This document provides an overview of cerebral venous sinus thrombosis (CVST), beginning with an introduction defining it as a blood clot within the dural sinuses or cerebral veins. It then covers the epidemiology, pathogenesis, clinical features, investigations, treatment, and prognosis of CVST. Some key points include that CVST accounts for 0.5-1% of stroke cases, affects more women than men and is more common in younger patients. Risk factors include oral contraceptives, genetic mutations, infections and cancers. Clinical features range from headaches to focal neurological deficits. Diagnosis involves imaging like CT, MRI or angiography. Treatment involves anticoagulation for 3-12 months and controlling increased intracranial pressure.

1. CEREBRAL VENOUS SINUS
THROMBOSIS
BY
Aminu Arzet
Department of Medicine
Nelson Mandela School of Medicine
University of K-Natal
Durban
22nd October,2015

2. CONTENTS
Introduction
Epidemiology
Pathogenesis
Clinical feature
Investigations
Treatment
Prognosis
Reference

3. Introduction
 Dural sinus thrombosis is also known as Cerebral venous
sinus thrombosis, or Cranial sinus thrombosis.
 It refers to presence of blood clot inside Dural sinuses and/or
cerebral veins
 Dural sinuses receive blood from internal and external veins
of the brain, also receive cerebrospinal fluid (CSF), then
ultimately empty into the internal jugular vein
 DST is a form of cerebro vascular accidents(CVA), and the
least common of all forms of stroke.

4. ANATOMY OF DURAL VENOUS SINUSES

5. Epidemiology
 DST account for 0.5% to 1% of all stroke cases.
 Roughly affect 5 people / 1 million.
 Prevalence of 3 – 9% across globe
 Commonest in Middle east, particularly Saudi Arabia, due high
prevalence of Behcet’s dx (an important risk factor for DST).
 Commoner in young then old - Ration 5:1
 Affect more women then men - Ratio 3:1

6. Etiology
 The exact etiology is not known
 How ever it can be conveniently linked to Virchow's triad:
blood stasis, changes in vessel wall, and changes in
composition of blood.

7. Continuation of Etiology
Risk Factors:
 Exogenous hormones; e.g oral Contraceptive (estrogen type)
 Genetic causes ; inherited thrombophilia's
 Mutation: Factor V Leiden Gene mutation and Prothrombin
G20210A Mutation
 Pregnancy and puerperium; particularly 3rd trimester
 Malignancy; Hematological /pressure symptom/chemo

8. Continuation of Etiology
 Infections; Mastoiditis,Sinusitis,Meningitis, ear/face infection
 Trauma to head/neck
 Head and neck surgical procedures
 Other Prothrombotic conditions:
- Antithrombin III, Protein C, and Protein S Deficiency
- Resistance to Activated Protein C
- Antiphospholipid and Anticardiolipin Antibodies
- Hyperhomocysteinemia
- Polycythemia vera

9. Continuation of Etiology
 Other risk factors:
- Nephrotic syndrome
- Bechet's disease
- Iron deficiency anemia
- Paroxysmal nocturnal hemoglobinuria / homocystinuria
- Heparin induced thrombocytopenia / TTP
- Sickle cell disease
- Inflammatory bowel disease
- Multiple myeloma
- Epidural blood patch/Lumbar puncture.

10. Pathogenesis
 Veins of the brain drain blood into Dural venous sinuses,
which forward the blood to the heart via internal jugular vein
 In DST blood clot/s is formed inside the veins of the brain and
the venous sinuses.
 Formation of clot/s inside the Dural sinuses/veins, blocks
outward movement of blood to the heart, with resultant
backflow, increased venous pressure, congestion and
engorgement of the blood vessels and near by brain tissues.

11. Continuation of Pathogenesis
 This leads to decreased capillary perfusion, disruption of
blood brain barrier, plasma leakage into interstitial space,
cerebral edema, venous infarction(damage to brain tissue
due to congestion), and eventfully small petechial
haemorrhages develop, which may coalesced into large
haematomas.
 Thrombosis of the sinuses also lead to decreased resorption
of CSF, stasis, and increased intracranial pressure, which
could lead intracranial hypertension.

12. Clinical features
 Clinical findings fall in to 2 categories:
1.Those due to increased ICT:
- Headache in up to 90% of pts
- The headache is diffused and often progresses in severity
over days to weeks, resembling Migraine.
- Minority of pts present with thunderclap headache - 25%.
- There could be associated vomiting , papilledema , and visual
disturbance.

13. Continuation of Clinical features
- Communicating hydrocephalus may develop (6.6%),
due to derangement of Arachnoid granulation
- Obstructive hydrocephalus is less common ;due to
ventricular hemorrhage.
2.Those due to brain infarction / hemorrhage:
- Focal sign; Monoparesis/hemiparesis, Aphasia, cranial nerve
palsy seizures
- Encephalopathy; Confusion, psychiatric like presentation,
- Drowsiness, stupor or coma

14. Continuation of Clinical features
3. Others:
- Fever
- Elevated BP
- Tachycardia/Bradycardia

15. Investigations
 Blood test:
- Baseline blood
- Septic screen/Viral screen
- DIC screen: D-dimer has high sensitivity (97.1%), and
specificity of 91.2%
- Clothing profile; PT/PTT
- Screening for potential Prothrombotic conditions; TTP, HIT, etc
- Lumbar Puncture; Elevated opening pressure in > 80%,
Elevated cell counts (50%) and protein (35%) can be seen.

16. Continuation of Investigations
Imaging:
1. Non Invasive Imaging:
- CT : Has sensitivity of 75-100% and a specificity of 81-100%
- MRI
- Ultrasonography
2. Invasive Imaging:
- Cerebral Angiography
- Direct Cerebral Venography.

17. Treatment
 Treatment of the underlying cause; if known
 Seizures Control:
- Seizures are present in 37% of adults and 48% of
children with diagnosis of DST
- Treatment is recommended after a single episode of
seizure
- Prophylactic antiepileptic drugs may be harmful

18. Treatment Continued
 Control of intracranial hypertension:
- Severe raised intracranial pressure (RIP) may require
therapeutic lumbar puncture
- Medication like Acetazolamide could be use
- Neurosurgical interventions like shunting and
Decompressive Hemicraniectomy may be offered if
necessary

19. Treatment Continuation
Antithrombotic therapy:
1. Anticoagulation:
- Heparin or low molecular weight heparin, fallowed by
Warfarin
- LMW heparin is preferred over Unfractionated heparin(UFH)
- Presence of ICH is not a contraindication
- Adjust dosage to achieve target INR of 2-3

20. Treatment Continuation
- Anticoagulation last 3-6 month for Provoked DST ,
associated with transient risk factor e.g hormonal
replacement therapy, pregnancy, etc
- Anticoagulate for 6 -12 month for Unprovoked CVT ; No
known risk factor
- Indefinite anticoagulation is recommended for
recurrent DST, DST with severe Thrombophilia or
Venous thrombo embolism(VTE) after DST

21. Continuation of Treatment
2. Thrombolysis :
- European Federation of Neurological Societies guideline
recommends thrombolysis only if patient deteriorate despite
adequate treatment
- Thrombolytic agents are given either systemically via vein, or
directly into the clot during angiography.
- Commonest drug use are Urokinase and tissue plasminogen
Activator (tp-A)

22. Treatment Continued
- Mechanical Thrombolysis is done using Balloon assisted
Thrombectomy
- Surgical thrombectomy is rarely done

23. Treatment Continuation
 Other treatments:
- Steroids are only use in case of vasogenic edema
- Steroid are not recommended, even in the presence of
parenchymal brain lesions on CT/MRI, unless needed for
another underlying fatal disease
- Antibiotics – indicated if there is associated infections
- Aspirin has no place in treatment of DST

24. PROGNOSIS
 About 80% of pts with DST recover completely or may have
minor residual symptoms or signs
 It has 5% mortality in early phase, and about 10% mortality
in late phase.
 The main cause of death in early phase include Herniation of
brain, Diffuse brain edema, Status epilepticus, Pulmonary
embolism
 Cause of death in later phase is generally due to underlying
cause like cancer or CNS infection.

25. Predictors of poor prognosis
- Central nervous system infection
- Any malignancy
- Thrombosis of the deep venous system
- Intra cranial Hemorrhage
- Depressed consciousness- GCS < 9 on admission
- Altered mental state
- Age >37 years
- Male gender

26. PROGNOSIS
 Dural Arteriovenous Fistula is another cause for poor
prognosis. It developed due to persistent dural sinus
occlusion with increased venous pressure.
 The fistula can close and cure if the sinus recanalizes.
A preexisting fistula can be the cause of CVT.
 Recanalization: Up to 85% DST reanalyze after 1 year
 Recurrence: Rate of recurrence of DST is 2 -4 %, while the
risk of recurrent venous thromboembolism in other locations
ranges from 4 - 7 %

27. THANK YOU

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