Cerebral venous infarct secondary to venous sinus thrombosis

Cranial MRI and MR venography (MRV) studies were performed on a 1.5T MRI scanner, with SE T1-weighted, FSE T2-weighted and FLAIR sequences in the sagittal, axial and coronal planes, and 3D-TOF for MRV. The MRI studies revealed heterogeneous hypointense signal changes on T1-weighted sequences, with mild hyperintense changes secondary to acute phase haemorrhagic components, and heterogeneous mixed signal intensity changes on T2-weighted and FLAIR sequences, representing hypointense acute phase haemorrhagic components (deoxyhaemoglobin state) associated with oedematous-ischaemic hyperintense areas in the left temporal lobe. The haemorrhagic infarct area in the acute phase caused a prominent mass effect, causing effacement of the left sylvian cistern, compression of the left-sided ventricles and neural parenchyma, leading to a subfalcian herniation of the midline structures. The underlying reason was detected as a T1-hyperintense and T2-hypointense acute thrombosis within the left transverse sinus. MRV studies demonstrated an occluded left transverse sinus.

Most commonly thrombosis develops within the dural venous sinuses, and the clot propagates into the cortical veins, leading to the obstruction of cortical venous drainage. Venous pressure increases, and causes breakdown of the brain-blood barrier with vasogenic oedema and haemorrhage. Finally, venous infarct with cytotoxic oedema ensues. The cerebral cortex is oedematous with petechial or gross haemorrhages.

Clinical presentation is variable from mild clinical symptoms to coma and death. Headache, nausea, vomiting, and neurological deficits related to the area of infarct are common findings.

Computed tomography (CT) studies reveal hyperdense dural sinuses and rarely cortical veins, related to the presence of clot within the lumen. Hyperdense petechial haemorrhages and hypodense oedema may be seen in the cortical grey matter and subcortical white matter. The best diagnostic sign is the empty delta sign on contrast-enhanced CT and MRI studies; this is characterised by enhancing dura surrounding a non-enhancing thrombus in the lumen. MRI is more sensitive in the detection of venous sinus occlusion and venous infarcts. Acute clot is usually iso- to mildly hyperintense on T1-weighted and hypointense on T2-weighted images. Venous infarct develops in more than 50% of cases with dural venous sinus thrombosis, characterised by gyral swelling and sulcal effacement. The affected gyri are hypointense on T1-weighted and hyperintense on T2-weighted sequences, however petechial or gross haemorrhages are associated in the cortico-subcortical areas with relevant signal intensity characteristics. MR venography studies show the occlusion of cortical venous sinuses with abnormal collateral channels.