Age and Body Size Reframe the Apparent Sex Gap in Cerebral Venous Thrombosis
Women with cerebral venous thrombosis have long been described as younger and more likely to present with headache than men. This Zurich cohort suggests part of that pattern may be an artifact of two basic clinical variables: age and body-mass index.
In 219 consecutive adults with confirmed cerebral venous thrombosis admitted between 2001 and 2021, women made up 132 cases, or 60.3% of the cohort. They were younger on average than men, at 47.3 versus 54.9 years, and had a lower body-mass index, 25.9 versus 27.8 kg/m2. Those differences matter because both age and adiposity influence thrombosis risk, inflammatory tone, and the pretest probability of headache-related presentations in routine neurology practice.
Headache and Cortical Vein Involvement Lost Statistical Ground After Adjustment
At first glance, women appeared to present differently. Headache was documented in 72.0% of women versus 57.5% of men, and cortical vein thrombosis appeared more common in women as well, at 14.4% versus 5.7%. The signal looked familiar, and it fit the long-standing impression that female patients with cerebral venous thrombosis are more likely to arrive with a painful, more diffuse symptom complex.
Once age and body-mass index were equalized, the picture changed sharply. The association between sex and headache disappeared, with an odds ratio of 1.17 and a 95% confidence interval from 0.54 to 2.54. Cortical vein thrombosis also lost statistical support after adjustment, with an odds ratio of 2.05 and a 95% confidence interval from 0.59 to 7.06.
The implication is straightforward: some of the observed sex difference in presentation is likely being driven by who gets CVT, not by sex itself. A younger and leaner female subgroup may be overrepresented among patients who come to attention with headache, while older and heavier men may be enriched for a different clinical mix. In a disorder as heterogeneous as CVT, baseline population structure can easily masquerade as a sex-specific phenotype.
Platelet Counts and Acute-Phase Markers Stayed Elevated in Women
Not every difference disappeared with adjustment. Two laboratory features remained tied to sex even after controlling for age, body-mass index, and calendar period. Women had higher platelet counts, by 56 × 10^9/L, with a 95% confidence interval from 26 to 86. They also more often showed elevated acute-phase markers without documented infection, 59.1% versus 33.3%, corresponding to an odds ratio of 2.91 with a 95% confidence interval from 1.44 to 5.87.
Those findings point toward a biology that cannot be explained away by age or adiposity alone. Platelets sit at the center of venous thrombosis, linking endothelial injury, coagulation activation, and inflammatory signaling. An acute-phase response without a clear infectious trigger raises the possibility of a broader prothrombotic inflammatory state, one that may differ by sex even when the clinical presentation does not.
The clinical message is not that women with CVT are uniformly more inflammatory in a causal sense. It is narrower. Some laboratory signatures of thrombosis risk remain sex-associated after major demographic differences are removed, which argues for further work on the biologic pathways behind venous clot formation rather than on bedside symptoms alone.
Outcome Measures Did Not Separate by Sex Among Assessed Patients
Follow-up data did not suggest a clinically meaningful outcome gap between men and women, at least among the patients who were assessed. Only 38% had six-month follow-up available, which immediately limits how confidently any long-term statement can be made. Even within that incomplete dataset, functional independence was nearly identical: 86.3% in women and 87.5% in men.
Residual headache, return to work, and recanalization likewise did not differ by sex among assessed patients. In practical terms, the sex-linked differences seen at presentation did not translate into a clear divergence in short-term recovery among those whose outcomes could actually be measured.
That finding matters at the bedside. The sex of the patient did not appear to dictate who recovered functionally, who returned to work, or who recanalized within the available follow-up window. The lingering concern is not a difference in recovery signal, but the sparse follow-up itself, which leaves substantial room for unmeasured outcome differences to remain hidden.
Why the Covariate Problem Matters in Cerebral Venous Thrombosis
This study is a reminder that sex-stratified neurology is vulnerable to confounding when age and body composition are unevenly distributed. CVT often reaches clinical attention in younger adults, and women are disproportionately represented in that age band. If investigators do not account for the background distribution of age and body-mass index, the final comparison can exaggerate sex-specific symptoms and understate shared pathophysiology.
The same logic applies to the laboratory findings. A higher platelet count and a nonspecific inflammatory response may reflect sex-linked biology, but they may also represent differences in the way thrombosis declares itself in men and women, or in the prevalence of unmeasured triggers across the two groups. The adjustment strategy used here reduces the risk of overinterpreting crude comparisons, while also preserving the signals most likely to be biologically real.
This was a single-center cohort from Zurich spanning two decades, so practice patterns, diagnostic methods, and referral behavior may have shifted over time. The study also remains a preprint and has not undergone peer review. Even so, the analysis usefully strips away two of the most obvious confounders and leaves a cleaner message: the familiar female excess of headache and cortical vein involvement in cerebral venous thrombosis may be partly demographic, while the platelet and inflammatory differences deserve further mechanistic attention.