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Background and Purpose CSF-venous fistulas (CVFs) are an increasingly recognised cause of spontaneous intracranial hypotension (SIH). Clinicians frequently encounter paradoxical normal or elevated lumbar puncture opening pressures and rebound intracranial hypertension (RIH) following treatment. Existing pathophysiological frameworks centred on venous engorgement and dural elastance do not completely explain these phenomena. This study applies first-principles physics to mathematically model CVF pressure-volume dynamics and explore the contributions of fistula geometry, CSF production rate, and dural stiffness to equilibrium states.Materials and Methods Iterative mathematical simulations were developed in Python based on first-principles fluid dynamics. A two-compartment model represented the CSF and paravertebral venous systems, incorporating a pressure-dependent one-way fistula valve. Adjustable parameters included initial CSF pressure, CSF production rate, fistula radius, outflow valve pressures, and a dural elastance coefficient. Dynamic equilibrium pressures and volumes were calculated iteratively and plotted against each parameter.Results Equilibrium CSF pressure was highly sensitive to fistula radius: large fistulas (radius > 2.0 mm) drove CSF pressure toward venous baseline (3 mmHg), whereas small fistulas (radius < 0.7 mm) allowed CSF pressure to stabilise at physiological levels (~15 mmHg) as alternative outflow mechanisms compensated. Intermediate fistulas produced equilibria between these extremes. Increasing CSF production rate elevated equilibrium pressure across all fistula sizes, an effect exacerbated at smaller radii due to higher outflow resistance. Dural elastance did not independently alter equilibrium pressure at a fixed fistula radius; however, increasing elastance markedly reduced equilibrium CSF volume, potentially masking true hypotension on volumetric assessments.Conclusions Current fistula-centric frameworks are insufficient to explain paradoxical opening pressures and rebound intracranial hypertension in CVF. Our model suggests these phenomena reflect global CSF dysregulation, encompassing upregulated production and secondary outflow dysfunction, rather than fistula anatomy alone. Clinically, established markers of global dysregulation such as elevated opening pressures and multiple fistulas may stratify patients at higher risk of recurrence or rebound hypertension, enabling more accurate prognostic counselling. Recurrence itself may be driven by increased dural elastance from multifactorial causes including connective tissue disease, pre-existing IIH, or chronic venous compensation; each representing a potentially treatable target independent of the fistula. Management of CVF should therefore extend beyond fistula occlusion to encompass assessment and treatment of underlying CSF volume-pressure dysregulation.Disclosures Y. Wardak: None. B. Shaygi: None. H. Kok: None. R. Chandra: None. A. Yazdabadi: None. A. Jhamb: None. J. Moore: None. P. Smith: None. J. Maingard: None. C. Gan: None. L. Slater: None. E. Barvulsky: None. M. Schembri: None. A. Gauden: None. J. Russell: None. A. Gonzalvo: None. A. Khabaza: None. D. Pavlin-Premrl: None. M. Brooks: None. C. Barras: None. H. Asadi: None.Abstract O-059 Figure 1