Findings
Head CT: Focal edema at the left temporooccipital junction.
CTA Head: Venous sinus thrombosis in the left transverse sinus.
Brain MRI: Moderate sized area of subcortical and cortical T2 prolongation at the left temporo-occipital junction, with evidence of blood product. No restricted diffusion. CTA Head: Venous sinus thrombosis in the left transverse sinus.
Differential diagnosis
- Venous thrombosis with hemorrhagic infarction
- Spontaneous intraparenchymal hemorrhage
- Low grade glioma
- AVM with hemorrhage
- Low grade late cerebritis
Diagnosis: Left transverse sinus and superficial cortical vein thrombosis with hemorrhagic subcortical brain infarction
Discussion
Occlusive venous disease is an important cause of cerebral ischemia and infarction and also intracranial hemorrhage. One readily thinks about arterial occlusion in the setting of ischemia and infarction, but venous occlusion is often forgotten and therefore can potentially go unrecognized. Additionally, venous occlusion can be a forgotten cause of intracranial hemorrhage. The identification of venous occlusive disease with or without associated hemorrhage is crucial because its treatment is considerably different than other etiologies of stroke and intracranial hemorrhage.
Venous thrombosis may occur in any or all of the following venous structures: the venous sinuses, superficial cortical veins, or the deep venous system. Typically, superficial cortical vein thrombosis is only seen in the seen in the setting of venous sinus thrombosis, and thrombosis of the deep venous system is relatively rare (albeit very serious). Approximately 1% of all strokes occur secondary to venous sinus thrombosis, and the most frequently thrombosed sinuses are the superior sagittal sinus, followed by the transverse, sigmoid and cavernous sinuses. There are numerous conditions associated with venous sinus thromboses and broadly speaking, these tend to be divided into septic or non-septic etiologies. One fourth of cases are of unknown cause. It is common for hemorrhage to be present within areas of venous infarction, whereas it is relatively uncommon to occur with arterial occlusion and infarction. In general, hemorrhagic cerebral infarctions are classified as primary or secondary with primary denoting those hemorrhages associated with intrinsic abnormalities of the blood vessel itself (elevated pressure, malformation, aneurysm, fistula, neoplasm) versus hemorrhages secondary to an ischemic event, or so-called hemorrhagic transformation. Suffice it here to say that venous occlusion and infarction is an important differential consideration in cases of intracranial hemorrhage. The treatment for venous occlusive disease and infarction is anticoagulation, even in the setting of hemorrhagic transformation, which is why the correct diagnosis is crucial to ensuring proper treatment. Clinical symptoms of venous thrombosis and infarction are variable and non-specific, even further highlighting the importance of the role of imaging in making the correct diagnosis.
Dural sinus thrombosis can be recognized on imaging as a hyperdense triangular density in the sinus on non contrasted head CT or as a filling defect in the sinus on contrasted studies (the "empty delta" sign in the sagittal sinus). On MR, acute venous sinus thrombosis can be isointense to brain on T1, making it subtle, but it is typically considerably brighter than a normal flow void. Potential pitfalls to consider include hypoplastic sinuses, normal flow void on MR, and arachnoid granulations. Cortical venous thrombosis can be demonstrated on non contrasted head CT as a hyperdense linear density over the cortical surface (the "cord sign"). Non contrasted head CT tends to be the initial imaging modality ordered, but MRI/MRV, CT angiography, or catheter angiography are the tests of choice for confirming the diagnosis.
Venous infarcts can be difficult to diagnose on imaging, but several features are important to keep in mind. The distribution of venous infarction is considerably different from arterial infarction. Venous infarctions tend to occur in subcortical locations, affecting white matter, as opposed to cortex. Therefore venous infarction should be considered when a non-arterial vascular territory has infracted, when an infarct is subcortical, and when no arterial thrombus (or if a venous thrombus) is identified. Venous infarcts may or may not have associated restricted diffusion and can have associated contrast enhancement. The differential diagnosis for venous infarcts also includes low grade glioma, encephalitis and late cerebritis.
