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Since the 2002 report of the Ocular Hypertension Treatment Study (OHTS) that central corneal thickness (CCT) was an independent and powerful predictive factor for glaucoma, we have seen an explosion of interest in CCT and its role in glaucoma. Investigators have generally taken two paths. The first has been to develop a 'correction nomogram' to allow the clinician to adjust Goldmann applanation tonometry (GAT) according to CCT. The second has been to link CCT to other parameters of the globe, perhaps to the lamina cribrosa itself.
It remains an open question whether such a CCT-IOP nomogram should be used in individual patientsKohlhaas et al. (302) in Dresden cannulated 125 otherwise normal eyes at the time of cataract surgery and correlated CCT, keratometry and axial length to the 'true' intracameral IOP. They report that there is an approximately 1 mmHg adjustment for each 25 micron difference from 550 microns and suggest their Dresden Correction Table will be useful for improving the accuracy of GAT. While the investigators are to be commended for having carefully used modern technology to perform a large cannulation study. It remains an open question whether such a nomogram should be used to correct measurements in individual patients. Several engineering models suggest that other characteristics of the cornea (such as stiffness and viscoelastic properties) have an impact on GAT accuracy that dwarfs CCT, that these properties vary independently of CCT and in fact vary with the true IOP. Recall that in a regression analysis, by definition half the data points lie above the regression line, half below. Thus for two patients with CCTs of 625 microns, correcting IOP downward by 3 mmHg (according to the Dresden table) may make sense for the individual with a thick, stiff cornea, but probably corrects in the wrong direction for an individual with a thick but more flexible cornea. Cannulation studies (and indeed large population studies like the OHTS) are useful for exploring the behavior of groups of patients, but applying a fixed algorithm to an individual patient is fraught with problems.
If CCT's impact in glaucoma risk is not fully explained by GAT error, is it linked to other biologically-plausible parameters that might be expressed at the nerve? Oliveira et al. (307) performed pachymetry and standardized radial ultrasound biomicroscopy in 140 eyes to see whether CCT was correlated to scleral thickness.
CCT was not related to scleral thickness
They did not find such a relationship and posit that their data fails to support the hypothesis that CCT is a surrogate for the thickness of the eye wall and lamina cribrosa. On the other hand, Congdon et al. (299) measured corneal hysteresis (a measure of the viscoelastic properties of the cornea) along with CCT and axial length in 230 subjects with glaucoma. They found that CCT was associated with the stage of glaucoma, and that lower corneal hysteresis was associated with progressive visual field worsening.
The recent finding that CCT is among the most heritable aspects of ocular structure,1 suggesting that CCT is genetically regulated, lends credence to the idea that CCT is linked somehow to glaucoma risk at a fundamental, biological level.
CCT is somehow linked to glaucoma risk at a fundamental, biological levelConflicting findings and approaches as represented by the studies above are typical of early work in any new field, as we begin to investigate potential biological links. The story of CCT and glaucoma is just starting to get interesting!