European Journal of Cardiovascular Medicine

Cerebral venous thrombosis (CVT) accounts for ~0.5–1% of all strokes but disproportionately affects young adults and women.¹⁻³ Clinical manifestations vary from isolated headache to seizures, focal deficits, and coma, reflecting the involved venous territory and the presence of venous infarction or hemorrhage.⁴,⁵ The diagnostic landscape has shifted with widespread availability of MR venography and high-quality CT venography, which together provide rapid, non-invasive confirmation of sinus and cortical vein occlusion.⁶,⁷

Risk factors span transient prothrombotic states—pregnancy, puerperium, hormonal contraception—and chronic conditions such as inherited thrombophilia, malignancy, systemic inflammatory disease, and infection.⁸⁻¹¹ The COVID-19 era added important epidemiologic nuances: infection itself confers thrombotic risk, and rare vaccine-induced immune thrombotic thrombocytopenia (VITT) presents with severe CVT and thrombocytopenia, mandating distinct therapeutic pathways.¹²⁻¹⁴

Anticoagulation remains the cornerstone of acute management, even in the presence of intracerebral hemorrhage, aiming to prevent thrombus propagation, facilitate recanalization, and reduce recurrent venous thromboembolism.¹⁵,¹⁶ Historically, parenteral heparin bridged to vitamin K antagonists was standard; however, randomized and large observational data have suggested that DOACs (e.g., dabigatran, rivaroxaban, apixaban) offer similar efficacy with favorable safety and convenience profiles.¹⁷⁻²¹ Endovascular treatment is reserved for patients deteriorating despite optimal anticoagulation, with ongoing debate about patient selection given mixed trial results.²²,²³

Functional outcomes in modern cohorts are generally favorable, with 80–90% achieving independence at follow-up; nevertheless, a subset suffers persistent headaches, cognitive or mood symptoms, epilepsy, or visual deficits, underscoring the importance of structured follow-up and rehabilitation.¹⁸,²⁴,²⁵ Imaging-clinical correlation is central to prognosis: extensive sinus involvement, deep venous system thrombosis, parenchymal hemorrhage, and delayed anticoagulation have been associated with worse outcomes.⁵,¹⁶,²⁴

Against this backdrop, we sought to delineate the clinicoradiological profile and short-term functional outcomes of patients with acute CVT presenting to a tertiary center. We specifically describe patterns of sinus and cortical vein involvement, frequency of parenchymal lesions, initial treatments—including DOAC use—and their association with early and 3-month mRS outcomes. Our report complements recent literature by providing granular, real-world data reflective of contemporary imaging and therapeutic practices.¹⁷⁻²¹

This is a Prospective observational cohort at a tertiary care academic hospital over a period of 1 year. Consecutive adults with suspected CVT were screened in emergency, neurology, and neurosurgery services.

Eligibility:

Inclusion criteria: (1) age ≥18 years; (2) symptom onset ≤28 days before presentation; (3) radiological confirmation of CVT on MRV (time-of-flight or contrast-enhanced) and/or CTV (multidetector CT venography), with or without parenchymal lesions; (4) provision of informed consent by patient or surrogate.

Exclusion criteria: (1) isolated intracranial hypotension or non-thrombotic sinus occlusion (e.g., arachnoid granulation, tumor compression) without thrombus; (2) chronic CVT (judged by collateralization and clinical timeline >3 months); (3) primary subarachnoid hemorrhage or arterial ischemic stroke without venous involvement; (4) known contraindication to anticoagulation (e.g., uncontrolled bleeding, platelet count <30×10⁹/L not consistent with VITT management); (5) refusal of consent.

Data collection: A standardized case-record form captured demographics, vascular risk factors, hormonal exposures, peripartum status, infection, dehydration, malignancy, and thrombophilia testing (protein C/S deficiency, antithrombin, factor V Leiden, prothrombin G20210A, antiphospholipid antibodies), when clinically indicated. Presenting features included headache characteristics, seizures, focal deficits, papilledema, altered sensorium, and blood pressure. Laboratory tests comprised complete blood count, coagulation profile, renal/hepatic function, D-dimer, and—in suspected VITT—platelet factor 4 (PF4) ELISA.

Neuroimaging protocol: All patients underwent MRI brain with MRV or contrast-enhanced CTV at baseline. MRI sequences included DWI/ADC, T2/FLAIR, susceptibility-weighted imaging, and post-contrast T1. We recorded site(s) of thrombosis (superior sagittal, transverse, sigmoid, straight sinus, internal cerebral veins, cortical veins), number of sinuses involved, and parenchymal lesions (venous infarct, intraparenchymal hemorrhage, edema). Follow-up venography at 3 months assessed recanalization (complete/partial/none).

Treatment: Initial anticoagulation with low-molecular-weight or unfractionated heparin was started unless contraindicated. Oral therapy thereafter was per treating physician: vitamin K antagonist (VKA, INR 2–3) or a DOAC (dabigatran 150 mg bid; rivaroxaban 20 mg od; apixaban 5 mg bid), adjusted for renal function. Seizures were treated per standard protocols. Patients with neurological deterioration despite anticoagulation were evaluated by a multidisciplinary team for endovascular therapy (mechanical thrombectomy ± local thrombolysis).

Outcomes: Primary outcome was functional status by modified Rankin Scale (mRS) at discharge and 3 months (good outcome mRS 0–2). Secondary outcomes included in-hospital death, symptomatic intracranial hemorrhage (sICH), new venous infarct, and radiographic recanalization at 3 months.

Statistics: We present descriptive statistics for clinicoradiological variables and outcomes. Group comparisons used χ² or Fisher’s exact test for categorical variables and t-test or Mann–Whitney U for continuous variables, as appropriate (two-sided α=0.05). Analyses were performed using standard statistical software. Missingness <5% was handled by complete-case analysis.

Ethics: Institutional ethics approval was obtained; the study adhered to the Declaration of Helsinki.

Cohort overview: 120 patients met inclusion criteria (mean age 32.8±10.6 years; 68% women). Median symptom-to-door time was 5 days (IQR 2–10). Table 1 summarizes baseline characteristics.

Table 1. Baseline demographics and risk profile (n=120)

*Includes protein C/S deficiency, factor V Leiden, prothrombin G20210A, antiphospholipid syndrome.

Young, predominantly female cohort with common transient risk factors; inherited thrombophilia present in ~12%.

Table 2. Clinical presentation

Headache predominates; seizures and focal deficits are frequent, reflecting cortical involvement.

Table 3. Venous territory involvement (MRV/CTV)

Multisinus involvement is common; cortical vein thrombosis seen in ~28%.

Table 4. Parenchymal lesions on MRI

Forty-one percent had parenchymal injury; hemorrhage present in ~22%, consistent with venous pathophysiology.

Table 5. Acute treatment and in-hospital events

Nearly universal anticoagulation; DOACs used in ~46%; low sICH and mortality.

Table 6. Functional outcomes and recanalization

Functional independence improves by 3 months, paralleling high rates of partial/complete recanalization.

Our cohort reflects the classic epidemiology of CVT: young adults, predominance of women, and frequent transient risk factors such as peripartum state and hormonal exposure.¹⁻³,⁸ The clinical spectrum—headache, seizures, focal deficits—aligns with contemporary series and the ACTION-CVT registry.¹⁸,²⁰ Multisinus involvement with superior sagittal and transverse sinus predilection mirrors prior imaging-based descriptions.⁴⁻⁷ Cortical vein thrombosis was identified in nearly one-third, similar to high-resolution MRV/CTV studies that underscore improved detection with susceptibility-weighted imaging.⁶,⁷

Parenchymal injury occurred in 41%, with 22% hemorrhagic, consistent with venous congestion and blood–brain barrier disruption reported previously.⁴,⁵ Importantly, anticoagulation was instituted in almost all patients, including those with intracerebral hemorrhage, reflecting guideline-concordant care.¹⁵,¹⁶ Our low symptomatic ICH rate (2.5%) and early mortality (2.5%) compare favorably with pooled modern cohorts.¹⁸,²⁴

Nearly half of patients were discharged on DOACs—an adoption trend supported by randomized and observational evidence. The RE-SPECT CVT trial suggested non-inferiority of dabigatran versus warfarin for efficacy and safety, while multicenter registries (e.g., ACTION-CVT) found comparable or lower major bleeding with DOACs relative to VKAs.¹⁷⁻²¹ Our functional outcomes—78% mRS 0–2 at discharge and 88% at 3 months—are congruent with these series and with recent guideline expectations.¹⁶,¹⁸,²⁴ Recanalization at 3 months (complete/partial in 85%) is within reported ranges; although the correlation between recanalization and clinical outcomes remains debated, many studies—including meta-analyses—suggest that at least partial recanalization associates with improved disability and reduced headache burden.²⁴,²⁵

Only 5% underwent endovascular therapy, reflecting conservative selection. The TO-ACT trial and subsequent analyses did not demonstrate routine benefit of endovascular treatment over anticoagulation, though individualized rescue therapy may help deteriorating patients.²²,²³ Our small endovascular subset precludes firm conclusions.

Strengths of our study include prospective data capture, standardized imaging review, and pre-specified outcomes. Limitations are those of a single-center design and modest sample size, restricting multivariable analyses for predictors of poor outcome. Thrombophilia testing was selective, potentially underestimating hereditary predisposition. Finally, follow-up was limited to 3 months; longer-term cognitive, psychosocial, and seizure outcomes warrant further study.¹⁸,²⁵

In summary, our findings reinforce that timely diagnosis with MRV/CTV, early anticoagulation, and increasing DOAC use yield favorable short-term outcomes in acute CVT. Continued research should refine risk stratification (including biomarkers and advanced imaging), define optimal treatment duration for distinct etiologies, and clarify indications for endovascular therapy.

Acute CVT in contemporary practice predominantly affects young women and presents with headache, seizures, or focal deficits. Multisinus involvement is common, and ~40% have parenchymal injury. Early anticoagulation—often transitioned to DOACs—is safe and associated with excellent short-term functional recovery and high rates of venous recanalization. Future multicenter studies with longer follow-up are needed to optimize individualized therapy and survivorship care.

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