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Thrombotic occlusion of deep cerebral veins
Usually affects both internal cerebral veins (ICVs) ± vein of Galen (VOG), straight sinus (SS)
May occur with more widespread dural sinus thrombosis
NECT
Hyperdense ICV ± VOG, SS
Hypodense thalami/basal ganglia (BG), loss of gray matter-white matter (WM) interfaces
Variable loss of deep gray-white interfaces; thalami seem to “disappear” into background WM hypodensity
± petechial hemorrhages
CECT
Loss of ICV enhancement, presence of enlarged collateral channels
“Shaggy,” irregular veins (collateral channels) in deep WM, around tentorium
MR
Acute clots hypointense on T2WI, “bloom” on T2*
Deep (medullary) WM veins prominent, tortuous on SWI
Protocol advice
If CT/CECT/CTV scans negative → MR with MRV
If MRV equivocal → DSA
Other bithalamic/basal ganglia lesions
Neoplasm (e.g., bithalamic astrocytoma)
Nonvenous ischemia (e.g., artery of Percheron infarct)
Toxic/metabolic disorders (e.g., CO poisoning)
Venous thrombosis = 1-2% of strokes; ICV thrombosis = 10% of venous “strokes”
Can present with headaches and coma
Deep cerebral venous thrombosis (DCVT)
Internal cerebral vein (ICV) thrombosis
Thrombotic occlusion of deep cerebral veins
Usually affects both ICVs ± vein of Galen (VOG), straight sinus (SS)
Often with widespread dural sinus thrombosis (DST)
Best diagnostic clue
Hyperdense ICV ± VOG, SS ± bithalamic hypodensity
Loss of deep gray-white matter interfaces
Thalami seem to “disappear” into background WM hypodensity
Location
ICV ± VOG, SS, basal veins of Rosenthal
Bilateral ICV thrombosis > > unilateral
Edema (venous congestion)
Deep gray nuclei, internal capsule, medullary white matter (WM)
Variable involvement of midbrain, upper cerebellum
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