mri and ct findings in cvt

1. IMAGING OF CEREBRAL VENOUS
THROMBOSIS
DR.ABHISHEK GUPTA

2. INTRODUCTION
• Cerebral venous thrombosis is a relatively
uncommon
• disorder, with an estimated annual incidence
• of between two and seven cases per million in the
• general population
• Accurate and prompt diagnosis of cerebral venous
thrombosis is crucial, because timely and
appropriate therapy can reverse the disease process
and significantly reduce the risk of acute
complications and longterm sequelae.

3. • Distribution of Thrombosed Cerebral Venous
• Structures :
• Location of Thrombus
• Superior sagittal sinus 63%
• Transverse sinus 57%
• Sigmoid sinus 15%
• Deep venous system 32%
• Internal cerebral vein 9%
• Vein of Galen 7%
• Straight sinus 15%
• Jugular bulb 8%
• Cortical vein 6%

4. Normal Venous Anatomy
• the cerebral venous system consists of the deep
venous system, superficial venous system, and dural
venous sinuses (with their superior and inferior
components)
• The superficial veins of the cerebrum empty into the
dural sinuses and are variable in morphologic structure
and location.
• Superiorly draining (ascending) superficial veins are
named for the area of cortex that they drain
• Inferiorly draining (descending) superficial veins
include
• the Labbe´ vein and
• the sylvian (superficial middle cerebral) veins

5. • The deep system includes:
• the vein of Galen,
• the internal cerebral veins, and their tributaries;
• the Rosenthal vein (basal vein) and its tributaries;
• and the medullary and subependymal veins,
• which drain the hemispheric white matter
• The deep system drains the inferior frontal lobe;
• most of the deep white matter of the frontal,
temporal, and parietal lobes;
• The corpus callosum; the upper brainstem; the
basal ganglia; and the thalamus

6. MIP image from contrast-enhanced MR venography, with a color overlay,
demonstrates the superiordural sinuses. They include the superior
sagittalsinus(green), inferior sagittal sinus (light blue), straight sinus
(dark purple), confluence of the sinuses (orange), transverse sinuses (dark blue), and
sigmoid sinuses (yellow). Theinternal jugular veins and bulbs (light purple) also are
depicted

7. Lateral MIP image from contrast-enhanced MR venography, with editing of the deep veins to improve the visibility of
the ascending veins that drain into the superior
sagittal sinus from the lateral hemispheric cortex (the frontopolar [1], anterior frontal [2], and posterior frontal [3]
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 Labbe´ vein [7], which drains into the transverse
sinus). The relative luminal diameters of the Trolard vein, Labbe´ vein, and superficial sylvian veins are reciprocal

8. Figure 3. Axial MR image series with a color overlay represents the major superficial cortical
venousdrainage territories . Most of the superior cerebrum (green) is drained primarily into the superior
sagittal sinus,which also receives drainage from the parasagittal cortical regions at lower levels. The sylvian
veins drain blood from the peri-insular region (yellow)into the basal duralsinuses. The transverse
sinusesreceive blood from the temporal, parietal, and occipitallobes (blue). The Labbe´ vein, if
dominant,may drain much of this territory. Parenchymal abnormalitiessuch as hemorrhage or edema in
this territory may be indicative of thrombosis of thetransverse sinus or Labbe´ vein.

9. Figure 4. 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

10. 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
occlusiontypically are found. The deep white matter (medullary)
venous drainage territory (blue) also is shown

11. Basal dural sinuses. Anteroposterior MIP image from contrast-enhanced MR venography, with the superficial
and deep veins removed for better visualization, shows the cavernous sinus complex (1) and, connecting
the lateral dural sinuses with the cavernous sinus, the superior petrosal sinuses (2), which arise from the
junction of the transverse and sigmoid sinuses and extend along the petrous ridge, and the inferior petrosal
sinuses(3), which arise from the distal portion of the sigmoid sinus or jugular bulb and extend along the
clivus. Alsovisible are the superficial middle cerebral vein (sylvian vein) (4), which in this case extends into the
cavernous sinus, and the emissary veins and occipital venous plexus complex (5).

12. summary
• Name Drains to
• Inferior sagittal sinus Straight sinus
• Superior sagittal sinus Typically becomes right transverse sinus
• Straight sinus Typically becomes left transverse sinus
• Occipital sinus Confluence of sinuses
• Confluence of sinuses Reference point, not an actual sinus
• Sphenoparietal sinuses Cavernous sinuses
• Cavernous sinuses Superior and inferior petrosal sinuses
• Superior petrosal sinus Transverse sinuses
• transverse sinuses Sigmoid sinus
• Inferior petrosal sinus Sigmoid sinus
• Sigmoid sinuses Internal jugular vein

13. DURAL VENOUS SINUSES

14. Definitions
• Thrombotic occlusion of intracranial
dural sinuses
• IMAging findings
• General Features
• • Best diagnostic clue
• o "Empty delta" on CECT, contrast-enhanced MR
• o Early imaging findings often subtle
• • Location: Thrombus in dural sinus +/- adjacent cortical
• vein(s)
• • Size: Variable
• • Morphology: Varies with age

15. • CT Findings
• • NECT
• o Hyperdense dural sinus> cortical vein ("cord sign")
• o Venous infarct in 50%
• • Cortical/subcortical petechial hemorrhages, edema
• • If SS/ICVs occlude, thalami/basal ganglia
• Hypodense •
• CECT
• o "Empty delta" sign in 25-30% of cases
• • Enhancing dura surrounds non enhancing
• thrombus
• o "Shaggy," irregular veins (collateral channels)
• • CTA: CT venogram (CTV) shows thrombus as filling
• defect(s) in dural sinus

16. • MR Findings
• • TlWI
• o Acute thrombus Tl isointense
• o Subacute thrombus becomes hyperintense
• • T2WI
• o Clot initially hypointense
• • Caution: If thrombus is hypointense, can mimic
• normal sinus "flow void" on T2WI
• o If venous infarct, mass effect with mixed
• hypo-/hyperintense signal in adjacent parenchyma
• o Subacute thrombus appears hyperintense
• o Chronically occluded, fibrotic sinus eventually
• appears isointense

17. • • PD/Intermediate
• o Loss of normal flow voids
• o More sensitive sequence than T2WI, less
sensitive
• than FLAIR
• • FLAIR
• o Thrombus hyperintense
• o Venous infarcts hyperintense

18. • • T2* GRE
• o Thrombus hypointense, "blooms"
• o Petechial and/or parenchymal hemorrhages
• hypointense
• • DWI
• o 40% have hyperintense clot in occluded vessel
• o DWI/ ADC findings in parenchyma variable,
• heterogeneous
• • Mixture of vasogenic + cytotoxic edema; cytotoxic
• edema may precede vasogenic
• • Parenchymal abnormalities more frequently
• reversible than in arterial occlusions

19. • Tl C+
• o Peripheral enhancement around acute clot
• o Chronic sinus thrombosis can enhance due to
• organizing fibrous tissue
• • MRV
• o Absence of flow in occluded sinus on 2D TOF MRV
• • "Frayed" or "shaggy" appearance of venous sinus
• • Abnormal collateral channels (e.g., enlarged
• medullary veins)
• o Tl hyperintense (subacute) clot can masquerade as
• flow on MRY, evaluate standard sequences and
• source images to exclude artifacts
• o Contrast-enhanced MRV (CE-MRV) better
• demonstrates thrombus, small vein detail, and
• collaterals, much faster than 2D TOF
• o PC MRV not limited by Tl hyperintense thrombus
• • MRS: Helpful if equivocal (differentiate from tumor)

20. • Angiographic Findings
• • Occlusion of involved sinus
• • Slow flow in adjacent patent cortical veins
• • Collateral venous drainage develops
• Imaging Recommendations
• • Best imaging tool
• o NECT, CECT scans +1- CTV as initial screening
• o MR, MRV (include T2*, DWI, T1 C+)
• • Protocol advice
• o If CT scan negative, MRI with MRV
• o If MRV equivocal, DSA

21. • I DIFFERENTIAL DIAGNOSIS
• Normal
• • Blood in vessels normally slightly hyperdense on
• NECT scans
• • Common in newborns (combination of unmyelinated
• low density brain, physiologic polycythemia)
• Anatomic variant
• • Congenital hypoplastic/absent transverse sinus
• (transverse sinus flow gaps 31%, usually non dominant
• sinus)
• • Right transverse sinus dominant 59%, left dominant
• in 25%, codominant in 16%
• • "High-splitting" tentorium
• • Fat in sinus

22. • "Giant" arachnoid granulation
• • Round/ovoid filling defect (clot typically long, linear)
• • CSF density/signal intensity
• • Arachnoid granulations normal in 24% of CECT, 13%
• ofMR
• o Transverse sinus most common location by imaging,
• L>R
• o SSSmost common location for arachnoid
• granulations on histopath (in lateral lacunae, not
• well seen by imaging)
• False "empty delta" sign
• • SDH, subdural empyema
• Neoplasm
• • Venous infarct can enhance, mimic neoplasm
• • Intravascular lymphomatosis (rare)

24. • PATHOLOGY
• General Features
• • Genetics
• o Genetics (inherited pre • Resistance to activated protein C (typically due to
• factor V Leiden mutation) = most common cause
• of sporadic CVT
• • Protein S deficiency
• • Prothrombin (factor II) gene mutation (G20210A)
• • Etiology
• o Wide spectrum of predisposing causes (> 100
• identified)
• • Trauma, infection, inflammation
• • Pregnancy, oral contraceptives
• • Metabolic (dehydration, thyrotoxicosis, cirrhosis,
• etc)
• • Hematological (coagulopathy)
• • Collagen-vascular disorders (e.g., APLA syndrome)
• • Vasculitis (e.g., Behcet)
• o Most common pattern: Thrombus disposing conditions)

25. • Most common pattern: Thrombus initially forms
in
• dural sinus
• • Clot propagates into cortical veins
• • Venous drainage obstructed, venous pressure
• elevated
• • BBBbreakdown with vasogenic edema,
• hemorrhage
• • Venous infarct with cytotoxic edema ensues

26. • Staging, Grading or Classification Criteria
• • Venous ischemia
• o Type 1: No abnormality
• o Type 2: High signal on T2WI!FLAIR; no
• enhancement
• o Type 3: High signal on T2WI!FLAIR;
enhancement
• present
• o Type 4: Hemorrhage or venous infarction

32. CORTICAL VENOUS THROMBOSIS
• Definitions
• • Superficial cerebral vein thrombotic occlusion
• with/without associated dural sinus thrombosis (DST)
• ~1/~AGINGiflNiOI.NGS
• General Features
• • Best diagnostic clue: "Cord sign" on NECT, T2* GRE
• • Location: Cortical veins (supra- > infratentorial)
• • Size: Varies from small to extensive clot
• • Morphology: Linear, cigar-shaped thrombus

33. • CT Findings
• • NECT
• o Hyperdense cortical vein ("cord sign") +/- DST
• o May have parenchymal abnormality
• • Petechial hemorrhage, edema
• • If internal cerebral veins (lCV) occlude, thalami
• and/or basal ganglia become hypodense
• • CECT
• o "Empty delta" sign in 25-30% of cases

34. • • Enhancing dura surrounds non enhancing
• thrombus
• o "Shaggy," irregular veins (collateral channels)
• • CTV
• o Depicts thrombus as filling defect in cortical
veins
• o Abnormal collateral channels (e.g., enlarged
• medullary veins)
• o Limited value in chronic CVT (organizing
• thrombosis also enhances)

35. • MR Findings
• • TlWI
• o Clot: Early Tl isointense, later hyperintense
• o Most conspicuous sequence if clot subacute
• o Venous infarct: Gyral swelling, hypointense edema,
• may be hemorrhagic
• • T2WI
• o Clot: Often T2 hypointense mimicking flow void,
• much later hyperintense
• o Venous infarct: Gyral swelling, hyperintense edema,
• may be hemorrhagic
• • FLAIR
• o Thrombus usually hyperintense
• o Best demonstrates hyperintense edema

36. • T2* GRE
• o Clot: Hypointense with blooming
• o Venous infarct: More sensitive for hemorrhage,
• often petechial • DWI
• o DWI/ ADC imaging findings heterogeneous
• dependent on presence of ischemia, type of edema,
• hemorrhage
• o Distinguishes cytotoxic from va sogenic edema
• o Restriction can be seen in clot properi occluded
• veins at time of diagnosis might be predictive of low
• rate of vessel recanalization 2 or 3 months later

37. • • T1 C+
• o Acute/early subacute clot: Peripheral enhancement
• outlines clot
• o Late clot: Thrombus, fibrous tissue often enhances
• o Venous infarct: Patchy enhancement
• • MRV
• o 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)
• o Contrast-enhanced MRV (CE-MRV)
• • Fasteri better depicts non enhancing thrombus &
• small veins than TOF

38. • o TOF limitations
• • Tl hyperintense thrombus falsely appears as
• patent flow on MIP
• • Must evaluate source images & conventional MRI
• sequences
• o Phase contrast MRV: Tl hyperintense thrombus not
• misrepresented as flow
• • MR Perfusion
• o T2* Gadolinium perfusion may show extensive
• venous congestion, but without perfusion deficits
• o May playa role in detecting venous congestion vs
• venous infarction in CVT

39. • Ultrasonographic Findings
• • Transcranial Doppler (TCD) ultrasound
• o Monitor venous flow velocities at ICU bedside
• o Follow therapy as decreasing velocities
• o Caveat: Normal venous velocities in serial
• measurements do not exclude a diagnosis of CVT
Angiographic Findings
• • Conventional: More accurate than MRI, particularly
• for isolated cortical vein thrombosis
• • Interventional: Treatment with thrombolytics and/or
• mechanical de clotting

40. • Imaging Recommendations
• • Best imaging tool
• o NECT, CECT scans +/- CTV
• o Conventional DSA most sensitive for CVT (useful
if
• intervention planned)
• • Protocol advice
• o If initial CT scan negative, MRI with MRV
• o If MR, MRV equivocal ...•DSA

41. • DIFFERENTIAL DIAGNOSIS
• Normal
• • Intravascular blood in vessels normally slightly
• hyperdense on NECT
• Anatomic variant
• • Congenital hypoplasia of transverse sinus
• • Vein of Trolard, Labbe, superficial middle cerebral vein
• have reciprocal relationship
• "Giant" arachnoid granulation
• • Round/ovoid filling defecti clot is long, linear
• • CSF density, signal intensity
• Cerebral hemorrhage
• • Mimics venous infarct
• • Amyloid, contusion, hypertensive

42. • [CLINICALISSl.JES· .
• Presentation
• • Most common signs/symptoms
• o Most common symptom is headache (95%)
• o Seizure (47%), paresis (43%), papilledema (41%)
• o Altered consciousness (39%), comatose (15%)
• o Isolated intracranial hypertension (20%)

43. • Natural History & Prognosis
• • Clinical diagnosis often elusive
• • Extremely variable outcome; asymptomatic to death
• • Up to 50% of cases progress to venous infarction
• • Pulmonary embolism is uncommon but carries a poor
• prognosis
• • Poor outcome associated with papilledema, altered
• consciousness, coma, age> 33, diagnostic delay> 10
• days, intracerebral hemorrhage, involvement of
• straight sinus
• • Good outcome associated with isolated intracranial
• hypertension presentation, delta sign on CT (leading

50. DEEP CEREBRAL VENOUS
THROMBOSIS
• Definitions
• • Thrombotic occlusion of deep cerebral veins
• • DCVT usually affects both lCVs +/- vein of
Galen (V of
• G), straight sinus (SS)
• • More widespread dural sinus thrombosis
(DST),
• cortical vein occlusion may occur

51. IMAGING FINDINGS
• • Best diagnostic clue: Hyperdense ICV on NECT +/-
• bithalamic hypodense edema, variable DST
• • Location
• o Clot in ICV +/- V of G, SS, basal veins of Rosenthal
• o Bilateral ICV thrombosis »> unilateral
• o Deep gray nuclei, internal capsule, medullary WM
• typically affected
• o Variable involvement of midbrain, upper cerebellum
• (V of G, SS territory)
• • Size: Parenchymal involvement varies in extent
• • Morphology: Cigar shaped, "cord-like"

52. • CT Findings
• • NECT
• o Hyperdense vein = "cord sign" +/- DST
• o +/- Parenchymal abnormality
• • If ICVs occlude, thalami/basal ganglia appear
• hypodense with loss of GM/WM interfaces
• • Petechial hemorrhages may be present
• • CECT
• o "Empty delta" (if DST)
• o "Shaggy," irregular veins (collateral channels) in
• deep WM, around tentorium
• • CTV
• o Loss of ICV enhancement, presence of enlarged
• collateral channels
• o Limited value in chronic organizing thrombosis as
• also enhances

53. • MR Findings
• • TlWI
• o Clot: Early Tl isointense, later hyperintense
• o Most conspicuous sequence if clot subacute
• o Venous hypertension: Hypointense swelling of
• thalami, basal ganglia
• o Venous infarct: Hypointense edema, may be
• hemorrhagic
• • T2WI
• o Clot: Often T2 hypointense mimicking flow void
• ("pseudo flow void"), much later hyperintense

54. • o Venous hypertension: Hyperintense swelling of
• thalami, basal ganglia
• • Corresponds to vasogenic +/- cytotoxic edema
• o Venous infarct: Parenchymal swelling, hyperintense
• edema, may be hemorrhagic
• • PLAIR
• o High signal in occluded veins
• o Best demonstrates hyperintense edema
• • T2* GRE
• o Clot: Hypointense with blooming
• o Venous infarct: More sensitive for hemorrhage,
• often petechial

55. • DWI
• o Distinguishes cytotoxic from vasogenic edema
• o DWlj ADC imaging findings heterogeneous
• o May restrict early (hyperintense BG/thalami)
• normalize later
• o Restriction can be seen in clot proper; occluded
• veins at time of diagnosis might be predictive of low
• rate of vessel recanalization 2 or 3 months later
• • T1 C+
• o Acute/early subacute clot: Peripheral enhancement
• outlines clot
• o Late clot: Thrombus, fibrous tissue often enhances
• o Venous stasis in deep WM (medullary) veins seen as
• linear enhancing foci radiating outwards from
• ventricles
• o Venous hypertension: No parenchymal
• enhancement
• o Parenchymal venous infarct: Patchy enhancement

56. • MRV
• o 2D time of flight (TOP) MRV shows "missing" ICVs,
• variable absent signal in V of G, SS
• • May see abnormal collateral channels
• o Contrast-enhanced MRV (CE-MRV)
• • Paster; better depicts non enhancing thrombus &
• small veins than TOP
• o TOP limitations
• • T1 hyperintense thrombus falsely appears as
• patent flow on MIP
• • Always evaluate source images & conventional
• MRI sequences

57. • o Phase contrast MRV: T1 hyperintense thrombus not
• misrepresented as flow
• • MRS: Reduced metabolites, lactate in infarcts may
help
• differentiate from non-vascular pathology (bithalamic
• glioma) in equivocal cases
• • MR perfusion
• o T2* Gadolinium perfusion may show extensive
• venous congestion, but without perfusion deficits
• o May playa role in detecting venous congestion vs
• venous infarction in CVT

58. • Angiographic Findings
• • Conventional
• o DSA more accurate than MRI
• o Unlike quite variable superficial veins, deep cerebral
• veins are always present on angiography
• • In DCVT, occluded ICVs don't opacify
• • Collateral venous channels (e.g., pterygoid veins)
• enlarge
• • Interventional: Treatment with thrombolytics and/or
• mechanical de clotting

59. • DIFFERENTIAL DIAGNO$I$
• Bilateral abnormalities of thalami, basal
• ganglia (e.g., glioma, toxic/metabolic
• disorders)
• • Tumors: Lymphoma, glioma
• o Normal venous system
• o Elevated choline
• o Vasogenic not cytotoxic edema
• • Toxic/metabolic: Carbon monoxide poisoning

60. • • Non-venous ischemic injury: Global hypoxia,
arterial
• (tip of basilar occlusion, artery of Percheron)
infarcts
• o Normal venous system
• o History of hypoxic event
• o Abnormal arterial evaluation

61. Axial NEeT shows bithalamic low density
edema/ischemia (arrows) and increased
density in
internal cerebral, thalamostriate veins &
straight sinus
from thrombosis (open arrows

62. Lateral DSA shows absence of deep cerebral
veins and
straight sinus consistent with deep cerebral
venous
thrombosis. The deep venous system should
always be
seen on DSA.