PURPOSE To compare intracranial pressure (ICP) in subjects with primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG; subset of POAG), and ocular hypertension (OHT) with that in subjects with no glaucoma. METHODS The study was a retrospective review of medical records of 62,468 subjects who had lumbar puncture between 1985 and 2007 at the Mayo Clinic. Of these, 57 POAG subjects, 11 NTG subjects (subset of POAG), 27 OHT subjects, and 105 control subjects met the criteria and were analyzed. A masked comparison of the relationship between ICP and other ocular and nonocular variables was performed by using univariate and multivariate analyses. RESULTS ICP was significantly lower in POAG compared with age-matched control subjects with no glaucoma (9.1 ± 0.77 mm Hg vs. 11.8 ± 0.71 mm Hg; P < 0.0001). Subjects with NTG also had reduced ICP compared with the control subjects (8.7 ± 1.16 mm Hg vs. 11.8 ± 0.71 mm Hg; P < 0.01). ICP was higher in OHT than in age-matched control subjects (12.6 ± 0.85 mm Hg vs. 10.6 ± 0.81 mm Hg; P < 0.05). CONCLUSIONS ICP is lower in POAG and NTG and elevated in OHT. ICP may play an important role in the development of POAG and NTG and in preventing the progression of OHT to POAG. Further prospective and experimental studies are warranted to determine whether ICP has a fundamental role in the pathogenesis of glaucoma.

The data indicate that the stiffness of glaucomatous HTM is significantly increased compared with that of normal HTM. Modeling exercises support substantial impairment in outflow facility with increased HTM stiffness. Alterations in the biophysical attributes of the HTM may participate directly in the onset and progression of glaucoma.

Cultured trabecular meshwork (TM) cells are a valuable model system to study the cellular mechanisms involved in the regulation of conventional outflow resistance and thus intraocular pressure; and their dysfunction resulting in ocular hypertension. In this review, we describe the standard procedures used for the isolation of TM cells from several animal species including humans, and the methods used to validate their identity. Having a set of standard practices for TM cells will increase the scientific rigor when used as a model, and enable other researchers to replicate and build upon previous findings.

Proteomic analysis of hAH identified 676 nonredundant proteins. More than 80% of these proteins are novel identifications. The elucidation of the aqueous proteome will establish a foundation for protein function analysis and identification of differentially expressed markers associated with diseases of the anterior segment.

Over a decade has passed since myocilin was identified as the first gene linked to early and late-onset primary open-angle glaucoma. During this time, considerable effort has been put forth to understand the functional role myocilin has in normal and glaucomatous eyes. Myocilin is expressed in many ocular and non-ocular tissues, is found in both intracellular and extracellular spaces, and has been linked to elevations in intraocular pressure. Mutations in the myocilin gene that have been associated with glaucoma appear to confer a gain-of-functional activity rather than loss of function. Unfortunately, what the normal function of myocilin is and how alterations in the function can confer a glaucoma phenotype have yet to be elucidated. We will review the current understanding of myocilin with special emphasis on the structural makeup of the myocilin gene and protein, its possible physiological roles internal and external to ocular cells, the regulation of intraocular pressure as evidenced through the use of perfusion culture systems and animal models, and as a causative agent in some forms of glaucoma.