Amblyopia from want of use, which formerly included all possible disturbances to vision, great and small, is now only accepted in two cases, for squint and congenital cataract, if the latter is not operated on very early in the first or second year of life.
The fact is simply this, that in congenital cataract even the most successful operation is frequently deceiving as to its issue without ophthalmoscopic report; this is the more disagreeable as the most exact reflection test before the operation fails to prove the existence of this defective sight. But does it follow from this, that congenital cataract has induced defective sight from want of use? We find the same defective vision also in congenital defective development of the transparent lenses (so-called luxation of the lens). On the whole, we often find several congenital defects in the same individual. The very circumstance that the cataract is congenital makes it probable that the defective sight is so also, or are we to take congenital cataract as being a guarantee against congenital amblyopia?
Von Graefe, who first considered this defective sight to be congenital, designated it in his later lectures as originating from want of use, probably in order to advise the earliest possible performance of an operation. There is no mention of his having brought forward evidence for this assertion; that the great master himself said it was enough, and the host of believers felt themselves to be the happy possessors of a new dogma.
A number of children appeared in my practice, in whom congenital cataract was needled by von Graefe in the first or second year of life with recovery of transparent media, who showed, however, the extremest degrees of defective vision when they were sufficiently intelligent to have their vision tested. Whoever is interested in this can find a number of such cases in the Royal Institution for the Blind at Steglitz, which I am accustomed to visit several times a year by request of the committee. On p. 91 I have related a case of monocular congenital defective sight in congenital cataract of both eyes.
Everywhere then the principle holds good, that whoever makes an assertion must be prepared to verify it; amblyopia from non-use is denoted as an inherited trouble, and still not a single observation exists which furnishes proof that an eye of previously ascertained good visual acuteness has become amblyopic in consequence of disuse, a fact I drew attention to ten years ago. Leber replies to this, he remembers "to have seen patients with complete amblyopia in the squinting eye, who stated that its visual faculty had been found to be good during an examination instituted years before." Is this intended as an observation? By that I mean is it a proof of facts, for the trustworthiness of which he holds himself responsible: in the handling of scientific questions I do not place the least reliance on the dim recollections of unnamed individuals. Even in personally conducted examinations we must be on our guard to avoid mistakes, and now we are confronted with mere recollections of tests of vision!
By means of the above observations the theory that "the peculiar variety of monocular amblyopia which is so frequent in monocular squint is hardly observed without squint" is sufficiently disproved.
Leber seeks to enfeeble Alfred Graefe's statement that the presence of extremely defective vision may sometimes be proved at a very early age, in children who have only squinted a short time (the rapid development of amblyopia in consequence of the squint really appears incredible), by the assertion "that just at the earliest age, when the activity of the optic nerve is not yet sufficiently strengthened by use, the conditions for producing amblyopia from non-use are most favorable with complete exclusion of one eye," but complete exclusion of the squinting eye does not take place even in extremely defective sight, as can easily be seen by the mirror test (p. 66) I described fourteen years ago. Which activities of the optic nerve apparatus are strengthened then by use? Perhaps visual acuteness? The physiological conditions of this are only to be sought in the anatomical structure, and the physiological arrangements of the retina or the visual organs, which cannot be changed much by use. What we can learn from the visual act relates solely to the conclusions which we are able to draw from sensual impressions; but visual acuteness, i. e. the faculty for the recognition of distinct points, is an anatomical, physiological gift, and not a thing to be acquired.
The opposing observation, that squint, even of monolateral character dating from earliest childhood, continued to the middle and later years of life, can still exist with very good visual faculty, may easily be explained by alternation from time to time. If that is so indeed, if squint begins during the presence of good visual acuteness, and nothing further is necessary to its maintenance than alternation from time to time, why should defective vision from non-use ever be developed? With good visual faculty on both sides alternations also occur from time to time.
Still more convincing are those cases which are numerous where the visual acuteness of the squinting eye only amounts to about 1/7 to 1/12, and where, on this account, there is no alternation. Were this defective sight acquired through non-use it must of necessity be progressive; it must exist in proportion to the duration of the squint. A moderate experience will suffice to show that this is not the case. And further, defective sight must continue progressive even after removal of the squint by operation, for by the operation nothing is changed in the relations of the binocular vision present in squint, which are dismissed with the one word, "suppression," by the advocates of defective vision from non-use.
Moreover, suppression may exist for years without the slightest disadvantage to the visual faculty.