Cerebral venous thrombosis
Updates to Article Attributes
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.
Epidemiology
Demographics of affected patients reflects underlying predisposing factors, which are identified in the majority of cases (87.5%) with many patients having more than one co-existent risk factors 2
- hormonal
- oral contraceptive pill: very common cause in female patients <50 years of age 2
- pregnancy
- puerperium
- steroids
- prothrombotic haematological conditions: 35% 2
- local factors
- skull abnormalities / trauma
- compressing mass: e.g. meningioma
- infection: especially mastoid sinus (dural sinus occlusive disease (DSOD )
- systemic illness
- dehydration: e.g. gastroentertitis
- sepsis
- malignancy
- connective tissue disorders
- idiopathic: 12.5% 2
Clinical presentation
Unlike most other intracranial vascular conditions, presentation can be highly variable and range from essentially asymptomatic to coma and death 1.
Symptoms include
- headaches
- decreased/altered conscious state
- decreased/altered vision
- nausea/vomiting
Signs include:
- papilloedema
- cranial nerve palsies
- focal neurological deficits
- seizures
- coma
Complications
Venous hypertension from poor outflow can lead to oedema, cerebral venous infarction(50% of cases) and even haemorrhage.
Radiographic features
CT
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 sinuessinuses and are especially common in the superior sagittal sinus and transverse sinus.
MRI
MRI is able to both visualizevisualise 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 infarction 1.
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.
DSA
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.
Treatment and prognosis
In approximately 50% of cases cerebral venous thrombosis progresses to venous infarction 1. Unlike arterial infarcts, venous infarcts usually present after some days 1:
- <2 days of symptom onset: 30%
- 2-30 days: 50%
- >30 days: 20%
The mainstay of treatment is heparin, even in the setting of haemorrhagic venous infarction 2,4. 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%) 2.
Interventional neuroradiologists can perform catheter directed thombolysis by using targeted thrombolytics in the affected sinuses.
Not surprisingly coma, haemorrhagic venous infarcts and co-existing malignancy correlate with poor outcome 2. Deep cerebral venous thrombosis also has a negative impact on prognosis due to usually bilateral involvement of the thalami 3.
-</ul><h4>Complications</h4><p> Venous hypertension from poor outflow can lead to oedema, <a href="/articles/venous-infarction">venous infarction </a>(50% of cases) and even haemorrhage.</p><h4>Radiographic features</h4><h5>CT</h5><p>Non-contrast CT, when not associated with venous haemorrhage or infarction can be a subtle finding, relying on hyperdensity of the sinus being identified <sup>1</sup>.</p><p>With contrast administration, especially with a <a href="/articles/ct-venogram">CT venogram</a>, then a filling defect in a sinus is sought. When in the sagittal sinus it is referred to as the '<a href="/articles/empty-delta-sign">empty delta sign</a>'. CTV has a reported sensitivity of 95% compared to DSA as the gold standard <sup>1</sup></p><p>Filling defects should not be confused with <a href="/articles/arachnoid-granulation">Pacchionian bodies</a> (arachnoid granulations) which can be seen in essentially all dural sinues and are especially common in the superior sagittal sinus and transverse sinus.</p><h5>MRI</h5><p>MRI is able to both visualize the clot as well as the sequelae. </p><p>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.</p><p>Cerebral oedema can be identified even in the absence of neurological dysfunction or infarction <sup>1</sup>.</p><p>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.</p><h5>DSA</h5><p>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.</p><h4>Treatment and prognosis</h4><p>In approximately 50% of cases cerebral venous thrombosis progresses to <a href="/articles/cerebral-venous-infarction">venous infarction</a> <sup>1</sup>. Unlike arterial infarcts, venous infarcts usually present after some days <sup>1</sup>:</p><ul>- +</ul><h4>Complications</h4><p> Venous hypertension from poor outflow can lead to oedema, <a title="Cerebral venous infarction" href="/articles/cerebral-venous-infarction">cerebral venous infarction</a> (50% of cases) and even haemorrhage.</p><h4>Radiographic features</h4><h5>CT</h5><p>Non-contrast CT, when not associated with venous haemorrhage or infarction can be a subtle finding, relying on hyperdensity of the sinus being identified <sup>1</sup>.</p><p>With contrast administration, especially with a <a href="/articles/ct-venogram">CT venogram</a>, then a filling defect in a sinus is sought. When in the sagittal sinus it is referred to as the '<a href="/articles/empty-delta-sign">empty delta sign</a>'. CTV has a reported sensitivity of 95% compared to DSA as the gold standard <sup>1</sup></p><p>Filling defects should not be confused with <a href="/articles/arachnoid-granulation">Pacchionian bodies</a> (arachnoid granulations) which can be seen in essentially all dural sinuses and are especially common in the superior sagittal sinus and transverse sinus.</p><h5>MRI</h5><p>MRI is able to both visualise the clot as well as the sequelae. </p><p>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.</p><p>Cerebral oedema can be identified even in the absence of neurological dysfunction or infarction <sup>1</sup>.</p><p>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.</p><h5>DSA</h5><p>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.</p><h4>Treatment and prognosis</h4><p>In approximately 50% of cases cerebral venous thrombosis progresses to <a href="/articles/cerebral-venous-infarction">venous infarction</a> <sup>1</sup>. Unlike arterial infarcts, venous infarcts usually present after some days <sup>1</sup>:</p><ul>
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