Cerebral venous thrombosis and infarct: Review of imaging manifestations

Findings of cerebral venous thrombosis can be subtle on imaging. When the clinical presentation is non-specific, a noncontrast CT is usually the first imaging exam performed. A hyperdense sinus may be the only sign of a thrombosed dural sinus in the absence of venous infarction (Figure 1A). In cases where a hyperdense sinus is suspected, a CT or MR venogram is performed which demonstrates a filling defect within the sinus in question (Figure 1B). When MRI of the brain is the initial exam, a T1 hyperintense thrombus or loss of T2 flow void effect may be found within the dural sinus (Figure 2). The gradient echo sequence may demonstrate susceptibility hypointensity within the thrombosed venous sinus (Figure 2C). However, the hyperdense sinus sign has a wide range in reported sensitivity of 25-64%,⁶ and is not consistently reliable due to variability of sinus attenuation.¹ The vertex and posterior fossa are locations where the superior sagittal, transverse and sigmoid sinuses reside, but are frequently obscured from beam hardening on noncontrast CT, contributing to the decreased reliability of the hyperdense sinus sign. Also, the offending vein is not always identified when small cortical veins are involved, presumably from recanalization after the subsequent insult by hemorrhage or infarct occurs.

Sometimes, only secondary signs of cortical swelling and infarct are apparent on noncontrast CT, raising the question of venous thrombosis. The earliest sign of venous infarct is gyral swelling, which is often extremely subtle and only appreciable by noticing the effacement of the adjacent sulci (Figure 3). Gray-white differentiation will be relatively preserved and frequently accentuated with the presence of vasogenic edema (Figure 4) mimicking an underlying mass. In contrast, arterial infarct presents with cytotoxic edema with blurring of the gray and white matter interface from edema distal from the point of occlusion (Figure 5). Vasogenic edema is best identified on T2 or T2 FLAIR-weighted sequences, which presents as T2 hyperintensity of the subcortical and periventricular white matter with sparing of the cerebral cortex. Differentiation of vasogenic and cytotoxic edema within a venous infarction, which can be present concurrently, is made with diffusion-weighted sequence (DWI), with restricted diffusion representing cytotoxic edema and T2 shine through representing vasogenic edema.

Venous infarcts can sometimes present with parenchymal hemorrhage and is estimated to occur in 30-40 % of patients with cerebral venous thrombosis.⁷ Hemorrhage is typically cortical or paramedian in location and not confined to a typical arterial vascular territory (Figures 6-8). In Figure 6, there is right temporal lobe cortical hemorrhage from a thrombosed inferior anastomotic vein (vein of Labbé), while in Figure 9 there is hematoma of the left occipital lobe from cortical vein thrombus. Diagnosis is sometimes hindered when the clinical history is obscured by trauma which may happen subsequent to the neurologic deficit as a result of the venous infarct and hemorrhage.

Noncontrast CT head and the T2* weighted MRI sequence are used to identify intraparenchymal hemorrhage with the greatest sensitivity.

History is critical to prompt diagnosis and essential to avoid misinterpretation. Figure 3 demonstrates a case of a young woman in her first trimester of pregnancy presenting with seizure. There was a high clinical suspicion for venous thrombosis because of the early gestational age of her pregnancy and her transient state of hypercoagulability. Left paramedian gyral swelling and a hyperdense superior sagittal sinus from thrombosis and subsequent venous cortical edema and infarct was the most reasonable diagnostic possibility. However, without the proper history, the imaging findings on this noncontrast CT are much more nonspecific, and can include encephalitis or post-ictal cerebral edema. Imaging findings of venous infarct can be extremely complex with concomitant findings of hyperdense vein or venous sinus, vasogenic edema and hemorrhage (Figure 9). Common competing differential possibilities are trauma, tumor and infection.

Trauma is the most common cause of parenchymal hemorrhage and may be a source of diagnostic confusion (Figure 10). However, traumatic hemorrhage usually occurs in typical locations such as the orbital frontal gyrus and temporal poles because of their relationship along the anterior and middle skull base and susceptibility to the greatest shearing forces. But parenchymal hemorrhage can occur anywhere at the impact, “coup” site with typical “contrecoup” hemorrhage occurring directly opposite. Figure 10 shows contrecoup parenchymal hemorrhage of the left orbital frontal gyrus and right temporal lobe with left frontal epidural hematoma (blood window). Direct (coup) impact the left temporal and occipital scalp result in temporal bone fracture and pneumocephalus.

Herpes encephalitis typically involves the temporal lobes with areas of hemorrhage. However, temporal lobe involvement is usually bilateral but asymmetric and the regions of hemorrhage are typically petechial, as demonstrated in Figure 11.

Infiltrating gliomas may sometimes mimic vasogenic edema.In Figure 12, there is an infiltrating tumor of the left temporal lobe, which is isointense to gray matter on T2, whereas the areas of vasogenic edema surrounding the tumor have increased T2 signal intensity.

Prompt diagnosis and treatment are key to a favorable outcome. In Figure 6, the initial CT of the vein of Labbé and transverse dural sinus thrombosis and hemorrhagic venous infarct was interpreted as right temporal lobe hemorrhage with subdural hematoma with concern for an underlying arteriovenous malformation. The thrombosed (hyperdense) right transverse sinus was misinterpreted as a subdural hematoma. The tubular hyperdensity next to the hematoma was a thrombosed inferior anastomotic vein (vein of Labbé). The subsequent MRI performed 12 hours later (Figure 7) performed for the possibility of an underlying mass reveals progression with infarction of the right temporal and occipital lobe superimposed on the temporal lobe hemorrhage. The subsequent CT (Figure 8), 18 hours after presentation shows new hemorrhage of the newly infarcted right temporal lobe with worsening edema and uncal herniation.

The main distinguishing factor between arterial and venous infarct is distribution. Figure 13 demonstrates a case of arterial infarct, with diffusion restriction in right inferior parietal lobule and temporal lobes, sparing the occipital lobe, in a typical distribution of posterior right middle cerebral artery territory. This is in contradistinction to the previous patient demonstrated in Figures 7 and 8, where there was also involvement of the occipital lobe, an area that is in the posterior cerebral arterial distribution. Infarct across multiple expected arterial territories suggests a venous rather than an arterial origin.