1. Cerebral venous sinus thrombosis (CVST) is a condition where blood clots form in the venous sinuses within the brain or in veins that drain blood from the brain. 2. CVST can cause headaches, seizures, focal neurological deficits, and altered mental status. Diagnosis is made through brain imaging like MRI or CTV that can identify clots. 3. Treatment involves anticoagulation to prevent further clotting as well as potentially thrombolysis to break up existing clots. Prognosis is generally good with many patients making a full or near full recovery.

1. Cerebral venous sinus
thrombosis
DR. MOHAMED ELSHAFEI
DR.LINK147@YAHOO.COM

2. Objectives
What`s CVST?
Is it rare?
How to diagnose?
How to treat ?
Prognosis ?
Questions?

3. Anatomy of venous drainage system
Major dural sinuses:
• Superior sagittal sinus, transverse, straight and
sigmoid sinuses.
Cortical veins:
• Vein of Labbe, which drains the temporal lobe.
• Vein of Trolard, which is the largest cortical vein that
drains into the superior sagittal sinus.
Deep veins:
• Internal cerebral and thalamostriate veins.
Cavernous sinus.

5. Incidence
< 2% of all strokes
Accounts for up to 50% of strokes during
pregnancy and puerperium
Important cause of stroke especially in
children and young adult
Male/female ratio = 1.29/1
Males uniform age distribution
Females 61% CVT in 20-35 age group

6. 72%
70%
14.5%
2.7%
27%
3%

7. Risk factors
Local conditions
- Brain and skull damage
- Intracranial and local regional infections (Mastoiditis)
Systemic conditions
- Hormonal (pregnancy or puerperium, OCP and steroid therapy)
- Surgery, immobilization
- Hematologic and hypercoagulable disorders
- Connective tissue disease
- Malignancy
- Systemic infection
- Dehydration
Idiopathic causes (25%)

8. Velocity
(stasis)
Vessel wall injury
Virchow Triad
Viscosity
(hypercoagulability)
INHERITED
THROMBOPHILIA
 Factor V leiden mutation
 Prothrombin gene
mutation
 Protein S deficiency
 Protein C deficiency
 Anti thrombin deficiency
 Homocysteinemia
 Dysfibrogenemia
ACQUIRED DISORDERS
 Malignancy
 CHF APLA
 surgery IBD PNH
 Trauma
 Nephrotic syndrome
 Polycythemia vera,
Myeloproliferative d/s
 Pregnancy , OCP’ s HRT
 HIV
 Multiple myeloma

9. Pathogenesis
Thrombosis of cerebral veins
Local effects caused by venous obstruction, oedema of brain (both cytotoxic and vasogenic) and infarction due to
elevated venous and capillary pressure complicated by haemorrhage
may be multiple and bilateral
Not respect arterial vascular territories
Thrombosis of major sinuses
obstruction leads to impaired absorption of CSF and intracranial hypertension
Intracranial hypertension occurs in 20%–40% of patients with cerebral venous thrombosis
and should be excluded in patients with the specific complex of symptoms

11. Clinical manifestations
3 main syndromes
I. ISOLATED INTRACRANIAL HYPERTENSION SYNDROME( Headache +/-
vomitings,papilledema,visual disturbances)
II. FOCAL SYNDROME( focal deficits, seizures, both)
III. ENCEPHALOPATHY ( mutlifocal signs, mental status changes, stupor or coma)

12. Clinical manifestations
Headache 75%
Papilledema 49%
Motor or sensory deficit 34%
Seizures 37%
Drowsiness, mental changes,confusion, or coma 30%
Dysphasia 12%
Multiple cranial nerve palsies 12%
Cerebellar incoordiantion 3%
Nystagmus 2%
Hearing loss 2%
Bilateral or alternating cortical signs 3%

13. Headache
most frequent symptom
common in young patients and women
Stabbing headache worst headache in life (thunderclap headache)
usually gradual in onset, often localised than diffuse but site of
headache has no relation to site of occluded vessel/ parenchymal lesion

14. Investigations
Labs :
oRoutine
od-dimer
oHypercoagulable screen
oSpecific underlying malignancy
Radiology
oCT / CTV
oMRI / MRV
oTCD
oEEG
oDSA

15. When to suspect CVST !?
High
risk

16. Dense clot sign
Empty delta sign

17. Flow void sign Cord sign

18. Superior sagittal sinus thrombosis

19. Vein of labbe thrombosis

20. Treatment
Anticoagulation
Thrombolysis
Endovascular thrombectomy
Antiepileptic
Antibiotics

21. ANTICOAGULATION
Initial anticoagulation by LMWH/ UFH( dose adjusted with a goal of 2-3 times control APTT) Later
oral Vitamin K Antagonists (Warfarin) Target INR- 2.0-3.0
Special situation of CVT with cerebral hemorrhage on presentation Anticoagulants appear to be
safe to use in adult patients with CVT who have intracranial hemorrhages, either intracerebral or
subarachnoid

22. ANTICOAGULATION
DURATION..
1) Provoked 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
severe thrombophilia  deficeincy of protein c/ protein S/ antithrombin, APLA, homozygous
factor V leiden, homozygousprothrombin G20210A
Testing for protein C, protein S, and anti-thrombin deficiency is generally indicated 2 to 4 weeks
after completion of anticoagulation. There is a very limited value of testing in the acute setting
or in patients taking warfarin

24. ENDOVASCULAR THROMBOLYSIS
Some patients with CVT worsen despite anticoagulant therapy.
Direct endovascular thrombolysis has been used as an alternative treatment in such cases.
Direct thrombolysis aims to dissolve the venous clot by delivering a thrombolytic substance
(urokinase or r-tPA) within the occluded sinus through an intravenous catheter.

25. Endovascular thrombectomy
In some cases, mechanical endovascular disruption of the thrombus has also been used

26. DECOMPRESSIVE HEMICRANIECTOMY
In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage
causing intractable intracranial hypertension, decompressive hemicraniectomy may be
considered

28. Complications
EARLY
1. Seizures
2. Hydrocephalus
3. Intracranial hypertension
LATE
Chronic headache
Visual loss
Epilepsy
Dural AV fistula

29. Early complications
1- SEIZURES
- 37% cases
-Treatment :
CONTROVERSAL  To initiate or await initial seizures before treatment
RECOMMENDATIONS :
-CVT and single seizure with parenchymal leisons  Early initiation of AED in pts for definite period is
recommended to prevent further seizure
-CVT with seizures withOUT parenchymal leison AED initiation is probably recommended
-Pts withOUT seizures routine use of AED not recommended

30. Early complications
2- HYDROCEPHALUS
Communicating/ Obstructive
If obstructive- ventriculostomy/ VP shunt

31. Early complications
3- INTRACRANIAL HYPERTENSION
- 40%
- Treatment:
Anticoagulation
LP
Acetazolamide
Decompressive craniotomy

32. Late complications
1- HEADACHE
- 50%
- Common complaint in follow up
- Persistent/severe headache  R/O 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

33. Late complications
2- VISUAL LOSS
3- SEIZURES
4- DURAL ARTERIOVENOUS FISTULA

34. CVT and PREGNANCY
One of risk factors because of hypercoagulable state
The greatest risk periods for CVT include the third trimester and the first 4 postpartum weeks
Cesarean delivery appears to be associated with a higher risk of CVT
women with a history of VTE appear to have an increased risk of thrombotic events
CVT is not a contraindication for future pregnancies

35. CVT and PREGNANCY
Recommendations
1. 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)
2. It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further
investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal
fetal medicine specialist are reasonable.
3. It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH
4. For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum
period is probably recommended

36. 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%.
Causes of death in acute phase is mostly neurologic  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
Neurological worsening may occur in 23% of patients, even several days after
diagnosis. Approximately one third of patients with neurological deterioration will have
new parenchymal lesions when neuroimaging is repeated

37. Prognosis
 PREDICTORS OF MORTALITY AT 30 DAYS
• Depressed consciousness
• Altered mental status
• Thrombosis of the deep venous
system
• Right hemisphere hemorrhage
• Posterior fossa lesions
 PREDICTORS OF POOR LONG-TERM PROGNOSIS
• Central nervous system infection
• Any malignancy
• Thrombosis of the deep venous system
• Hemorrhage on head CT or MRI
• Glasgow coma scale score <9 on admission
• Mental status abnormality
• Age >37 years
• Male gender

38. Prognosis
Recanalization :
-In a systematic review of 5 small studies, recanalization rates of CVT at 3
months and 1 year of follow-up were 84% and 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.
-In adults, recanalization of the occluded sinus is not related to outcome after
CVT.
-A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to
assess for recanalization of the occluded cortical vein/sinuses in stable
patients

39. Prognosis
Recurrence
- The risk of recurrent CVT is approximately 2 -4 %
- while the risk of recurrent venous thromboembolism in other locations ranges from 4 - 7 %

41. Case 1
Male patient 38 years old known epileptic on phenytoin but not compliant , ESRD on regular
dialysis , develop headache and seizure during dialysis session which resolved without
intervention and patient stated that he forgot to take his medication , after 2 days patient
develop same condition on next session however resolved on iv diazepam and patient was sent
to ER for neurological evaluation, brain imaging done and showed next pics
What is next step in management?

42. Case 1

43. Case 2
Female patient pregnant G2P1 14 weeks pregnancy has repeated severe vomiting that indicates
her admission, on second day of admission patient had slow response to orders no apparent
focal neurological deficit no witnessed seizures , mri brain is done showed next picture
What is your diagnosis ?
What is your management plan?
What is your advice for next pregnancy?

44. Case 2

45. Case 3
Male patient 30 years old no past medical history presented to ER with status epilepticus which
was refractory to regular medication, after sedation ct brain done and showed bilateral frontal
and parasaggital hemorrhagic insult
What`s your next step in diagnosis ?
How long should anticoagulation is needed?

46. Case 3