Abstract
OBJECTIVE: This study aimed to evaluate the choroid plexus volume in patients with spontaneous intracranial hypotension (SIH), including the lateral, third, and fourth ventricles, and explore its potential relationship with clinical characteristics. BACKGROUND: SIH is caused by cerebrospinal fluid (CSF) leaks. The choroid plexus is predominantly responsible for CSF production and has been implicated in altered CSF dynamics in various neurological conditions. METHODS: This retrospective case control study included 25 patients with SIH who were diagnosed between 2022 and 2024 from a single tertiary center. In addition, 25 age- and sex-matched healthy controls were included. Choroid plexus volumes were manually segmented from 3D contrast-enhanced magnetization-prepared rapid acquisition gradient echo MRI sequences using 3D Slicer. The total intracranial volume was also calculated. Clinical data, including the Bern score and Headache Impact Test-6 score, were collected from patients with SIH. Group differences in choroid plexus volumes were assessed using a generalized linear mixed model for the lateral ventricles and multivariable linear regression for the third and fourth ventricles, adjusting for age, sex, body mass index, and total intracranial volume. Associations with clinical variables were evaluated using univariable linear regression. RESULTS: After adjusting for covariates, the choroid plexus volume in the lateral ventricles was significantly higher in patients with SIH compared to that in healthy controls (unstandardized regression coefficient = 201.81 mm(3), p = 0.016). However, no significant differences were observed in the choroid plexus volumes of the third (p = 0.617) and fourth ventricles (p = 0.314). Additionally, choroid plexus volume was not associated with disease duration (p = 0.292), Bern score (p = 0.580), and Headache Impact Test-6 score (p = 0.539) in patients with SIH. CONCLUSION: The lateral ventricular choroid plexus is enlarged in patients with SIH, which may represent a compensatory response to CSF hypovolemia.