforator arterial circulation and deep medullary venous egress consistent with moyamoya vasculopathy. [Yes/No]
There is hyperemic pial circulation with contrast leak consistent with dysautoregulation. [Yes/No]
There is evidence of dural sinus filling defect (empty delta sign) indicating thrombosis within one or more dural sinuses on the post contrast T1. [Yes/No]
There is evidence of pial venous collateral veins (typically appear serpiginous, enlarged size, draining the reversed directiong, with the size changed from being larger next to the dural sinus to being larger at there inception site on the post constrast T1 MR). [Yes/No]
There is prominence of any of the pial/dural anastomotic sites (i.e. vertex venous lacunae, tenorial confluences, or cavernous sinus/retropharyngeal venous plexus) on the post contrast T1-w sequence. [Yes/No]
There is evidence of mural enhancement or actual luminal filling defect within a cortical or central vein indicating acute thrombus on post contrast T1. [Yes/No]
There is evidence of mural enhancement or intraluminal filling defect indicating thrombosis in an ophthalmic vein on post contrast T1. [Yes/No]
There is evidence of dural sinus filling defect indicating thrombosis within the cavernous sinus and either its afferent input or efferent egress veins on the post contrast T1. [Yes/No]
There is contrast enhancement (contrast leak) which follows the parenchymal Virchow-Robin spaces surrounding the small metarterioles consistent with angiitis. This may create a patterns suggesting small nodule when viewed in axial plane. [Yes/No]
There is evidence of unexpected regional cortical vein enlargement (arterialization of otherwise NL veins), consistent with the combination of a dural AV fistula plus dural sinus stenosis/thrombosis on post contrast T1. [Yes/No]
There is evidence of skull base destruction (infection/tumor) leading to cavernous or dural sinus thrombosis. [Yes/No]
There is evidence of hemorrhagic conversion. [Yes/No]
Other
No other findings abnormalities are noted. [Yes/No]
