ANATOMY OF CEREBRAL VEINS AND ITS APPLICATION IN CLINICAL MEDICINE-CEREBRAL VENOUS THROMBOSIS

PRESENTER – DR AMAR PATIL

PG MEDICINE

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.

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.

SUPERFICIAL OREXTERNAL CEREBRAL VEINS

Drain the surface (cortex) of cerebral hemisphere:

3 groups:

Superior cerebral veins

Middle cerebral veins

Inferior cerebral veins.

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.

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.

INFERIOR CEREBRAL VEINS

Drains :

Inferior surface,

Lower parts of medial and superolateralsurfaces.

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

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.

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.

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.

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.

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.

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.

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.

CAVERNOUS SINUSES

These large sinuses are about 2 cm long and 1 cm wide. They are located on each side of sellaturcica 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.

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)

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.

DEEP VEINSVEINS

Thalamostriate vein Septal vein

Internal Cerebral vein (2)

Basal vein ofRosenthal (2)

Occipital vein

PosteriorPericallosal

vein

Mesencephalicvein

PrecentralCerebellar

vein

Vein of Galen Inferior Sagittal Sinus

Straight Sinus

CEREBRAL VENOUS THROMBOSIS(CVT )

Epidemiology

Puerperal CVT and non-puerperal CVT

Etiology and risk factors.

Clinical features

management

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.

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.

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) .

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.

PUERPERAL CVT

Epidemiology

Incidence

Presentation

statistics

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.

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.

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.

EPIDEMIOLOGY

In the largest hospital-based prospective cohort study from India (Nizam'sInstitute 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.

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.

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.

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.

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.

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.

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.

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

NON PUERPERAL CVT

Epidemiology and incidence

Etiology

Risk factors

Clinical presentation

Management .

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.

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.

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 C&S deficiency, Factor V leiden

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.

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

RISK FACTORS

Nonmodifiable

Age

Gender

Race – undetermined.

Heredity

Modifiable

Postmenopausal replacement therapy

Oral contraceptives

Infection

Hypertension

Diabetes

• Hypercholesterolemia

• Obesity • Alcohol

consumption • Homocysteine • Cancer

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

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.

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%).

PATHOGENESIS

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 )

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 mimicingsubarachnoid 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 .

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.

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.

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.

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.

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.

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.

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 .

MANAGEMENT OF CVT

Laboratory StudiesCurrent 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.

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.

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.

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.

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.

The empty delta (empty triangle) sign. This is seen on CT after contrast administration, as a bright triangle surrounding a central hypodensecore.

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.

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 haemorrhagicinfarctions which are either small or large, single or multiple.

Diffuse edema of the brain may be seen.

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.

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

MRV

Magnetic Resonance Venography

MRV has become the imaging modality most widely used to establish the diagnosis of CVT.

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.

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.

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.

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.

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.)

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)

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

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.

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.

Subsctance Indication Aim Doasge Duration

Acetaminophen

Mild headache Necessary pain relief 200-1000mg tid On demand

Tramadol Severe headache

Necessary pain relief 50-100 mg tidorally

On demand

OTHER TREATMENTS

FIBRINOLYTIC THERAPY.

DIRECT CATHETER ABLATION.

MECHANICAL THROMBECTOMY / THROMBOLYSIS.

SURGERY.

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.

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.

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.

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.

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.

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.

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 TranstentorialHerniation, Diffuse brain edema, Status epilepticus, Medical complications, Pulmonary embolism.

Cause of death in later phase is generally due to underlying cause like cancer.

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.

Thank you

REFERENCES

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