Left Temporal Lobe Hematomas Caused By Transvers And Sigmoid Sinus Thrombosis

Clinical History

A 20 year old woman presented at the emergency department complaining of sudden onset of severe headache which followed by loss of consciousness.

Imaging Findings

An otherwise healthy 20 year old woman suffered from sudden onset of severe headachce followed by loss of consciousness and was admitted to the emergency department. Her prior neurological history was unremarkable. Initial unenhanced CT imaging showed left temporal intra-parenchymal haemorrhage with surrounding edema. The haemorrhagic areas was not fall into any specific arterial territory (Fig. 1a). The left sigmoid sinus was relatively hyperdense on unenhanced images that suggests a thrombus and on enhanced images the thrombus seen as filling defect (Fig. 1a, b). A subsequent cranial MR and MR venogram was performed. Hematomas are centrally hyperintense and have a hypointense halo on T1-weighted images (Fig. 2a). On T2-weighted images hematomas are centrally hypointense with a hyperintense surrounding edema (Fig. 2b). On gradient-echo images hematomas are more prominent (Fig. 2c). Diffusion-weighted images shows elevated interstitial tissue water content, suggestive of vasogenic brain edema in the perihematoma tissue (Fig. 2d). Coronal T2-weighted images show replacement of signal void by thrombus in left sigmoid and transvers sinus and iso-hypointens hematoma with hyperintense edema in left temporal lobe (Fig. 3a, b). 2D TOF MR venography shows no flow in left transvers and sigmoid sinuses and contrast-enhanced MR venography confirms the absence of blood flow in the left transvers and sigmoid sinuses. The other venous sinuses are patent (Fig. 4 a-c).

Discussion

Cerebral venous thrombosis (CVT) are responsible for about 10% of all cerebral ischemic lesions and approximately 2.4% of strokes in young adults [1, 2]. The estimated annual incidance of CVT is 3-4 per million in general population and female/male ratio is 1.5:5 [3]. The superior sagittal sinus is the most commonly effected side and followed by the transverse, sigmoid, and straight sinuses [4]. One third of patients demonstrate more than one sinus involvement [5]. The etiologic factors of CVT are often multifactorial and differs to the patient age [6]. The most common causes are hypercoagulable states, severe dehydratation, infection, oral contraceptives, hormone replacement therapy, pregnancy and puerperium [4, 7].
The clinical presentation of CVT is generally nonspecific. Headache is the first and the most frequent symptom. Other clinical manifestations are focal neurologic deficits, seizures, papilledema, and altered consciousness [4, 7]. Hence the clinical symptoms are nonspecific, diagnosis is based on both direct and indirect imaging findings.
“Dense clot sign” is direct visualization of thrombosis in dural sinuses on non-contrast-enhanced cranial CT, and cord sign (hyperdense bridging vein) and empty-delta sign on contrast-enhanced cranial CT are the direct signs of CVT which could only be seen in one third of the cases. Indirect signs (focal or diffuse brain swelling, parenchymal bleeding, and tentorial and falcian enhancement) are often nonspecific. Hemorrhagic areas in CVT, do not typically correspond to expected localizations of hypertensive bleedings or the known arterial territories [5, 6, 8].
Thrombosis in the sagittal sinus often leads to parenchymal change in the parasagittal region. Temporal lobe infarction is seen in Labbé’s vein thrombosis and in deep venous thrombosis bilateral or unilateral infarction in the thalami, basal ganglia, and internal capsule is typical. Infarctions could be hemorrhagic or nonhemorrhagic [6]. Intraparenchymal hematoma occurence rate is 35-40% [5].
Unenhanced CT generally shows only the indirect signs and the most specific indirect finding is venous infarction. The presence of multiple isolated lesions, involvement of a subcortical region with sparing of the cortex, or extension more than one arterial distribution, is highly suspicious for a venous cause [6].

Venous thrombus may be directly visualized on MRI. Conventional MRI sequences demonstates patent dural sinuses as a flow void and the thrombus may be seen as absence of a flow void, which is often best seen on T2-weighted and FLAIR images. The abnormal signal intensity of the thrombus follows the signal characteristics of intracranial hemorrhage. Brain swelling and hemorrhagic or nonhemorrhagic infarction are the indirect signs of venous thrombosis on MRI which are similar to the findings on CT. Although conventional MRI sequences often provide sufficient information to make a diagnosis of CVT, the diagnosis can be further confirmed by MR venography [6].
MR venography can be performed with the phase contrast technique or the time-of-flight (TOF) technique. Hence contrast-enhanced MR venography is less likely to be affected by complex flow, it is superior to unenhenced MR venography [6].

Differential Diagnosis List

Final Diagnosis

Temporal lobe hematomas caused by transvers and sigmoid sinus thrombosis.

URL:	https://eurorad.org/case/7001
DOI:	10.1594/EURORAD/CASE.7001
ISSN:	1563-4086