Amblyopia
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
Amblyopia refers to visual weakness not explainable by anatomical abnormalities, optical defects, or pathological changes in the eye's internal structures. The article describes various forms including congenital, hysterical, toxic (from alcohol, wood alcohol, quinine, lead, and carbon disulfide), and their treatments.
Encyclopedia article (1928–1936)
AMBLYOPIA (from Greek amblyopia—dull vision), weakness of vision; like amaurosis (see), it refers to those visual disorders which at the present time cannot be explained by either anatomical abnormalities, optical imperfections of the eye, or any pathological changes in the internal membranes of the eye. Therefore, it is understandable that over time, in connection with the progress achieved in ophthalmology and with the improvement of research techniques, the circle of various forms of A. is constantly narrowing, since it becomes increasingly possible to establish a more or less precise pathological-anatomical diagnosis. First of all, mention should be made of congenital A. (amblyopia congenita). People are not infrequently encountered in whom one eye sees significantly worse than the other throughout life, and sometimes this is discovered already in childhood, and sometimes later, accidentally, during examination of the visual acuity of both eyes. The cause of such A. is considered to be the underdevelopment of the visual-nerve apparatus and unknown pathological processes in the fetal period or in early childhood. Königstein and Schleich indicate, as the cause of congenital A., the not infrequent hemorrhages into the retina of newborns during the act of childbirth; these hemorrhages can resorb without a trace or leave behind weakness in the function of the retina without any ophthalmoscopically visible traces. Congenital A. can be inherited (Blatt). It is known that three anomalies, namely: anisometropia (Averbakh), amblyopia, and strabismus, which are developmental defects, are inherited. Congenital A. does not require any special treatment. However, prolonged exercises of the amblyopic eye (bandaging the healthy eye, instilling atropine into it, exercises with a stereoscope and amblyoscope) can give certain results in terms of improving visual acuity. Such cases have been described by a number of authors. Congenital A. can be present in both eyes from the start. The question of amblyopia ex anopsia, i.e., A. from disuse, has not yet been finally resolved. A number of authors have completely abandoned this form of A., considering it to be the congenital A. described above. Hysterical A. (and amaurosis) in hysteria is a purely functional disorder, manifesting either as the only symptom of the illness (monosymptomatic hysteria) or accompanied by various hysterical stigmata. A. is observed in both sexes, but more often in women; according to Kerneis, a/ of all cases are observed in women between the ages of 16 and 25. Visual disturbances reach various degrees; A. in hysteria usually manifests as a greater or lesser reduction in central vision, concentric narrowing of the visual field with a characteristic change in the boundaries of the visual field for individual colors (violation of the normal type of boundaries; patients often give the widest visual field for the color red) and in disturbances of color perception in general. A rarer form is hemianopia; in hysteria, both homonymous and heteronymous forms are encountered. The question of the condition of the pupils remains open to this day. Some authors have even described a complete absence of reaction to light in this disease. Upon repeated examinations, patients often give completely different data. Bilateral A. with a duration of 1 to 8 months is more common, but cases have been described where the duration of the illness is counted in decades (2 cases of Harlan). In the treatment of hysterical visual disorders, the causal factor is primarily taken into account. Psychotherapy, hypnosis, electrotherapy, and strychnine are recommended. A. and amaurosis of toxic origin, i.e., changes in the optic nerve and retina caused by poisoning. The use of a number of harmful substances—alcoholic beverages, tobacco, etc.—causes visual disturbances called amblyopia alcoholica potatorum and amblyopia nicotina. As a rule, it is a matter of chronic poisoning by toxins, more often in men (aged 40 to 50) than in women. A. in acute poisonings is described much less frequently. Both eyes are affected, but sometimes to varying degrees; the changes manifest as a decline in central vision, the appearance of incomplete central scotomas, disturbance of color perception, mainly for red and green colors, in the central parts of the visual field, with preservation at the periphery. In severe cases, the scotoma can occupy the entire visual field and A. can turn into amaurosis. Ophthalmoscopic examination gives either a negative result or sometimes hyperemia of the optic nerve papilla is observed, pallor of its temporal part, and in far-advanced cases even atrophy of the optic nerve. The pathological anatomy of toxic amblyopias, developed by Uhthoff, Vossius, and others, has clarified that their basis is chronic neuritis, which gradually leads to atrophy of those bundles of the optic nerve that supply the fovea centralis. Interstitial inflammation usually begins at the foramen opticum and then descends, but later ascending atrophy of the optic nerve can also develop. Histological studies have shown that there is degeneration and atrophy of nerve fibers and hypertrophy of connective tissue. As for prognosis, it is unfavorable in cases of intoxication A. with absolute central scotoma and marked narrowing of the visual field. In milder cases, improvement in vision and restoration of color perception are possible. Treatment consists in complete abstention from alcoholic beverages or tobacco. Some authors recommend iodine and bromine preparations, injections of urotropin. Mention should be made separately of A. and amaurosis from wood alcohol. Its harmful effect is manifested both with internal use and with inhalation of its vapors and with rubbing it into the skin. The widespread falsification of alcoholic beverages, various types of balsams, perfumes, on the one hand, and the widespread use of wood alcohol in technology, on the other, have often caused poisonings in recent years. For this reason, the question is also of interest from the point of view of professional hazards. The toxic dose of wood alcohol for humans is very small: 5-8 g already causes blindness, 30 g is a fatal dose. The characteristic signs are—general weakness, depressed psyche, rapidly developing blindness with headaches and acute gastroenteritis. Kazas draws attention to the complete absence of an excitation period and convulsions. In the chronic form—the same phenomena, but less pronounced. Characteristic are the stages of fluctuation of amaurosis and A., i.e., cessation of the process, partial restoration of vision, occasionally even to normal, for 2-3 months, and then again a gradual decline in vision. The eyes can be affected to varying degrees. The fundus of the eye is either normal or hyperemia, papillitis are noted, with gradual development of atrophy of the optic nerve. The prognosis is mostly poor. Treatment—dry-air baths, injections of strychnine into the temple area, iodine preparations. Therapy of acute poisoning (Kazas)—administration of potassium permanganate under the skin of the abdomen in the form of a 2% aqueous sterile solution, in an amount of 25 cubic cm and even more, neutralization of acidosis with alkalis; they also recommend sodium citrate, to reduce edema—salts, for example, calcium chloride. Quinine amblyopia. Taking large doses of quinine internally can cause A. and amaurosis. In mild cases, no changes are found in the fundus of the eye, in more severe cases—narrowing of the retinal vessels (ischaemia retinae), pallor of the optic nerve papillae, a sharp decrease in vision, concentric narrowing of the visual field, disturbance of color perception and adaptation, violation of the normal pupillary reaction to light, decreased sensitivity of the cornea. At the same time, dulling of hearing and even complete deafness are observed. Blindness can last for months, and then central vision gradually recovers, but the visual field remains more or less permanently narrowed. Histologically, degeneration of the ganglion cells of the retina has been noted. Treatment—inhalation of amyl nitrite to dilate the vessels, strengthening agents. A. from lead poisoning (amb. saturnina) usually affects both eyes and develops suddenly or gradually. Visual disturbances manifest as a sharp decrease in visual acuity and narrowing of the visual field (concentric). Ophthalmoscopic examination sometimes shows a complete absence of pathological changes in the fundus of the eye, more often a picture of neuroretinitis. Also described: paralysis of the internal and external eye muscles, paralysis of accommodation, retinitis albuminurica. In chronic forms, the outcome can be atrophy of the optic nerves. The diagnosis of this form of A. is facilitated by the presence of other signs of lead poisoning (convulsions, colic, etc.). Treatment—etiological. General therapy, as in lead poisoning (see Lead). Further described are cases of A. from inhalation of carbon disulfide-CS2 vapors (in rubber production), manifesting as a decrease in central vision with preservation of normal boundaries of the visual field and central scotoma for colors. Ophthalmoscopically, pallor and blurring of the boundaries of the optic nerve papilla are noted.
Amblyopia has also been described in poisoning by harmful gases (CO3, CO2, CH4), mercury preparations, opium, chloral hydrate, sodium salicylate, aniline, veronal, and a number of other chemical substances. Visual disturbances in general diseases should include uremic and diabetic amblyopia and amaurosis as a result of auto-intoxication. Uremic amaurosis, always bilateral, is probably due to changes in the brain center (cortical layer of the occipital lobes), and is often observed in scarlatinal nephritis, in albuminuria of pregnancy, in eclampsia in the postpartum period, and rarely in chronic nephritis. Blindness sets in rapidly and suddenly; rarely is it preceded by a gradual decline in vision over several days. The pupillary reaction is preserved in most cases. The fundus of the eye is completely normal. If the uremic attack passes, vision is restored quickly and completely. Some authors, however, have noted persistent defects in the visual field. Treatment consists in treating uremia. In diabetes, visual disturbances in the form of central scotoma with decreased central vision while peripheral vision is normal, as well as cases of narrowing of the visual field, have been described. Ophthalmoscopically, either no changes or signs of atrophy of the optic nerve are found. With the disappearance of sugar in the urine, vision also improves. The cause of amblyopia and amaurosis can also be abundant hemorrhages (pulmonary, uterine, hemorrhoidal, nasal, in the gastrointestinal tract, traumatic, etc.). In this case, the decline in vision occurs either suddenly and always bilaterally, or amblyopia develops gradually and consists of a sharp decline in central vision with the presence of a large positive central scotoma. The ophthalmoscope in some cases shows a completely normal fundus of the eye, in others a clear picture of neuroretinitis. Sometimes hemorrhages into the retina are added. As an outcome of the disease, atrophy of the optic nerve is also possible. Treatment consists in treating the underlying disease. Cases of malarial amblyopia are not uncommon, characterized by temporary, then more permanent visual disturbances. A connection has been noted between amblyopia and diseases of the teeth, nose, ear and accessory sinuses, and with infectious diseases (influenza, typhus, encephalitis, etc.).
N. Moshovova.
Amblyopia and amaurosis are also observed from mechanical causes, mainly in increased intracranial pressure, which causes changes in the optic nerve at the place of its passage from the orbit into the cranial cavity through the optic foramen, first hindering the proper circulation of blood in the optic nerve and thereby causing phenomena of stagnation, and then by direct pressure on the fibers of the optic nerve. In the initial stage, there is a decrease in vision, and then when stagnation turns into atrophy, complete blindness develops. Increased intracranial pressure is observed in new formations in the brain, in hydrocephalus, in hemorrhages into the ventricles or at the base of the skull. Changes in vision are usually bilateral, more pronounced on the side of the lesion. Amblyopia and amaurosis accompany various diseases of the central nervous system: infectious (encephalitis, myelitis, syphilis of the brain) due to inflammation of the optic nerve itself; tabes (atrophy of the optic nerve) and various other diseases affecting one part of the visual conducting pathway from the retina to the cerebral cortex, as a result of which the transmission of visual perceptions to the visual centers is interrupted. When the optic nerve is involved in the process, changes in vision occur in the corresponding eye; but when other parts of the visual pathway are involved in the disease, half of the vision is lost in each eye, i.e., there is so-called hemianopia (see).
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“Amblyopia.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/amblyopia/