(Hyperdense veins, SSSthrombosis, partial recanalisation on thrombolysis)
Cerebral venous thrombosis refers to occlusion of venous channels in the cranial cavity, including both dural venous thrombosis, cortical vein thrombosis and deep cerebral vein thrombosis.
The presentation is similar, and often dural sinus and deep and cortical vein thrombosis co-exist
Prothrombotic haematological conditions
Unlike most other intracranial vascular conditions, presentation can be highly variable and range from essentially asymptomatic to coma and death 1.
Venous hypertension from poor outflow can lead to oedema, venous infarction (50% of cases) and even haemorrhage
Non-contrast CT, when not associated with venous haemorrhage or infarction can be a subtle finding, relying on hyperdensity of the sinus being identified 1
With contrast administration, especially with a CT venogram, then a filling defect in a sinus is sought. When in the sagittal sinus it is referred to as the ‘empty delta sign‘. CTV has a reported sensitivity of 95% compared to DSA as the gold standard 1
Filling defects should not be confused with Pacchionian bodies (arachnoid granulations) which can be seen in essentially all dural sinues and are especially common in the superior sagittal sinus and transverse sinus.
MRI is able to both visualize the clot as well as the sequelae.
The clot acutely is iso intense on T1 and hypo intense on T2 (this can mimic a flow void), with sub acute clot becoming hyper intense on T1.
Cerebral oedema can be identified even in the absence of neurological dysfunction or infarction1.
MRV will demonstrate lack of flow. 2D Time of Flight (TOF) venography is routinely performed in suspected cases. Contrast MR venography has more sensitive in detecting dural venous sinus thrombosis than TOF venography. Hypoplastic dural sinuses and low flow areas remain a major problem with 2D TOF.
Although digital subtraction angiography has historically been the gold standard, the relative lack of experienced angiographers, and invasive nature of the examination has led to a dramatic decline in it’s use as a primary mode of diagnosing cerebral venous thrombosis.
In approximately 50% of cases cerebral venous thrombosis progresses to venous infarction 1. Unlike arterial infarcts, venous infarcts usually present after some days 1:
The mainstay of treatment is heparin, even in the setting of haemorrhagic venous infarction. The natural history of cerebral venous thrombosis is highly variable, with some patients having minimal or no symptoms and an uneventful recovery ( ~ 65%), whereas others have a fulminant course culminating in extensive venous infarction and dependency or death (~20%) .
Interventional neuroradiologists can perform catheter directed thombolysis by using targeted thrombolytics in the affected sinuses.
(catheter directed thrombolysis and recanalisation)
Catheter-directed thrombolysis is a minimally invasive treatment that dissolves abnormal blood clots in blood vessels to help improve blood flow and prevent damage to tissues and organs.
When blood does not flow smoothly through a vessel, it can begin to coagulate, turning from a free-flowing liquid to a semi-solid gel, or blood clots. A blood clot, or thrombus, that forms within a blood vessel may continue to grow, blocking off the blood supply to certain parts of the body and causing damage to tissues and organs. In some patients, blood clots come from one site, dislodge, travel downstream, and lodge in relatively small vessels causing a blockage, or embolization. Untreated, a vascular blockage due to thrombosis or embolization, can result in the loss of an organ or extremity, with potentially life-threatening consequences.
In a catheter-directed thrombolysis procedure, x-ray imaging is used to help guide a special medication or medical device to the site of blood clots to dissolve the blockage.
Technically successful thrombolysis requires that the catheter be placed in a stable position near the clot. This means that the catheter tip is situated so that the clot-dissolving agent can reach the site of the obstruction. In some cases, the procedure is not technically possible. It is important to understand that clot removal alone cannot repair tissue already damaged by lack of circulation. Further treatment may be required, both for the underlying condition that caused the clot and for any damage to affected organs or other tissues.
Not surprisingly coma, haemorrhagic venous infarcts and co-existing malignancy correlate with poor outcome. Deep cerebral venous thrombosis also has a negative impact on prognosis due to usually bilateral involvement of the thalami.