Aseptic thrombosis of the superior sagittal sinus
This 32 year old female presented with sudden onset of severe headache, nausea and vomiting. She had taken oral contraceptives for several years.
At physical examination a mild right hemiparesis, as well as an ipsilateral 6th nerve palsy was noted. There was also a bilateral papilledema.
Emergency CT scan was performed in another hospital and the diagnosis of thrombosis of the superior sagittal And left transverse sinuses was suggested. Follow-up on the next day confirmed the diagnosis.
After transfer, a combined MRI-MRA examination was carried out. Follow-up MRI-MRA examination 3 weeks later demonstrated partial recanalization of the thrombosed dural sinuses. The patient subsequently improved clinically.
(Aseptic thrombosis of the superior sagittal sinus, 0.5 T)
Examination 1
Fig.1 Transverse non-enhanced CT images. The hyperdense appearance ("cord sign") of the superior sagittal sinus (arrow) is well appreciated. Less well seen is the very subtle hyperintensity of the right transverse sinus (left upper image).
Fig.2 Transverse contrast-enhanced CT images. Absence of enhancement ("empty delta sign") is clearly seen in the superior sagittal sinus as well as in the right transverse sinus, suggesting the diagnosis of thrombosis.
Examination 2 (1 day follow-up)
Fig.3 Transverse non-enhanced brain CT images. The hyperdense appearance ("cord sign") of the superior sagittal sinus and especially of the right transverse sinus is more marked here.
Fig.4 Transverse contrast-enhanced brain CT images. The abnormal dural and tentorial enhancement reflects collateral circulation and venous congestion.
Examination 3 (one-week follow-up)
Fig.5 Sagittal T1-weighted spin-echo image. The subacute thrombus in the superior sagittal and left transverse sinuses is characterized by short T1 relaxation time and therefore increased signal intensity. Note a thrombosed ascending cortical vein in the right parietal region (arrow).
Fig.6 Transverse proton-density weighted fast spin-echo images. Compare the normal signal void of the straight sinus to the high signal intensity of the superior and right transverse sinuses.
Fig.7 Transverse T2-weighted fast spin-echo images. Small abnormal signal intensity areas are seen in the brain parenchyma adjacent to the thrombosed superior sagittal sinus bilaterally (venous infarction). Otherwise same observations as on Fig.3.
Fig.8 Coronal T1-weighted spin-echo images. The bilateral juxtasinusal parenchymal lesions exhibit high signal intensity on these images as well and hence suggest hemorrhagic venous infarctions. Compare the appearance of the transverse sinuses, the left presenting with a normal signal void and the right being hyperintense due to thrombosis. Note also the previously seen thrombosed left parietal cortical vein.
Fig.9 Coronal T1-weighted spin-echo images. All of the dural sinuses, including both transverse sinuses appear to be thrombosed on these images, suggesting occlusion of the initial portion of the left transverse sinus as well. However, this high intravascular signal from the left transverse sinus is limited to the entry slices of the stack only, and thus can also correspond to flow-related enhancement and reflect slow flow (See Effects of spin motion on the MR signal: basic flow phenomena: Time-of-Flight effects: In-flow effects: Flow-related enhancement).
Fig.10 Sagittal (above) and transverse (below) 2D PC MR angiograms. These rapid (Tac: 36 sec for each) survey images confirm occlusion of the superior and right transverse sinuses and patency of the left transverse sinus. The left transverse sinus assures drainage of the deep midline venous system.
Fig.11 Sagittal averaged modulus (left) and corresponding magnitude of complex differences (right) type images from a non-enhanced 3D PC MRA acquisition (Venc: 20 cm/s, Tac: 10 min) showing absence of flow in the superior sagittal sinus and patency of the internal cerebral veins (blue arrows), the straight sinus (green arrows) and the left transverse sinus (yellow arrow). Note that the appearance of the venous structures on the averaged modulus images does not predict patency or occlusion (both the thrombosed superior sagittal sinus and the patent internal cerebral vein exhibit high intravascular signal) because on these (T1-weighted gradient-echo) images contrast is based either on differences in T1 relaxation times for stationary tissues and/or inflow effects without phase-based information for vascular structures (See Phase Contrast MR angiography: Image types). Therefore, when evaluating the significance of intravascular signal on averaged modulus images, they should always be interpreted by simultaneous comparison with their corresponding magnitude of complex differences image pairs.
Fig.12 Sagittal MIP reconstruction (above) and a directional phase difference MPR image (below) from the 3D PC MRA acquisition data set. The patent vascular structures in the projection of the superior sagittal sinus are probably parallel collateral cortical veins. Note the signal drop-outs (yellow) within the left transverse sinus at the junction of the vein of Labbe which reflects rapid phase dispersion due to turbulent flow and should not be mistaken for thrombosis. Flow direction is normal (identical to that in the pericallosal artery) in the deep midline venous structures.
Fig.13 Transverse source images from a 3D TOF MRA acquisition. Both the patent left (flow-related enhancement) and the thrombosed right (subacute thrombus with short T1 relaxation time) transverse sinuses present as high signal intensity structures.
Fig.14 Coronal targeted MIP reconstruction of the transverse and sigmoid sinuses from the 3D TOF MRA acquisition data set. Demonstration of the T1-contamination phenomenon: the thrombus in the right transverse sinus has a short T1 relaxation time, therefore remains visible due to incomplete background signal suppression and mimics flow on the MIP image (yellow arrows), indistinguishable from the normal flow-related enhancement in the left transverse sinus (blue arrows). This is a typical problem with the Time-of-Flight technique and a potential pitfall in the evaluation of intracranial venous thrombosis.
Examination 4 (three-week follow-up)
Fig.15 Sagittal T1-weighted spin-echo images. The superior sagittal sinus exhibits intermediate signal intensity, consistent with an organized chronic thrombosis (See Intracranial occlusive venous pathologies: MRA of intracranial dural sinus thrombosis: Image analysis).
Fig.16 Transverse proton-density weighted fast spin-echo images. The superior sagittal sinus still appears as a high signal intensity structure, however a small punctate signal void (arrow) is noted within its lumen, suggesting the commencement of recanalization.
Fig.17 Transverse T2-weighted fast spin-echo images. Normalization of the previously abnormal signal intensity areas in the brain parenchyma adjacent to the superior sagittal sinus. Otherwise same observations as on Fig.16.
Fig.18 Sagittal survey 2D PC MR angiogram (Venc: 20 cm/s, Tac: 1 min) and a corresponding directional phase difference reconstruction. The thin recanalization channel as well as the normal flow direction within the superior sagittal sinus are well appreciated on these images.
Fig.19 Sagittal ("anatomical") averaged modulus (left) and corresponding ("flow") magnitude of complex differences (right) type images from a Gadolinium-enhanced 3D PC MRA acquisition (Venc: 20 cm/s, Tac: 12 min). The organized thrombus shows marked enhancement on the "anatomical" images. Recanalization within the thrombus is detected however upon analysis of the "flow" images.
Fig.20 Sagittal survey 2D PC (above) and 3D PC (below) MR angiograms for comparison. Both clearly show the recanalization of the superior sagittal sinus.
Fig.21 Oblique targeted MIP reconstructions of the torcular of Herophilus showing the irregular and narrow recanalization channel within the superior sagittal sinus and right transverse sinus (arrows).
Video 1.
3D demonstration of the intracranial vessels (3D PC MRA acquisition) showing the recanalization of the superior sagittal and the right transverse sinus.
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