Is stagnant cerebrospinal fluid involved in the pathophysiology of normal tension glaucoma.

Current concepts of the pathophysiology of normal tension glaucoma (NTG) include intraocular pressure, vascular dysregulation and the concept of a translaminar pressure gradient. Studies on NTG performed with cisternography demonstrated an impaired cerebrospinal fluid (CSF) dynamics in the subarachnoid space of the optic nerve sheath, most pronounced behind the lamina cribrosa. Stagnant CSF might be another risk factor for NTG.

Impaired cerebrospinal fluid dynamics along the entire optic nerve in normal-tension glaucoma.

PURPOSE: To investigate the cerebrospinal fluid (CSF) dynamics along the entire optic nerve (ON) in patients with normal-tension glaucoma (NTG). METHODS: Retrospective analysis of computed tomographic (CT) cisternographies in Caucasian patients with NTG. Fifty-six patients (99 of 112 eyes) fulfilled the diagnostic criteria of NTG and underwent CT-cisternography. Twelve subjects without NTG (24 eyes) served as controls. Contrast-loaded cerebrospinal fluid (CLCSF) density measurements in Hounsfield units (HU) were performed at four defined regions along the ON and in the basal cistern. RESULTS: In NTG patients, the mean density CLCSF in the bulbar segment measured 76 ± 49 HU right and 88 ± 74 HU left, in the mid-orbital segment 117 ± 92 HU right and 119 ± 73 HU left, in the intracanalicular ON portion 209 ± 88 HU right and 216 ± 101 HU left, in the intracranial ON portion 290 ± 106 HU right and 286 ± 118 HU left and in the basal cistern 517 ± 213 HU. The distribution of CLCSF along the ON showed a statistically significant reduction in the intraorbital ON segments in NTG patients compared to controls without NTG with the far largest difference within the retrobulbar segment (-150 HU right and -117 HU left; right: p < 0.001, left: p < 0.001). CONCLUSION: This study demonstrates a gradual reduction in CLCSF towards the retrobulbar segment in NTG, while in controls without NTG, no reduction in CLCSF was measured within the orbital segments. Impaired CSF dynamics along the ON may contribute to the pathophysiology of NTG.