EYE, DISEASES OF. The specially important diseases of the eye are those which temporarily or permanently interfere with sight. (See BLINDNESS, CAUSES OF.) In considering the subject it must be remembered that (I) the eye is a double organ, while (2) either eye may have its own trouble.
I. Normally, the two eyes act together. Impressions made upon either retina, to the one side of a vertical line through the centre, the fovea centralis, before giving rise to conscious perception cause a stimulation of the same area in the brain. Impressions formed simultaneously, for instance, on the right side of the right retina and on corresponding areas of the right side of the lef t retina, are conveyed to the same spots in the right occipital lobe of the brain. Pathological processes, therefore, which are local ized in the right or left occipital lobes, or along any part of the course of the fibres which pass from the right or left optic tracts to these "visual centres," cause defects in function of the right or left halves of the two retinae. Hemianopia, or half-blindness, arising from these pathological changes, is of very varying degrees of severity, according to the nature and extent of the particular lesion. The blind areas in the two fields of vision, corresponding to the outward projection of the paralysed retinal areas, are al ways symmetrical both in shape and degree. The central lesion may for instance be very small, but at the same time destructive to the nerve tissue. This will be revealed as a sector-shaped or insular symmetrical complete blindness in the fields of vision to the opposite side. Or a large central area, or an area comprising many or all of the nerve fibres which pass to the visual centre on one side, may be involved in a lesion which causes impairment of function, but no actual destruction of the nerve tissue. There is thus caused a symmetrical weakening of vision (amblyopia) in the opposite fields. In such cases the colour vision is so much more evidently affected than the sense of form that the condition has been called hemiachromato Asia or half-colour blindness. Hemianopia may be caused by haemorrhage, embolism, or tu mour growth which either directly involves the visual nerve ele ments or affects them by compression and by inflammation. Transitory hemianopia is rare and is frequently of toxic origin.
The two eyes also act as if they were one in accommodating. It is impossible for the two eyes to accommodate simultaneously to different extents, so that where there is, as occasionally hap pens, a difference in focus between them, this difference remains the same for all distances for which they are adapted. In such cases, therefore, both eyes cannot ever be accurately adapted at the same time, though either may be alone. It often happens as a consequence that the one eye is used to receive the sharpest images of distant, and the other of near objects. Any pathological change which leads to an interference in the accommodating power of one eye alone must have its origin in a lesion which lies peripherally to the nucleus of the third cranial nerve. Such a lesion is usually one of the third nerve itself. Consequently, a unilateral accommodation paresis is almost invariably associated with paresis of some of the oculo-motor muscles. A bilateral accommodation paresis is not uncommon. It is due to a nuclear or more central cerebral disturbance. Unlike a hemianopia, which is mostly permanent, a double accommodation paresis is fre quently transitory. It is often a post-diphtheritic condition, ap pearing alone or associated with other paresis.
Both eyes are also, normally, associated in their movements. They move in response to a stimulus or a combination of stimuli, emanating from different centres of the brain, but always equally distributed to the corresponding muscles in both eyes, so that the two lines of fixation meet at the succession of points on which attention is directed. The movements are thus associated in the same direction, to the right or left, upwards or downwards, etc. In addition, owing to the space which separates the two eyes, convergent movements, caused by stimuli equally distributed be tween the two internal recti, are required for the fixation of nearer and nearer-lying objects. These movements would not be neces sary in the case of a single eye. It would merely have to accom modate. The converging movements of the double eye occur in association with accommodation, and thus a close connection be comes established between the stimuli to accommodation and con vergence. All combinations of convergent and associated move ments are constantly taking place normally.
Associated and convergent movements may be interfered with pathologically in different ways. Cerebral lesions may lead to their impairment or complete abolition, or they may give rise to involuntary spasmodic action, as the result of paralysing or irri tating the centres from which the various co-ordinated impulses are controlled or emanate. Lesions which do not involve the centres may prevent the response to associated impulses in one eye alone by interfering with the functional activity of one or more of the nerves along which the stimuli are conveyed. Paraly sis of oculo-motor nerves is thus a common cause of defects of association in the movements of the double eye. The great ad vantage of simultaneous binocular vision—viz., the appreciation of depth, or stereoscopic vision—is thus lost for some, or it may be all, directions of fixation. Instead of seeing singly with two eyes, there is then double-vision (diplopia). This persists so long as the defect of association continues, or so long as the habit of mentally suppressing the image of the faultily-directed eye is not acquired.
In the absence of any nerve lesions, central or other, interfer ing with their associated movements the eyes continue throughout life to respond equally to the stimuli which cause these move ments, even when, owing to a visual defect of the one eye, binocu lar vision has become impossible. It is otherwise, however, with the proper co-ordination of convergent movements. These are primarily regulated by the unconscious desire for binocular vision, and more or less firmly associated with accommodation. When one eye becomes blind, or when binocular vision for other reasons is lost, the impulse is gradually, as it were, unlearnt. This is the cause of divergent concomitant squint. Under somewhat similar conditions a degree of convergence, which is in excess of the re quirements of fixation, may be acquired from different causes. This gives rise to convergent concomitant squint.
For Astigmatism, etc., see the article VISION.
The dioptric media, or the transparent portions which are con cerned in the transmission of light to, and the formation of images upon, the retina, are the following : the cornea, the aque ous humour, the crystalline lens and the vitreous humour. Loss of transparency in any of these media leads to blurring of the retinal images of external objects. In addition to loss of trans parency the cornea may have its curvature altered by pathological processes. This necessarily causes imperfection of sight. The crystalline lens, on the other hand, may be dislocated, and thus cause image distortion.
Inflammation of the cornea may be primary or secondary, i.e., the inflammatory changes may be directly connected with one or more foci of inflammation in the cornea itself or the focus or foci may be in some other part of the eye. Only the very super ficial forms of primary keratitis, those confined to the epithelial layer, leave no permanent change; there is otherwise always a loss of tissue resulting from the inflammation and this loss is made up for by more or less densely intransparent connective tissue (neb ula, leucoma). These according to their site and extent cause greater or less visual disturbance. Primary keratitis may be ul cerative or non-ulcerative, superficial or deep, diffuse or circum scribed, vascularized or non-vascularized. It may be complicated by deeper inflammations of the eye such as iritis and cyclitis. In some cases the anterior chamber is invaded by pus (hypopyon). The healing of a corneal ulcer is characterized by the disappear ance of pain where this has been a symptom and by the rounding off of its sharp margins as epithelium spreads over them from the surrounding healthy parts. Ulcers tend to extend either in depth or superficially, rarely in both manners at the same time. A deep ulcer leads to perforation with more or less serious con sequences according to the extent of the perforation. Of ten an eye bears permanent traces of a perforation in adhesion of the iris to the back of a corneal scar or in changes in the lens capsule (capsular cataract). In other cases the ulcerated cornea may yield to pressure from within, which causes it to bulge forwards (staphyloma).
The principal causes of primary keratitis are injuries and in fection from the conjunctiva. Injuries are most serious when the body causing the wound is septic or when micro-organisms from some other source, often the conjunctiva and tear-sac, effect a lodgement before healing of the wound has sufficiently ad vanced. In infected cases a complication with iritis is not un common owing to the penetration of toxines into the anterior chamber.
Primary Keratitis.—Inflammations of the cornea are the most important diseases of the eye. Treatment of primary keratitis must vary according to the cause. Generally speaking the aim should be to render the ulcerated portions as aseptic as possible without using applications which are apt to cause a great deal of irritation and thus interfere with healing. On this account it is important to be able to recognize when healing is taking place, for then rest, and frequent irrigation of the conjunctiva with sterilized water at the body temperature, and occasional mild antiseptic irrigation of the nasal mucous membrane is all that is required. It is dangerous to overtreat.
Among the many local antiseptics may be mentioned the actual cautery, chlorine water, freshly prepared silver nitrate or protargol, and the yellow oxide of mercury. These agents are not equally applicable in any given case. For instance, the actual cautery is employed only in the case of the deeper septic ulcers, in which the destruction of tissue is already considerable and tending to spread further. Again the yellow oxide of mercury should only be used in the more superficial, tuberculous forms of inflammation.
Secondary Keratitis takes the form of an interstitial deposit of leucocytes between the layers of the cornea as well as often of vascularization, sometimes intense, from the deeper network of vessels (anterior ciliary) surrounding the cornea. The duration of a secondary keratitis often lasts many months. More or less complete restoration of transparency is the rule, however, eventually.
No local treatment is called for except shading of the eyes and in most cases use of a mydriatic to prevent adhesions when the iris is involved. Inherited syphilis, tuberculous and other inflam mations are the causes of secondary keratitis.
Neuro-paralytic Keratitis.—When the fifth nerve (sensory) is paralysed there is a tendency for the cornea to become in flamed. Different forms of inflammation may then occur which all show a marked slowness in healing. The explanation of neuro paralytic keratitis is that in the insensitive condition of the cornea it is less guarded against injuries. The prognosis is necessarily bad. The treatment consists in as far as possible protecting the eye from external influences and frequently irrigating with anti septic lotions.
Certain degenerative changes occur in the cornea. In kera toconus or conical cornea, the normal curvature of the cornea becomes altered with consequent impairment of vision. Other degenerative changes are arcus senilis, a whitish opacity due to fatty degeneration, extending round the corneal margin, varying in thickness in different subjects and usually only met with in old people : transverse calcareous film, consisting of a finely punctiform opacity extending, in a tolerably uniformly wide band, occupying the zone of the cornea which is left uncovered when the lids are half closed.
Deep scleritis with its attendant complications is a more serious disease. Etiologically it is equally obscure. Both eyes are almost always attacked. It more generally occurs in young people, mostly in young women. It is more persistent and less subject to periods of intermission than episcleritis. Eventually it leads to weakening of the sclerotic coat causing it to yield to the intraocular pressure. Vision suffers from extension of the infiltration to the cornea, or from iritis with its attendant adhesions, or from anterior cho roiditis, and sometimes also from secondary glaucoma. Iri dectomy, especially if done early in the process, may be of use.
The symptoms to which the inflammation may give rise are dread of light (photophobia), pain, generally most severe at night and often very great, lacrimation, more or less impairment of sight. An acute attack of iritis usually lasts about six weeks. Some cases become chronic and last much longer. Others are chronic from the first, and in one clinical type, in which the cil iary body is also affected, viz., iritis serosa, there is usually little injection of the eye or pain, so that the patient's attention may only be directed to the eye by gradual impairment of sight. In some cases, particularly in men, there is recurrence at longer or shorter intervals of attacks of iritis (recurrent iritis). In these cases, as well as in all cases of plastic iritis, serious consequences to sight are apt to follow from adhesion of the iris to the lens capsule and occlusion of the pupil by exudation.
Inflammation of the ciliary body, cyclitis, is frequently asso ciated with iritis. This association is probable in all cases where there are deposits on the posterior surface of the cornea. It is certain where there are changes in the intra-ocular tension. Of ten in cyclitis there is a very marked diminution in tension. Cyclitis is also present when the degree of visual disturbance is greater than can be accounted for by the visible changes in the pupil and anterior chamber. The exudation may, as in iritis, be serous, plastic or purulent. It passes from the two free surfaces of the ciliary body into the posterior aqueous, and into the vitreous, chambers. This produces more or less intransparency of the vitreous humour, a constant sign of cyclitis. Where there has been excessive exudation into the vitreous, subsequent shrinking and liquefaction take place, leading to detachment of the retina and consequent blindness. The most serious form of iridocyclitis is that which may follow penetrating wounds of the eye. This may lead to a similar inflammation of the other eye (sympathetic ophthalmia) which ends in its complete destruction.
The treatment of iritis necessarily differs to some extent ac cording to the cause. The general treatment applicable to all cases need only be here considered. The aim should be to put the eye as far as possible at rest, to prevent the formation of adhe sions and alleviate the pain. An attempt should be made to keep the pupil thoroughly dilated with atropine as long as any circum corneal injection lasts. If a case of iritis be left to itself or treated without the use of a mydriatic, posterior synechiae almost inva riably form. Some fibrinous exudation may even organize into a membrane stretching across, and more or less completely occlud ing, the pupil. Synechiae, though not of themselves causing im pairment of vision, increase the risk that the eye runs from sub sequent attacks of iritis. It should, however, be remembered that as the main call for a mydriatic is to prevent synechiae, the raison d'ętre for its use no longer exists when, having been begun too late, the pupil cannot properly be dilated by it. Under these conditions it may even do harm. The eyes should also be kept shaded from the light by the use of a shade or neutral-tinted glasses. During an attack any use of the eyes for reading, sewing or work of any kind calling for accommodation must be prohib ited. This applies equally to the case of inflammation in one eye alone and in both.
Pain is best relieved by hot fomentations, cocaine, and in many cases the internal use of salicin or phenacetin. The treatment sometimes required for cases of old iritis is iridectomy. The op eration is called for in two different classes of cases. In the first place, to improve vision where the pupil is small, and to a great extent occluded, though the condition has not so far led to seri ous nutritive changes; and in the second place, with the object of preventing the complete destruction of vision threatened by either the existing condition or the danger of recurrence of the inflamma tion. Iridectomy for iritis should be performed when the inflam mation has entirely subsided. The portion of iris excised should be large. The operation is urgently called for where the condition of iris bombans exists.
Iris tumours, either simple or malignant, are rare. A frequent result of a severe blow on the eye is a separation of a portion of the iris from its peripheral attachment. Of congenital anomalies the most common are a cleft condition (coloboma) and more or less persistence of the foetal pupillary membrane.
In glaucoma there is an increase of intra-ocular tension, which acts injuriously on the optic nerve end and its ramifications in the retina. The cause of the rise of tension is partly congestive, partly mechanical. The effect of glaucoma, when untreated, is to cause ever-increasing loss of sight, although the time occupied by the process before it leads to complete blindness varies within such extraordinary wide limits as from a few hours to many years. The onset of glaucoma is characterized by subjective flashes of light or a halo around objects and stony hardness of the eyeball to touch. Such symptoms call for immediate treatment, instillation of pilocarpine to contract the pupil to the utmost and thus dilate the lymphatic canal of Petit (see EYE, ANATOMY OF) or iridec tomy. The uveal tract may be the site of sarcoma.
The retina is subject to inflammation, to detachment from the choroid, to haemorrhages from the blood-vessels and to tumour.
Retinal inflammation may primarily affect either the nerve ele ments or the connective tissue framework. The former is usually associated with some general disease such as albuminuria or dia betes and is bilateral. The tissue changes are oedema, the f orma tion of exudative patches, and haemorrhage. Where the connec tive tissue elements are primarily affected, the condition is a slow one, similar to sclerosis of the central nervous system. The gradual blindness which this causes is due to compression of the retinal nerve elements by the connective tissue hyperplasia, which is always associated with characteristic changes in the disposition of the retinal pigment. This retinal sclerosis is generally known as retinitis pigmentosa, a disease with hereditary predisposition. Haemorrhages into the retina are met with in phlebitis of the cen tral retinal vein, which is almost invariably unilateral, and in cer tain conditions of the blood, as pernicious anaemia, when they are always bilateral.
The optic nerve is subject to inflammation (optic neuritis) and atrophy. Double optic neuritis, affecting, however, only the intra ocular ends of the nerves, is an almost constant accompaniment of brain tumour. Unilateral neuritis has a different causation, depending upon an inflammation, mainly perineuritic, of the nerve in the orbit. It is analogous to peripheral inflammation of other nerves, such as the third, fourth, sixth and seventh cranial nerves.
Hyperaemia of the conjunctiva where not followed by inflam mation causes more or less lacrimation but no alteration in the character of its secretion. The hyperaemia may be acute and transitory or chronic. Much depends upon the cause as well as upon the persistence of the irritation which sets it up.
Traumata, the presence of foreign bodies in the conjunctival sac, or the irritations of superficial chalky infarcts in the Mei bomian ducts, cause more or less severe transitory congestion. Continued subjection to irritating particles of dust, etc., causes a more continued hyperaemia, often circumscribed and less pro nounced. Bad air also causes a chronic hyperaemia in which it is common to find a follicular hyperplasia. Long exposure to too intense light, astigmatism and other ocular defects which cause asthenopia lead also to chronic hyperaemia. Anaemic individuals often suffer from hyperaemia of this nature.
The treatment of conjunctival hyperaemia consists first in the removal of the cause when it can be discovered. Often this is difficult. The application of hot sterilized water is useful.
The treatment should have the primary object of preventing implication of the cornea and extension to the other eye.
Catarrhal conjunctivitis, which is characterized by an increased mucoid secretion accompanying the hyperaemia, is usually bilater al and may be either acute or chronic. Acute conjunctivitis lasts as a rule only for a week or two : the chronic type may persist, with or without exacerbations, for years. The subjective symp toms vary in intensity with the severity of the inflammation.
There is always troublesome "burning" in the eyes with a tired, heavy feeling in the lids. This is aggravated by reading. In acute cases, indeed, reading is impossible. In all cases the symptoms are also more marked if the eyes have been tied up, though this may produce a temporary relief.
A special variety of acute catarrhal conjunctivitis is the so called hay-fever (q.v.; see ANAPHYLAXIS) . Other ectogenetic causes are mostly microbic. The most common are the Morax Axenfeld and the Koch-Weeks conjunctivitis.
The Morax-Axenfeld bacillus sets up a contagious conjuncti vitis which affects individuals of all ages and conditions. The in flammation is usually chronic, at most subacute. It is often suf ficiently characteristic to be recognized without a microscopical examination of the secretions. In typical cases the lid margin, palpebral conjunctiva, and it may be a patch of ocular con junctiva at the outer or inner angle are alone hyperaemic : the secretion is not copious and is mostly found as a greyish coagu lum lying at the inner lid-margin. The subjective symptoms are usually slight. Complications with other varieties of catarrhal conjunctivitis are not uncommon. This mild form of conjuncti vitis generally lasts for many months, subject to more or less complete disappearanQe followed by recurrences. It can be rapid ly cured by the use of an oxide of zinc ointment, which should be continued for some time after the appearances have altogether passed off.
The conjunctivitis caused by the Koch-Weeks microbe is still more common. It is a more acute type, affects mostly children, and is very contagious and often epidemic. Here the hyperaemia involves both the ocular and the palpebral conjunctiva, and us ually there is considerable swelling of the lids and a copious se cretion. Both eyes are always affected. Occasionally the en gorged conjunctival vessels give way, causing numerous small extravasations (ecchymoses). Complications with phlyctenulae (vide infra) are common in children. The acute symptoms last for a week or ten days, after which the course is more chronic. Treatment with nitrate of silver in solution is generally satis factory. Less frequent microbic causes yield to the same treat ment.
A form of epidemic muco-purulent conjunctivitis is not uncom mon, in which the swelling of the conjunctival folds and lids is much more marked and the secretions copious. It is less amen able to treatment and also apt to be complicated by corneal ul ceration. The microbe which gives rise to this condition has not been definitely established. This inflammation is also known as school ophthalmia. It is extremely contagious, so that isolation of cases becomes necessary. The treatment with weak solutions of sub-acetate of lead during the acute stage, provided there be no corneal complication, and subsequently with a weak solution of tannic acid, may be recommended.
Purulent Conjunctivitis.—Some of the severer forms of catarrhal conjunctivitis are accompanied not only by much swell ing of both conjunctiva and lids but also by a muco-purulent se cretion. Nevertheless there is a sufficiently sharply-defined clin ical difference between the catarrhal and purulent types of in flammation. In purulent conjunctivitis the oedema of the lids is always marked, often excessive, the hyperaemia of the whole conjunctiva is intense : the membrane is also infiltrated and swol len (chemosis), the papillae enlarged and the secretion almost wholly purulent. Although this variety of conjunctivitis is prin cipally due to infection by gonococci, other microbes, which more frequently set up a catarrhal type, may lead to the purulent form.
All forms are contagious, and transference of the secretion to other eyes usually sets up the same type of severe inflammation. Infection mostly takes place by direct transference through the hands, or secretions containing gonococci either from the eye or some other mucous membrane. The poison may also be carried by flies. The dried secretion loses its virulence.
In new-born children (ophthalmia neonatorum) infection takes place from the maternal passages during birth. Notwithstanding the great changes which occur during the progress of a purulent conjunctivitis, there is on recovery a complete restitutio ad integ rum so far as the conjunctiva is concerned. Owing to the tend ency to severe ulceration of the cornea, more or less interference with sight may result before the inflammation has passed off. This is a special danger in adults. For this reason, when only one eye is affected the first point to be attended to in the treatment is to secure the second eye from contagion by efficient occlusion. The appliance known as Buller's shield, a watch-glass strapped down by plaster, is the best for this purpose. It not only admits of the patient seeing with the sound eye but allows the other to remain under direct observation. The treatment otherwise con sists in frequent removal of the secretions from the affected eye, and the use of nitrate of silver solution as a bactericide applied directly to the conjunctival surface; sometimes it is necessary to cut away the chemotic conjunctiva immediately surrounding the cornea. When the cornea has become affected efforts may be made with the thermo-cautery or otherwise to limit the area of destruction and thus admit of something being done to improve the vision after all inflammation has subsided.
Phlyctenular conjunctivitis is an acute inflammation of the ocular conjunctiva, in which little blebs or phlyctenules form in the vicinity of the corneal margin and on the epithelial continu ation of the conjunctiva which covers the cornea. The inflamma tion is distributed in little circumscribed foci and not diffused as in all other forms of conjunctivitis. In it the conjunctival secre tion is not altered, unless there should exist wt the same time a complication with some other form of conjunctivitis. This con dition is most frequent in children, particularly if ill-nourished or recovering from some illness, e.g., measles. The susceptibility occurs in fact mainly where there exists what used to be called a "strumous" diathesis. This basis has to do with the susceptibility only, at all events to begin with. The local changes are not tuber culous; their exact origin has not been clearly established. They are in all probability produced by staphylococci.
Many children with phlyctenular conjunctivitis suffer after a short time from eczematous excoriation of the skin of the nos trils, the result of lacrimation. Another frequently distressing symptom is a pronounced dread of light (photophobia), which often leads to convulsive and very persistent closing of the lids (blepharospasm) . Indeed the relief of the photophobia is often the most important point to be considered in the treatment of phlyctenular conjunctivitis. Photophobia may be very severe when the local changes are slight. The best local application is yellow oxide of mercury.
Granular Conjunctivitis.—This disease, also known as trachoma, is characterized by an inflammatory infiltration of the adenoid tissue of the conjunctiva. The inflammation is accom panied by the formation of so-called granules, and by a hyperplasia of the papillae. The changes further lead in the course of time to cicatricial transformations, so that a gradual and progressive atrophy of the conjunctiva results. The disease takes its origin most frequently in the conjunctival fold of the upper lid, but eventually as a rule involves the cornea and the deeper tissues of the lid, particularly the tarsus.
The cause of trachoma is a filter-passing virus (q.v.). In a distinctive affection when fully established, differential diag nosis from other forms of conjunctivitis, particularly those with much follicular enlargement or purulent from the first, may be difficult. Trachoma is mostly chronic. When occurring in an acute form it is more amenable to treatment and less likely to end in cicatricial changes. Fully half the cases of trachoma ex tend to the cornea and produce superficial vascularized infiltra tion (pannus). The veiling which pannus produces causes more or less defect of sight.
Various methods of treatment are in use for trachoma. Ex pression by means of roller-forceps or repeated grattage are amongst the more effective means of surgical treatment, while local applications of copper sulphate or of alum are useful in suitable cases. Recently, the beta radiation from radium emana tion enclosed in specially shaped applicators has been used with good effect.
Of non-inflammatory conjunctival affections reference may be made to the following: Amyloid degeneration, in which waxy-looking masses grow from the palpebral conjunctiva of both lids, often attaining very considerable dimensions. The condition is not uncommon in China and elsewhere in the East.
Lastly, short reference must be made to the commonest malig nant new growths affecting the eye (see TUMOUR). These are melanoma, starting in the choroid, glio-sarcoma starting in the optic nerve or its retinal expansion, epithelioma starting in the conjunctiva, and sarcoma, usually spindle or round celled, starting in the bones of the orbit. (G. A. B.)