We read with interest the paper by Sun and associates, which corroborates prior reports of rises in corneal hysteresis following reductions in intraocular pressure (IOP), but were surprised that they did not consider that the association they found could be related to their method of measurement.

The ocular response analyzer uses an air puff to deform the cornea into a slight concavity and an electro-optical system to detect the timing of the corneal deflection from which the IOP can be determined. The air puff switches off shortly after the first applanation spike. This standardizes the degree of indentation but means that the pressure applied to the cornea is determined by a combination of the IOP and the structural resistance of the eye. By manually adjusting the pressure of the air puff, it is possible to induce artificial changes in hysteresis (Asaoka R, et al. IOVS 2008;49:ARVO E-Abstract 703).

In our center, we examined consecutive records of 30 previously untreated subjects with glaucoma or ocular hypertension diagnosed by a single fellowship-trained glaucoma specialist (A.W.) and assigned to a 1-eye trial of either travoprost or bimatoprost. IOP and corneal biomechanical parameters were measured at baseline and at follow-up (mean 53 days) using a Goldmann tonometer, Pascal dynamic contour tonometer (DCT), and ocular response analyzer. Data for the first treated eye were analyzed using the corresponding eye as control.

Using Student t tests, we found that our results were similar to those of Sun and associates. Significant decreases in Goldmann IOP (24 to 17 mm Hg, P = .0000003) in intervention eyes occurred alongside significant increases in corneal hysteresis (8.06 to 9.04 mm Hg, P = .00007). However, when we modeled the data in a mixed model using Pascal DCT intraocular pressure and central corneal thickness as covariates we found that the change in corneal hysteresis did not reach conventional levels of statistical significance ( P = .78). We conclude that the introduction of prostaglandin analogues increases corneal hysteresis as measured by the ocular response analyzer but not independently of IOP.

Cross-sectional surveys have correlated corneal hysteresis with IOP, central corneal thickness, and axial length. The effect of IOP appears to be modest within the normal range, but these factors may be clinically relevant at high intraocular pressures, and research into air puff dynamics and hysteresis values at extremes of range is ongoing. It may be possible to use a correction factor to limit the influence of IOP on hysteresis measurement, but until one has been properly validated, it would seem prudent to consider inclusion of these variables as covariates in studies examining large variations in IOP.