THE testimony of the experiments described in the preceding chapters to the effect that the lens is not a factor in accommodation is confirmed by numerous observations on the eyes of adults and children, with normal vision, errors of refraction, or amblyopia, and on the eyes of adults after the removal of the lens for cataract.
It has already been pointed out that the instillation of atropine into the eye is supposed to prevent accommodation by paralyzing the muscle credited with controlling the shape of the lens. That it has this effect is stated in every text-book on the subject, (see note 1) and the drug is daily used in the fitting of glasses for the purpose of eliminating the supposed influence of the lens upon refractive states.
In about nine cases out of ten the conditions resulting from the instillation of atropine into the eye fit the theory upon which its use is based; but in the tenth case they do not, and every ophthalmologist of any experience has noted some of these tenth cases. Many of them are reported in the literature, and many of them have come under my own observation. According to the theory, atropine ought to bring out latent hypermetropia in eyes either apparently normal, or manifestly hypermetropic, provided, of course, the patient is of the age during which the lens is supposed to retain its elasticity. The fact is that it sometimes produces myopia, or changes hypermetropia into myopia, and that it will produce both myopia and hypermetropia in persons over seventy years of age, when the lens is supposed to be as hard as a stone, as well as in cases in which the lens is hard with incipient cataract. Patients with eyes apparently normal will, after the use of atropine, develop hypermetropic astigmatism, or myopic astigmatism, or compound myopic astigmatism, or mixed astigmatism (see note 2). In other cases the drug will not interfere with the accommodation, or alter the refraction in any way. Furthermore, when the vision has been lowered by atropine the subjects have often become able, simply by resting their eyes, to read diamond type at six inches. Yet atropine is supposed to rest the eyes by affording relief to an overworked muscle.
In the treatment of squint and amblyopia I have often used atropine in the better eye for more than a year, in order to encourage the use of the amblyopic eye; and at the end of this time, while still under the influence of atropine, such eyes have become able in a few hours, or less, to read diamond type at six inches (see Chapter XXII). The following are examples of many similar cases that might be cited:
A boy of ten had hypermetropia in both eyes, that of the left or better eye amounting to three diopters. When atropine was instilled into this eye the hypermetropia was increased to four and a half diopters, and the vision lowered to 20/200. With a convex glass of four and a half diopters the patient obtained normal vision for the distance, and with the addition of another convex glass of four diopters he was able to read diamond type at ten inches (best). The atropine was used for a year, the pupil being dilated continually to the maximum. Meantime the right eye was being treated by methods to be described later. Usually in such cases the eye which is not being specifically treated improves to some extent with the others, but in this case it did not. At the end of the year the vision of the right eye had become normal; but that of the left eye remained precisely what it was at the beginning, being still 20/200 without glasses for the distance, while reading without glasses was impossible and the degree of the hypermetropia had not changed. Still under the influence of the atropine and still with the pupil dilated to the maximum, this eye was now treated separately; and in half an hour its vision had become normal both for the distance and the nearpoint, diamond type being read at six inches, all without glasses. According to the accepted theories, the ciliary muscle of this eye must not only have been completely paralyzed at the time, but must have been in a state of complete paralysis for a year. Yet the eye not only overcame four and a half diopters of hypermetropia, but added six diopters of accommodation, making a total of ten and a half. It remains for those who adhere to the accepted theories to say how such facts can be reconciled with them.
Equally, if not more remarkable, was the case of a little girl of six who had two and a half diopters of hypermetropia in her right or better eye, and six in the other, with one diopter of astigmatism. With the better eye under the influence of atropine and the pupil dilated to the maximum, both eyes were treated together for more than a year, and at the end of that time, the right being still under the influence of the atropine, both became able to read diamond type at six inches, the right doing it better, if anything, than the left. Thus, in spite of the atropine, the right eye not only overcame two and a half diopters of hypermetropia, but added six diopters of accommodation, making a total of eight and a half. In order to eliminate all possibility of latent hypermetropia in the left eye – which in the beginning had six diopters – the atropine was now used in this eye and discontinued in the other, the eye education being continued as before. Under the influence of the drug there was a slight return of the hypermetropia; but the vision quickly became normal again, and although the atropine was used daily for more than a year, the pupil being continually dilated to the maximum, it remained so, diamond type being read at six inches without glasses during the whole period. It is difficult for me to conceive how the ciliary muscle could have had anything to do with the ability of this patient to accommodate after atropine had been used in each eye separately for a year or more at a time.
According to the current theory, atropine paralyzes the ciliary muscle and thus, by preventing a change of curvature in the lens, prevents accommodation. When accommodation occurs, therefore, after the prolonged use of atropine, it is evident that it must be due to some factor or factors other than the lens and the ciliary muscle. The evidence of such cases against the accepted theories is, in fact, overwhelming; and according to these theories the other factors cited in this chapter are equally inexplicable. All of these facts, however, are in entire accord with the results of my experiments on the eye muscles of animals and my observations regarding the behavior of images reflected from various parts of the eyeball. They strikingly confirm, too, the testimony of the experiments with atropine, which showed that the accommodation could not be paralyzed completely and permanently unless the atropine was injected deep into the orbit, so as to reach the oblique muscles, the real muscles of accommodation, while hypermetropia could not be prevented when the eyeball was stimulated with electricity without a similar use of atropine, resulting in the paralysis of the recti muscles.
As has already been noted, the fact that after the removal of the lens for cataract the eye often appears to accommodate just as well as it did before is well known. Many of these cases have come under my own observation. Such patients have not only read diamond type with only their distance glasses on, at thirteen and ten inches and at a less distance, but one man was able to read without any glass at all. In all these cases the retinoscope demonstrated that the apparent act of accommodation was real, being accomplished, not by the “interpretation of circles of diffusion,” or by any of the other methods by which this inconvenient phenomenon is commonly explained, but by an accurate adjustment of the focus to the distances concerned.
The cure of presbyopia (see Chapter XX) must also be added to the clinical testimony against the accepted theory of accommodation. On the theory that the lens is a factor in accommodation such cures would be manifestly impossible. The fact that rest of the eyes improves the sight in presbyopia has been noted by others, and has been attributed to the supposed fact that the rested ciliary muscle is able for a brief period to influence the hardened lens; but while it is conceivable that this might happen in the early stages of the condition and for a few moments, it is not conceivable that permanent relief should be obtained by this means, or that lenses which are, as the saying goes, as “hard as a stone,” should be influenced, even momentarily.
A truth is strengthened by an accumulation of facts. A working hypothesis is proved not to be a truth if a single fact is not in harmony with it. The accepted theories of accommodation and of the cause of errors of refraction require that a multitude of facts shall be explained away. During more than thirty years of clinical experience, I have not observed a single fact that was not in harmony with the belief that the lens and the ciliary muscle have nothing to do with accommodation and that the changes in the shape of the eyeball upon which errors of refraction depend are not permanent. My clinical observations have of themselves been sufficient to demonstrate this fact. They have also been sufficient to show how errors of refraction can be produced at will, and how they may be cured, temporarily in a few minutes, and permanently by continued treatment.
1. Certain substances have the power of producing dilation of the pupil (mydriasis) and hence are termed mydriatics. At the same time they act upon the ciliary body diminishing and when applied in sufficient strength completely paralyzing the power of accommodation thus rendering the eye for some time unalterably focused for the farthest point – Herman Snellen Jr.: Mydriatics and Myotics System of Diseases of the Eye, edited by Norris and Oliver, 1897-1900, vol. ii, p. 30.
2. In simple hypermetropic astigmatism one principal meridian is normal and the other, at right angles to it, is flatter. In simple myopic astigmatism the contrary is the case.; one principle meridian is normal and the other, at right angles to it more convex. In mixed astigmatism one principal meridian is too flat the other too convex. In compound hypermetropic astigmatism both principal meridians are flatter than normal one more so than the other. In compound myopic astigmatism both are more convex than normal, one more so than the other.