A mechanism underlying dural and subdural fluid disorders: Reframing pathophysiology through the unified transdural-pressure gradient model.

Subdural hygroma, chronic subdural hematoma (SDH), and diffuse pachymeningeal enhancement have long been viewed as separate disorders—arising from cerebrospinal fluid (CSF) leakage into the subdural space, repeated microbleeds from such vessels as bridging veins, or venous engorgement and inflammation, respectively. This review proposes a unified framework in which the net transdural pressure gradient governs meningeal permeability and drives the formation of dural and subdural fluid collections. Widening of this pressure gradient increases transcapillary water flow; to accommodate the elevated flux, endothelial permeability rises accordingly. When venous and lymphatic drainage suffice, the result is only mild dural edema; when drainage cannot keep pace, filtrate dissects along the path of least resistance—into the dural border cell (DBC) layer—producing a subdural hygroma. In parallel, sustained or high-magnitude gradients trigger mechanotransductive angiogenesis, also to accommodate the increased water flow, through the formation of fragile neovessels prone to leakage of plasma proteins and erythrocytes—either transforming an existing hygroma into a watery, low-density subdural hematoma or creating a hematoma de novo. Subdural fluid disorders, therefore, represent variable branching gradient-dependent manifestations of a single hemodynamic mechanism. Evidence from spontaneous intracranial hypotension (SIH), shunt over-drainage, aging brains, and the characteristic pan-dural enhancement seen even after unilateral craniotomy, together with findings from middle meningeal artery embolization (MMAE), converges to support this unified model.