1. Santa Clara Valley Medical Center, San Jose, CA
Pictorial review of intracranial MRV techniques, pitfalls, and common pathologies involving the cerebral venous system
Jennifer Trinh, MD
Rajul Pandit, MD
Mahesh R. Patel, MD
Santa Clara Valley Medical Center, San Jose, CA
Control #806
eEdE-44

2. Disclosures
There are no financial disclosures.

3. Objectives
Know the advantages and disadvantages of two non-contrast based MR venography (MRV) techniques and their pitfalls
Review the anatomy of the cerebral venous system
Know the common sites of cerebral venous thrombosis (CVT)
Illustrate common etiologies of CVT and occlusion

4. Introduction
The cerebral venous system can be difficult to evaluate due to artifacts, variant anatomy, and overlapping signal intensities of venous flow.
Several MRV methods are available to image the intracranial venous system.
These methods include both non-contrast and contrast based techniques.
Cerebral venous sys consists of deep venous sys, superficial venous sys, dural venous sinuses

5. MRV Techniques
Two non-contrast based MRV techniques are utilized at our institution.
2-D time of flight (TOF) MRV is obtained with the source data in the coronal plane.
3-D phase contrast MRV is obtained with the source data in the sagittal plane.
Contrast-enhanced MRV is another technique that is used at other institutions.
This technique relies on the paramagnetic effect of intravenous gadolinium to shorten T1 and provide intravascular contrast enhancement.
2D TOF has excellent sensitivity to slow flow and their diminished sensitivity to signal loss from saturation effects compared with the sensitivities of three-dimensional TOF techniques
Venous flow in the plane of image acquisition may produce saturation and resultant nulling of the venous signal at TOF MRV, a potential pitfall for image interpretation and diagnosis
Pitfalls
TOF
Signal loss within the venous structure in areas where the venous flow is in the plane of image acquisition may resemble thrombotic occlusion.
It may be difficult to distinguish a hypoplastic or atretric sinus from thrombosis.
Phase contrast - Arterial inflow may obscure venous anatomy.

6. Signal Generation in Non-Contrast MRV
Time of Flight
TOF uses flow phenomenon for signal generation. Blood flowing into the slice is not saturated and appears bright relative to the dark (suppressed) background. A saturation band is applied above the slice to suppress inflowing arterial signal.
Phase Contrast
Spins that are moving in the same direction as a magnetic field gradient develop a phase shift that is proportional to the velocity of the spins. Bipolar gradients (two gradients with equal magnitude but opposite direction) are used to encode the velocity of the spins.
The signal in the vein depends on the velocity of the flowing blood and the velocity encoding by the technician.
2D TOF has excellent sensitivity to slow flow and their diminished sensitivity to signal loss from saturation effects compared with the sensitivities of three-dimensional TOF techniques
Venous flow in the plane of image acquisition may produce saturation and resultant nulling of the venous signal at TOF MRV, a potential pitfall for image interpretation and diagnosis
Pitfalls
TOF
Signal loss within the venous structure in areas where the venous flow is in the plane of image acquisition may resemble thrombotic occlusion.
It may be difficult to distinguish a hypoplastic or atretric sinus from thrombosis.
Phase contrast - Arterial inflow may obscure venous anatomy.

7. Comparison of MRV Techniques
Advantages
Disadvantages
TOF
Shorter imaging time
No special pulse sequences are required
More prone to false-positives from in-plane flow
Phase contrast
Better background suppression
Can detect flow in all 3 orthogonal planes
Better flow quantification
No false-negatives due to methemoglobin
More sensitive to motion artifacts and turbulent flow
More arterial signal
Contrast enhanced
Less likely to give false-positives due to slow or complex flow
Potential false negatives due to methemoglobin or enhancing chronic thrombus
Signal loss on unenhanced MRV may result from in-plane flow, extremely slow flow, or complex flow, mimicking thrombosis.
Contrast enhanced MRV better at depicting dural venous sinuses because of a decrease in the effects of turbulent flow on vessel contrast.

8. Internal jugular veins
Anatomy
TOF
Phase Contrast
Superior Sagittal Sinus
Superior Sagittal Sinus
Vein of Galen
Vein of Galen
Internal cerebral vein
Internal cerebral vein
Straight sinus
Straight sinus
Internal jugular veins
Transverse sinus
Internal jugular vein
Sigmoid sinus
Transverse sinus
Sigmoid sinus

9. Cerebral Venous System & Most Frequent Location of Thrombosis
TOF
Phase Contrast
Superior Sagittal Sinus
Superior Sagittal Sinus (62%)
Cortical veins (17%)
Vein of Galen
Vein of Galen
Internal cerebral vein
Internal cerebral vein (12%)
Straight sinus (18%)
Straight sinus
Internal jugular veins (12%)
Transverse sinus (45%)
Internal jugular vein
Sigmoid sinus
Transverse sinus
Sigmoid sinus

10. artifacts

11. In Plane Flow Artifact TOF Phase Contrast Teaching Points:
Common sites of signal loss include:
The distal portion of the SSS, which is located in the coronal plane, on coronal TOF MRV.
The horizontal portion of the SSS, the junction of the vein of Galen with the straight sinus, and the portions of the transverse sinus that are located in the axial plane on axial TOF MRV.
In plane artifact
In flow signal loss in the distal SSS in TOF sequence
Phase contrast imaging shows the SSS is patent

12. Obscuration of the internal cerebral veins by arterial inflow
TOF
Phase Contrast
Only one internal cerebral vein is visualized. The other is obscured by arterial inflow
Internal cerebral veins
TOF: In flow signal loss in SS
3D Velocity: Internal cerebral veins not visualized
Arterial inflow in carotids

13. Arachnoid Granulations
Phase Contrast
Teaching Points:
Arachnoid granulations are small protrusions through the dura mater.
They occur throughout the dural sinus, but most commonly in the transverse and superior sagittal sinus.
Imaging shows a focal, well-defined, round filling defect with a characteristic anatomic distribution.
Normal patent flow immediately proximal and distal to the filling defects further supports arachnoid granulations.
Well defined extrinsic filling defect in the right transverse sinus
TOF
TOF Source Data

14. Hypoplastic transverse sinus
TOF
Phase Contrast
Hypoplastic, but patent rt transv sinus
Apparent signal loss in the transverse sinus is due to hypoplastic sinus
Source TOF data shows a hypoplastic sinus
Hypoplastic right transverse sinus on phase contrast
Teaching Points:
Hypoplasia or aplasia of one of the transverse sinuses is common.
Do not mistake for a sinus thrombosis!
Evaluate the source data.
If there is a CT, evaluate the jugular foramen size. A hypoplastic transverse sinus will also have a small jugular foramen.

15. Pathologies

16. Venous Sinus Thrombosis
64 year old female with headaches.
Teaching Points:
Mechanisms that lead to cerebral venous thrombosis include direct involvement of the dural sinus (e.g. infection, trauma, tumor infiltration), hypercoagulable states, increased blood viscosity (e.g. dehydration), or venous stasis.
Absence of a flow void and the presence of abnormal signal in the sinus is a primary finding of thrombosis on MRI. This should be further evaluated by MRV as slow or turbulent flow can also cause abnormal signal.
An acute thrombus can be very hypointense on T2 and mimic a flow void.
MRI:  focal signal abnormality w/in lt lateral transverse sinus.  centrally T2 hypointense, susp for thrombosis
MRV: lt lateral transv sinus, sigmoid, IJ are only partially seen, c/w partial venous thrombosis
Normal right transverse sinus flow void
Abnormal low T2 signal in the left lateral transverse sinus.
Left lateral transverse, sigmoid, and IJ are not seen, consistent with thrombosis.

17. Cortical Vein Thrombosis due to Spontaneous Intracranial Hypotension
46 year old female with orthostatic headaches for 10 days.
CT: Dense cortical veins.
Sag T1W: Sagging of cerebellar tonsils and posterior fossa structures with crowding of foramen magnum.
Axial GRE, FLAIR, T1WC+: blooming in the thrombosed cortical veins, subarachnoid hemorrhage in the parietal lobes, subdural hematomas, slit-like ventricles, and diffuse dural enhancement.
CT: prom cortical veins at b/l cerebral convexitities
Possible small b/l subdral collections
diminutive ventricles + cisterns, particularly quad plate cistern
MRI:  Subarachnoid hemor in b/l fronto parietal lobes along the convexity.  B/l subdural hematomas.  Small vents & mild effacement of the cisterns
Sagging of cerebellar tonsils and posterior fossa structures w/ crowding of foramen magnum
flattening of ventral surface of pons along the clivus, best seen on sagittal view
downward sagging of the optic chiasm along the roof of the sella
abnml hypointense sig on GRE w/in dilated cortical veins along the convexity b/l
Overall, findings s/o intracranial hypoTN w/ small size vents and overall deceased vol of CSF in basal cisterns
MRIC+:  diffuse dural enhm
dilated nonenhancing cortical veins in the convexity b/lly, likely rep thrombosis
slitlike vents
MRV:  no deep venous sinus thrombosis.  Mult dilated cortical veins along convexity, susp for cortical v thrombosis

18. Cortical Vein Thrombosis due to Spontaneous Intracranial Hypotension
Dilated cortical vein
Teaching Points:
Dense cortical veins (cord sign) on CT is a sign of cortical venous thrombosis.
Imaging signs of intracranial hypotension include diffuse cerebral edema, cerebellar tonsillar herniation, sagging of the brainstem, and dural enhancement.
Undiagnosed intracranial hypotension can result in subdural hematomas, subarachnoid hemorrhage, and dural venous sinus thrombosis.
Isolated cortical vein thrombosis is rare. It may be associated with coagulation abnormalities or chronic inflammatory conditions such as inflammatory bowel disease.
CT: prom cortical veins at b/l cerebral convexitities
Possible small b/l subdral collections
diminutive ventricles + cisterns, particularly quad plate cistern
MRI:  Subarachnoid hemor in b/l fronto parietal lobes along the convexity.  B/l subdural hematomas.  Small vents & mild effacement of the cisterns
Sagging of cerebellar tonsils and posterior fossa structures w/ crowding of foramen magnum
flattening of ventral surface of pons along the clivus, best seen on sagittal view
downward sagging of the optic chiasm along the roof of the sella
abnml hypointense sig on GRE w/in dilated cortical veins along the convexity b/l
Overall, findings s/o intracranial hypoTN w/ small size vents and overall deceased vol of CSF in basal cisterns
MRIC+:  diffuse dural enhm
dilated nonenhancing cortical veins in the convexity b/lly, likely rep thrombosis
slitlike vents
MRV:  no deep venous sinus thrombosis.  Mult dilated cortical veins along convexity, susp for cortical v thrombosis
No deep venous sinus thrombosis. 
Multiple dilated cortical veins along convexity.

19. Venous Infarction
2 day old term infant with ongoing dusky spells of unclear etiology.
Marked restricted diffusion in the temporal lobe, consistent with acute infarction.
2 day old unclear etiology, ? Hypercoagulable state
40w0d, via Vaginal, Spontaneous Delivery, episodes of duskiness while at rest
Term infant born to serologies negative mother with chorioamnionitis, s/p antibiotics once 15 minutes prior to birth. Now with four episodes cyanosis and floppiness; also with persistent hypoglycemia
2 day old term infant with maternal Chorioamnionitis and several episodes of cyanosis and ? Apnea. With ongoing dusky spells here in the NICU for no apparent reason
Marked restricted diffusion w/ hem in lt temp lobe likely due to venous infarct, which often presents with hemor in acute setting
Hemorrhagic transformation of arterial infarct usu occurs later
Infarction in caudate could be due to thrombosis of deep cerebral veins, which are not evaluated
MRV: Lt transverse sinus thrombosis. Hypoplasia of lt sigmoid sinus & IJ
T1 hypointense, T2 hypointense signal with the area of infarction with blooming on GRE, consistent with hemorrhagic venous infarction. Venous infarcts often present with hemorrhage in the acute setting. Hemorrhagic transformation of an arterial infarct is less common and usually occurs later.

20. Venous Infarction & Thrombosis
MRV from the same patient.
TOF
Phase Contrast
MRV: Lt transverse sinus thrombosis. Hypoplasia of lt sigmoid sinus & IJ
Artifactual loss of signal in the posterior SSS on TOF. SSS is patent on 3D velocity imaging.
Filling defect in the left transverse sinus, consistent with thrombus.
Hypoplastic left sigmoid sinus and IJ vein, better seen on phase contrast MRV.
Teaching Points:
Suspect venous infarct in a young patient, if the infarct does not correspond to a a vascular territory, if there is a round area of hemorrhage, if it spares the cortex, or is in a bilateral parasagittal location.
Evaluate the venous sinuses for a thrombus if there is a venous infarct.

21. Venous thrombosis due to venous epidural hematoma
15 year old male brought in after a gang fight.
Occipital fracture causing a venous epidural hematoma
Transverse sinus thrombosis fr venous epidural hematoma. Occipital condyle fx
CTV: filling defects starting fr transverse sigmoid sinus jxn to upper jugular vein, likely rep clot. Medial aspect of rt transv sinsu not visualized, may be injured. Active venous bleeding in the venous epidural hematoma.
MRV: Occlusion of rt transv venous confluence. Distally, the transverse sinus and IJV are diminutive, but faintly patent.
Cervical protion of lt IJV not well seen. ? Narrowing vs occlusion. Emissary vein, providing an alternative drainage
Probable clot in the right transverse and sigmoid sinus junction
Active venous hemorrhage within the epidural hematoma
Normal left venous sinuses
Medial aspect of right transverse sinus not visualized and may be injured.

22. Venous thrombosis due to venous epidural hematoma
MRV from the same patient.
MRV: Occlusion of rt transv venous confluence. Distally, the transverse sinus and IJV are diminutive, but faintly patent.
Cervical portion of lt IJV not well seen. ? Narrowing vs occlusion. Emissary vein, providing an alternative drainage
Occlusion of the right transverse venous confluence.
Cervical portion of left IJ vein not visualized and may be narrowed or occluded. There is an emissary vein providing an alternative drainage.
Source data shows the distal right transverse sinus is diminutive, but patent.

23. Mastoiditis with Right Internal Jugular Vein Thrombosis
Attenuated transverse & sigmoid sinuses
No signal in right IJ vein
Normal left IJ vein
No signal in right IJ vein
Normal left IJ vein
Hx: b/l otomastoiditis
Loss of signal in the rt INJV, concerning for thrombosis
Attenuation of the rt transverse and sigmoid sinus, c/w proximal R IJ occlusion
Involvement of the sinus due to adjacent infectious process is a known cause for venous sinus thrombosis
Teaching Points:
Venous sinus thrombosis is a complication of mastoiditis, although the incidence has declined due to antibiotic therapy.
The sigmoid sinus and internal jugular vein should be carefully evaluated for thrombosis.
Thrombosed right IJ vein
Normal left IJ vein
Flow present proximal to thrombosis

24. Compression from a Meningioma
CTV: Left parafalcine meningioma compressing the sagittal sinus. Difficult to exclude focal thrombosis or invasion. Sagittal sinus around the mass is patent.
T1WC+: Homogenously enhancing left parafalcine extra-axial mass that compresses the sagittal sinus at its dural attachment.

25. Compression from a Meningioma
Teaching Point:
If a mass compresses the venous sinus, a venogram should be performed to evaluate for thrombosis and invasion.
MRV MIP and source data: Mild irregularity and narrowing of the superior sagittal sinus at the region of the meningioma due to compression. No significant thrombosis or occlusion.

26. Compression from a Meningioma
T1WC+: Homogenously enhancing mass in the superior vermian cistern with a broad based dural tail extending along the tentorium.
MRV: Narrowing of the posterior two thirds of the straight sinus due to mass effect from the meningioma.

27. Occlusion from a Meningioma
62 year old female with headache and papilledema.
T1WC+: Homogenously enhancing extra-axial mass in the posterior left cerebellopontine angle cistern. The mass closely abuts the left transverse sinus as it turns into the sigmoid sinus.

28. Occlusion from a Meningioma
MRV from the same patient.
Occlusion of the left transverse sinus at the level of the mass.
Flow is seen in the left IJ vein at the skull base.
Source data better depicts flow in the left sigmoid sinus and IJ vein

29. Thrombosis from a Schwannoma
Filling defect in
Areas of segmental narrowing of rt transverse sinus w/ attenuation of rt IJV
Short segment narrowing of lt transverse sinus, likely mass effect from vestibular schwannoma
Filling defect in the right transverse sinus due to thrombus
Bilateral schwannomas
MRV shows thrombus in the distal right transverse sinus and narrowing in bilateral transverse sinuses due to mass effect. The right internal jugular vein is diminutive.

30. Occlusion from Squamous Cell Carcinoma
70 year old male with chronic right mastoiditis and subperiosteal abscess.
SCC of rt mastoid, temporal bone, EAC – Ruiz
MRI: Enh of rt sigmoid and trv sinus. Loss of flow void w/ abnml T1 hypointense sig. Heteregon enh mass centered in the rt mastoid
MRV: Rt IJ, distal trv, sigmoid sinuses not vis, c/w occlusion
TW1C+: Enhancing right mastoid mass.
T2W: Central T2 hypointense signal in the right transverse sinus.
TOF MRV: Distal right transverse, sigmoid sinus, and IJ vein are not seen, consistent with occlusion.

31. Thrombosis from RCC Metastasis
CT: ST mass and osseous destruction of rt occipital condyle, clivus, hypoglossal canal, jugular foramen, petrous apex.
MRI: Filling defect in rt transv sinus, likely due to thrombosis. Lytic heteregen enh mass in rt jugular foramen w/ mult flow voids. Occlusion of jugular foramen w/ enlarged IJ, which has abnml signal indicating thrombosis
MRV: Filling defects in rt TS, c/w clot. Long segment of absent signal in rt sigmoid & IJV, c/w thrombosis and occlusion.
Nonenhanced CT: Soft tissue mass with osseous destruction of right occipital condyle, hypoglossal canal, and jugular foramen.
T1WC+ with fat saturation: Enhancing mass in the jugular foramen with occlusion of the jugular foramen.

32. Thrombosis from RCC Metastasis
CT: ST mass and osseous destruction of rt occipital condyle, clivus, hypoglossal canal, jugular foramen, petrous apex.
MRI: Filling defect in rt transv sinus, likely due to thrombosis. Lytic heteregen enh mass in rt jugular foramen w/ mult flow voids. Occlusion of jugular foramen w/ enlarged IJ, which has abnml signal indicating thrombosis
MRV: Filling defects in rt TS, c/w clot. Long segment of absent signal in rt sigmoid & IJV, c/w thrombosis and occlusion.
T1WC+: Filling defect in the right transverse sinus, consistent with clot.
T2W: Enlarged right IJ vein with abnormal signal, consistent with thrombosis.
TOF MRV: Filling defect in the right transverse sinus, consistent with clot.
Long segment of absent signal in right sigmoid & IJ vein, consistent with thrombosis and occlusion.

33. Occlusion from Epidermoid
CT: Lobulated extra-axial mass in the left occipital region with serpeginous ring and arc like calcifications within the mass. The mass erodes the occipital bone and posterior aspect of the temporal bone.
Axial ADC map does not show low ADC signal.
There are areas of high T1 and low GRE signal, consistent with hemorrhagic blood products.
The majority of the mass is T2 hyperintense.
The mass abuts the transverse and sigmoid.
Path: Epidermoid
Lobulated extra-axial mass in lt occipital region w areas of high T1 w/ low GRE, c/w hemorrhagic blood products. Majority is T2 hyperintense. No restricted diffusion. Mass abuts lt transverse and sigmoid sinuses  occluded on MRV.
Serpiginous ring and arc like calcs w/in the mass. Mass erodes the occipital bone and posterior aspect of the temporal bone. Ddx hemangiopericytoma, chondrosarcoma, chordoma, meningioma.

34. Occlusion from Epidermoid
MRV from the same patient.
TOF
Phase Contrast
Teaching Points:
The differential diagnosis of an extra-axial mass with ring and arc like calcifications include hemangiopericytoma, chondrosarcoma, chordoma, and aggressive meningioma.
This is an atypical appearance of an epidermoid, which did not demonstrate restricted diffusion.
MRV shows occlusion of the left transverse and sigmoid sinuses.

35. Management of Cerebral Venous Thrombosis
Endovascular therapy may be considered in patients with absolute contraindications for anticoagulation therapy or failure of initial therapeutic doses of anticoagulant therapy.
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 physicians in the initial management of CVT. Anticoagulation remains the principal therapy and is aimed at preventing thrombus propagation and increasing recanalization. This algorithm is not comprehensive, nor applicable to all clinical scenarios and patient management must be individualized. Limited evidence is available on the benefits of decompressive hemicraniectomy and endovascular therapy for the management of CVT as reflected by the low grade and level of recommendations. Anticipated future advances in imaging techniques, new pharmacological agents and endovascular procedures may provide other therapeutic alternatives to be considered in patients with CVT, and in the future these guidelines will be periodically updated to reflect the changing evidence. CVST indicates cerebral venous and sinus thrombosis; LMWH, low molecular weight heparin; Tx, therapy; ICH, intracerebral hemorrhage; CTV, CT venogram; MRV, MR venogram. †Intracranial hemorrhage that occurred as the consequence of CVST is not a contraindication for anticoagulation. ‡Endovascular therapy may be considered in patients with absolute contraindications for anticoagulation therapy or failure of initial therapeutic doses of anticoagulant therapy.
Gustavo Saposnik et al. Stroke. 2011;42:

36. Summary
Familiarity with common pitfalls of MRV will assist in the accurate interpretation and diagnosis of the intracranial venous system.
Correlating imaging findings on different MRV sequences and reviewing the source data can avoid diagnostic pitfalls associated with all imaging techniques.
Knowledge of the typical and subtle imaging features of common pathologies of the cerebral venous sinuses will lead to prompt diagnosis and treatment, which can improve prognosis.

37. References
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Poon CS, Chang JK, Swarnkar A, Johnson MH, Wasenko J. Radiologic diagnosis of cerebral venous thrombosis: pictorial review. AJR Am J Roentgenol. 2007;189(6 Suppl):S64-75
Ayanzen RH, Bird CR, Keller PJ et al. Cerebral MR venography: normal anatomy and potential diagnostic pitfalls. AJNR Am J Neuroradiol 2000:21:74–78
Glockner JF, Lee CU. Magnetic Resonance Venography. Appl Radiol. 2010:39:36-42
Rollins N, Ison C, Booth T, Chia J. MR Venography in the Pediatric Patient. AJNR Am J Neuroradiol. 2005;26(1):50-5
Carr JC, Carroll TJ (2012). Magnetic Resonance Angiography: Principles and Applications. Chicago, IL: Springer.
Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(4):

38. Contact Information
Jennifer Trinh, MD
Department of Radiology
Santa Clara Valley Medical Center
751 S. Bascom Ave.
San Jose, CA 95125