cerebral venous thrombosis

1. CEREBRAL VENOUS
SINUS THROMBOSIS

2. ANATOMY OF DURAL VENOUS SINUSES

3. Dural venous sinuses -
 These are endothelial lined spaces between
the outer peri-osteal and the inner
meningeal layers of the dura mater that
eventually lead to the internal jugular veins.
 All the cerebral , cerebellar ,brainstem
veins along with diploic & emissary veins
drain into dural venous sinuses.

5. Dural venous sinuses
Unpaired sinuses
 Sup.sagittal sinus
 Inf. Sagittal sinus
 Straight sinus
 Occipital sinus
 Basilar sinus
 Confluence of sinuses
Paired sinuses
 Transverse sinuses (rt. and Lf )
 Sigmoid sinuses (rt and Lf )
 Cavernous
 Sphenoparietal
 Sup .petrosal
 Inf . Pertrosal

6. Superior sagittal sinus -
 It is present in the superior border of the falx cerebri and receives cerebral
veins from the superior surface of cerebral hemisphere ,diploic and
emissary veins & veins from falx cerebri . It ends at the confluence of
sinuses and drains into the right transverse sinus.
Inferior sagittal sinus –
 It is present in the inferior border of falx cerebri and few cerebral veins &
veins from falx cerebri .It ends posteriorly near the tentorium cerebelli and
forms the straight sinus after joining with the great cerebral vein(of galen).
 The straight sinus runs along falx cerebri and tentorium cerebelli and
drains at the confluence of sinuses into the left transverse sinus.

7. Confluence of sinuses, transverse and sigmoid sinuses -
 The superior sagittal , occipital and straight sinus drain into the confluence
of sinuses which is present at the internal occipital protruberance and
drains into right and left transverse sinuses .
 The transverse sinuses run along the occipital bone and receives blood from
superior petrosal sinus ,veins of inferior part of cerebral hemispheres and
ends as the sigmoid sinus which inturn drains into the internal jugular
vein.
Superior and inferior petrosal sinuses –
 Superior petrosal sinus originates from the cavernous sinus and drains into
the transverse sinus and runs along the superior margin of the petrous part
of temporal bone .
 Inf .petrosal sinus drains the cavernous sinus into the internal jugular vein.

10. Cavernous sinuses –
 These are paired sinuses lying against the lateral aspect of the sphenoid
bone on either side of the sella turcica . It receives blood not only from the
cerebral veins but also from the opthalmic vein . Inter-cavernous sinuses
connect the two cavernous sinuses .
 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)

12. Cerebral veno-sinus thrombosis
It is the thrombosis of the draining venous sinuses
of the cerebral cortex and the least common of all
other types of cerebro vascular accidents .

13. • This condition frequently affects young adults and children . More
commonly effecting women than men with a f:m ratio of 3:1 most
probably due to the presence of gender specific risk factors like
pregnancy , puerperium and OC pills & HRT .
• It is one of the leading causes of maternal mortality and morbidity
with cases of puerperal CVT occuring 10 -12 times more frequently
in India than the west .
• In ISCVT it was found that the mean age of patients with CVT was
39yrs with only 8% of subjects being >65 yrs .

14. Aetiology-
The exact etiology in most of the cases is unclear but many possible
risk factors have been identified . These may either be transien tor
permanent .
 Prothrombotic conditions either genetic or acquired
 OC pills especially 3 generation pills with desogestrel
 Pregnancy and puerperium
 Malignancy
 Infections –head,face &ear (cavernous ,transverse and sigmoid )
and meningitis .
 Head injuries and mechanical precipitants(surgical procedures )
In more than 85% pts one of the risk factors has been identified most
often prothrombotic states .where as infections were present only in
6-12% of the patients.

15. Pathogenesis –
Two basic mechanisms for the development of symptoms have been identified
to be responsible for the clinical features in CVT –
 Thrombosis of cerebral veins or sinuses leading to cerebral parenchymal
lesions or dysfunctios .
 Occlusion of dural venous sinus resulting in decreased CSF absorption and
elevated intracranial pressure .
Obstruction of venous structures > increased venous pressure >decreased
capillary perfusion >increased cerebral blood vol. >disruption of blood
brain barrier >plasma leakage into interstitial space>cerebral
edema,parenchymal changes ,venous haemorrhage .

16. Clinical features -
The clinical presentation of CVT is highly variable with acute /subacute
/chronic presentation .
• The symptoms and signs of CVT depends on the sinuses involved, the pace
of occlusion, involvement of cortical veins and presence of collaterals
,paranchymal changes and the patients age .
• Symptoms of CVT have been grouped under three major clinical
syndromes-
 Isolated intracranial hypertension syndrome( headache with or without
vomiting ,papilledema ,and visual problems )
 Focal syndrome (focal deficits or seizures or both)
 Encephalopathy ( multifocal signs ,mental status changes ,stupor or
coma )

17. Headache –
This is the most common and least specific of all symptoms of CVT .in the
ISCVT study 89% of pts presented with headache .Headdache is usually the
first symptome is CVT .
• headache is gradual in onset , increase over a period of days to weeks ,
severe in intensity.
• It is more often localised than diffuse .
• 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 .

18. Focal signs and symptoms –
 Motor weakness with monoparesis or hemiparesis is the most common
focal deficit associated with CVT .
 Aphasia is especially associated with left lateral sinus thrombosis .
Seizures –
focal or generalised seizures including status epilepticus are more common
in CVT than in any other type of stroke .
Encephlopathy –
disturbances of consiousness and cognitive dysfunctions such as delirium
,apathy , frontal lobe syndrome ,multifocal deficits can be present .

19. Presentation of isolated sinus and vein
thrombosis -
 Cavernous sinus thrombosis –ocular signs predominate :ocular
pain,chemosis,proptosis and ocular palsies .
 Sagittal sinus occlusion –motor deficits ,bilateral deficits ,seizures .
 Lateral sinus occlusion –isolated intracranial hypertension . If left lateral
sinus thrombus is present aphasia is seen .
 Jugular vein obstruction –isolated pulsating tinnitus .
 Deep venous system occlusion – severe signs &symptoms with coma
,mental problems and motor deficits which are often bilateral .But if limited
thrombosis is present then the symptoms are mild .
 Lateral sinus and jugular vein thrombosis –multiple cranial nerve palsies .

20. INVSTIGATIONS
I . NEUROIMAGING
II .LABORATORY TESTS

21. NEUROIMAGING-Neuroimaging
features include findings that suggest primary
underlying pathology of venous thrombosis and associated
paranchymal lesions( focal areas of edema, haemorrhagic venous
infarction , diffuse brain edema)
MRI –
MRI using gradiend echo t2 susceptiblity weighted sequences in
combination with MR venography is most sensitive for
demonstrating thrombus and occluded dural sinus and vein.the
charecteristics of MRI deend on the age of the thrombus-
• First 5 days thrombus appears isointense (t1) and hypointense (t2)
• Beyond 5 days thrombus becomes more apparent in both t1 and t2 weighted
images .

22.  Paranchymal brain lesions secondary to venous thrombus including brain
swelling,edema,venous infarctions appear hypo or isointense on t1
weighted images and hyperintense on t2 weighted images .
 Haemorrhagic infarcts appear hyperintense in both MRI sequences .
MR venography –
This is useful in demonstrating absence of flow in cerebral venous sinuses .

27. Head CT-CT
is often the first investigation to be performed in clinical practice and is
used to rule out other acute or subacute cerebral disorders.
 The following are direct signs of CVT demonstrated in CT –
 Dense triangle sign –seen as hyperdensity with triangular shape at the posterior end of
superior saggital sinus caused by venous thrombus .
 Empty delta sign – seen in head CT with contrast as a triangular patter of contrast
enhancement surrounding a central region lacking contrast enhancement .
 Cord sign – as linear or curvilinear hyperdensity over the cerebral cortex caused by
thrombosed cerebral veins .
Indirect signs of CVT on CT include demonstration of contrast
enhancement of falx and tentorium ,dilated trans cerebral veins
,paranchymal abnormalities .
Non-haeemorrhagic lesions including focal areas of hypodensity caused by
edema or venous infarction .

28. Dense clot sign
Empty delta sign

36. Laboratory tests-
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 )
 Lumbar puncture –to exclude meningitis in pts with CVT . More therapeutic
advantage than diagnostic .

37. TREATMENT OF CVT
Treatment is to be started as soon as the diagnosis is confirmed
and consists of –
1. Treating the underlying cause when known
2. Control of seizures and intracranial hypertension
3. Antithrombotic therapy

38. Cerebral venous thrombosis can result in death or permanent
disability but usually has a favorable outcome .
 Predictors of mortality at 30 days include –
• Depressed consciousness
• Altered mental status
• Thrombosis of deep venous system
• Right hemisphere haemorrhage
• Posterior fossa lesions
Transtentorial herniation secondary to haemorrhage is the main cause of acute
death in CVT.
Otherr causes include –status epilepticus ,diffuse brain edema ,pulmonary
embolism and other medical complications .

39.  Predictors of poor prognosis includes –
 Central nervous system infection
 Malignancy
 Thrombosis of deep venous system
 Haemorrhage on head CT or MRI
 Glasgow coma score <9 at admission
 Mental status abnormalities
 Age >37 yrs
 Male gender

40. TREATMENT PLAN –
1. ACUTE ANTITHROMBOTIC TREATMENT –
the goals of this are-
• To recanalize the occluded veins
• To prevent the propagation of the thrombus
• To treat underlying prothrombotic state
The main treatment option to achieve these goals is anticoagulation using
heparin or LMWH (i.v/s.c)
 Anticoagulants appear to be safe in adults who have intracranial
haemorrhages .
 AHA/ASA guidelines for CVT management conclude that initial treatment
with weight adjusted LMWH /dose adjusted unfractioned heparin in full
anticoagulant dose followed by vit.k antagonists is reasonable regardless of
presence of ICH.with recommended target INR is 2-3 .

41. 2.ACUTE SYMPTOMATIC TREATMENT –
i.Elevated ICP and herniation –
• Elevating the head end
• Administration of mannitol
• Hyperventilation to a target paCO2 of 30-35 mm hg
• Impending herniation of unilateral hemispheric lesions
hemicraniotomy can be life saving .
• Therapeutic lumbar puncture to decrease csf pressure and offer
headache relief .
ii.Seizures –
• Recurrent seizures are likely to develop in those who present with
seizures or with supra tentorial lesions therefore anti epileptic drugs
profhylaxis are recommended for these patients .Valproate is
preferred to phenetoin due to fewer drug interactions with oral
anticoagulants .

42. 2. Management after acute phase -
The aim of continuing anticoagulants after the acute phase is to
prevent recurrence.
 It is recommended that anticoagulant therapy with warfarin should
be given for a minimum of 3 months after acute CVT aiming at an
INR target of 2.5(2-3).
 European guidelines recommend –
• 3 mnts treatment with oral anticoagulants for a patient with initial CVT
secondary to a transient risk factor.
• 6-12 mnts of ral anticoagulants for patients with idiopathic CVT and those
with mild thrombophilia .
• Indefinite therapy for patients with recurrent CVT and one episode of CVT
and severe thrombophilia