Ablyopia, Amaurosis, And Disturbances Of Vision Without Ophthalmoscopic Change.

Amblyopia Of The Visual Field, Scotomas, And Hemianopia
by casey a. wood, m. d.,
of chicago, ill.

THE terms amblyopia ( dull, and eye i. e. obscurity of vision) and amaurosis (dark, a marked blindness) have, since the days of Hippocrates, been applied to different degrees of loss of sight without sensible change in the ocular structures. The invention of the ophthalmoscope and the use of the microscope have greatly diminished the number of these affections, but there still remain "functional " diseases of the eye designated either by the dimness of vision (amblyopia) or decided loss of sight (amaurosis) that forms the most prominent symptom. Eyes blind from inflammatory diseases, as well as from certain congenital changes in the fundi, may also be described as anaerobic.

Congenital Amblyopia. When an eye has never taken part in the visual act, as in cases of early squint, congenital cataract, corneal scars, or other obstruction to the light rays, the accompanying dim vision may be altogether or partly the result of simple non use ; hence the terms amblyopia, exanopsia, and argamblyopia (Gould). In such cases, especially in squint, where the defective sight is largely due to the presence of high degrees of hyperopia or astigmatism, or both, correction of this ametropia, with exercise of' the eye, may result in much improvement of sight or even in a return to normal vision. In other instances, however, correcting lenses do not' help, and we may then conclude, even in the absence of positive signs, that structural changes or defects exist, probably in some portion of the extra bulbar nervous apparatus.

In still another class of cases careful examinations with the mirror show in the nerve head, retina, or choroid slight departures from the normal appearances. The papilla especially may be irregularly shaped or dimmed in outline, while the perimeter reveals scotomata and peripheral contractions of the field. Such anomalies as colobomata of the opticus, choroid, retina, and iris, as well as non development of the whole eyeball (microphthalmos), are usually associated with, and are described as, examples of congenital amblyopia. Many of the ocular diseases of extra uterine life also affect the fetal eye. Among these are glaucoma, iritis, chorio retinitis, and diseases of the optic nerve, all of which have been classed with the congenital amblyopias.

Congenital Amblyopia for Colors (Subnormal Color sense; Colorblindness). Total absence of the color sense (achromatopsia) is rare as a congenital condition and apart from disease, but it occurs to some extent and for some colors in about 3 per cent. of the whole population. It is quite rare (0.20 per cent.) in women, is sometimes hereditary, and is almost always bilateral.

By far the commonest form of color blindness is exhibited when the individual fails to detect the red and green in mixtures containing these colors. As a result of this defective color sense, or dyschromatopsia the pure greens are readily mistaken for grays and shades of red, and vice versa.

A less numerous class name correctly most of the saturated primary colors, but are very liable to miscall all or most of the color mixtures. They see little or no difference between orange and red, blue and purple, or violet and blue. In other words, they perceive in a compound only the predominating color. Artificial light generally adds to the difficulty which these persons experience in selecting colors.

The nomenclature of color blindness is built upon various theories of color perception ; thus, the two forms of dyschromatopsia just described may be designated " red green " and " blue yellow " blindness, or we may, with propriety, speak of red, green, and violet dyschromatopsia (see also pages 98 100).

Whether the structural defects that give rise to the various forms of subnormal color perception exist at the periphery or in the central portions of the optic tract, they are equally incurable (see also Appendix, page 603).

Reflex Amblyopia. Both amblyopia and amaurosis have resulted from “reflex irritations” conveyed from remote organs, but, such cases are rare. Loss of sight has been attributed to diseases of the reproductive organs, spinal cord, and digestive apparatus. Well authenticated examples of amblyopia from intestinal worms, decayed teeth, diseases of the nasopharynx and its neighboring cavities (especially neoplasms and inueo purulent collections) have also been recorded. In most of these cases there were no fundus changes, and improvement or cure followed successful treatment Of the distant lesion.

The etiology of reflex amblyopia is very obscure, and we must, for the continue to hold to the vague hypothesis of vaso motor disturbances, affecting the nutrition of the retina in some instances and of the central ganglia in others, until similar mysteries of ‘’functional disorders “elsewhere are cleared up. Probably some of these alleged reflex manifestations are really unrecognized cases of hysterical amblyopia.

Uremic Amblyopia, or Amaurosis. This loss of vision occurs occasionally in the toxemia of Bright's disease, but is most frequently noted in those states of the system where albuminuria is found as a transient condition viz. in pregnancy and the late stage of scarlatina. It affects both eyes, comes on suddenly, often lasts but a short time, and disappears as quickly as it came. It is almost always associated with other uremic symptoms, especially with convulsions, headache, vomiting, and coma. The blindness, which may be complete, is probably due to a temporary affection of the visual centers produced by the uremia.

The prognosis is uniformly favorable. Permanent blindness results only when organic lesions of the nerve and retina (albuminuric retinitis and optic neuritis) are present.

Ophthalmoscopically, nothing is to be seen in the retina, although several writers describe fullness of the vessels and a swollen appearance of the papilla.

The treatment is that of uremia.

Glycosuric Amblyopia Apart from the cataract of diabetic patients and those retinal and optic nerve lesions that so closely resemble the fundus changes found in Bright's disease, there is sometimes observed a dimness of vision that simulates the amblyopia from tobacco and alcohol. There are, in these cases, no alterations visible with the mirror, but central scotomata for red and green can always be mapped out.

As the writer has elsewhere' pointed out, the diagnosis is somewhat difficult when the diabetic patient is a smoker, but in such instances the color defect often extends to blue and white. In time white becomes involved at the periphery of the field also a condition of things never found in pure tobacco or alcohol amblyopia.

The pathology is obscure, but Horner's views of the causation of alcohol tobacco blindness may find acceptance in the case of glycosuric amblyopia that it is due to malnutrition of the macular fibers, in this instance brought about by glucose in the blood.

The prognosis, unlike that of tobacco amblyopia, which it resembles, is grave; in spite of treatment (of the diabetes) the case usually goes on to simple optic nerve atrophy and terminates in total loss of sight.

Malarial Amblyopia. It has been observed that during the course of intermittent fever and other diseases of malarial origin an amblyopia accompanied by fundus changes, and usually affecting one eye, may set in. The attacks are generally of short duration, but in some instances persist for weeks. The dim Vision is commonly attributed to the action of the malarial poison upon the optic nerve and retina. It must not be forgotten, in this connection, that quinin, so universally administered in malarial diseases, is known to produce a temporary amblyopia quite apart from the well known, serious fundus lesions of quinin Amaurosis, and the writer is convinced that some of the reported cases of malarial amblyopia, are merely examples of the ocular symptoms of a mild quinin intoxication.

True malarial amblyopia improves under quinin and other antiperiodics, and complete recovery is the rule.

Amblyopia from Loss of Blood. The optic nerve bears even a temporary anemia very badly, and many secondary alterations in its tissues may be directly traced to malnutrition of a kind that would be successfully resisted by other nerves of special sense. Instances of a temporary loss of vision following excessive hemorrhage are quite common, especially from ulcer of the stomach or intestines. Postpartum flooding may also produce this form of amblyopia. An attack of dim vision may be the forerunner of optic atrophy (usually preceded by optic neuritis.) setting in a week or ten days after the loss of blood. The papilla, at the time of the bleeding, is quite pale and the arteries are small.

Treatment. The treatment of the primary amblyopia is the transfusion of blood or the intravenous injection of physiological salt solution. Diffusible stimulants and rest in bed, with small and repeated quantities of easily assimilated food, should be prescribed. These should be followed by tonic mixtures of iron and strychnin the remedies employed for the relief of the later eye troubles following profuse hemorrhage must be regulated by the form the fundus lesions assume.

Amblyopia from the Abuse of Drugs. The poisonous agents that produce ocular symptoms are so numerous that anything like a complete account of all of them would be inappropriate here. In the following list the most important ones are italicized : tobacco, alcohol, carbon disulphid, iodoform, lead salts, quinin, salicylic acid and other salicylates, cocain, snakevenom, mydriatic alkaloids, ptomains, carbolic acid, male fern, aconite, chloral, santonin, picric acid, digitalis, tea, coffee, chocolate, gelsemium, ergot, coaltar products, arsenic, naphthalin, potassium bromid, ergot, amyl nitrite, nitrobenzol, mercurial compounds, silver nitrate, antipyrin, curare, and a large number of other drugs.

Etiology and Pathology. Tobacco , alcohol , and tobacco alcohol intoxications present by far the commonest examples of toxic amblyopia. It is now admitted that alcohol or tobacco alone may produce partial loss of vis¬ion, but inasmuch as the smoker is usually a drinker and as the alcoholic commonly smokes, we almost always have to deal with mixed examples of intoxication.

Sachs (with the English school) believes that alcohol predisposes to tobacco poisoning by producing dyspepsia. Horner is convinced that neither alcohol nor tobacco; as such, produces the pathological changes found in the opticus. Together these drugs produce a chronic gastric catarrh, which, in its turn, brings on a chronic anemia of the Optic nerve, terminating in the retro bulbar neuritis characteristic of alcohol and tobacco amblyopia.

Samelsohn, Uhtboff, and others have demonstrated by autopsies that the essential lesion in this disease is an axial, interstitial neuritis, beginning somewhere between the papilla and brain, and probably extending thence both toward the center and the periphery (see Plate 7 ). The fibers affected are those that supply the macular region one fourth or one third of the whole number. The axis cylinder and the true nervous elements mostly escape. The trabecular tissues enclosing these increases both as to number and size and press upon the nerve fibers, bringing about their partial atrophy, just as the connective elements in cirrhosed liver and fibroid phthisis encroach upon the more highly organized tissues of the liver and lungs.

Recently, Nuel has revived the theory that central toxic scotoma is not primarily a neuritis of the macular bundle, but a disease of the macula lutea, causing degeneration of its cells, and that the optic nerve changes are secondary to the destruction of the nerve cells of the macula. Usher and Dean have observed macular fiber degeneration follow experimentally produced retinal lesions.

The majority of these cases occur in persons, over forty years of age; examples of the disease in the female sex are uncommon, and we must remember that this form of toxic amblyopia occurs only in those who have an idiosyncrasy toward tobacco or alcohol.

Symptoms. The symptom most complained of is 1, misty" vision; the patient speaks of " seeing through a fog" or " through smoke." Even difficulty in reading or doing any other form of earlier than this be finds near work, for which be usually seeks glasses or requests to have his reading lenses changed. His visual acuity for both distance and near may fall as low as 6 and J., 14. He now fails to distinguish red and green objects, and on examination with the perimeter negative central scotomata, in the form of horizontal ovals extending from the blind spots and including the fixation points, can be mapped out (Figs. 269 and 270). Blue and white are rarely affected in pure cases of tobacco amblyopia.

Owing to the situation of the scotomata, most patients are day blind and see best with a dilated pupil i. e. toward evening or in a dimly lighted room.

The mirror sometimes reveals alterations in the disk. When these are absent it may be assumed that the atrophic changes have not yet reached the nerve head. The most constant signs are hyperemia of the papilla in the early stages of the disease, and later a triangular atrophic area, occupying the temporal third of the nerve bead and corresponding to the macular bundle of fibers.

Diagnosis. The diagnosis of the retro bulbar neuritis produced by tobacco and alcohol rests upon the account just given.' The disease may be mistaken for non toxic orbital axial neuritis, disseminated sclerosis, locomotor ataxia, and scotomatous atrophy of the optic disk. Everything considered, it is not difficult to differentiate these forms of ocular disease (see also page 447).

Ubthoff thus summarizes the points of diagnosis between the retro bulbar neuritis of tobacco and alcohol and that due to other causes, such as syphilis, rheumatism, disorders of menstruation, cold, diabetes, etc.' as follows: 1. In true toxic amblyopia the central scotomata are almost invariably confined to red and green. 2. The scotomata and visual disturbances are bilateral, and the former are confined to the center of the field. 3. Vision does not fall below 6/200. The form of the scotoma is that of an oval including both blind spot and fixation point, with its long axis lying above the horizontal meridian. 5. The vision becomes gradually less. 6. The disease affect& men above forty years of age. 7. Pain is noticed on extreme ocular movements in essential retro bulbar neuritis, but is invariably absent in the toxic form.

De Schweinitz says of the non toxic variety that there is a history of chilling of the body, excessive exertion, suppression of menses, or of infectious diseases, rheumatism, etc. ; there is no special relation to sex or age. The visual acuity is greatly disturbed; sometimes there is complete blindness. Often there is a positive scotoma tending to pass to the nasal side of the fixation point, and not specially oval or horizontal. Peripheral contraction of the field for white and colors may be present, with woolliness of the whole disk and distention of the veins. It is often rapid in onset, and is frequently slow in responding to treatment.

Prognosis. This is favorable, even when the blindness has lasted for a long time. When total abstinence from the toxic agent is persistently practised and there is no other Optic nerve disease, sight should, with judicious management, be restored in from six weeks to three months.

Treatment. This consists, first, of all, in stopping the use of tobacco and alcohol in all their forms. It must be remembered that the amblyopia is but part of a general intoxication and that chronic gastric catarrh is usually present. The digestive power is consequently often weak, and it should be fortified by appropriate means. Proper food, exercise, bathing, and regulation of the bowels are valuable adjuncts to tonic remedies. The Turkish bath has a decided value, especially in alcoholic cases. The chief aim should be to furnish a supply of good blood to the badly nourished optic nerve. Most of the so called specifies, nux vomica and strychnin particularly, are very useful, especially with pallor of the disk and when general toxic symptoms are present. Usually full doses of the elixir of pepsin, bismuth, and strychnin may be given internally. This treatment is accompanied by hypodermic injections of strychnine that are gradually increased in strength until toxic symptoms are produced. The dose is then to be diminished one fourth, and so continued for several weeks. When there is an edematous or hyperemic papilla, potassium iodid may be substituted for the strychnin. 'When not otherwise contraindicated and the Turkish bath cannot be readily taken, the hot pack, combined with hypodermic injections of pilocarpin (gr.1/8) twice a week, is very useful, and certainly cuts short the duration of the amblyopia. Lead amblyopia. Lead and its salts not infrequently produce amblyopia and amaurosis. These cases are most commonly found in painters, employes of paint and lead works, plumbers, as well as in persons poisoned from eating canned food or drinking water polluted with plumbic compounds.

The poison brings about so many changes in the brain and kidneys, as well as in the optic nerve, that it is often difficult to say whether the eye alterations are due to the direct action of the lead on the optic nerve, retina, and visual centers, or whether they are secondary to the other organic lesions. In any event, it is probable that the ocular changes begin in the terminal vessels of the eye as a fatty metamorphosis or obliterating endarteritis, and that subsequently the tissues supplied by these vessels undergo secondary metamorphoses.

These alterations affect the retina and papilla, and may be studied ophthalmoscopically. The commonest sign is optic nerve atrophy with woolly disks and small vessels. Vision is always greatly affected, both at the center and periphery. In another class of cases there is optic neuritis, with the usual appearances in and about the nerve head; in still another retro bulbar degeneration sets in. Finally, there are states of transient amblyopia without ophthalmoscopic change indeed, patients suffering from atrophy due to lead poisoning often give a history of antecedent "attacks" of dim vision. These Gowers regards as analogous to the temporary amaurosis of diabetes and uremia, and thinks they are due to the direct effect of the lead salts upon the visual centers. In doubtful cases the excreta should be examined for lead. Oliver relates a case of progressive blindness where the urine, saliva, and nasal mucus revealed the presence of lead. In a case reported by the writer there were marked optic nerve atrophy, with restricted fields (see Figs. 271 and 272), and almost complete oculo motor paresis on the left side.

Prognosis is favorable in the early stages of transient amblyopia, but very unfavorable when optic inflammation or atrophy has set in.

Treatment consists in the instant removal of the source of the poison, the administration of small doses of magnesium sulphate, the use of Turkish baths, and pilocarpin injections. Strychnin before a meal and potassium iodid after it are usually employed, but the former should be omitted when active inflammation is present.

Quinin amaurosis. Quinin, like lead, may be responsible for both a temporary amblyopia and an amaurosis with characteristic fundus changes. The blindness, in the latter instance, comes on suddenly, is often complete, and may last for several days. The pupils are widely dilated, and do not react to light, although they may to accommodation.

The ophthalmoscope shows an absolute anemia of the fundus. The papilla is chalky white, and no trace of retinal vessels can be discovered. This remarkable condition is accompanied by other signs and symptoms of cinchonism, although permanent blindness is excessively rare. In severe cases the optic nerve rarely recovers entirely from the poisonous effects of the drug, and the patient henceforth exhibits decided limitations of the field (Fig. 273), often defective central vision, and usually evidences of retinal ischemia. Usually, large doses of the drug are required to produce amaurosis; but in some susceptible individuals even physiological doses have produced temporary blindness.

We are mainly indebted to Brunner and de Sehweinitz for experimental proof that the amaurosis is due to a species of 11 edema of the optic nerve tissue between the chiasm and eyeball and the influence of quinin on the vaso motor apparatus, which cause excessive constriction of the peripheral circulation, and finally local changes in the vessels (endovasculitis) and atrophy of the optic nerve fibers" (Figs. 273 and 274). De Bono believes that quinin intoxicates the protoplasmic elements of the retina, acting as a depressant poison on the rods and cones. Holden has demonstrated that the primary action of the drug is upon the ganglion cells of the retina.

The treatment of quinin amaurosis is much the sattle as that of tobacco amblyopia. Nitrite of amyl inhalations give temporary relief.

Ptomaln poisoning; Botttlismus; Allantiasis. The putrefactive alkaloids found in 11 high " game, decomposed sausage, uncooked meat, and rotten fish (as well as the leukomains of poisonous fungi, snakes, and shellfish) occasionally produce amblyopia as one of the symptoms of intoxication. Brieger found ethylenediamin to be the active principle in several cases of poisoning from decomposed food.

Symptoms. These closely resemble those of belladonna poisoning; the dim vision is transitory and it is uniformly due to bilateral paresis of accommodation with marked mydriasis. Ptosis is also a common symptom. All the extrinsic ocular muscles ma be paralyzed, from bilateral and nearly complete ophthalmoplegia externa to paresis of a single muscle. There are no fundus changes. When death does not occur and the paralyses persist, these are the result of basilar meningitis or nuclear hemorrhages. The treatment is the same as that suited to atropin poisoning.

Male fern amblyopia and amaurosis are not uncommon from acute poisoning with this drug, but the ocular sy mptoms (except that of blindness) and the fundus changes recorded have been far from uniform. Widely dilated pupils, followed by optic nerve atrophy, are most commonly observed. De Schweinitz and others have experimented on the lower animals with negative results; but Nuel and others have produced optic nerve degeneration by administering extract of' male fern to animals.

Toxic Asthenopia. Some time ago the writer ventured the opinion that the employment of certain intoxicants, some of them drugs and beverages in every day use, is not infrequently followed by minor defects of vision, tile true nature of which is unsuspected by the patient or his medical attendant. These symptoms, which are commonly included in the term "asthenopia," show themselves especially as a decrease in the amplitude of accommodation and convergence. Evidences of this muscular weakness may be seen in the transient intoxication from quinin, the salicylates, iodids, bromids, alcohol, tobacco, coffee, tea, chocolate, and such forms of decomposed food as “high " game, " strong " cheese, etc. The asthenopic symptoms occasionally observed in some forms of dyspepsia probably also constitute a toxic amblyopia due to ptomain poisoning. They properly belong to those milder types of allantiasis where the eye signs are not sufficiently marked to be recognized by the unskilled observer.

Hysterical Amblyopia. This curious form of blindness is most commonly observed in girls and women, but typical examples are not unusual in men and children. The most constant symptom is amaurosis of one eye without fundus changes. This peculiar loss of visual power sometimes follows injuries (traumatic hysteria, traumatic neurosis) in hysterical subjects, but it more frequently comes on without warning. The pupil usually reacts to light, but it may be dilated and motionless. The patient is often partially or totally color blind. Sometimes there is a central scotoma.

There are nearly always other hysterical symptoms present, especially hemianesthesia (usually variable and incomplete) of the affected side, loss of the pharyngeal and corneal reflexes, ptosis, monocular diplopia, micropsia and megalopsia and blepbarospasm. the field for red and green is often larger than that for white. Sometimes there is complete reversal of the natural order of the color fields, blue or white being smallest, red next in size, while the field for green is largest of all (for diagrams see page 487).

Diagnosis. This is sometimes difficult, especially in recent cases. It is well known, for example, that the hysterical amblyope can be made to see. An instance of this occurred in a case known to the writer where a hysterical subject sited for damages on account of injury to the head causing blindness to the right eye. Malingering was set up as a defense, because it was shown that the patient saw with the supposed blind eye when examined by prisms and a light at twenty feet. In all cases of unexplained monocular blindness without fundus alterations hysteria should be suspected, and one should be on the lookout for its other manifestations.

Prognosis is favorable, but the amaurosis may persist for years. Treatment should be directed to the hysterical state generally. Electricity, massage, outdoor exercise, and tonics furnish the best results.

Pretended Amblyopia; Malingering. It is comparatively easy to detect a pretended monocular amblyopia or amaurosis, but difficult to uncover the deception of the person who claims to be blind in both eyes. He mar be exposed by watching him when he does not expect it, by flashing a bright light on his face, or by making feints to strike him for the purpose of elicit¬ing the lid or iris reflex. As Swanzy points out, one cannot depend, for detection of the malingerer, upon the pupillary reactions, because the pupils contract to light, even when the patient is quite blind, if the lesion be situated at the cortical center or in the fibers that connect it with the corpora quadrigemina. Recently Priestley Smith and E. Jackson have suggested a simple test for feigned binocular blindness: Place a lighted candle in front of the subject; now hold a six degree prism with its base to the temple before one eye; if both eyes see the one behind the prism will move inward, and on removing the prism will move outward, the other eye remaining fixed.

Many plans have been devised for the detection of simulated monocular blindness, but, on the whole, Snellen's colored letter test for distant binocular vision is the most valuable. The suspect should be watched that he does not close the alleged blind eye during the examination. A frame holding transparent letters, colored alternately red and green and adapted to five or six meters' distance, is hung in a window or is highly illuminated from behind. A reversible spectacle frame, fitted with a plane red glass on one side and a green glass on the other, is placed on the subject's face. The red letters can be distinguished only by the eye covered with the red glass (which shuts out the green rays), and the green letters can be read through the green glass only, because the red glass cuts off the green rays. If the subject reads red and green types with both eyes open, or during several trials, reads letters of a color that does not correspond with that of the glass in front of his admittedly sound eye, he must have seen with the alleged blind eye.

Dr. Harlan has suggested that a + 16 D. lens be placed before the eye acknowledged by the subject to be normal, and a 0.25 D. sphere before the alleged blind eye. The suspect is now asked to read the ordinary distant, test types. If he succeeds, he is a malingerer, because the high degree convex lens has made it impossible for him to see with the sound eye, and of course the weak concave glass does not interfere with vision. An additional control test may now be made by placing a book or a towel over the + 16 D. lens. The malingerer will declare his inability to read any of the letters, thus further exposing his attempted fraud.

Prism or diplopia tests are advised by some observers. The subject is seated before a point of light six meters distant. The supposed blind eye is covered with a frosted glass, and the apex of a 6' prism, directed up or down, is slowly advanced to the pupillary center of the sound eye, and the suspected person is asked to recognize the double images of the monocular diplopia thus produced. This maneuver is repeated, with the prism pointed in various directions, until he becomes accustomed to the idea of diplopia. A weak concave lens is now substituted for the frosted glass, and the suspect is examined by Stevens's phorometer or by simple prisms in the manner commonly advised for testing the extrinsic ocular muscles. If he now perceives double images, he must see binocularly, and may be pronounced a malingerer.

Snow blindness. This is a form of amblyopia produced by the blinding reflections of the sun upon the naked eye of persons (usually strangers) exposed to the brilliant snow fields of northern latitudes or mountain resorts. The dazzling at length causes contracted pupils and retinal congestion. Central and peripheral limitations of the field of vision have been observed, as well as a lessening of the visual acuity, especially for near work.

The most common effect of this exposure is, however, a peculiar form of hyperemia and edema of the conjunctiva. This is accompanied by swollen lids, lachrymation, burning pain in the eyeballs, photophobia, and blepharospasm symptoms attributed to “sun burn” rather than to the effects of the light rays. The writer has had occasion to study various grades of snow blindness in Northern Canada and among the members of a party who spent some time on the Mer de Glace.

The light rays from electric furnaces and are candles are capable of producing practically the same symptoms, constituting the so called electric ophthalmia. Those who are much concerned with the Roentgen X rays may suffer in a similar manner.

The eyes remain sensitive to light and show signs of retinal fatigue for some days, and the conjunctivitis may persist, requiring treatment proper to that condition. Rest in a darkened room, with atropin and hot applications, seems to give most relief to the retinal and corneal symptoms.

Erythropsia, or red vision, is most commonly seen after cataract extraction. It has also been observed in poisoning by santonin (which may also produce xanthopsia or yellow vision), and as a phosphene experience in persons suffering from optic nerve atrophy and glaucoma. These exhibitions of color may be due both to central irritation and to excitation of the retinal elements.' Potassium bromid has been recommended for this symptom. After cataract extraction patients often complain of a "glaring white haze" which seems to cover all objects. An uncommon phenomenon, described by Becker and Swan M. Burnett, is kyanopsia, or blue vision. According to the latter author, it is especially observed by patients with more or less amber colored cataractous lenses', the blue appearance depending upon fatigue of the retina from long continued exposure to yellow light, giving blue as a residual sensation in white light.'

Micropsia and Megalopsia. In hysteria, in some diseases affecting the macular region, and after the correction of marked ametropia, objects may appear smaller or larger than usual, and these visual abnormalities are sometimes accompanied by distortion of the images. In the foregoing class of cases the rods and cones are either actually separated or pressed together as a consequence of retinal infiltration, or the contrast effect of corrected refractive errors may convey the impression of altered size. As Parinaud has shown, when these phenomena are experienced by hysterical amblyopes they are probably the effect of a variable accommodative spasm.

Night blindness (Functional Night blindness; Hemeralopia,' preferably Nyctalopia). This symptom is seen as a functional disturbance, probably due to diminished sensibility of the retina or rather imperfect adaptation powers of the retina unassociated with visible change in the background.

It has been observed as an epidemic affecting scorbutic soldiers and sailors who, in addition to insufficient feeding, have been exposed for a long time to the glare of the sun Simeon Snell has seen it among the pupils of the English public schools. Among the poor and ill nourished Russian peasants night blindness has been frequently noticed, particularly during the fasts of Lent. It has been attributed to miasmatic influences by Adamuck. Not only do nyctalopes see badly on dull or dark days and well OD bright days, but they suffer from other ocular troubles, the chief of which is a peculiar wasting disease of the conjunctiva xeroplitbalmia (see page 296).

The treatment of the condition that gives rise to the night blindness is called for a generous diet, ferruginous tonics, cod liver oil, roundings, and protection from bright light.

Day blindness (Nyctalopia, preferably Hemeralopia). In almost all the forms of central amblyopia (see page 460) patients see best on dull days or in a dimly lighted room. The explanation of this is that with a weak illumination the pupils are dilated, and most rays fall upon unaffected portions of the retina: bright light, on the other band, contracts the pupils and the asensitive foveal region only is presented to objects. Persons from whom light has long been excluded exhibit this symptom, and it is said to be congenital in others.

Hemeralopia also occurs in retinitis nyetalopia, coloboma of the iris, and in albinism.

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