Astigmatism and neural development.

A. , lmost 90 years ago, George Martin, an ophthalmologist from Bordeaux, reported that even after optical correction with cylindrical lenses many astigmats continued to see lines of one orientation less clearly than others. This condition, which he referred to as "astigmatic amblyopia," was characterized by the fact that the lines that were seen clearest, as well as those that appeared most blurred, were parallel to the principal meridians of the astigmatism. Quantitative tests revealed that after full optical correction of the refractive error, acuity may be normal for stimuli parallel to one of the principal meridians of the astigmatism but could be degraded by as much as a factor of two for perpendicular stimuli. Possibly because of the widespread use of Snellen letters or similar test targets which contain contours of several different orientations, the existence of this condition remained largely ignored in the clinical literature until quite recently. Its rediscovery a few years ago has contributed in no small way to the current debate concerning the role exerted by the visual input early in life on the development of neurons in the mammalian visual cortex and, as such, provides an interesting example of the sort of beneficial interaction between clinical and basic research that is emphasized by the title of the JOURNAL. The frequent occurrence of amblyopia in association with conditions as diverse as strabismus, anisometropia, and opacities of the ocular media led clinicians to suspect that poor or unequal visual stimulation of the two eyes in early life may result in abnormal visual development. This suspicion was implicit in terms such as amblyopia of arrest or amblyopia ex anopsia that have been used in past designations for amblyopia. An explanation along similar lines was also offered by Martin to account for astigmatic amblyopia. He regarded the meridional differences in acuity as being due to asymmetric development of the visual system because of the astigmatic visual input in early life. Although the connection between visual input and amblyopia had been suspected for some time, the mechanisms by which these visual deficits arose remained largely a matter for speculation until the pioneering demonstrations by Hubel and Wiesel of the plasticity of binocular connections in the mammalian visual cortex during early postnatal life. On the basis of their important work over the last 15 years, we now know that binocular connections are functionally present at birth but nevertheless need to be refined by concordant binocular visual experience during a "sensitive period" early in life. If for a time during this period concordant binocular visual input is prevented either by monocular occlusion or by a surgically induced strabismus, the vast majority of cortical neurons lose functional connections with one eye. It can be safely assumed that dramatic changes in neural organization such as these may underlie some of the perceptual deficits experienced by amblyopic and strabismic patients. The magnitude of change in the ocular dominance of cortical cells led naturally to experiments to determine whether the distribution of other properties of cortical neurons could be altered by biased early visual exposure. Perhaps the best known of these experiments were those of Hirsch and Spinelli and of Blakemore and Cooper which examined the effects of restricting the visual input of young kittens to stripes of a single orientation. Although there were significant procedural differences between the two studies, particularly with regard to the means by which the early visual input of the animals was restricted, both groups reported that the distribution of preferred orientations of orientation-selective cortical neurons was dra-