anatomoy of ceebral veins...sinuses..presentation..puerperal and Non puerperal CVt... management

1. ANATOMY OF CEREBRAL VEINS AND ITS APPLICATION IN
CLINICAL MEDICINE-CEREBRAL VENOUS THROMBOSIS
PRESENTER – DR AMAR PATIL
PG MEDICINE

2. PREVIEW
 Anatomy of Cerebral Veins and Sinuses.
 Epidemiology of Cerebral Vein and Sinus Thrombosis.
(Puerperal and nonpuerperal)
 Risk Factors of Cerebral Vein and Sinus Thrombosis.
 Clinical Presentations of Cerebral Vein and Sinus Thrombosis.
 Radiological Diagnosis of Cerebral Venous Thrombosis.
 Treatment of Cerebral Venous and Sinus Thrombosis.
 Interventional Neuroradiology in the Treatment of Cerebral Venous
Thrombosis.
 Complications of Cerebral Vein and Sinus Thrombosis.
 Long-Term Prognosis of Cerebral Vein and Sinus Thrombosis.

3. ANATOMY OF CEREBRAL VEINS
 The cerebral veins are divided into
 The superficial and
 Deep groups.
 The superficial group drains the cortical surfaces.
 The deep group drains the deep white and gray matter and collects into
channels that course through the walls of the ventricles and basal cisterns
to drain into the internal cerebral, basal, and great veins.

4. SUPERFICIAL OR
EXTERNAL CEREBRAL VEINS
 Drain the surface (cortex) of cerebral hemisphere:
 3 groups:
 Superior cerebral veins
 Middle cerebral veins
 Inferior cerebral veins.

5.  Superior cerebral veins
 8 to 12 in number
 Drain- Superolateral and
Medial surface
 Ascends upwards ->
Arachnoidmater ->Subdural space-
> Superior saggital sinus.
 Middle cerebral veins
 Four in number : 2 on each side
 Superficial middle cerebral vein
 Deep middle cerebral vein.

6.  Superficial middle cerebral vein :
 Lies superficially in lateral sulcus.
Anteriorly, drains into cavernous
sinus.
 Posteriorly, communicates with
Superior sagittal sinus through
superior anastomotic vein (of
Troland).
 With Transverse sinus via inferior
anastomotic vein of Labbe.
 Deep Middle Cerebral Vein
 Lies deep in lateral sulcus.Joins
anterior cerebral vein to form the
basal vein.

7. INFERIOR CEREBRAL VEINS
 Drains :
 Inferior surface,
 Lower parts of medial
and superolateral
surfaces.

8. BASAL VEIN OF ROSENTHAL
 Basal vein of Rosenthal:
 Formed at base of brain
 By union of three veins:
 (1) Anterior cerebral
vein:Accompanies anterior
cerebral artery. Drains
medial surface.
 (2) Deep middle cerebral vein
 (3) Striate vein
 Basal vein terminate into Great
cerebral vein of Galen

9. GREAT CEREBRAL VEIN OF GALEN
 Length 2cm
 Union of 2 internal
cerebral vein
 Receives two basal
veins.
 Two internal cerebral
veins joins to form->
Great cerebral vein of
Galen-> Straight sinus.

10. DURAL SINUSES AND VEINS
 The dural sinuses receive cerebral veins from the superficial and deep parts.
 These are: (1) superior and inferior sagittal
 (2) straight
 (3) transverse
 (4) tentorial
 (5) cavernous
 (6) superior petrosal.

11. SUPERIOR AND INFERIOR SAGITTAL SINUSES
 Superior sagittal sinus
superiorly attached to the
falx cerebri ends with crista
galli. In about 60% of cases,
superior sagittal sinus ends
by becoming the right
transverse sinus.
 At the termination of the
superior sagittal sinus is a
dilatation, known as
confluence of the sinuses. It
is also known as torcula
herophili.

12.  The superior sagittal sinus also communicates with veins in the scalp through
emissary veins that pass through the parietal foramina. The cortical veins may
pass directly to the superior sagittal sinus, or they may join the meningeal
sinuses, which empty into the superior sagittal sinus.
 Inferior sagittal sinus occupies the posterior two thirds of the free inferior
edge of the falx cerebri. It ends by joining the great cerebral vein to form
straight sinus.

13. STRAIGHT SINUS
 This venous sinus is formed by
the union of the inferior sagittal
sinus with the great cerebral
vein.
 It is attached to the tentorium
cerebelli. It may drain into
either the transverse sinus or,
most commonly, the left
transverse sinus.

14. TRANSVERSE SINUSES
 These venous sinuses pass laterally
from the confluence of the sinuses in
the attached border of the tentorium
cerebelli.
 The right transverse sinus, which is
usually larger, receives the majority of
the drainage from the superior sagittal
sinus. Receive blood from superficial
parts of the brain.
 Left transverse sinus, left sigmoid sinus
and left internal jugular vein contain
blood mainly from the deep parts of
the brain drained by the internal
cerebral, basal and great veins.

15. TENTORIAL SINUSES
 These sinuses divide into the medial and lateral groups.
 The medial group drains into transverse sinuses and
 The lateral group drains into both straight and transverse sinuses.

16. CAVERNOUS SINUSES
 These large sinuses are about 2
cm long and 1 cm wide. They are
located on each side of sella
turcica and the body of the
sphenoid bone.
 There are many trabeculae that
contain blood channels.
 Each cavernous sinus receives
blood from the superior and
inferior ophthalmic veins, the
superficial middle cerebral vein in
the lateral fissure of the cerebral
hemispheres.

17.  Many important structures pass
through the sinus –
 Internal carotid artery
 Abducent nerve (vi)
 Structures present in the lateral
wall of the sinus include
 Occulomotor nerve(iii)
 Trochlear nerve (iv)
 Opthalmic nerve (v 1)
 Maxillary nerve (v 2)

18. PETROSAL SINUSES
 These venous sinuses are small
channels that drain the
cavernous sinuses.
 They run from the posterior
ends of the cavernous sinuses to
the transverse sinuses. Both of
petrosal sinuses lie in the
attached margins of the
tentorium cerebelli.

19. DEEP VEINSVEINS
Thalamostriate vein Septal vein
Internal Cerebral
vein (2)
Basal vein of
Rosenthal (2)
Occipital
vein
Posterior
Pericallosal
vein
Mesencephalic
vein
Precentral
Cerebellar
vein
Vein of Galen Inferior Sagittal Sinus
Straight Sinus

20. CEREBRAL VENOUS THROMBOSIS(CVT )
 Epidemiology
 Puerperal CVT and non-puerperal CVT
 Etiology and risk factors.
 Clinical features
 management

21. DIFFERENCE BETWEEN ARTERIAL AND VENOUS STROKE
Arterial stroke
 Mechanism- Vascular damage,
involves pertaining to the site of
involvement.
 Pathology- at the site of endothelial
injury, usually occlude the blood flow.
 Clinical presentation- acute or
insidious onset(usually hours), deficit
will be maximum at onset in embolic
stroke.
Venous stroke
 Mechanism –venous stasis, decreased
fibrinolytic activity.
 Pathology – at the area of stasis,
invariably occlude the blood flow, can
cause venous thromboembolism.
 Clinical presentation – slowly
progressive(generally days), less severe,
associated with headache, seizures or
LOC.

22. CVT- INTRODUCTION
 Cerebral venous thrombosis(CVT) is the presence of
acute thrombosis (a blood clot) in the dural venous sinuses, which
drain blood from the brain.
 It involves the thrombosis of the cortical veins and the draining
venous sinuses, either alone or in combination.
 Cerebral venous thrombosis is an uncommon cause of stroke with
extremely varied clinical presentations, predisposing factors, imaging
findings, and outcomes.
 The first description of CVT, appearing in the French literature in
1825, was by Ribes, in a 45-year old man who died after a 6-month
history of severe headache, epilepsy, and delirium.

23.  Venous infarctions in the course of venous thrombosis (involving sinuses,
deep and superficial veins) are much rarer than ischemic strokes of arterial
etiology (2.7 per million in general population) and constitute about 0.5–1%
of causes of all strokes.
 They most often occur in young patients, more frequently in women (about
75% of patients) .

24. WHEN TO SUSPECT CVT?
 Gradual onset.
 History of cranial nerve palsies, diplopia, tinnitus.
 Headache –throbbing type or band like or thunder clap also associated with
vomiting.(without any neurological signs difficult to diagnose)
 History of seizures.
 Patient in altered sensorium or in coma.
 History of cancer, recent head injury, recurrent venous thrombosis,
autoimmune diseases such as systemic lupus erythematous, puerperium
and/or pregnancy and the use of oral contraceptives should all raise the
attention of the physician for a possible CVT.

25. PUERPERAL CVT
 Epidemiology
 Incidence
 Presentation
 statistics

26. PUERPERAL CVT
 Puerperium and pregnancy, as predisposing factors for CVT, are well
known. Most of the pregnancy-related CVT occurs in the third trimester or
puerperium.
 During pregnancy and for 6-8 weeks after birth, women are at increased
risk of developing venous thromboembolic (VTE) events.
 Pregnancy induces several Prothrombotic changes in the coagulation
system that persists at least during early puerperium. Hypercoagulability
worsens after delivery as a result of anemia, volume depletion,
dehydration and trauma.

27.  Physiological changes during pregnancy include increase in red cell mass
and plasma volume with dilutional anemia.
 The plasma levels of protein S decline progressively during pregnancy
while protein C levels remain unchanged.
 There is also increase in D-dimer levels in late pregnancy due to
increased thrombin generation and fibrinolysis. Coagulation factors may
be elevated during postpartum state up to 12 weeks.
 These changes during pregnancy and postpartum period confer a higher
risk of venous thrombosis.

28. EPIDEMIOLOGY
What is the Magnitude of the Problem in India?
 It has been thought that the incidence of puerperal CVT may be more in
India compared to the western countries. This was probably due to the
reporting of many large series of puerperal CVT from India in the 70's and
80's.
 Vascular diseases are the most common disorders of the brain. They mainly
affect older population, but in 25% of cases they also occur in patients
younger than 55 years old.

29. EPIDEMIOLOGY
 In the largest hospital-based prospective cohort study from India (Nizam's
Institute Venous Stroke Registry [NIVSR]) by Narayan et al., 428 consecutive
patients with CVT were enrolled over a period of 8 years from a tertiary care
hospital from South India, the mean age of the patients in this study was
31.3 years.
 Most of the earlier case series from India reported a higher proportion of
women suffering from CVT than men.
 In 1957, Padmavati et al., for the first time from India, reported 15 cases of
CVT in puerperium in an epidemiological study evaluating the causes of
hemiplegia in 44 women. It was at that time recognized as a diagnosis which
was mostly made at autopsy and considered lethal.

30. EPIDEMIOLOGY
 In a study by Nagaraja et al., A large hospital-based case series of 317 patients
with CVT recruited over a period of 8 years during the 80's had only 15 male
patients.
 This gender bias was usually attributed to gender-specific risk factors like the
usage of oral contraceptives (OCPs) and the influence of other factors such as
pregnancy, puerperium, and hormone replacement therapy.
 In contrast to this, the recent case series from India do not show this trend of
female dominance.

31. EPIDEMIOLOGY
 In the study of 428 patients of CVT recruited from a tertiary care hospital of
Hyderabad, Narayan et al., had a larger proportion of males than
females.(M=53.7% F= 46.3%)
 Showing a similar trend, a large prospective study by Pai N et al., which
recruited 612 consecutive patients of CVT from various hospitals of Mumbai
had a male to female ratio of 3:2.
 The plausible reason for this change in gender trends over the last two
decades could be the improvement in obstetric care.

32. INCIDENCE OF PUERPERAL CVT
 In the recent years with improving health-care system, there is a reduction in
the pregnancy-related CVT. The occurrence of pregnancy-related venous
thrombosis has been reported to be 9.8% to 17% of all the CVT.
 The prevalence of CVT in Indian population is about 4.5/1000 obstetric
admissions.
 CVT is more common in primigravidae.
 In 1984, Srinivasan, reported 135 cases of stroke in women, of whom only 6
had an arterial stroke, and the rest had a CVT.

33.  In the recent times, a change in this trend has been noted. The NIVSR cohort
study and the study by Pai et al., have reported only 9.8% and 8% patients in
the postpartum or pregnant state, respectively.
 CVT was found to be 12 times more common in India than in Western
countries. An angiographically proven study reported that 50% of the total
cases of stroke in young women were related to pregnancy and puerperium,
95% of which were due to CVT.

34. RISK FACTORS
 Increasing maternal age, increased duration of hospital stay, cesarean
delivery, instrument-assisted delivery, hypertension, infections, and
excessive vomiting in pregnancy increase the risk of developing CVT.
 Cultural practices such as water deprivation, unhygienic home deliveries,
anemia, and malnutrition have been proposed to promote pregnancy-
related CVT in India.
 Nagaraja et al., (2007) stated that the pregnancy and puerperium increase
the risk of thrombotic events, and these risks are likely to be increased in
women who are carriers of thrombophilic gene polymorphisms.

35. CLINICAL PRESENTATION-PUERPERAL CVT
 In contrast to the arterial stroke, which can be easily diagnosed clinically in a
majority of the cases, CVT has no single pattern of presentation, and it may be
difficult to diagnose it on clinical grounds alone.
 Clinical findings in CVT fall into two major categories: Those related to
increased intracranial pressure due to impaired venous drainage; and, those
related to focal brain injury from venous ischemia/infarction or hemorrhage.

36. CLINICAL PRESENTATIONS IN VARIOUS INDIAN STUDIES.
Symptoms(%) Nagaraja D
al(n=76)
Srinivasan K
et al(n=135)
Narayana et
al(n=428)
Pai et
al(n=628)
Headache 72 78 88.3 61.9
Fever 22 15 5.4 -
Seizuers 68 64 39.9 31.2
Altered
sensorium
93.4 43 14.5 -
Focal deficits 65.4 47.4 27.3 47.7
Papilloedema 27 15.5 63.4 62.4

37. NON PUERPERAL CVT
 Epidemiology and incidence
 Etiology
 Risk factors
 Clinical presentation
 Management .

38. EPIDEMIOLOGY
 CVST is a disease with potentially serious consequences and usually
affecting young to middle-aged people. Strokes in the young account for
nearly 30% of all cases of stroke in India and cerebral venous thrombosis
(CVT) accounts for 10-20% of these cases.
 Banerjee et al., in an autopsy series in late 1980's found that CVT
accounted for almost 10% of all strokes in India.
 In a hospital-based study from South India in the 1980's, 15% of strokes
were in individuals <40 years of age and CVT accounted for 15-20% of
these cases.

39. INCIDENCE
 CVST represents 0.5%-1% of all strokes.
 various study revealed significant number of patients affected by CVST in
2nd and 3rddecade of life, predominantly affecting female population,
approximately one third.
 Most common sinus affected in male is sigmoid and transverse sinus
thrombosis. Sagittal sinus is most commonly affected in female population.

40. CAUSES OF CVT
Infective Causes Non Infective Causes
Local – Intracranial infections like
abscess, subdural empyema and
meningitis.
Local – Head injury, Post
Neurosurgery, Tumours like
cholesteatoma, meningioma)
Regional infection – Otitis,
Sinusitis, Orbital cellulitis.
OBGY – Pregnancy, Post Partum,
OCP’s
General – Bacterial sepsis,
Typhoid, TB, Mycoplasma
pneumonia, hepatitis virus B and
C
Any surgery
Severe dehydration of any cause
Inherited Thrombophilia – Anti-
thrombin C deficiency, Protein

41. CAUSES OF CVT
Non infective causes - contd
Acquired coagulation disorders –
Nephrotic syndrome, APLA,
Homocystinemia
Inflammatory diseases like SLE,
Behcet’s disease
Medications – IV or intrathecal
Drugs
Oral contraceptives
Hormone replacement therapy
Androgens.

42. CAUSES OF CVT
Blood disorders
Leukaemia
Anemia
Myeloproliferative disorders
Polycythemia
Sickle-cell trait
Thrombotic thrombocytopenic purpura
Heparin-induced thrombocytopenia
Coagulopathies
Protein S, protein C deficiency
Antithrombin III deficiency
Factor V Leiden deficiency.
Antiphospholipid antibodies

43. RISK FACTORS
 Nonmodifiable
 Age
 Gender
 Race – undetermined.
 Heredity
 Modifiable
 Postmenopausal replacement therapy
 Oral contraceptives
 Infection
 Hypertension
 Diabetes
• Hypercholesterolemi
a
• Obesity
• Alcohol
consumption
• Homocysteine
• Cancer

44. POLYCYTHEMIA AND THROMBOSIS
 PV is a myeloproliferative disorder manifested by overproduction of erythrocytes,
granulocytes, and megakaryocytes.
 The incidence of thrombosis and bleeding in PV was reported to be 12-39% and 1.7-
20%, respectively.
 In PV, arterial, venous or microcirculatory thrombosis may occur. The frequency of
venous events is less than for arterial ones
 5. Elliott MA, Tefferi A. Thrombosis and haemorrhage in polycythaemia vera and essential thrombocythaemia. Br J
Haematol. 2005;128:275–290

45. ANEMIA AND CVT
 Several mechanisms have been proposed to explain the association between
IDA and thrombosis, as iron is an important regulator of thrombopoiesis: low
iron levels disinhibit megakaryocyte activity , which provokes secondary
thrombocytosis, thus leading to a hypercoagulable state.
 In addition, microcytosis alters red cells deformability, which increases
viscosity and possibly the risk of venous thrombosis.
 Finally, anemic hypoxia secondary to iron deficiency may occur as the
oxygen-carrying capacity of erythrocytes decreases, especially in situations
where the metabolic demands are increased.
 All these conditions lead to a turbulent blood flow, causing platelets to come
more frequently in contact with the endothelial lining.

46. ANEMIA AND CVT
 In a study by Anand Viswanathan et al.,in 121 prospectively recruited
patients with noninfectious causes of CVT and 120 healthy age- and sex-
matched controls.
 Severe anemia (hemoglobin <9 g/dL) was more common in patients with
CVT than in controls (14 vs. 2 patients; P=0.005).
 Most patients with severe anemia were female (n=15; 94%).

47. PATHOGENESIS

48. CLINICAL PRESENTATIONS OF CEREBRAL VEIN AND SINUS THROMBOSIS.
 The presenting features of CVT usually depend on the sinuses involved,
speed of occlusion, involvement of the cortical veins and the presence of
collaterals.
 Symptoms of CVT have been grouped under three major clinical
syndromes-
 1- Isolated intracranial hypertension syndrome( headache with or without
vomiting ,papilledema ,and visual problems )
 2- Focal syndrome (focal deficits or seizures or both)
 3- Encephalopathy ( multifocal signs ,mental status changes ,stupor or
coma )

49. ISOLATED INTRACRANIAL HYPERTENSION SYNDROME
 Headache is the most common and least specific of all symptoms of CVT . It
is usually the first symptom in CVT .
 Headache is gradual in onset , increase over a period of days to weeks ,
severe in intensity sometimes throbbing type.
 Bilateral diffuse associated with vomiting.
 In some patients it may be severe thunderclap type of headache mimicing
subarachnoid haemorrhage .
 In patients with raised ICP it is severe, diffuse ,generalized pain which
worsens on valsalva manouver and recumbence. Visual obscurations may
occur coinciding with these bouts .
 It may resemble migrane with aura .

50.  Patients affected by cerebral venous thrombosis
can present with threatened vision, visual
obscuration, visual loss and constriction of the
visual field.
 Papilledema on fundoscopy can be initially
evidenced as optic disc swelling, elevating and
blurring.
 Furthermore, papilledema is commonly
associated with other signs of intracranial
hypertension such as headache, vomiting and
bradycardia.
 In the absence of treatment, papilledema is
known to lead to optic atrophy.

51. FOCAL SYNDROME (FOCAL DEFICITS OR SEIZURES OR BOTH)
 Seizures the next commonest symptom occur in about 40 to 70% of
patients with sinus thrombosis.
 They may be focal but more commonly generalized.
 Life threatening status epilepticus or clusters may be seen in 20% patients.
 Neurological signs develop in 50% of patients with sinus thrombosis and
include monoparesis, or hemiparesis.
 Focal neurological deficits such as paresis, dysphasia, visual-spatial
disorders, and homonymous hemianopia are common symptoms in 15% of
patients affected by cerebral venous thrombosis and they can be observed
in up to 50% during the course of the disease.

52. FOCAL SYNDROME
 Cranial nerve palsies are reported in 12% of all cases of cerebral venous
thrombosis.
 The cranial nerves that have been described to be involved are III, IV, V, VI,
VII, VIII, IX, X and XI, and the involvement can be multiple or single.
 In patients with lateral sinus thrombosis, diplopia due to VI nerve palsy
and signs of V nerve irritation with temporal and retro-orbital pain, it has
also long been known as the Gradenigo syndrome, suggesting
involvement of the nerves at the petrous apex.

53. FOCAL SYNDROME
 In rare cases, cranial nerve palsies can be the only sign of cerebral venous
thrombosis, especially when there is the involvement of the
transverse/sigmoid sinus (VI, VII and VIII cranial nerves) .
 The unilateral or bilateral VI cranial nerve involvement can also be due to
the intracranial hypertension itself.
 The involvement of the III, IV, V and VI cranial nerves can be due to the
thrombosis of the anterior cavernous sinus.
 An involvement of the IX, X and XI cranial nerves is possible when the
location of the thrombosis is in the posterior cavernous sinus or the
internal jugular vein, or the deep venous system or the cerebellar veins.

54. CAVERNOUS SINUS SYNDROME
 Cavernous sinus thrombosis is rare and represents about 0.5–2% of all
cerebral venous thrombosis it can have infective etiology especially in
younger patients, and has characteristic clinical features.
 Cavernous sinus thrombosis, often secondary to infection from orbital
cellulitis (frequently Staphylococcus aureus), a cutaneous source on the face,
or sinusitis (especially with mucormycosis in diabetic patients), is the most
frequent cause;.
 other etiologies include aneurysm of the carotid artery, a carotid-cavernous
fistula (orbital bruit may be present), meningioma, nasopharyngeal carcinoma
and other tumors.

55. CAVERNOUS SINUS SYNDROME
 Often, the onset in the anterior cavernous sinus
thrombosis is abrupt with headache, ocular pain,
chemosis, proptosis, ocular nerve palsy (III, IV, VI and
the ophthalmic division of V) and fever in the case of
infective etiology.
 In some cases, ocular nerve palsy can be the
exclusive symptom. Posterior cavernous sinus
thrombosis, spreading to the inferior petrosal sinus,
may cause palsies of cranial nerves VI, IX, X and XI
without proptosis.

56. ENCEPHALOPATHY
 A generalized encephalopathic illness without localizing signs or recognizable
features of raised intracranial pressure is another pattern of presentation.
 A depressed level of consciousness is the most constant finding, varying from
drowsiness to deep coma.
 Disturbances of consciousness and cognitive dysfunctions such as delirium
,apathy , frontal lobe syndrome ,multifocal deficits can be present .

57. MANAGEMENT OF CVT
 Laboratory Studies
Current guidelines from AHA/ASA recommend routine blood studies
consisting of
 Complete blood picture
 Prothrombin time
 Activated partial thromboplastin time
 Other investigations –
 D-dimer testing ( elevated levels support the diagnosis of CVT however
normal levels do not exclude the diagnosis ).
 Values of D-dimer levels >500 ng/mL may be significant.

58.  Testing for protein C, protein S, and Antithrombin deficiency is generally
indicated 2 to 4 weeks after completion of anticoagulation.
 ESR,ANA-systemic lupus erythematosus, Wegener granulomatosis, and
temporal arteritis.

59. RADIOLOGICAL
 The imaging findings in CVT can be generally divided into indirect and
direct signs of CVT .
 The findings include ‘direct signs’, i.e. primarily caused by the thrombosis of
veins and sinuses and ‘indirect signs’ when they are secondary to the
effects of thrombosis.

60. DIRECT SIGNS OF CVT ON CT SCAN
 The cord/dense sign.
 In 2–25% of patients, the
fresh thrombus can be
visualized as a subtle focus of
hyperdensity within the
occluded sinus on plain CT.
 This is best seen within the
large straight and superior
sagittal sinuses.

61.  The dense delta (filled
triangle) sign.
 This is seen on plain CT, as
a dense triangle (from
hyperdense thrombus)
within the superior sagittal
sinus.
 It is seen in up to 60% of
patients.

62.  The empty delta (empty triangle) sign.
This is seen on CT after contrast
administration, as a bright triangle
surrounding a central hypodense
core.
 It represents contrast enhancement of
the dilated collaterals surrounding
the clot. It is seen in 25–52% of
patients with sagittal, straight, and
lateral sinus thrombosis.

63. INDIRECT SIGNS OF CVT ON CT SCAN
 Indirect signs are more frequent. Venous stasis and hyperaemia caused by
occlusion of the sinuses.
 Irregular hyperdense or mixed density lesions suggestive of haemorrhagic
infarctions which are either small or large, single or multiple.
 Diffuse edema of the brain may be seen.

64. MAGNETIC RESONANCE IMAGING
 At a very early acute stage (day 1–3), there is an absence of flow void and the
thrombi appear isointense on T1- and hypointense on T2-weighted images.
 At the subacute stage (day 4–21), the thrombus becomes hyperintense,
initially on T1- (day 4–9) then on T2-weighted images (day 10–15).
 At the chronic stage (21–35 days), the MRI pattern is more variable. The
thrombosed sinus can either remain totally or partially occluded or can
recanalize.

65. Gadolinium-enhanced MRI showing decreased flow in
the left transverse sinus (a), and a corresponding ‘empty
delta sign’ (b).

66. MRV
 Magnetic Resonance
Venography
 MRV has become the
imaging modality most
widely used to establish the
diagnosis of CVT.

68. MANAGEMENT
 The main issues in CVT is the progression of thrombosis with resultant
cerebral edema, raised intra-cranial hypertension, central or uncal herniation
and death.
 If the vital parameters are maintained during acute phase, alternative channels
open up and re-canalization of sinuses occur naturally.
 So the main stay of treatment evolves round decreasing cerebral edema and
ICH and prevention of progression of thrombosis.

69. PUERPERAL CVT- TREATMENT
 In a study by Nagaraja et al., prospectively randomized 57 women with
puerperal CVT from South India into a treatment group and a placebo group.
 Twenty-nine patients received IV unfractionated heparin (UFH), 5000 IU every
6 h, and then dose-adjusted to reach aPTT of 1.5 times the initial value, and
28 subjects were in the control group.
 Two patients in the control group died, and one had a residual paresis at 6
months. In the heparin group, all patients recovered.

70.  In an open-label trial by Nagaraja et al., On 150 patients with CVT, 73 received
low-dose heparin (2500 thrice daily) and 77 did not receive heparin.
 There was a reduction of death (8 vs. 18; P < 0.001) and increase in complete
recovery (34 vs. 14; P < 0.001) in the group which received heparin compared
to that which did not receive heparin.

71. TREATMENT STRATEGIES
 For women with CVT during pregnancy, LMWH in full anticoagulant doses
should be continued throughout pregnancy, and LMWH or vitamin K
antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6
weeks postpartum (for a total minimum duration of therapy of 6 months)
 It is to advise women with a history of CVT that future pregnancy is not
contraindicated.

72. TREATMENT
 Heparin : indicated During the acute stage.
 Dosage : IV Bolus of 3,000–5,000 IU, then 1,000–1,500, IU (average 1,200IU)
per hour.
 Aim: until aPTT is doubled.
 Until clinical condition is stable (continuous stabilization of symptoms or
complete remission usually within 10–14 days.)

73. TREATMENT
 LMWH : During the acute stage
 Dosage : antifactor Xa U/kg per 24 h.
 Duration : Until clinical condition is stable (continuous stabilization of
symptoms or complete remission usually within 10–14 days)

74. ORAL ANTICOAGULANT
 Warfarin : Subacute stage
 Days 1 and 2,10 mg/day
- 3rd day, according to INR values
 Aim : Target INR 2.0–3.0
 Duration (1) Povoked CVT - 3-6 months
(associated with transient risk factor)
(2) Unprovoked CVT - 6-12 months
(3) recurrent/ CVT with severe THROMBOPHILIA / VTE after
CVT- indefinite anticoagulation

75. AED
 Phenytoin : Prophylactic in patients at risk for seizures, and in all patients
after the first seizure.
 Aim : Avoidance of seizure in acute phase and to prevent status epilepticus.
 Dosage : 500-1000mg IV over 4-6hrs after first seizure.
- For prophylaxis 300mg tid orally
 Prolonged treatment with AED for 1 year may be advised for patients with
early seizures and hemorrhagic lesions on admission brain scan, whereas in
patients without these risk factors AED therapy may be tapered off
gradually after the acute stage.

76. ANTI OEDEMA
 Mannitol 20% : Critical rise of ICP, threatened herniation
 Aim : Reduction of ICP
 Dosage : 125ml IV over 15-20min. 4-6 times/day,
 Duration : Usually for 48-72 hours.

77. Subsctance Indication Aim Doasge Duration
Acetaminoph
en
Mild headache Necessary pain relief 200-1000mg tid On demand
Tramadol Severe
headache
Necessary pain relief 50-100 mg tid
orally
On demand

78. OTHER TREATMENTS
 FIBRINOLYTIC THERAPY.
 DIRECT CATHETER ABLATION.
 MECHANICAL THROMBECTOMY / THROMBOLYSIS.
 SURGERY.

79. THROMBOLYTIC THERAPY
 Infusion of a thrombolytic agent into the dural venous sinus utilizing
microcatheter technique.
 Limited to specialized centers ,should be considered for patients with
significant deficit.
 Leads to breaks up the thrombus.
 Particulate debris is directed into an effluent lumen for collection into
a disposable bag.

80.  Alteplase
 1 mg/cm infused via venous sinus catheter throughout clot, then 1-2 mg/hr.
 Urokinase
 250,000 U/hr instilled directly or via venous sinus catheter; additional doses
50,000 U; total dose 1,000,000 U over 2 hr.
 Streptokinase
 Loading dose: 1000-3000 IU/kg; followed by infusion of 1000-1500 IU/kg/h;
CVT, administered by direct infusion via catheter.

81. DECOMPRESSIVE HEMICRANIECTOMY
 In patients with neurological deterioration due to severe mass effect or
intracranial haemorrhage causing intractable intracranial hypertension,
decompressive hemicraniectomy may be considered.
 In a recent retrospective study by Srinivas D et al., in 2012 among 34 patients
(the largest series currently) who underwent decompressive craniectomy, 26
(76.4%) achieved a favorable outcome.

82. COMPLICATIONS
1 EARLY
2 LATE
 1)EARLY
a) SEIZURES- 37% cases
 RECOMMENDATIONS
 Early initiation of AED in patients with CVT and single seizure with
parenchymal leisons for definite period is recommended to
prevent furthur seizure.
 CVT with seizures without parenchymal lesion AED initiation is
probably recommended.
 Patients without seizures routine use of AED is not recommended.

83. b) HYDROCEPHALUS
Communicating/ Obstructive
If obstructive- ventriculostomy/ VP shunt
c) INTRACRANIAL HYPERTENSION
 Seen in about 40% of patients with CVT.
 Treatment includes – Anticoagulation.
- Lumbar Puncture.
- Decompressive craniotomy.

84. LATE COMPLICATIONS
 HEADACHE- observed in 50% patients coming for follow up.
 Persistent or severe headache- rule out recurrence or intracranial HTN.
 In patients with a history of CVT who complain of new, persisting, or severe
headache, evaluation for CVT recurrence and intracranial hypertension should
be considered.
 VISUAL LOSS.
 SEIZURES.
 DURAL ARTERIOVENOUS FISTULA.

85. PROGNOSIS
 CVT is associated with a good outcome (complete recovery or minor
residual symptoms or signs) in close to 80 % of patients.
 Nevertheless, approximately 5% of patients die in the acute phase of the
disorder, and longer-term mortality is nearly 10%.
 The main cause of acute death with CVT is neurologic, most often from
brain herniation.
 Causes of death in acute phase may be because of Transtentorial
Herniation, Diffuse brain edema, Status epilepticus, Medical complications,
Pulmonary embolism.
 Cause of death in later phase is generally due to underlying cause like
cancer.

86. RECANALIZATION
 The recanalization rates of CVT at 3 months and 1 year of follow-up are
approximately 80% to 85%,respectively.
 The highest rates of recanalization are observed in deep cerebral veins and
cavernous sinus thrombosis and the lowest rates in lateral sinus thrombosis.
 A follow-up CTV or MRV at 3 to 6 months after diagnosis is done to assess for
recanalization of the occluded cortical vein/sinuses in stable patients.

87. Thank you

88. REFERENCES
 Narayan D, Kaul S, Ravishankar K, Suryaprabha T, Bandaru VC, Mridula KR, et al. Risk factors, clinical profile, and
long-term outcome of 428 patients of cerebral sinus venous thrombosis: Insights from Nizam′s Institute
Venous Stroke Registry, Hyderabad (India). Neurol India 2012;60:154-9.
 Nagaraja D, Taly AB. Cerebral venous thrombosis. J Assoc Physicians India 1987;35:876.
 Pai N, Ghosh K, Shetty S. Hereditary thrombophilia in cerebral venous thrombosis: A study from India. Blood
Coagul Fibrinolysis 2013;24:540-3.
 Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F; ISCVT Investigators. Prognosis of cerebral vein
and dural sinus thrombosis: Results of the International Study on Cerebral Vein and Dural Sinus Thrombosis
(ISCVT). Stroke 2004;35:664-70.
 Nagaraja D, Rao BS, Rao BSS, Taly AB, Subhash MN. Randomized controlled trial of heparin in puerperal
cerebral venous/sinus thrombosis.NIMHANS J 1995;13:111-5.
 vishwanadhan et al. Anemia as a risk factor for cerebral venous thrombosis? An old hypothesis revisited:
Results of a prospective study. J Neurol 2007 Jun; 254:729.
 Nagaraja D, Haridas T, Taly AB, Veerendrakumar M, SubbuKrishna DK. Puerperal cerebral venous thrombosis:
Therapeutic benefit of low dose heparin. Neurol India 1999;47:43-6
 T. Ogata, M. Kamouchi, T. Kitazono et al., “Cerebral venous thrombosis associated with iron deficiency
anemia,” Journal of Stroke and Cerebrovascular Diseases, vol. 17, no. 6, pp. 426–428, 2008.