Laszlo Mechtler, MD

1/16/2012

Summary

Normal anatomy

Normal varients

Incidental findings

Laszlo Mechtler MD Venous disease

Co-director of Neuroimaging 1. Deep venous thrombosis 2. Cortical venous thrombosis Dent Neurologic Institute 3. Jugular vein thrombosis 4. CCSVI Buffalo NY 5. Benign Intracranial Hypertension 6. Venous obstruction due to neoplasm 7. Vein of Galan Malformation

(21).Gre Green – Superior sagittal sinus

Yellow- Basal dural sinuses

Blue- Transverse sinuses

1 1/16/2012

superior sagittal sinus

frontopolar [1], anterior frontal [2], superior sagittal sinus and posterior frontal [3] veins inferior sagittal sinus

straight sinus

confluence of the sinuses

transverse sinuses

sigmoid sinuses

internal jugular veins Trolard vein [superior anastomotic vein] [4]; and anterior parietal veins [5]) and the larger named veins on the lateral surface of the cerebrum (the superficial sylvian vein [superficial middle cerebral vein] [6], which typically drains into the sphenoparietal sinus or the cavernous sinus, and the Labbé vein [7

Lateral MIP image from contrast-enhanced MR venography shows the major components of the deep venous system: the thalamostriate vein (1), septal vein (2), internal cerebral vein (3), basal vein (Rosenthal vein) (4), and vein of Galen (5).

1), septal vein (2), internal cerebral vein (3), basal vein (Rosenthal vein) (4), and vein of Galen (5).

2 1/16/2012

vein of Trolard – large anastomotic cerebral vein that courses cephalad from the sylvian fissure to the superior sagittal sinus – more dominant on the nondominant side vein of Labbe – courses posterolaterally from the sylvian fissure to the transverse sinus – more prominent on the dominant side

Axial MR image with color overlay shows the drainage territory of the deep cerebral veins (internal cerebral vein, vein of Galen) (pink), in which parenchymal abnormalities due to deep venous occlusion typically arePink- found. Vein of Galen via internal cerebral vein

Blue-Medullary veins

Leach J L et al. Radiographics 2006;26:S19-S41

3 1/16/2012

Occipital sinus Superior sagittal sinus angulation

SSS

torcula

Transverse sinuses were found to be right (A), left (B), and codominant (C) in 59%, 25%, and 16% of the cases examined, respectively.

4 1/16/2012

To differentiate whether there is a hypoplastic transverse sinus or thrombosed sinus, you need to look at the source images……dx-thrombosis of the When you suspect, that there is a hypoplastic transverse sinus, left transverse sinus then you should look at the size of the jugular foramen.

The superior sagittal sinus (straight arrow), straight sinus Sinus Pericranii (arrowhead ), and vein of Galen (curved arrow) are clearly depicted, and were seen in all 100 cases studied, without flow gaps.

Anomalous communication between intracranial (IC) and extracranial venous circulation

The right vein of Labbe (C, arrow) was seen in 91% of the cases. The right vein of Trolard (D, arrow), depicted as a large tributary to the superior sagittal sinus, was seen in only 37% of the Best diagnostic clue: Vascular scalp lesion cases communicating with underlying DVS

5 1/16/2012

Classic appearance of arachnoid granulations.

pacchionian bodies

Arachnoid Granulations

• MR Findings

• T1WI: Venous sinus defect isointense to CSF Pathology • T2WI • Hyperintense, homogeneous lesion, surrounded Mutations in chromosome 9p by normal flow void of major venous sinus Most common cerebral vascular malformation at autopsy • Single or multiple 15-20% occur with co-existing CM • T1WI C+: Focal nonenhancing venous sinus lesion Radially oriented dilated medullary veins surrounded by enhancing blood within sinus Venous radicals are separated by normal brain • MRV • Focal smooth filling defect within venous sinus on Clinical Issues source images or multi-planar reformations Usually asymptomatic • Venous flow is normal proximal & distal to lesion Stenosis or thrombosis of draining vein increases hemorrhage risk

6 1/16/2012

• MR Findings in DVA • T1WI • Can be normal if DVA is small • Variable signal depending on size, flow • "Flow void" appearance possible • Hemorrhage may occur if associated with CM or with draining vein thromboses • Best diagnostic clue: "Medusa head" (dilated medullary white matter • T2WI veins) draining into solitary major venous trunk • ±"Flow void" • Location • ± Blood products • FLAIR: Usually normal; may show hyperintense region if venous ischemia or hemorrhage • Periventricular white matter: Main venous trunk drains into deep present venous system • T2* GRE • Usually into the thalamostriate/ependymal vein in the lateral • Hypointensity may bloom if co-existing CM present with short T2 hemorrhagic products • Hypointense blooming may also occur from intravascular conversion of oxyhemoglobin to aspect of the lateral ventricle deoxyhemoglobin due to slow flow • Near frontal horn = most common site • DWI • Other: Adjacent to fourth ventricle • Usually normal • Subcortical white matter: Main venous trunk drains into the dural • Rare: Acute venous infarct seen as hyperintense area of restricted diffusion • T1WI C+ venous sinuses • Strong enhancement • Supratentorial: Usually into the superficial sagittal sinus • Stellate, tubular vessels converge on collector vein • Infratentorial: Usually into the transverse sinus • Collector vein drains into dural sinus/ependymal vein • MRA • Size: Varies (may be extensive) but usually < 2-3 cm • Arterial phase usually normal • Morphology • Contrast-enhanced MRA may demonstrate slow-flow DVA • Umbrella-like collection of enlarged medullary (white matter) veins • MRV: Delineates "Medusa head" and drainage pattern • Large "collector" vein drains into dural sinus or deep ependymal vein • MRS: Normal; deoxyhemoglobin or short T2 hemorrhagic products may result in peak broadening • Usually solitary • Can be multiple in blue rubber-bleb nevus syndrome

7 1/16/2012

Terminology

Congenital cerebral vascular anomaly with angiogenically mature venous elements

Imaging Findings

Best diagnostic clue: "Medusa head" (dilated medullary white matter veins) draining into solitary major venous trunk Collector vein drains into dural sinus/ependymal vein Protocol advice: Include T2* sequence to look for hemorrhage, mixed CM

Top Differential Diagnoses

AVM, Cavernous Malformation, Capillary Telangiectasia Vascular Neoplasm Dural Sinus Occlusion (with Venous Stasis, Collateral Drainage) Sturge-Weber Syndrome

DVA SUMMARY

• Large area of brain parenchyma

• Paucity of connecting or bridging veins

• Single, dominant “transcortical vein”

• Multiple smaller veins drain into the “head”

• Probable increased venous pressure

• Associated with Cavernous Malformations

• Hemorrhage likely from the CCM

8 1/16/2012

• MR • Acute thrombus isointense on T1WI • Hypointense on T2WI (can mimic flow void) • T2* GRE best (clot usually blooms)

Deep Cerebral Venous Thrombosis

• MRV • 2D time of flight (TOF) MRV shows "missing" ICVs, variably absent signal in VOG, SS • May see abnormal collateral channels • Contrast-enhanced MRV (CE-MRV) • Faster; better depicts nonenhancing thrombus and small veins than TOF • TOF limitations • T1 hyperintense thrombus falsely appears as patent flow on MIP • Always evaluate source images and conventional MR sequences • Phase contrast MRV: T1 hyperintense thrombus not misrepresented as flow

Venous infarcts - vein of Labbe

9 1/16/2012

Deep Cerebral Venous Thrombosis Deep Cerebral Venous Thrombosis

• Best imaging tool • Best imaging tool • NECT/CECT ± CTV venogram • NECT/CECT ± CTV venogram • CT • CT • Hyperdense ICV ± bithalamic hypodensity • Hyperdense ICV ± bithalamic hypodensity • Variable loss of deep gray-white interfaces • Variable loss of deep gray-white interfaces • ± petechial hemorrhages • ± petechial hemorrhages • Protocol advice • Protocol advice • If CT/CECT/CTV scans negative → MR with MRV • If CT/CECT/CTV scans negative → MR with MRV • If MRV equivocal → DSA • If MRV equivocal → DSA • MR: Clot hypointense, "blooms" on T2 • MR: Clot hypointense, "blooms" on T2

abnormal high signal in the internal cerebral veins and straight sinus on the T1-weighted images. The diagnosis is bilateral infarctions in the basal ganglia due to deep cerebral venous thrombosis

10 1/16/2012

angiography demonstrated occlusion of all major sinuses. An IV catheter was advanced directly to the occluded sinuses, and 40 mg of tissue plasminogen activator was injected, which resulted in restoration On the left a lateral and oblique MIP image from a normal contrast- of the sinus flow enhanced MR venography. Notice the prominent vein of Trolard (red arrow) and vein of Labbe (blue arrow).

MR Findings

T1WI: Subacute to chronic phase: Tubular mass in the posterolateral CS with high signal on T1 images secondary to T1 shortening from the paramagnetic effect of methemoglobin

T2WI Acute-subacute phase: May have a bizarre tumorous MRV: Absent signal in the region of appearance, especially in coronal plane; adjacent fat thrombosis; may have artifactual signal from appears infiltrated incorporation of high signal methemoglobin High signal from methemoglobin can be seen within thrombus on TOF MRV → underestimate Loss of normal flow void extent of thrombosis Edema in the retropharyngeal space

T1WI C+: Filling defect in the IJV

11 1/16/2012

• MR Findings in CVT • T1WI • Thrombus is isointense early, hyperintense later • ± venous infarct • Gyral swelling, edema hypointense • Iso- to slightly hyperintense foci if hemorrhagic • T2WI • NECT • Thrombus hypointense acutely, hyperintense much later • Acute clot can mimic flow void • Venous infarct • "Cord" sign (hyperdense vein) • Gyral swelling, edema hyperintense • Involved veins usually enlarged (distended with • Hypointense foci if hemorrhagic clot), irregular • FLAIR • • Thrombus usually hyperintense ± petechial parenchymal hemorrhage, edema • Parenchymal edema hyperintense • T2* GRE • CECT • GRE most sensitive sequence for thrombus • Hypointense ("black"), cord-like • SWI not as helpful due to intrinsic hypointensity of normal veins • If DST, "empty delta" sign (25-30% of cases) • DWI • CTV: Thrombi may be seen as filling defects • DWI/ADC varies with ischemia, type of edema, hemorrhage • Distinguishes cytotoxic from vasogenic edema • Restriction can be seen in clot itself • T1WI C+ • Thin (1 mm) 3D volume acquisition • Acute/early subacute clot: Peripheral enhancement outlines clot • Late clot: Thrombus, fibrous tissue often enhances • Venous infarct: Patchy enhancement

• MRV Protocol advice • 2D time of flight (TOF) MRV depicts thrombus as sinus discontinuity, loss of vascular flow signal • May see abnormal collateral channels (e.g., enlarged medullary veins) • Occluded veins at time of diagnosis may predict low rate of → vessel recanalization 2 or 3 months later If CT negative MR with T1WI C+, GRE, MRV • Contrast-enhanced MRV (CE-MRV) • Faster; better depicts nonenhancing thrombus and small veins than TOF If MR, MRV equivocal → DSA • TOF limitations • T1 hyperintense thrombus (subacute) may mimic patent flow on MIP (false-negative MRV) • Must evaluate source images and conventional MR sequences to exclude potential false-negatives

• Phase contrast MRV: T1 hyperintense thrombus not misrepresented as flow

12 1/16/2012

Etiology of CVT CVT • No cause identified in 20-25% of cases • Most common pattern • Wide spectrum of predisposing causes (> • Thrombus initially forms in dural 100 identified) sinus • Clot propagates into cortical • Trauma, infection, inflammation, veins malignancy • Venous drainage obstructed →↑ • Pregnancy, oral contraceptives venous pressure • Metabolic (dehydration, thyrotoxicosis, • Blood-brain barrier breakdown cirrhosis, hyperhomocysteinemia, etc.) with vasogenic edema, • Hematological (coagulopathy) hemorrhage • Collagen-vascular disorders (e.g., APLA • Venous infarct with cytotoxic syndrome) edema ensues • Vasculitis (e.g., Behçet) • Isolated CVT without DST occurs • Drugs (androgens, ecstasy) but is uncommon

13 1/16/2012

CVT Natural History & Prognosis of CVT • Clinical diagnosis often elusive • Most common signs/symptoms • Extremely variable outcome; asymptomatic to death • Up to 50% of cases progress to venous infarction • Headache (95%) • Pulmonary embolism is uncommon but carries poor prognosis • Seizure (47%), paresis (43%), papilledema • Poor outcome associated with papilledema, altered consciousness, coma, (41%) age > 33 years, diagnostic delay > 10 days, intracerebral hemorrhage, • Altered consciousness (39%), comatose involvement of straight sinus (15%) • Good outcome associated with isolated intracranial hypertension • Isolated intracranial hypertension (20%) presentation, "delta" sign on CT (leading to earlier diagnosis) • D-dimer is useful in patients with suspected • 1 year following CVT, 40% have lifestyle restrictions, 40% are unable to CVT; patients with positive test results should resume previous level of economic activity, 35% have altered be urgently sent for MR imaging consciousness, 6% are dependent • Overall mortality = 10%; recurrence as high as 12% • Other signs/symptoms: Focal neurologic deficits; depend on location • Treatment • Heparin ± TPA • Endovascular thrombolysis; thrombolytic &/or mechanical disruption

Age and sex distribution of cerebral venous and sinus thrombosis (CVT) in adults. Image Interpretation Pearls of CVT

• 2D TOF MRV should not be interpreted without comparing conventional sequences (particularly T1)

• Must do NECT concurrently with CECT or CTV to exclude false- negative contrast study due to hyperdense thrombus

• Consider "cord" sign for early and accurate diagnosis

• Subtle early imaging findings often overlooked

• Include T2* GRE sequence on MR/MRV

Saposnik G et al. Stroke 2011;42:1158-1192

1 1/16/2012

Magnetic resonance venogram showing the cerebral venous system and most frequent (%) location of cerebral venous and sinus thrombosis, as reported in the International Study on Cerebral Venous and Dural Sinuses Thrombosis (n=624).44.

Saposnik G et al. Stroke 2011;42:1158-1192

Proposed algorithm for the management of CVT. The CVT writing group recognize the challenges facing primary care, emergency physicians and general neurologists in the diagnosis and management of CVT. The aim of this algorithm is to provide guidance to physi...

Saposnik G et al. Stroke 2011;42:1158-1192

2 1/16/2012

(a, b) Lateral MR venograms show the coronal (vertical white line in a) and axial (horizontal (a) Contrast-enhanced CT image in a patient with superior sagittal sinus thrombosis shows white line in b) planes of image data acquisition used for TOF MR venography. a central filling defect in the superior sagittal sinus (arrow), surrounded by intensely enhanced dura mater.