Chronic subdural hematoma (CSDH) — a blood collection beneath the skull's inner lining — is projected to become the most common cranial neurosurgical condition in adults by 2030. This minireview systematically maps CSDH pathogenesis onto López-Otín's twelve hallmarks of aging. Two hallmarks have strong direct evidence: chronic inflammaging signatures permeate hematoma fluid, and dysregulated paracrine signaling dominates the outer neomembrane. Cellular senescence earns moderate-evidence status, with the senescence-associated secretory phenotype's cytokine and matrix-remodeling profile closely mirroring the CSDH cavity milieu — though no study has yet confirmed senescent cells in resected tissue. Genomic instability, telomere attrition, epigenetic alterations, and stem cell exhaustion remain entirely unstudied.
The real significance here is conceptual reorientation. CSDH has been treated almost exclusively as a plumbing problem — drain the blood, discharge the patient — despite alarmingly high recurrence rates near 20%. Positioning it within geroscience opens mechanistic questions that surgery alone cannot answer. The 2024 middle meningeal artery embolization trials and the positive ATOCH atorvastatin trial already hint that biology matters beyond anatomy. If senescent cells in the neomembrane drive recurrent fluid accumulation, senolytics like dasatinib-quercetin could theoretically prevent reaccumulation rather than just evacuate existing hematoma. This is a review, not primary data, so its contribution is a research roadmap rather than causal proof. Still, the framework is timely: an aging global population means surgical capacity alone cannot absorb the coming CSDH wave.
