Circle of Willis Configuration Is Not Associated with Early Neurological Deterioration in Lacunar Stroke

Lacunar strokes, caused by occlusion of small penetrating arteries, account for approximately 25% of all ischemic strokes. Despite often mild initial presentations, up to 30% of patients experience early neurological deterioration (END), a worsening of neurological status within the first 72 hours. Although mechanisms like branch atheromatous disease (BAD), edema, or hemodynamic instability have been implicated, the role of proximal collateral circulation, particularly the Circle of Willis (CoW), in modulating END risk in lacunar stroke remains unclear. This study aimed to investigate the association between CoW anatomical configuration and END in patients with lacunar infarcts.

We conducted a retrospective analysis of 245 patients with acute ischemic stroke attributed to small vessel disease, admitted to a single tertiary care center from 2020 to 2024. Clinical, laboratory, and imaging data were extracted from institutional registries. END was defined as a ≥2-point increase in NIHSS within 72 hours in the absence of other causes. CoW anatomy was assessed via CTA or MRA. Univariate and multivariable logistic regression analyses were used to evaluate predictors of END.

Among the 245 patients included, 50 (20.4%) experienced END. Compared to those without END, patients in the END group had a significantly higher prevalence of peripheral artery disease (PAD), higher pulse pressure (PP) and ejection fraction, larger infarct volumes, and a greater frequency of ataxia. No differences were observed in age, sex, race, vascular risk factors (except PAD), or initial NIHSS scores. Radiographically, infarct side (left vs. right), territory (anterior vs. posterior), and CoW configuration, did not differ significantly between groups, except that a fetal PCA was more common in the END group (46% vs. 29.7%, p = 0.03). Multivariable logistic regression identified PAD (OR = 6.54, 95% CI: 1.61-26.57, p = 0.009), infarct volume (OR = 2.25, 95% CI: 1.30-3.91, p = 0.004), and ataxia at presentation (OR = 3.03, 95% CI: 1.40-6.93, p = 0.005) as independent predictors of END. PP showed a borderline association (OR = 1.02, p = 0.083), while the remaining variables, including fetal PCA were not significant.

In acute lacunar stroke, END was associated with vascular comorbidities (PAD), clinical signs of strategic pathway disruption (ataxia), and larger infarct volumes, but not with Circle of Willis configuration. These findings suggest that END in small vessel stroke is more strongly influenced by local disease processes and infarct burden than by proximal arterial anatomy. Recognizing these risk factors may help clinicians identify high-risk patients and tailor early monitoring and treatment strategies.