Early Neurological Deterioration in Subcortical Infarcts: A Narrative Review

Background/Objectives: Early neurological deterioration (END) is a frequent and clinically relevant complication in patients with a single small subcortical infarction (SSI), including lacunar infarction and branch atheromatous disease (BAD). Despite initially mild symptoms, END occurs in approximately 20–25% of cases and is strongly associated with poor functional outcomes. However, definitions, mechanisms, predictors, and therapeutic strategies remain heterogeneous. This review aims to synthesize current evidence regarding the incidence, pathophysiology, predictors, and management of END in SSI. Methods: We performed a narrative review of published studies addressing END in patients with lacunar stroke or SSI. We analyzed data on END definitions and incidence, imaging and clinical predictors, proposed pathophysiological mechanisms, and preventive and rescue therapeutic strategies. Results: END definitions vary across studies, most commonly defined as a ≥2-point increase in the National Institutes of Health Stroke Scale within 48–72 h. Hemodynamic compromise due to proximal perforator pathology, particularly in BAD, appears central to END development. Advanced imaging studies demonstrate perfusion abnormalities beyond the infarct core, supporting the concept of a “lacunar penumbra.” Lesion topology, proximal infarct patterns, parent artery plaques, larger infarct size, and vertical extension are consistent imaging predictors. Clinical factors such as diabetes mellitus, higher baseline severity, systemic inflammation, and increased arterial stiffness further modulate risk. Preventive strategies, including early dual antiplatelet therapy and intensified antithrombotic regimens, show promising signals, while induced hypertension may benefit selected patients as a rescue therapy. However, evidence remains largely observational or derived from subgroup analyses. Conclusions: END in SSI is a multifactorial and potentially modifiable process driven by interactions between proximal vascular pathology, hemodynamic failure, and tissue vulnerability. Standardized definitions, MRI-based phenotyping, and mechanism-driven trials are needed to optimize risk stratification and develop targeted preventive and rescue strategies.