Purpose: Active emmetropization describes the process by which young eyes regulate their growth to eliminate refractive errors. The purpose of this study was to re-investigate the role of the brain in compensation to imposed hyperopic defocus (negative lenses), specifically, to assess whether a retina-brain link and/or an intact ciliary nerve are required for this emmetropizing response. Data from previous related studies are equivocal.
Methods: Unilateral lesion surgery involving either or both optic nerve section (ONS) and ciliary nerve section (CNS), was performed on 2-3 day old White-Leghorn chicks to interrupt communication between the eye (retina in the case of ONS) and brain. After a recovery period of 4 days, lesioned eyes were fitted with either -5 or -15 D lenses or diffusers (6-9 per group). An additional lesion group underwent unilateral CNS and was fitted with -5 D lenses bilaterally. Finally 3 groups that underwent the same unilateral optical treatments but no surgery were included as controls for analyzing lesion-induced changes. Complete sets of measurements, involving retinoscopy for refractive errors, and high frequency A-scan ultrasonography for axial ocular dimensions, were made at the beginning (baseline), and end of a 4 day treatment period. Additional ultrasonography data were collected after 1 and 2 days of treatment. Optical treatment effects were expressed as changes in interocular differences from baseline values.
Results: All three lesions produced hyperopic shifts in refraction (evident in baseline values), although this effect was minimal for the ONS+CNS group. Choroidal thickening as well as increased anterior chamber depth and lens thinning were observed in all cases but vitreous chamber depth was reduced in only the ONS group. In response to the -5 D lens, the control (nonlesioned) group showed nearly complete compensation, while full compensation was not achieved to the -15 D lens over this short treatment period. The diffuser group showed the largest change, which was also in the direction of myopia. Both the ONS and CNS groups showed near normal compensation, as indexed by the changes in refractive errors relative to their respective baseline values. In contrast, the ONS+CNS lens groups overcompensated, by 130% and 54% for the -5 D and the -15 D lens groups respectively. Form deprivation responses were slightly exaggerated in both ONS and ONS+CNS groups, the latter group again showing the largest response. Enhanced vitreous chamber growth was evident under all conditions and correlated well with the refractive changes across the groups.
Discussion: The data imply that an intact retina-brain link is not required for compensation to hyperopic defocus and thus emmetropization. However, the data also imply interactions between higher centers and the eye. The emmetropization set-point appears to be recalibrated after ONS surgery. The data also indicate a role of the ciliary nerve as an important conduit for signals that exercise a restraining influence on eye growth.