Vein of Trolard thrombosis with venous infarction (CT perfusion)

Case contributed by Craig Hacking
Diagnosis certain


Dysphasia, dysarthria, right upper limb paresthesia and reduced power. 5 days post partum. ?CVA

Patient Data

Age: 30 years
Gender: Female

No intra- or extra-axial hemorrhage. No space-occupying lesion, mass effect or midline shift evident. The ventricles and CSF spaces appear normal. 

Subtle hypodensity and loss of grey-white matter differentiation in the left precentral and postcentral gyri. There is a prominent hyperdense cortical vein (dense vein sign) in the region representing the superior anastomotic vein (of Trolard). No dense artery sign.

No evidence of dissection or thrombus within the carotid arteries or vertebrobasilar system. Normal appearance of the circle of Willis. No aneurysm identified. Fenestrated right A2 origin.

The previously identified cortical vein (vein of Trolard) within the left frontoparietal region demonstrates no contrast enhancement in keeping with thrombosis. Normal contrast enhancement within the dural venous sinuses and internal cerebral veins.

A wedge-shaped focus of abnormal perfusion is seen within the left frontoparietal area at the vertex with decreased cerebral blood flow (CBF), increased mean transit time (MTT) and time to drain, and increased cerebral blood volume (CBV). This in keeping with a penumbra.

Cortically based gyriform restricted diffusion within the left parietal lobe (postcentral gyrus), corresponding to the perfusion abnormalities demonstrated on the CT and in keeping with acute infarction. Associated increased T2/FLAIR signal within the affected swollen gyri. An enlarged left superficial cortical vein (the vein of Trolard) shows susceptibility-weighted abnormality representing thrombosis.

Increased FLAIR signal within some parietal and frontal sulci just anterior to the infarct with associated susceptibility weighted artifact, in keeping with a small volume acute sulcal subarachnoid hemorrhage.

No further foci of abnormal restricted diffusion. Otherwise normal signal intensity of the neuroparenchyma. Neuroparenchymal volume is preserved. The ventricular system is within normal limits for age.


Acute infarct within the cortex of the left parietal lobe secondary to thrombosis of the vein of Trolard. Small volume of adjacent acute sulcal subarachnoid hemorrhage but no intraparenchymal hemorrhage.

Case Discussion

This case nicely demonstrates the vascular territory of the superior anastomotic vein (of Trolard) and the typical CT and MRI features of cortical venous thrombosis and infarction.

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