Chronic subdural hematoma (CSDH) is traditionally described as a post-traumatic blood collection within the subdural space; however, both its anatomical localization and pathophysiology have been increasingly questioned. Ultrastructural and histopathological evidence demonstrates that no true subdural space exists under physiological conditions and that CSDH originates instead within the dural border cell (DBC) layer, a mechanically fragile and biologically active meningeal interface. Accordingly, chronic “subdural” hematoma may be more accurately interpreted as an intradural border cell lesion. Beyond anatomy, CSDH is a dynamic, self-sustaining disease driven by chronic inflammation, pathological angiogenesis, vascular immaturity, and localized hemostatic dysregulation. Hypoxia-induced HIF-1α/VEGF activation promotes fragile, hyperpermeable neovessels, while local hyperfibrinolysis and kallikrein–kinin activation prevent stable clot formation, driving recurrent microbleeding and plasma exudation. Consequently, hematoma persistence and recurrence represent a biological failure rather than a purely technical surgical shortcoming. This conceptual shift provides a coherent rationale for dural-targeted therapies, including middle meningeal artery embolization and pharmacological modulation of angiogenesis and fibrinolysis. Reframing CSDH as a chronic intradural and biologically active disorder has important implications for terminology, classification, and the development of mechanism-oriented, multidisciplinary management strategies.