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Updated: Jul 5, 2026

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
Published on: April 24, 2020
Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma
John P Berdahl1, R Rand Allingham, Douglas H Johnson
1Duke University Eye Center, Durham, North Carolina 27710, USA. johnberdahl@gmail.com
Cerebrospinal fluid pressure is significantly lower in patients with primary open-angle glaucoma (POAG). This finding suggests cerebrospinal fluid pressure may contribute to POAG development.
Area of Science:
- Ophthalmology
- Neurology
Background:
- Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
- The pathogenesis of POAG is multifactorial, involving intraocular pressure (IOP) and potentially other systemic factors.
- Cerebrospinal fluid (CSF) pressure is a potential systemic factor influencing ocular physiology.
Purpose of the Study:
- To compare CSF pressure between patients diagnosed with POAG and a control group without glaucoma.
- To investigate the relationship between CSF pressure and glaucoma severity indicators.
Main Methods:
- A case-control study was conducted using data from 31,786 subjects who underwent lumbar puncture.
- The study analyzed 28 POAG patients and 49 non-glaucoma controls.
- Retrospective chart review and statistical analyses (univariate and multivariate) were employed.
Main Results:
- Mean CSF pressure was significantly lower in POAG patients (9.2+/-2.9 mmHg) compared to controls (13.0+/-4.2 mmHg; P<0.00005).
- Lower CSF pressure in POAG patients was consistent across different LP indications and age groups.
- Optic disc cup-to-disc ratio independently correlated with IOP, CSF pressure, and translaminar pressure difference, with larger ratios associated with lower CSF pressure.
Conclusions:
- CSF pressure is demonstrably lower in individuals with POAG.
- These findings support the hypothesis that reduced CSF pressure may play a role in the development of POAG.
- Further research into the interplay of CSF pressure and POAG pathogenesis is warranted.
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