Chronic subdural hematoma as failed resolution at the aged dura-subdural interface: Immune-vascular mechanisms,...

Chronic subdural hematoma (CSDH) is a frequent disorder of older adults, yet its persistence and recurrence are not fully explained by retained clot, bridging-vein injury, or technical failure of evacuation. We propose an aging-informed failed-resolution framework for interpreting CSDH persistence and recurrence at the aged dura-subdural interface. In this model, brain atrophy can maintain a residual subdural space, while frailty, multimorbidity, immune aging, vascular aging, and local fibrinolytic excess may lower the threshold for persistent membrane activity and delayed resolution. These host-level vulnerabilities are proposed to shape the outer-membrane environment, where macrophage and dendritic-cell recruitment, cytokine signaling, pathological angiogenesis, vascular leakage, recurrent microhemorrhage, and fibrin turnover may interact as an immune-vascular-fibrinolytic niche. We distinguish direct CSDH evidence from aging-derived mechanisms that remain inferential. Current CT and MRI phenotypes define hematoma burden, architecture, mass effect, and membrane enhancement, but they do not yet identify biological endotypes or select treatment. Peripheral inflammatory indices, coagulation-fibrinolysis markers, hematoma-fluid mediators, and single-cell profiling should be interpreted according to biological proximity, age-related confounding, and treatment-response validation. Burr-hole evacuation with drainage remains the standard for symptomatic mass effect. Middle meningeal artery embolization (MMAE) currently has the most developed evidence base among membrane-directed adjuncts, whereas corticosteroid trials show that nonselective anti-inflammatory therapy can reduce reoperation yet worsen patient-centered outcomes. A key next step is to link frailty, lesion activity, functional recovery, safety, and treatment response in aging-informed cohorts and trials.