Flow dynamics of cerebrospinal fluid between the intracranial cavity and the subarachnoid space of the optic nerve measured with a diffusion magnetic resonance imaging sequence in patients with normal tension glaucoma

摘要

Abstract Importance This study offers a new approach for the quantification of CSF dynamics. Background Non‐invasive method to quantify the CSF dynamics in the subarachnoid space of the optic nerve is highly desirable. The aim of the study was to measure slow‐flow CSF velocities in healthy controls and normal tension glaucoma patients between the intracranial cavity and the subarachnoid space of the optic nerve. Design Prospective observational study. Participants Eleven age‐matched healthy volunteers and 15 normal tension glaucoma patients. Methods Using phase contrast images, the phase shift in MRI diffusion images can be used to determine the flow velocity. Flow‐range ratio between the intracranial cavity and the subarachnoid space of the optic nerve was calculated. Main Outcome Measure Flow‐range ratio between the intracranial cavity and the subarachnoid space of the optic nerve was calculated. Results First, phantom measurements were provided to validate the slow‐flow velocity calculations. Second, flow‐range ratio was validated for the healthy controls (0.63?± 0.05), with the range being similar for the right and left optic nerve ( P = 0.1). Statistically significant results were obtained ( P 0.05) when comparing the flow‐range ratio in the optic nerve of healthy controls ( n =?22 eyes, 0.63?± 0.05) with the flow‐range ratio in pathological optic nerves ( n =?23, 0.55?± 0.08) of normal tension glaucoma patients. MANOVA revealed no dependency between flow‐range ratio and patient dependent variables. Conclusion and Relevance Diffusion‐weighted imaging provides a method to evaluate CSF flow within the subarachnoid space of the optic nerve in a non‐invasive manner. Compared to healthy controls, patients with normal tension glaucoma measure a significantly lower flow‐range ratio. This finding suggests a possible role of impaired CSF dynamics in the pathophysiology in normal tension glaucoma.