Albumin quotient is associated with subdural effusion and lower CSF opening pressure in spontaneous intracranial hypotension

Spontaneous intracranial hypotension (SIH) is characterized by cerebrospinal fluid (CSF) leakage and reduced CSF volume, yet its effects on blood–CSF barrier function remain poorly understood. The CSF/serum albumin quotient (QAlb) is an established marker reflecting blood–CSF barrier function and CSF dynamics. We investigated QAlb in patients with SIH and its associations with clinical, CSF pressure, and neuroimaging features. We retrospectively reviewed patients with SIH who underwent dynamic myelography at a tertiary referral center between August 2024 and July 2026. Patients with available CSF and serum albumin measurements were included, while those with possible traumatic lumbar puncture, defined as a CSF red blood cell count > 200/µL, were excluded. QAlb was calculated as the ratio of CSF albumin (mg/dL) to serum albumin (g/dL) and expressed as ×10 − 3 . Associations between QAlb and clinical and imaging variables were assessed using univariable and multivariable linear regression. Sensitivity analyses were performed using log-transformed QAlb and after excluding patients with subdural hematoma. A total of 69 patients were included (mean age, 42.0 ± 11.1 years; 40.6% male). The median QAlb was 5.5 × 10 − 3 (interquartile range [IQR], 4.3–8.9), and the median CSF opening pressure was 110 mmH 2 O (IQR 70–130). In multivariable analysis, male sex (β = 2.260; P = 0.009) and subdural effusion (β = 4.038; P = 0.001) were independently associated with higher QAlb, whereas CSF opening pressure was inversely associated with QAlb (β = −0.017 per mmH 2 O; P = 0.028). These associations remained consistent after logarithmic transformation of QAlb and after excluding 8 patients with subdural hematoma. Higher QAlb in SIH was independently associated with lower CSF opening pressure and subdural effusion, but not with overall brain MRI severity or other clinical variables. These findings provide initial evidence of altered blood–CSF barrier function in SIH and suggest that QAlb may reflect pathophysiological changes related to reduced CSF pressure and subdural effusion.