In this study we investigated the impact of accommodation on axial and oblique astigmatism along 12 meridians of the central 30° of visual field and explored the compensation of corneal first-surface astigmatism by the remainder of the eye's optical system. Our experimental evidence revealed no systematic effect of accommodation on either axial or oblique astigmatism for two adult populations (myopic and emmetropic eyes). Although a few subjects exhibited systematic changes in axial astigmatism during accommodation, the dioptric value of these changes was much smaller than the amount of accommodation. For most subjects, axial and oblique astigmatism of the whole eye are both less than for the cornea alone, which indicates a compensatory role for internal optics at all accommodative states in both central and peripheral vision. A new method for determining the eye's optical axis based on visual field maps of oblique astigmatism revealed that, on average, the optical axis is 4.8° temporal and 0.39° superior to the foveal line-of-sight in object space, which agrees with previous results obtained by different methodologies and implies that foveal astigmatism includes a small amount of oblique astigmatism (0.06 D on average). Customized optical models of each eye revealed that oblique astigmatism of the corneal first surface is negligible along the pupillary axis for emmetropic and myopic eyes. Individual variation in the eye's optical axis is due in part to misalignment of the corneal and internal components that is consistent with tilting of the crystalline lens relative to the pupillary axis.

The interaction between oblique and axial astigmatism was investigated analytically (generalized Coddington's equations) and numerically (ray tracing) for a theoretical eye model with a single refracting surface. A linear vector-summation rule for power vector descriptions of axial and oblique astigmatism was found to account for their interaction over the central 90° diameter of the visual field. This linear summation rule was further validated experimentally using a physical eye model measured with a laboratory scanning aberrometer. We then used the linear summation rule to evaluate the relative contributions of axial and oblique astigmatism to the total astigmatism measured across the central visual field. In the central visual field, axial astigmatism dominates because the oblique astigmatism is negligible near the optical axis. At intermediate eccentricities, axial and oblique astigmatism may have equal magnitude but orthogonal axes, which nullifies total astigmatism at two locations in the visual field. At more peripheral locations, oblique astigmatism dominates axial astigmatism, and the axes of total astigmatism become radially oriented, which is a trait of oblique astigmatism. When eccentricity is specified relative to a foveal line-of-sight that is displaced from the eye's optical axis, asymmetries in the visual field map of total astigmatism can be used to locate the optical axis empirically and to estimate the relative contributions of axial and oblique astigmatism at any retinal location, including the fovea. We anticipate the linear summation rule will benefit many topics in vision science (e.g., peripheral correction, emmetropization, meridional amblyopia) by providing improved understanding of how axial and oblique astigmatism interact to produce net astigmatism.

Purpose Oblique astigmatism is a prominent optical aberration of peripheral vision caused by oblique incidence of rays striking the refracting surfaces of the cornea and crystalline lens. We inquired whether oblique astigmatism from these two sources should be expected, theoretically, to have the same or opposite signs across the visual field at various states of accommodation. Methods Oblique astigmatism was computed across the central visual field for a rotationally-symmetric schematic-eye using optical design software. Accommodative state was varied by altering the apical radius of curvature and separation of the biconvex lens’s two aspheric surfaces in a manner consistent with published biometry. Oblique astigmatism was evaluated separately for the whole eye, the cornea, and the isolated lens over a wide range of surface curvatures and asphericity values associated with the accommodating lens. We also computed internal oblique astigmatism by subtracting corneal oblique astigmatism from whole-eye oblique astigmatism. Results A visual field map of oblique astigmatism for the cornea in the Navarro model follows the classic, textbook description of radially-oriented axes everywhere in the field. Despite large changes in surface properties during accommodation, intrinsic astigmatism of the isolated human lens for collimated light is also radially oriented and nearly independent of accommodation both in theory and in real eyes. However, the magnitude of ocular oblique astigmatism is smaller than that of the cornea alone, indicating partial compensation by the internal optics. This implies internal oblique astigmatism (which includes wavefront propagation from the posterior surface of the cornea to the anterior surface of the lens and intrinsic lens astigmatism) must have tangentially-oriented axes. This non-classical pattern of tangential axes for internal astigmatism was traced to the influence of corneal power on the angles of incidence of rays striking the internal lens. Conclusions Partial compensation of corneal astigmatism by internal optics is due mainly to the highly converging nature of wavefronts incident upon the lens resulting from corneal refraction. The degree of compensation is quadratically dependent on eccentricity but is expected to diminish as the eye accommodates. Neutralising the cornea by index-matching defeats internal compensation, revealing classical, radially-oriented oblique astigmatism in the isolated lens.

Choroideremia is an X-linked, blinding retinal degeneration with progressive loss of photoreceptors, retinal pigment epithelial (RPE) cells, and choriocapillaris. To study the extent to which these layers are disrupted in affected males and female carriers, we performed multimodal adaptive optics imaging to better visualize the in vivo pathogenesis of choroideremia in the living human eye. We demonstrate the presence of subclinical, widespread enlarged RPE cells present in all subjects imaged. In the fovea, the last area to be affected in choroideremia, we found greater disruption to the RPE than to either the photoreceptor or choriocapillaris layers. The unexpected finding of patches of photoreceptors that were fluorescently-labeled, but structurally and functionally normal, suggests that the RPE blood barrier function may be altered in choroideremia. Finally, we introduce a strategy for detecting enlarged cells using conventional ophthalmic imaging instrumentation. These findings establish that there is subclinical polymegathism of RPE cells in choroideremia.