Cerebral venous thrombosis: an evidence-based review

Introduction

Cerebral venous thrombosis is thrombosis of the dural venous sinuses, the cortical veins, the deep cerebral veins, or a combination of these. It accounts for 0·5–3% of all strokes.¹⁵ It differs from arterial stroke in whom it strikes and why: most patients are young, three-quarters are women, and the usual causes are hormonal exposure, inherited or acquired thrombophilia, cancer and infection rather than atherosclerosis.^3,16 Its treatment is anticoagulation, which makes it a haematological disease as much as a neurological one.

Three developments since the last European guideline in 2017¹⁷ justify a new synthesis. First, direct oral anticoagulants have been tested in a randomised trial in adults,⁹ a feasibility trial,¹⁸ a paediatric trial,¹⁹ and large observational cohorts.⁸ Second, the one randomised trial of endovascular treatment has reported,¹¹ as has a prospective cohort of decompressive surgery.¹² Third, in 2021 vaccine-induced immune thrombotic thrombocytopenia (VITT) produced a cluster of severe cerebral venous thrombosis with a distinct, antibody-mediated mechanism.^13,20,21 The American Heart Association (AHA) updated its scientific statement in 2024.^15,22 This review sets out what is known, how strong the evidence is, and where guidance has moved.

Epidemiology

Population-based estimates from the past 15 years are higher than older figures from hospital series. A cross-sectional study of 19 hospitals serving 3·1 million people in the Netherlands found an incidence of 1·32 per 100 000 person-years (95% CI 1·06–1·61), rising to 2·78 per 100 000 in women aged 31–50 years.²³ In Adelaide, Australia, a search of more than 250 000 neuroimaging reports gave 15·7 per million per year (12·9–19·0).²⁴ A Norwegian hospital catchment gave 1·75 per 100 000 per year (1·36–2·23),²⁵ and discharge data from Piedmont, Italy, gave 11·6 per million, with 15·1 per million in women and 7·8 per million in men, peaking at 27·0 per million in women aged 40–44 years.²

The largest dataset comes from state inpatient databases in New York and Florida (5567 cases, 2006–16). Incidence was 13·9–20·2 per million per year, 20·3–26·9 per million in women and 6·8–16·8 in men, and 24·0–32·6 per million in women aged 18–44 years. It rose over the decade, driven by men and by women aged 45 years and older; incidence in young women did not change. Incidence was higher in Black than in White patients.¹ Part of this rise probably reflects wider use of MR and CT venography; how much is not known.

In children, the Canadian Pediatric Ischemic Stroke Registry estimated 0·67 per 100 000 children per year, with neonates most often affected.²⁶ More recent US data give 1·1 per 100 000 per year, 6·4 per 100 000 in infants, and an annual rise of 3·8% (95% CI 0·2–7·6).²⁷

All of these estimates come from Europe, North America and Australia. We found no population-based study from the Arabian Peninsula. Estimates made for one population's mix of oral contraceptive use, obesity, inherited thrombophilia and infection should not be carried to another without checking them.

Risk factors

At least one risk factor is found in most patients, and often more than one. Table 1 gives the size of each association from the strongest available study.

Hormonal factors

Oral contraceptives are the most common risk factor in women of reproductive age, and they multiply other risks. In two case–control studies published in 1998, oral contraceptive use combined with a prothrombotic defect gave odds ratios of about 30 and 149.^29,30 Obesity adds to the risk only in women who take oral contraceptives, in a dose-dependent way.³¹ In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), 75% of the 624 patients were women, and 65% of these had a sex-specific risk factor: oral contraceptives, pregnancy, the puerperium or hormone replacement. Women with such a factor had better outcomes than men, and the absence of a sex-specific factor predicted poor outcome in women (OR 3·7, 1·9–7·4).¹⁶

Cancer and myeloproliferative neoplasms

Cancer raises the risk of cerebral venous thrombosis about five-fold overall and 25-fold for haematological cancers, most strongly in the first year after diagnosis.³² The reverse also holds. In 2649 Dutch patients with a first cerebral venous thrombosis, the standardised incidence ratio for a new cancer was 3·35 (2·41–4·55) in the first year and 1·40 (1·14–1·69) at 10 years. The 10-year cumulative incidence was 5·9% overall and 13·5% in men aged 50 years or older.³⁸ Cancer is also a leading cause of death after the acute phase.³⁹

For the haematologist, myeloproliferative neoplasms matter because they may be unrecognised at presentation. In a small Italian series of 44 patients with myeloproliferative neoplasms and thrombosis at unusual sites, 86·4% carried JAK2 V617F.⁴⁰ That figure describes patients already known to have a neoplasm; it is not the prevalence of JAK2 V617F in cerebral venous thrombosis, which we could not establish from a large study. In ISCVT, polycythaemia or thrombocythaemia predicted recurrent venous thromboembolism (HR 4·4, 1·6–12·7).⁴¹ Paroxysmal nocturnal haemoglobinuria is rarer but important. In a French series of 15 patients, cerebral venous thrombosis was the first sign of the disease in four, and recurrent thrombosis reached 50% at 6 years, occurring only in patients who received neither eculizumab nor a stem-cell transplant.⁴²

Mechanism

Two processes produce the clinical picture (mechanistic evidence, reviewed elsewhere^43,44). Thrombosis of a large sinus impairs venous drainage and absorption of cerebrospinal fluid, which raises intracranial pressure and produces headache, papilloedema and visual loss. Occlusion of cortical or deep veins raises local venous pressure, which causes vasogenic and cytotoxic oedema, venous infarction and haemorrhage. Parenchymal lesions, haemorrhagic or not, carry a worse prognosis than their absence: in ISCVT, 23·6% of patients had non-haemorrhagic lesions, and their outcome lay between that of patients with no lesion and those with haemorrhage.⁴⁵ The haemorrhage is caused by venous congestion, which is why it is not a reason to withhold anticoagulation (see below).

Clinical presentation

Presentation varies more than in arterial stroke, and onset is often subacute. Headache is the most common symptom, reported by 83% of patients in a Norwegian cohort, with nausea in 45%, motor deficits in 32% and seizures in 32%.²⁵ About 10% of patients able to report symptoms have no headache. These patients are older, more often men and more often have cancer; seizures (58% vs 32%) and paresis are more common and papilloedema less common.⁴⁶ Seizures at presentation occurred in 34% of a Portuguese prospective registry⁴⁷ and 47% of an Indian cohort, including ten patients in status epilepticus.⁴⁸ A supratentorial parenchymal lesion is the most consistent predictor of seizures (OR 3·7–4·7).^47,48 Four clinical patterns are described: isolated intracranial hypertension, focal deficits with or without seizures, encephalopathy (typical of deep venous thrombosis), and cavernous sinus syndrome.⁴³ In ISCVT the median delay from onset to diagnosis was 7 days. Delay did not change functional outcome overall, but persistent visual deficits were more frequent with later diagnosis, and in patients with isolated intracranial hypertension delay was associated with death or dependency.⁴⁹

In children, seizures (58%) and diffuse neurological signs (76%) predominate, and venous infarcts are seen in 41%.²⁶

Diagnosis

Imaging

The diagnosis requires demonstration of thrombus or absent flow in a sinus or vein. The European Stroke Organisation (ESO) guideline recommends magnetic resonance venography or CT venography to confirm it,¹⁷ and the AHA statement takes the same position.¹⁵ Non-contrast CT is not enough. In a blinded multicentre study of 285 patients and 303 controls, readers' visual impression of thrombosis on non-contrast CT had a sensitivity of 41–73% and a specificity of 97–100%. The best quantitative marker reached only 76% sensitivity at a 20% false-positive rate, so non-contrast CT misses about one case in four.⁴ On susceptibility-weighted and T2* sequences, the “brush sign” marks a higher thrombus burden and more parenchymal lesions but does not predict 3-month outcome.⁵⁰

D-dimer

A meta-analysis of 14 studies (1134 patients) gave a pooled sensitivity of 93·9% (87·5–97·1) and specificity of 89·7% (86·5–92·2) for D-dimer. False-negative results were more common in patients with isolated headache, longer symptom duration and limited sinus involvement,⁵ which are the patients in whom the diagnosis is most often in doubt. A normal D-dimer therefore lowers the probability but does not exclude the disease when clinical suspicion is high.

Tests for the cause

The ESO guideline suggests not screening all patients for thrombophilia or cancer.¹⁷ Two findings argue for targeted testing. Severe thrombophilia (deficiency of antithrombin, protein C or protein S, antiphospholipid syndrome, or combined defects) predicted recurrent venous thromboembolism outside the brain (adjusted HR 4·71, 1·34–16·5), though not recurrent cerebral venous thrombosis.⁵¹ The excess of cancer after cerebral venous thrombosis is concentrated in the first year and in older men.³⁸ Panel 1 gives a practical approach. It is our opinion, drawn from the studies cited here; it has not been tested prospectively.

Acute treatment

Anticoagulation with heparin

Two randomised trials underpin anticoagulation. In the first, 20 patients were randomly assigned to dose-adjusted intravenous unfractionated heparin or placebo. At 3 months, 8 of 10 patients on heparin had recovered completely against 1 of 10 on placebo, and 3 placebo patients died.⁵² In the second, 60 patients were randomly assigned to subcutaneous nadroparin or placebo for 3 weeks. Poor outcome at 12 weeks occurred in 13% vs 21% (risk difference −7%, −26 to 12), which was not significant.⁵³ A Cochrane meta-analysis of the two trials (79 patients) gave a relative risk of death of 0·33 (0·08–1·21) and of death or dependency of 0·46 (0·16–1·31), an absolute reduction of 13%. Neither estimate was significant, but no new symptomatic intracranial haemorrhage occurred with anticoagulation.⁶ On this evidence and on consistent observational data, the ESO guideline makes a strong recommendation for parenteral anticoagulation in acute cerebral venous thrombosis.¹⁷ This is a strong recommendation built on low-certainty evidence, and it is unlikely to be tested against placebo again.

Anticoagulation in the presence of haemorrhage

Intracerebral haemorrhage at presentation is where clinicians most often hesitate. Haemorrhage on admission CT predicts poor outcome (HR 1·9 in ISCVT).³ Anticoagulation should still be given. The first trial's retrospective arm reported mortality of 15% in 27 patients with haemorrhage who received heparin against 69% in 13 who did not,⁵² and the nadroparin trial included patients with haemorrhage without new symptomatic bleeding.⁵³ No trial has randomised patients with haemorrhage specifically, and the evidence remains observational. The treatment is aimed at the venous obstruction that causes the bleeding, not at the bleeding itself.

Low-molecular-weight or unfractionated heparin

One randomised trial compared the two. In 66 patients, all 6 in-hospital deaths occurred with unfractionated heparin and none with low-molecular-weight heparin; complete recovery at 3 months was numerically more frequent with low-molecular-weight heparin (30 of 34 vs 20 of 32), which was not significant.⁷ In a non-randomised analysis of ISCVT, low-molecular-weight heparin was associated with functional independence at 6 months (adjusted OR 2·4, 1·0–5·7) and, in patients with parenchymal lesions, with fewer new haemorrhages (adjusted OR 0·19, 0·04–0·99).⁵⁴ This second study is often cited as if it were randomised; it was not. The ESO guideline suggests low-molecular-weight heparin in preference.¹⁷ Unfractionated heparin keeps a place when rapid reversal may be needed, for example before possible decompressive surgery. The paediatric guideline of the American Society of Hematology (ASH) and International Society on Thrombosis and Haemostasis (ISTH) makes this explicit for children with haemorrhage from venous congestion.⁵⁵

Anticoagulation after the acute phase

Direct oral anticoagulants or warfarin

After 5–15 days of heparin, patients have traditionally taken a vitamin K antagonist. Table 2 summarises the evidence for direct oral anticoagulants (DOACs).

The evidence points one way but is not conclusive. The only randomised trial in adults with a clinical comparison (RE-SPECT CVT) had 120 patients and no recurrences, so it could exclude neither benefit nor harm.⁹ The largest cohort, ACTION-CVT, found similar recurrence and a lower rate of major haemorrhage with DOACs,⁸ but patients kept on warfarin may have been sicker, and the authors called for randomised confirmation. Meta-analyses that mix observational and randomised data favour DOACs,^56,57 whereas the most recent meta-analysis restricted to randomised trials found fewer bleeds overall with DOACs but a non-significant signal of more recurrence, with low certainty for every outcome.¹⁰ This discordance should be stated plainly. Adding observational data narrows the confidence intervals, and it also brings confounding by indication into the estimate.

Guidance has moved. The 2017 ESO guideline, written before any of these data, suggested not using DOACs.¹⁷ The 2024 AHA statement reviewed the newer evidence.¹⁵ In children, the ASH/ISTH 2024 guideline suggests DOACs over standard anticoagulants for venous thromboembolism generally, on low-certainty evidence drawn mostly from children without cerebral venous thrombosis.⁵⁵ In our reading, a DOAC is a reasonable alternative to warfarin after initial heparin in adults with cerebral venous thrombosis, and its practical advantages weigh heavily in favour. The CVT-specific data do not cover pregnancy, breastfeeding or antiphospholipid syndrome. In those groups, choice of agent rests on extrapolation from venous thromboembolism at other sites.

Duration

No randomised trial has defined how long to anticoagulate, and the ESO guideline explicitly made no recommendation.¹⁷ The EXCOA-CVT cluster-randomised trial is comparing 3–6 months with 12 months of anticoagulation, with a planned sample of 1428 patients and symptomatic venous thromboembolism as the primary outcome.⁵⁸ We found no published results as of September 2026.

Observational data describe the risk that treatment duration has to balance. In ISCVT, 5·8% of patients had a further venous thromboembolic event over a median of 13·9 months (4·1 per 100 person-years), and 2·2% had recurrent cerebral venous thrombosis. Two-thirds of events occurred in the first year. Male sex (HR 2·6) and polycythaemia or thrombocythaemia (HR 4·4) predicted recurrence.⁴¹ In an Italian cohort followed for a median of 6 years after anticoagulation stopped, recurrent cerebral venous thrombosis occurred at 0·53 per 100 person-years and any venous thromboembolism at 2·03 per 100 person-years. Male sex was a strong predictor (adjusted HR 9·66), and severe thrombophilia predicted recurrence outside the brain.⁵¹ In a multicentre cohort of 706 patients, recurrence rose from 23·6 to 35·1 per 1000 patient-years after anticoagulation was withdrawn, and previous venous thromboembolism was the only independent predictor (HR 2·70).⁵⁹

Current practice is 3–12 months for a first event with a transient provoking factor, with longer or indefinite treatment considered for recurrence, severe thrombophilia, active cancer or a myeloproliferative neoplasm. These thresholds are a convention built from these cohorts and from venous thromboembolism at other sites; they are not trial-derived.

Severe disease

Endovascular treatment

The TO-ACT trial randomly assigned 67 patients with at least one predictor of poor prognosis to endovascular treatment plus standard care or standard care alone. It was stopped early for futility. At 12 months, a modified Rankin Scale score of 0–1 was reached by 67% vs 68% (RR 0·99, 0·71–1·38). Mortality was 12% vs 3% and symptomatic intracranial haemorrhage 3% vs 9%; neither difference was significant.¹¹ Meta-analyses of uncontrolled series report a good functional outcome in 82·6–85% and mortality of 5–6·7%.^60,61 An earlier systematic review of 235 patients reported mortality of 14·3%.⁶² These single-arm figures reflect selection and publication bias, and they cannot be set against the randomised result. On current evidence, endovascular treatment is a rescue option for patients who worsen despite adequate anticoagulation, at centres with experience. It should not be used as a first-line treatment. The ASH/ISTH paediatric guideline reaches the same position, citing TO-ACT.⁵⁵

Decompressive surgery

For patients with a large parenchymal lesion and impending herniation, decompressive surgery is lifesaving. In a registry and individual-patient review of 69 patients, 56·5% were independent (modified Rankin Scale 0–2) at a median of 12 months and 15·9% died; three of nine patients with bilateral fixed pupils recovered completely.⁶³ The prospective DECOMPRESS2 cohort (118 patients, 15 centres) found death or severe disability in 39% at 12 months, death in 33·9% and independence in 35·6%. Coma predicted a poor outcome (OR 2·39, 1·03–5·56). Most surviving patients (78·9%) and caregivers (87·1%) judged the surgery worthwhile.¹² Survivors carry a real burden. At 12 months, 84% reported problems in at least one quality-of-life domain,⁶⁴ and 23% had a seizure within a year of surgery, most while taking antiseizure medication.⁶⁵ Restarting anticoagulation within 24 hours of surgery was not associated with more bleeding or thrombosis than later restarting (OR 0·86, 0·24–3·04), although the study was small.⁶⁶ The ESO guideline recommends decompressive surgery to prevent death from herniation.¹⁷

Seizures, corticosteroids and intracranial pressure

The ESO guideline suggests antiseizure medication for patients who have had an early seizure and have a supratentorial lesion. It makes no recommendation on primary prophylaxis or prevention of late seizures.¹⁷ Late seizures occurred in 9·5% of the Portuguese registry.⁴⁷ No randomised trial of antiseizure prophylaxis exists.

Corticosteroids should not be given for the thrombosis itself. In ISCVT they did not improve outcome, and in patients without parenchymal lesions they were associated with a worse prognosis (OR 4·2, 1·6–11·6).⁶⁷ The ESO guideline suggests against them.¹⁷

The ESO guideline also suggests not using acetazolamide to reduce death or dependency.¹⁷ That is a different question from the management of papilloedema that threatens vision. There, acetazolamide, therapeutic lumbar puncture and, if these fail, cerebrospinal fluid shunting are used by convention, extrapolated from idiopathic intracranial hypertension rather than tested in cerebral venous thrombosis.⁶⁸ Readers of the guideline should not take its wording as advice against acetazolamide for threatened vision.

Special situations

Vaccine-induced immune thrombotic thrombocytopenia

In April 2021, three case series described thrombosis with thrombocytopenia 5–24 days after the ChAdOx1 nCoV-19 vaccine, most often cerebral venous thrombosis, with high titres of antibodies to platelet factor 4 (PF4) in patients never exposed to heparin.^13,20,21 The antibodies form immune complexes with PF4 that activate platelets through the Fc receptor, independently of heparin, in a picture that mimics autoimmune heparin-induced thrombocytopenia.^20,69 In vitro, platelet activation was blocked by high-dose heparin, Fc-receptor blockade and immunoglobulin.²⁰

The cerebral venous thrombosis of VITT is severe. In an international registry, in-hospital mortality was 47% with VITT against 3·9% in cerebral venous thrombosis before the pandemic.⁷⁰ In the UK cohort that defined the clinical criteria, overall mortality was 22%. Cerebral venous thrombosis increased the odds of death 2·7-fold, and mortality reached 73% in patients with a platelet count below 30 × 10⁹/L and intracranial haemorrhage.⁷¹ Treatment changed outcomes. In a UK multicentre cohort, death or dependency was lower in patients given a non-heparin anticoagulant (36% vs 75%) and in those given intravenous immunoglobulin (40% vs 73%).¹⁴ Reported mortality fell from 47% to 22% once the syndrome was recognised.⁷² Of patients who survived the acute phase, 88% became functionally independent and no new thrombosis occurred.⁷³ Decompressive surgery in VITT carried an in-hospital mortality of 65%, and 94% in patients in coma before surgery,⁷⁴ and half of the patients given endovascular treatment died, although this was not independently associated with mortality after adjustment.⁷⁵

The earliest UK series recommended avoiding platelet transfusion and giving a non-heparin anticoagulant and intravenous immunoglobulin.¹³ The German Society of Thrombosis and Haemostasis Research issued guidance to the same effect,⁷⁶ and serial laboratory studies showed a fall in antibody-mediated platelet activation after immunoglobulin.⁷⁷ Testing needs care. PF4 enzyme immunoassays are more than 95% sensitive for VITT antibodies, whereas some rapid immunoassays used for heparin-induced thrombocytopenia detect fewer than 25% of cases.⁶⁹ A negative rapid test does not exclude VITT. Panel 2 sets out the approach. The same principles apply to cerebral venous thrombosis complicating classic heparin-induced thrombocytopenia, which occurs in 1·6% of patients with HIT and carries an in-hospital mortality of 33%.³³

COVID-19

Early reports of cerebral venous thrombosis in COVID-19 described in-hospital mortality of 40%.³⁴ A later registry comparison found more severe presentations but no significant difference in in-hospital mortality (7% vs 3%; adjusted OR 2·6, 0·7–9) or independence at 6 months compared with pre-pandemic patients.⁷⁸ Across 171 centres in 49 countries, admissions for cerebral venous thrombosis did not rise in the first pandemic year, and COVID-19 was present in 7·6% of cerebral venous thrombosis admissions.³⁵

Pregnancy and contraception

Pregnancy and the puerperium are among the sex-specific risk factors seen in women with cerebral venous thrombosis, and these women have a better prognosis than other patients.¹⁶ By convention, low-molecular-weight heparin is the anticoagulant used in pregnancy. A systematic review of 13 studies found recurrent cerebral venous thrombosis in 9 per 1000 subsequent pregnancies (3–33) and other venous thromboembolism in 27 per 1000 (12–61). Spontaneous abortion occurred in 17·7% and did not differ significantly with antithrombotic prophylaxis.⁷⁹ The absolute risk is low but well above background. The ESO guideline suggests that later pregnancies are safe, that prophylactic low-molecular-weight heparin should be considered throughout pregnancy and the puerperium, and that oestrogen-containing contraceptives should be avoided after cerebral venous thrombosis.¹⁷

Children and neonates

Whether to anticoagulate children, and especially neonates, has been debated more than in adults. In a prospective Toronto cohort, thrombus propagated in 28% of neonates and 37% of children not anticoagulated, against 4% and 7% of those anticoagulated. Major haemorrhage on treatment occurred in 6%: 14% with pre-existing haemorrhage and 2% without.⁸⁰ In 104 neonates, lack of anticoagulation predicted propagation (RR 13), and 61% had a poor outcome, meaning death or any deficit, at a median of 2·5 years.⁸¹ In a European cohort, anaemia or microcytosis was as common as a prothrombotic disorder, and 62% of children had sequelae.³⁷

The ASH/ISTH 2024 guideline suggests anticoagulation rather than none for children with cerebral sinovenous thrombosis, with or without haemorrhage secondary to venous congestion. The recommendation is conditional and rests on very low certainty evidence. In the guideline's pooled data, mortality in non-neonates was 1·4% with anticoagulation against 11·0% without (RR 0·12, 0·04–0·36). The panel downgraded its 2018 strong recommendation to a conditional one, citing heterogeneity of cause and bleeding risk.^55,82 It suggests anticoagulation alone rather than thrombolysis, reserving thrombolysis for deterioration despite anticoagulation, and a short half-life agent such as unfractionated heparin when bleeding risk is high.⁵⁵ In EINSTEIN-Jr CVT, rivaroxaban gave results similar to standard treatment.¹⁹

Prognosis

Most patients do well. In ISCVT, 57·1% had no symptoms and 86·6% were independent at a median of 16 months; 8·3% died.³ A multicentre cohort of 706 patients reported complete recovery in 89·1% and mortality of 2·8% at a median of 40 months.⁵⁹ In the largest recent cohort (1525 adults), mortality was 3·4% at 30 days and 5·6% at 1 year. Early deaths were mostly from haemorrhage or herniation (48·1%) and cancer (21·2%); late deaths were mostly from cancer (38·2%).³⁹

Predictors of death or dependency in ISCVT were age over 37 years, male sex, coma, mental status disorder, haemorrhage on admission, deep venous system thrombosis, central nervous system infection and cancer.³ Two newer scores perform better. The IN-REvASC score, derived in 1025 patients, predicted poor 90-day outcome with an area under the curve of 0·84 against 0·71 for the older ISCVT-based score; active cancer was the strongest predictor (OR 11·20).⁸³ The SI₂NCAL₂C score, from 1454 patients, gave C-statistics of 0·80 for poor 6-month outcome and 0·84 for 30-day and 1-year mortality.⁸⁴ Both need external validation before they guide individual decisions.

Uncertainties and future research

An international research agenda published in 2024 sets out the open questions.⁸⁵ Five matter most to practising haematologists.

• Duration of anticoagulation. EXCOA-CVT should answer the main question; until it reports, duration rests on convention.⁵⁸
• DOACs. The randomised evidence comes from six small trials with 428 patients in total, and randomised-only and mixed meta-analyses disagree on recurrence.^10,57 A trial powered for recurrence and intracranial haemorrhage would settle whether DOACs are equivalent or better.
• Endovascular treatment. TO-ACT was small and stopped early.¹¹ Whether any subgroup benefits, and how it should be selected, is not known.
• Haematological work-up. The yield of screening for myeloproliferative neoplasms, paroxysmal nocturnal haemoglobinuria and occult cancer in unselected patients has not been measured prospectively.
• Populations without data. Almost all evidence comes from high-income countries. The Middle East, Africa and much of Asia lack population-based incidence data, and quality of life after decompressive surgery was worse in patients living in middle-income countries.⁶⁴

Conclusion

Cerebral venous thrombosis is more common than once thought, and most patients recover. The basis of treatment has not changed in three decades: prompt diagnosis by venography and anticoagulation with heparin, including when haemorrhage is present. What has changed is the evidence around that basis. DOACs are now a reasonable alternative to warfarin, endovascular treatment has not shown benefit in its only trial, decompressive surgery saves lives, and VITT has shown that thrombocytopenia at presentation changes the treatment entirely. The questions that remain, on duration, on DOACs and on endovascular selection, each need a trial rather than more cohorts.

References

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