which differ considerably from our measurement conditions (abnormally thick or thin cornea, for example…), errors of several millimeters are to be expected” [1]. Given the paucity of published data at the time, 500 µm seemed a reasonable assumption for the “average” patient. We now know CCT varies greatly among the general population, to a degree that impacts the accuracy of GAT in daily practice.

10.1.2  The Influence of CCT on Tonometry

The first indication that CCT varied enough in otherwise normal eyes to influence GAT came from Ehlers, who in 1975 cannulated 29 eyes undergoing cataract surgery and correlated CCT to the difference between “true” and GAT-measured IOP [2]. His study demonstrated that GAT error could indeed be as large as 5 or 6 mmHg in otherwise normal eyes, and that GAT appeared most accurate with a CCT of 520 µm. His study had significant limitations, including the relatively small number of patients and (in retrospect) the racial homogeneity of his population; nonetheless, his findings spurred other investigations that suggested that CCT-induced GAT error might be important in ocular hypertension and normal tension glaucoma [3–6]. Unfortunately the significance of this early work did not gain widespread recognition until the publications of the Ocular Hypertension Treatment Study (OHTS).

Goldmann tonometry measures the force necessary to flatten a fixed area of the central cornea and uses this force to estimate the value of IOP. The forces opposing applanation include both IOP and the structural resistance of the cornea. It seems intuitive that a thicker cornea will resist applanation more than a thin cornea, but the reality is more complex. The structural resistance of the cornea represents a combination of its “stiffness,” viscoelastic properties, and thickness. Several engineering models of the cornea suggest that variations in the material properties of the cornea (i.e., viscoelastic properties, Young’s modulus – an engineering term for inherent properties) probably dwarf the effect of CCT on GAT measurements [7, 8]. These models suggest that if the material properties of the cornea were constant, variations in CCT from the mid400s to mid-600s would explain only some ±4 mmHg in variance from “true” (directly-measured) IOP, and

that variations in material properties may explain ±10 to 15 mmHg in GAT error.

Summary for the Clinician

››Goldmann applanation assumed a constant CCT in the population; however CCT varies to a degree that impacts the accuracy of the Goldmann applanation.

››Engineering models suggest that material properties of the cornea likely dwarf the effect of CCT on the Goldmann applanation (10–15 mmHg variance from true IOP due to material properties and ±4 mmHg due to CCT).

10.2  How Does Central Corneal

Thickness Vary?

10.2.1  CCT in Different Populations

The earliest surveys of corneal thickness were primarily performed in Caucasian Scandinavian populations [9–11]. While these and other early studies demonstrated that CCT varied more within normal populations than previously appreciated, it wasn’t until much later that population-based differences were recognized among different racial groups. La Rosa and colleagues showed that as a group African American male veterans had thinner corneas than their Caucasian counterparts [12] as did African American participants in the OHTS compared to Caucasian participants [13]. The Barbados Eye Survey reported that black participants had thinner corneas than white participants [14]. The population-based Los Angeles Latino Eye Study found CCTs among their Hispanic patients intermediate between values reported for African American and Caucasian populations [15]. What underlies these racial differences? Racial and ethnic categorization is imprecise – there are no genetic alleles that define a unique population or race. On the other hand, the prevalence of certain alleles does vary among populations. Toh et al. in Australia recently showed that CCT is among the most highly heritable aspect of ocular structure [16], suggesting that the gene(s) controlling ocular structure and more specifically corneal thickness may vary among populations.