Key result
Branch atheromatous disease linked to ~20.7-fold higher odds of early neurological deterioration vs SAD.
Why the study?
Early neurological deterioration is common after acute isolated pontine infarction, but the relative associations of imaging phenotype and metabolic or coagulation markers with this outcome remain uncertain.
Are operational brain MRI imaging phenotypes (BAD and LAA vs SAD) and metabolic or coagulation markers (TyG index, diabetes, thrombin time) independently associated with early neurological deterioration within 7 days in patients with acute isolated pontine infarction?
Cohort (n=162)
Two independent neuroradiologists, blinded to clinical data and outcomes, reviewed all images
No
Are operational brain MRI imaging phenotypes (BAD and LAA vs SAD) and metabolic or coagulation markers (TyG index, diabetes, thrombin time) independently associated with early neurological deterioration within 7 days in patients with acute isolated pontine infarction?
In patients with acute isolated pontine infarction, branch atheromatous disease and large artery atherosclerosis imaging phenotypes strongly predict early neurological deterioration, warranting closer early clinical surveillance, whereas the triglyceride-glucose index is not independently predictive once adjusted for imaging phenotype.
Answers are grounded in this paper and cite their sources.
Imaging phenotypes may aid risk stratification in pontine infarction; leaves open prospective validation before clinical adoption.
Background Early neurological deterioration (END) is common after acute isolated pontine infarction (IPI), but the relative associations of imaging phenotype and metabolic or coagulation markers with END remain uncertain. We evaluated these domains and developed an exploratory prediction model. Methods We retrospectively analyzed 162 patients with acute IPI. END was a ≥2-point increase in total National Institutes of Health Stroke Scale (NIHSS) score or a ≥1-point increase in NIHSS motor item 5 or 6 from the admission baseline within 7 days after admission. Imaging was modeled nominally (BAD, LAA, or SAD; SAD as reference). Primary associations were estimated by Firth logistic regression. Four prespecified Firth models were compared by AUC, and the full model underwent 1,000-resample bootstrap validation. Results END occurred in 49 patients (30.2%). In the full Firth model, BAD (OR 20.70, 95% CI 7.10–70.04; P < 0.001) and LAA (OR 5.06, 95% CI 1.84–15.41; P = 0.001), relative to SAD, were associated with END. Thrombin time (TT) was also associated with END (OR 1.34 per second, 95% CI 1.04–1.73; P = 0.020); diabetes showed borderline evidence of association ( P = 0.057), whereas TyG was not independently associated ( P = 0.603). The apparent AUC was 0.652 (95% CI 0.562–0.742) for the base model, 0.814 (95% CI 0.745–0.883) for the base-plus-imaging model, 0.716 (95% CI 0.631–0.802) for the base-plus-metabolic/coagulation model, and 0.852 (95% CI 0.792–0.911) for the full model. Discrimination did not differ significantly between the base-plus-imaging and base-plus-metabolic/coagulation models (ΔAUC 0.098, bootstrap 95% CI −0.015–0.180; paired DeLong P = 0.066). All 1,000 bootstrap iterations succeeded; the optimism-corrected AUC was 0.818, with a calibration intercept of −0.023, calibration slope of 0.870, and Brier score of 0.162. Conclusion In this cohort, BAD and LAA imaging phenotypes were independently associated with END, whereas TyG was not independently associated. However, the direct discrimination advantage of the imaging model over the metabolic/coagulation model was not statistically established. The association with TT is exploratory, and the full model and nomogram require external validation before clinical use.
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陈燕翔 et al. (2026) conducted a cohort in Acute isolated pontine infarction (IPI) (n=162). Branch atheromatous disease (BAD) and large artery atherosclerosis (LAA) imaging phenotypes, metabolic markers (TyG, diabetes), and thrombin time (TT) vs. Small artery disease (SAD) imaging phenotype (reference group) was evaluated on Early neurological deterioration (END), defined as a ≥2-point increase in total NIHSS score or a ≥1-point increase in NIHSS motor item 5 or 6 from admission baseline within 7 days (OR 20.70, 95% CI 7.10-70.04, p=<0.001). Branch atheromatous disease (OR 20.70, P<0.001) and large artery atherosclerosis (OR 5.06, P=0.001) imaging phenotypes were independently associated with early neurological deterioration vs small artery disease.
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