Altered emmetropization in response to specific visual manipulations is a consistent finding in a diverse range of animals, including chicken,
16,17 tree shrew (Siegwart JT, et al.
IOVS 1993;34:ARVO Abstract 2482),
18 guinea pig,
19,20 and monkey,
21,22 with myopia being the product of both spatial form deprivation and imposed hyperopic defocus. The early finding that the eyes of young chicks adjust their growth to compensate for imposed optical defocus has since been generalized to other animal models. With imposed hyperopic defocus (negative lenses), eyes increase in axial length, and with myopia defocus (positive lenses), the elongation slows (Siegwart JT, et al.
IOVS 1993;34:ARVO Abstract 2482).
17,20,22 Evidence of a role of the peripheral retina in eye growth regulation also comes from early studies in the chick, followed by recent studies in the monkey. In chicks, form deprivation treatments restricted to one half of the visual field cause excessive eye growth only in the affected field,
23 and similar field-dependent changes occur when optical defocus is limited in its extent.
24 In monkeys, isolated central (foveal) laser lesioning has shown that eyes can recover from induced myopia,
25 implying that the peripheral retina alone is capable of guiding emmetropization. In more recent studies, limiting either form deprivation or optical defocus to a hemifield was reported to induce asymmetric eye growth, consistent with appropriately localized responses.
26,27 However, despite the emerging evidence of a role for the peripheral retina in guiding eye growth, the nature of the interactions between peripheral and central retinal regions as determinants of eye shape and their respective influences on central (on-axis) refractive errors remains inconclusive.