The behavior of the amblyopic eye under reduced illumination and the theory of functional amblyopia.

Abstract

What has been presented about the response of amblyopic eyes may be summarized as follows. In thephotopic state eyes with functional amblyopia are characterized, in comparison to normal eyes, by reduced visual acuity; unsteadiness of fixation; reduced physiologic contrast; increased spatial summation in the central retinal areas; normal CFF. In themesopic and scotopic state the threshold of amblyopic eyes is virtually normal, foveally and peripherally, in rods and cones; fixation is as steady as in the normal eyes; visual acuity and contrast function approach the normal, or are even better, for a given level of adaptation. What do these facts signify for thetheory of functional amblyopia? They would appear to indicate that the loss of physiologic superiority of the fovea in amblyopia is comparable to the similar loss in the dark adapted state. In other words,the fovea of the amblyopic eye acts in the photopic state as if the eye were dark adapted. This conclusion is further support for the view which I have often expressed that nothing qualitatively new is added in the visual act of the squinter and that all observed phenomena in these patients are exaggerations or perversions of physiologically pre-formed functions. With regard to themechanism inducing functional amblyopia, one must assume that somehow the mechanisms underlying the functional changes observed in dark adaptation are made use of to produce the clinical picture which we call functional, strabismic amblyopia. The retinas, and the whole of the visual system, are not abnormalper se. The abnormality resides in the fact that the fovea of the amblyopic eye gives in themselves normal,scotopic responses in thephotopic state. This statement does not say anything about the seat of the lesion. It could, in principle, be located in any part of the retina (including its photopigments) or the visual pathways. Neither the explanations given bybest & bohnen (1956), nor the theory ofmiller (1954, 1955) andgrosvenor (1954), imply that the control of these mechanisms resides necessarily in the retina itself. It is, in fact, very likely that the situation is much more complex, with an intercession by many neural structures concerned with vision, including a possible interaction between the two eyes. It should be kept in mind that what has been said here relates strictly tofunctional amblyopia. Eyes in which the amblyopia is due to clearly established organic changes behave very differently from eyes with functional amblyopia which makes their study as useful, as a control, as the study of normal eyes.