At the onset of the lens-rearing period, the eyes of the experimental and control monkeys were, on average, moderately hyperopic, and there were no between-group differences in refractive error or vitreous chamber depth (two-sample
t-test,
P = 0.59 for refractive error;
P = 0.62 for vitreous chamber depth), nor were there any systematic interocular refractive error differences in either the experimental or control groups (paired
t-test;
P > 0.14). Over time, the two eyes of each control monkey grew in a coordinated manner toward a low degree of hyperopia, the ideal optical state for young monkeys.
12 14 15 This emmetropization process was very successful so that by 4 to 5 months of age 90% of the control monkeys had refractive errors between +1.13 and +3.68 D of hyperopia
(Fig. 1) .
If unrestricted central vision was sufficient to mediate emmetropization, peripheral form deprivation should have no effect on refractive development. However, peripheral form deprivation consistently disrupted the emmetropization process. As illustrated in
Figure 1 , shortly after the onset of peripheral form deprivation, three of the six animals that wore diffusers with 4-mm apertures and four of the six animals viewing through 8-mm apertures exhibited relative myopic errors that were outside the range of refractive errors exhibited by the control animals. The refractive changes were symmetric in the two eyes of a given animal (mean interocular difference: right eye − left eye = −0.06 ± 0.57 D, paired
t-test,
P = 0.31; also see
Figs. 3 4 5 ) and the animals that wore the diffusers with the smaller central apertures exhibited slightly larger amounts of myopia (average = −0.44 D more myopia), although these differences were not significant (two-sample
t-test,
P = 0.76). At the end of the lens-rearing period, the experimental monkeys as a group exhibited a much broader than normal range of refractive errors, with 9 of the 12 treated monkeys showing refractive errors that fell outside the 10th and 90th percentile limits for the age-matched control animals (
Fig. 1 , right). Although 1 of these treated monkeys was more hyperopic than normal, 8 of these 9 treated animals exhibited relative myopic errors and the refractive errors in all 12 of the treated monkeys were significantly less hyperopic/more myopic than those of the control monkeys (mean = +0.03 ± 2.39 D vs. +2.39 ± 0.92 D; two-sample
t-test,
P = 0.006; median = +0.38 D vs. +2.35 D, Mann-Whitney test,
P = 0.003). It is not known why the one animal became relatively hyperopic, whereas most of the treated animals became myopic. There was nothing notable in the history of this animal that could explain the difference. However, it has been reported that form deprivation of the entire retina also produces hyperopia in a small proportion of infant monkeys.
47 59 60
The relative myopic errors came about because peripheral form deprivation accelerated the eye’s axial elongation rate
(Fig. 2) . At the end of the lens-rearing period, four of the treated monkeys had vitreous chambers that were longer than those of any of the control animals and the refractive errors for all the treated monkeys were inversely correlated with vitreous chamber depth (
r 2 = 0.61,
P = 0.003). The mean and median vitreous chamber depths in the treated monkeys were longer than those for control animals; but, primarily due to the variability in the treatment groups, these differences were not significant (mean = 10.01 mm vs. 9.73 mm, two-sample
t-test,
P = 0.16; median = 10.07 mm vs. 9.74 mm, Mann-Whitney test,
P = 0.08). However, in the eight treated monkeys that exhibited relative myopic refractive errors that fell outside the 10th- and 90th-percentile limits of the control animals, the vitreous chambers were significantly longer than normal (mean = 10.23 ± 0.57 mm vs. 9.73 ± 0.26 mm, two-sample
t-test,
P = 0.05; median = 10.22 mm vs. 9.74 mm, Mann-Whitney test,
P = 0.008).
As previously observed in monkeys with axial myopia produced by form deprivation of the entire retina,
53 the experimental monkeys were capable of recovering from the induced refractive errors. For example, at the end of the diffuser-rearing period, monkey LEI exhibited approximately −2.0 D of myopia in each eye (
Fig. 3 , top). However, after lens removal and the restoration of unrestricted vision, there was a decrease in the rate of axial growth, and the refractive errors of both eyes subsequently shifted in a systematic and coordinated manner back toward the normal range.
If the fovea played a dominant role in this recovery process, one would expect that foveal ablation would delay and/or decrease the effectiveness of the recovery in the treated eye. However, on the contrary, the recovery process was unaffected by the foveal ablations, regardless of whether relative hyperopic or myopic refractive errors had developed in the treated animals during the lens-rearing period. For example, during the lens-rearing period, monkey MIT (
Fig. 4 , left) exhibited faster than normal axial growth rates and a substantial degree of myopia in each eye. In contrast, monkey LAU exhibited slower than normal axial growth rates during the lens-rearing period and became relatively hyperopic (
Fig. 4 , right). Regardless, after the onset of unrestricted vision and the photoablation of the fovea in one eye, there were clear changes in the vitreous chamber elongation rates in both eyes (a decrease in monkey MIT and an increase in monkey LAU) and both eyes of each of these monkeys showed more normal refractive errors. The key finding was that the recovery process was very similar in the intact and laser-treated eyes.
The similarity of the recovery process in the intact and laser-treated eyes is emphasized in
Figure 5 , which shows longitudinal, interocular differences in refractive error for all seven of the lens-reared monkeys that had foveal ablations in one eye. At the onset of the recovery period, several of the monkeys (e.g., monkeys MIT and NOL) exhibited anisometropia that was slightly outside the control range; however, in each case, the degree of anisometropia decreased with time. For the other laser-treated monkeys, there were no systematic differences between the two eyes throughout the recovery period. Instead, the observed anisometropias in the laser-treated monkeys were typically within the range of anisometropias observed in control monkeys. Consequently, at 300 days of age, when the recovery process was complete, there was not a significant difference in the refractive errors of the laser-treated and fellow nontreated eyes (+0.80 ± 0.71 D vs. +0.79 ± 0.76 D; paired
t-test,
P = 0.91). Moreover, the average degree of anisometropia manifested by the laser-treated monkeys (0.29 ± 0.24 D) was comparable to that exhibited by the experimental monkeys with intact eyes (0.14 ± 0.17 D; two-sample
t-test,
P = 0.24) and the age-equivalent control monkeys (0.18 ± 0.22 D; two-sample
t-test,
P = 0.33).