Pontine Infarct Imaging Phenotypes Linked to Early Deterioration

Key Takeaways

• At a single center in China, 30.2% of adults with acute isolated pontine infarction experienced early neurological deterioration within seven days.
• Branch atheromatous disease and large artery atherosclerosis imaging phenotypes were significantly associated with deterioration relative to small artery disease.
• Longer thrombin time was significantly associated with deterioration, diabetes showed borderline evidence, and the triglyceride-glucose index was not independently associated.
• Imaging augmentation yielded higher observed discrimination than metabolic/coagulation augmentation, but the direct difference was not statistically significant.

Neurological deficits can worsen during the first week after an acute isolated pontine infarction (IPI). Investigators evaluated imaging and laboratory features in patients with this condition.

Chen and colleagues retrospectively examined an acute isolated pontine infarction cohort of 162 adults at Xiaolan People's Hospital of Zhongshan, Guangdong, China. Patients were admitted from March 2021 through April 2025 within 72 hours of symptom onset; diffusion-weighted imaging (DWI) confirmed infarction confined to the pons within 48 hours of admission. Branch atheromatous disease (BAD) denoted ventral-surface extension without at least 50% stenosis. Large artery atherosclerosis (LAA) denoted at least 50% vertebral or basilar stenosis. Small artery disease (SAD) denoted a small, deep lesion without ventral extension or significant vertebrobasilar stenosis. These were imaging categories, not confirmed causes. Two neuroradiologists independently classified scans while blinded to clinical information and outcomes, resolving disagreements by consensus.

Early neurological deterioration (END) meant a rise from admission of at least two total National Institutes of Health Stroke Scale (NIHSS) points or one point in motor item 5 or 6 during seven days of daily assessments. Firth-penalized logistic regression assessed adjusted associations using SAD as reference. Separate discrimination models compared admission modified Rankin Scale (mRS) and NIHSS alone, that base plus imaging, that base plus diabetes, triglyceride-glucose index (TyG), and thrombin time (TT), and the full combination. Candidate predictors preceded documented deterioration.

END occurred in 49 patients. Relative to SAD in the full adjusted model, BAD had an odds ratio (OR) of 20.70 (95% confidence interval [CI] 7.10–70.04; P < 0.001). LAA had an OR of 5.06 (95% CI 1.84–15.41; P = 0.001). TT was also associated with END, with an adjusted OR of 1.34 per second (95% CI 1.04–1.73; P = 0.020). Diabetes showed borderline evidence of association, whereas TyG was not independently associated.

The imaging-augmented model had an apparent area under the curve (AUC) of 0.814, versus 0.716 for the metabolic/coagulation-augmented model. The direct difference was not statistically significant: ΔAUC 0.098 (bootstrap 95% CI −0.015–0.180; paired DeLong P = 0.066). Imaging augmentation improved discrimination over the base model, but that comparison does not establish superiority over metabolic/coagulation augmentation.

The full model had an apparent AUC of 0.852 and an optimism-corrected AUC of 0.818 after internal bootstrap validation.

Retrospective selection at one center and residual confounding limit interpretation. The imaging categories are not confirmed etiologies, and the TT association is exploratory rather than evidence of a treatment target. Bootstrap checking was internal; neither the nomogram nor exploratory decision-curve analysis establishes clinical utility or transportability without independent external validation.

Clinician Questions

Did atrial fibrillation exclude patients from the acute isolated pontine infarction cohort?

Chen and colleagues excluded adults whose acute isolated pontine infarction was adjudicated as a cardioembolic index stroke, not everyone with atrial fibrillation. Some adults with atrial fibrillation remained because their pontine infarctions were not adjudicated cardioembolic.

Does longer thrombin time after isolated pontine infarction prove thrombin activation?

No. In acute isolated pontine infarction, thrombin time measures the time to fibrin formation in vitro after exogenous thrombin is added to plasma; fibrinogen quantity or function and other laboratory or clinical influences can affect it. Its association with early neurological deterioration does not establish in vivo thrombin activation, a local clotting mechanism, or a treatment target.

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