New Dural MRI Sign Tracks With Intracranial Atherosclerotic Burden
A newly described MRI finding, the para-ISS dural space enhancement sign, appeared far more often than expected in contrast-enhanced intracranial vessel-wall imaging and showed a strong relationship with intracranial atherosclerosis. The signal is centered at the free inferior margin of the falx cerebri adjacent to the inferior sagittal sinus, where enhancement extends beyond the venous lumen itself. In practical radiology terms, this creates a recognizable dural pattern rather than a nonspecific haze of contrast uptake.
The sign was present in 609 of 811 patients, a detection rate of 75.1%. Prevalence rose steadily with age, from 50.0% in those younger than 40 years to 81.7% in patients older than 70 years. In a field where many incidental enhancement patterns are dismissed as artifactual or anatomically unimportant, this one behaved like a structured imaging biomarker tied to vascular disease burden.
A Graded Relationship With Plaque Severity
The strongest univariate correlate was vulnerable intracranial plaque, with an odds ratio of 8.29 and a 95% confidence interval of 5.54 to 12.40. Detection climbed across plaque grades in a dose-response pattern: 38.7% at grade 0, 77.2% at grade 1, and 90.3% at grade 2. That progression is difficult to explain by chance alone and is exactly the kind of monotonic imaging association that tends to signal a biologically relevant process rather than a coincidental co-occurrence.
A direct bedside implication follows from the anatomy. The falx cerebri and the adjacent dural venous structures are not isolated from the vascular milieu of the intracranial compartment. If atherosclerotic disease alters arterial wall biology, downstream inflammatory signaling, microvascular permeability, or adjacent dural perfusion, the dura may enhance in a patterned way near the inferior sagittal sinus. The authors’ data do not prove the mechanism, but the alignment of enhancement severity with plaque burden makes an atherosclerosis-related dural pathway plausible.
Why the Pattern Matters More Than the Absolute Prevalence
Several associations survived multivariable modeling even after adjustment for age and sex. Vulnerable plaque remained independently associated with the sign, as did plaque grade, age, and inpatient status. Per grade increase, plaque grade carried an odds ratio of 2.84. Age also remained a significant correlate, with an odds ratio of 1.38 per standard deviation, while inpatient status showed an odds ratio of 3.18. The cross-validated model reached an AUC of 0.755, which is substantial for a single imaging sign measured across a heterogeneous clinical population.
A single sentence captures the clinical tension here: this is not just a common finding, it is a common finding that tracks with disease severity. The difference matters because high-prevalence incidental signs are often ignored unless they preserve a graded relationship with pathology. Here, the relationship persisted across machine-learning and regression approaches, which strengthens confidence that the pattern is not an analytical artifact.
Anatomical Concordance Favored Anterior-Circulation Disease
The association was stronger for anterior-circulation plaque than for posterior-circulation plaque, with odds ratios of 4.42 and 2.76, respectively. That topographic concordance supports the idea that the enhancement is not random dural reactivity but may reflect a regional vascular or inflammatory signature linked to intracranial atherosclerotic biology. When an imaging sign is anatomically selective in this way, its value rises because it suggests the radiologist is seeing a vascular footprint rather than a generalized inflammatory background.
Moyamoya disease moved in the opposite direction and was inversely associated with the sign, with an odds ratio of 0.25. That inverse relationship is informative because moyamoya and atherosclerotic disease do not share the same vessel-wall behavior. The finding argues against a nonspecific “any vasculopathy” explanation and instead points toward a process more tightly coupled to atherosclerotic burden.
How the Cohort Was Built and Why the Statistics Hold Up
Investigators reviewed consecutive contrast-enhanced intracranial vessel-wall MRI examinations collected between May 2015 and December 2025. Of 875 examinations, 835 were evaluable, representing 811 patients. For the primary analyses, only the first outcome-evaluable examination per patient was used, limiting duplicate patient influence on the core results. The sign itself was defined with unusual specificity: enhancement had to occur strictly at the falx free margin adjacent to the inferior sagittal sinus and exceed the venous lumen.
To test robustness, 47 demographic, clinical-history, and imaging variables were assessed with univariate testing and Benjamini-Hochberg false discovery rate correction. Multivariable logistic regression was then triangulated with LASSO and random forest, while patient-grouped 5-fold cross-validation assessed model stability. Inter-reader agreement was high, with Cohen’s kappa of 0.93, suggesting the sign can be recognized consistently rather than subjectively stretched to fit one reader’s expectations.
What This Means for Intracranial Vessel-Wall Imaging
The most important clinical consequence is not immediate treatment change. This is a preprint, not a peer-reviewed practice-changing study, and the authors do not present outcome data showing that the sign predicts stroke, recurrent ischemia, or response to therapy. Even so, the imaging signal is strong enough to deserve attention during routine vessel-wall MRI interpretation, especially in older patients and in those already known to harbor intracranial plaque.
Radiologists and neurologists may eventually use the sign as a companion marker of intracranial atherosclerotic burden, particularly when plaque burden is difficult to quantify across multiple arterial segments. A dural enhancement pattern could help identify patients whose disease extends beyond a single focal stenosis and into a broader intracranial vascular phenotype. The biologic plausibility is reinforced by the graded plaque association, but prospective validation will need to determine whether the sign changes risk stratification, management intensity, or follow-up imaging decisions.
For now, the practical message is narrower: a frequent and reproducible enhancement pattern at the inferior sagittal sinus margin appears to travel with intracranial atherosclerotic burden, especially vulnerable plaque. Whether it becomes a useful marker in routine neuroradiology will depend on prospective studies that test reproducibility, mechanism, and prognostic value in independent cohorts.