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Chapter VI The Optic Nerve And Retina.

Anatomy. The optic nerve arises from the brain at the posterior and inferior aspect of the optic thalamus; on account of its form it has been called the 11 optic tract." After having passed round the cerebral peduncle, the optic tract intercrosses, at least partially, in the median line, with its fellow of the opposite side to form the optic chiasma.

From this junction arise the two optic nerves, which run outwards to the optic foramina, through which they pass into the orbit. Here the course of the nerve has almost the form of the letter S, and has a length Of 28 to 29 millimetres to its ocular insertion, which is situated about 4 millimetres to the inner side of, and somewhat below the centre of, the posterior sclerotic hemisphere.

The principal connections of the optic nerve with different parts of the central organs have been indicated by Stilling, who has traced nerve bundles from the thalamus directly up to the corp. quadrigemina, and from the tract up to the cerebral peduncle. Other bundles coming from the tract follow the internal side of the corp. geniculatun~ to the inferior olive, to the origin of the oculornotorius, and to the crus cerebelli. Gratiolet and Meyriert have noticed numerous bundles traced from the thalar6s up to the white substance of the occipital lobe. Thus we obtain the anatomical explanations of hemianopsia (vide infra) in affections and wounds of certain parts of the occipital lobe (Munk), and of affections of the optic nerve in spinal diseases. Semi decussation in the chiasma takes place in such a way that the lateral bundles of the tract pass directly into the nerve of the same side; but the bundles of the middle intercross with those of the other tract, and pass into the nerve of the opposite side. The intercrossing bundles are the more numerous, and supply with their nervous fibres the nasal parts (including the point of fixation) of both retina, while the lateral bundles supply the temporal parts.

Till they reach the point of junction, the optic tracts are composed of medullated fibres without neurilemma. At the chiasma the pia mater furnishes an envelope which accompanies the optic nerves to the eyeball, and which sends cellular partitions into the thickness of the nerve, thus dividing the nerve into several secondary bundles. At the optic foramen the nerve receives a new fibrous envelope, which is a prolongation of the cranial dura mater. This covering is composed of two concentric layers viz., the external sheath, which is the thicker, and the internal sheath. Between these two layers there is a space which communicates at the optic foramen with the cerebral arachnoid space (Schwalbe).

The two sheaths unite to form the sclerotic, the fibres of the external sheath bending at an obtuse angle and becoming lost in the external and middle layers of the sclerotic, whilst the internal sheath, representing the neuilemma, comes to the intraocular surface of the sclerotic and becomes lost in its internal layer. We have thus a fibrous ring, which is slightly prominent, and which also gives a point of attachment for the choroid. The optic nerve pierces this ring with a diminution of its diameter from 3 to 1,5 millimetres, to enter the eyeball, where it helps to form the retina (Fig. 85)

The central artery of the optic nerve arises either directly from

OPTIC NERVE ENTRANCE.

the ophthalmic artery, or from a ciliary or muscular branch of that artery. It pierces the envelopes of the nerve at a short distance behind the sclerotic, and enters the central canal, in which it runs forward till it reaches the intraocular extremity of the optic nerve (o ti a i a). p c p ap I

At the papilla the artery terminates in two branches which extend, the one upwards, the other downwards; and these branches again divide dichotomously on the optic papilla or near its margin, so that there are four arterial branches diverging over the retina.

The veins of the retina, as a rule, unite into four large veins, two superior and two inferior, which converge towards the optic papilla. These four veins, by their union at the margin of the papilla, form two branches, which generally become united into one near the point of emergence of the central artery, but which may remain separate to the lamina cribrosa, in tile neighborhood of' the papilla. In addition. to the central vessels, we also find a certain number of small arterial and venous vessels which anastomose with each other. A few of these vessels, which supply nourishment to the optic nerve, arise from the central vessels, but the majority of them come from the ciliary and muscular arteries; it is by them that the vessels of the papilla and retina communicate with the ciliary vessels of the posterior part of the sclerotic.

The retina extends between the vitreous body and the choroid, from the optic nerve to the zonule of Zinn. Becoming thinner, it is united to the zonule; and, if its periphery be separated, it is found to be finely dentated. '0 Hence, this region has been called the ora serrata This termination, however, is only an artificial one, for traces of the retina may be found on the hyaloid membrane, to which the periphery of the retina is firmly fixed.

The thickness of the retina at its centre is about .04 millimetre, but this gradually diminishes, so that in its equatorial regions it is reduced to one half, and, at the ora serrata to a quarter of its thickness at the centre.

The histological structure of the retina is very complicated. It consists of nerve and cellular elements, intimately combined, and sometimes difficult to distinguish in the exceedingly small and delicate details of this membrane.

1. Nerv6 Tissue of the Retina. We can distinguish various layers of nerve tissue which, beginning with the one 111ext to the choroid, are arranged in the following order:

(a) layer of rods and cones (Fig. 86, 9). Each of these elements Is provided with I fibrous or elongated filamentous appendage (7), Which communicates with the elements of' the following layer

(b) The external granular layer is divided into three viz., the granular layer (7), the intergranular layer (6), and the cellular layer (5). These layers are separated perpendicularly by the fibres which support the rods and cones, and which are intimately connected with the elements of the granular layer.

These fibres also enter :

The molecular layer (4), which is composed of a network of very fine and slender nerve filaments. This layer gives origin to the external prolongations of the ganglion cells, and these cells form, again,

(d) The ganglion layer (3) ; and the internal offsets of the ganglia enter, finally,

(e) The nerve fibrous layer (2).

II. The cellular tissue is composed of fibres and membranes which give support to the nerve elements of the retina. We have, first of all, the membrana limitans (I), the innermost layer of the retina, the internal surface of which is in contact with the hyaloid membrane of the vitreous humor. From its external surface arise the numerous and broad based radial fibres of muller, which almost all pierce the retina perpendicularly to the direction of the nerve fibres from the optic nerve, dividing them into bundles. The radial fibres then pass into the layer of ganglion cells, which they surround with filamentous prolongations. In the molecular layer the radial fibres form a very small meshed network. In the granular layer, they surround the cells with large meshes. Again, in the intergranular layer, they divide into a very fine network, and, passing through the outer nuclear layer as simple fibres, unite at the external limit of that membrane. This termination of the retinal cellular tissue has been called the I I membrana limitans externa " (Max Schultze). It is fenestrated, so as to give passage to the prolongations of the rods and cones.

In these radial fibres, whose course through the retinal has just been described, we find nuclei situated almost exclusively amongst the cells of the granular layer. They are ovoid, and their long axes coincide with the direction of the fibres ; they also contain nucleoli.

We can easily see that the cellular tissue sustains and gives support to the nerve elements ; but it is the nerve elements that determine the shape of the cellular tissue. Thus, when the nerve elements 'are globular, as in the case of the ganglion cells, the cellular tissue forms cavities ; but, when the nerve tissue is fibrous, the cellular tissue forms a network.

The structure of the retina is subject to a few modifications in the arrangement of the various elements near the periphery of the membrane, at the optic nerve papilla, and at the yellow spot and fovea centralis.

The gradual thinning of the retina from the centre towards the periphery affects, at first, almost all the layers of the membrane to an equal extent. Beginning at the equator, the granular layer and the layer of ganglion cells are the first to disappear; the layer of rods also disappears at the ora serrata, so that at that point the retina only contains cellular tissue.

At the entrance of the optic nerve, the retina contains only nerve fibres, which, having passed through the opening in the sclerotic and choroid, become deflected at a right angle to form the innermost layer of the retina. The external layers also take origin in this situation sometimes their margin is very thin, and they gradually increase in thickness; while, on the other hand, their margin is occasionally thick and well defined.

At its entrance, the optic nerve measures on an average 1.5 millimetre diameter; it is round or slightly oval. At the centre of the papilla, the divergence of the nerve fibres causes a small hollow pbysiological excavation (Fig. 83), which is generally the point of emergence of the central vessels of the retina. Sometimes this excavation is placed eccentrically.

The nerve fibres of the retina, which are, in reality, only a fan like cxpansion of the optic nerve, are in the optic nerve itself separated into bundles by cellular portions which arise from the envelope of the optic nerve. These cellular partitions stop at tile sclerotic opening,where they form the fenestrated membrane (Fig. 85, L. cr. Lamina cribrosa), which is partly connected with the choroid, and partly with the sclerotic, from the former of which it sometimes receives a few pigment cells, visible to the ophthalmoscope. Thus, beginning at the fenestrated membrane, the nerve fibres become perfectly transparent, having there lost the medullary envelope which makes their outline opaque.

At the centre of the retina we find the yellow spot (macula lutea), and at the centre of the yellow spot we find the fovea centralis. The yellow spot is about two millimetres in diameter, and is slightly oval in the horizontal diameter ; in this region, especially at the level of the fovea centralis, the cellular tissue is much diminished. All the nerve fibres coming to this spot terminate in a very thin and almost imperceptible layer; the ganglion cells are here very numerous; the thickness of the nuclear layer is diminished, and replaced by the very much elongated filaments of the cones. The rods gradually disappear as we approach the macula, so that here we only find cones. It should also be mentioned that the radial fibres, which traverse the retina perpendicularly to its surface, in the macula change their direction, and converge towards the fovea centralis.

The external layers of the retina include, as has been proved by Boll, a colored substance, the retinal purple, which renders it pink, and vanishes rapidly through the influence of light. Under the same influence the internal extremities of the cones become shorter, as Engelmann assures us, again becoming larger in the darkness. These changes are produced in both eyes, even when one of them only is exposed to light, while the other is kept in darkness; and they are also to be observed when both eyes are kept in darkness, the light acting only on part of the skin, for instance, on the back. After destruction of the brain, the effect of the light is produced only on the eye which is directly exposed, and not on the other kept in darkness.

As to the vessels of the retina, they come from the central arteries and veins of the optic nerve, which divide primarily on the optic papilla and then on the retina, forming with the retinal capillaries an almost independent system, connected with the choroidal vascular system only by the arterial circle of the sclerotic, which surrounds the optic nerve and sends vessels into the choroid and retina. In addition to these, we find numerous small arteries, veins and capillaries, passing from the margin of the choroid into the optic nerve, and anastomosing with the capillary network that surrounds the bundles of nerve fibres. The arteries and veins of the retina are generally found behind the layer of nerve fibres ; in the region of the optic papilla they pass behind the membrana limitans; the capillaries extend to all the other layers.

The vessels surrounding the macula, as in a circle, provide it with delicate ramifications ending in capillaries in the immediate neighborhood of the fovea centralis, which is, however, itself entirely devoid of blood vessels.

The ophthalmoscopic image of the normal optic papilla (Fig. 87) has been described at P 35

DISEASES OF THE RETINA.

ART. I. Hyperernia and Anemia of the Retina.

Hyperernia cannot be considered as a distinct disease, but rather as a symptom of very various affections. It is so much the more difficult to define, that the degree of distention of the vessels, which is its leading feature, is subject to very considerable physiological variation, so that a reliable diagnosis can only be obtained by comparing the two eyes.

Arterial, or active, hyperamia is characterized by an abnormal redness of the optic papilla, which is due to the dilatation of the small vessels embedded in its substance. Venous, or passive, byperemia, again, is distinguished by the tortuosity of the veins, and by their being increased to double or triple their ordinary size. They are distended with blood, and are of a dark red color. In very pronounced cases, this hyperemia is accompanied by slight serous exudation, which is recognized as a grayish streak along the venous trunks.

The functional disturbances are: Great sensibility of the eye to light, a sensation of fatigue whilst working, and the apparition of luminous points of dazzling; passive hyperemia is most generally accompanied by an actual diminution of the acuteness of vision, which is due to the before mentioned serous exudation.

These forms of hyperemia are, as a rule, merely passing, and vanish with the trivial cause which has excited them.

When they form one of the prodromata or a concomitant of some ocular affection, their progress is naturally connected with that of the disease itself.

The circumstances which determine the hyperemia, also decide the prognosis.

Etiology. Active hyperemia is observed contemporaneously with a pericorneal injection, whenever the conjunctiva is much irritated ; when the iris or choroid is congested ; or, again, when the eye has been exposed to great conditions dazzling, or has been overworked under hurtful conditions.

Venous hyperemia is found in diseases of the retina, or owes its existence to affections of the general circulation (diseases of the heart, liver, dysmenorrhea), or mechanical obstacles in the course of the central or ophthalmic vein or venous sinuses (orbital tumors, tumors of the brain, etc.). Finally, retinal hyperemia has been noticed at the same time as severe headache in the first stage of constitutional syphilis.

Treatment. Apart from any indication furnished by the exciting cause, an eye affected with hyperemia requires rest, and to be protected from a bright light by darkening the room, or by the use of very dark colored preserves. Cold compresses may also be employed, and, if necessary, light purgation, or even the artificial leech, observing the precautions already laid down.

Anemia of the retina, characterized by discoloration of the optic papilla and an abnormal contraction of the retinal vessels, cannot be considered as invariably a symptom of a cholorotic anemia. It is rather the consequence of some disturbance of the circulation, such as compression of the vessels in the optic nerve or orbit. When this compression is not merely passing, it rapidly produces other alterations, such as edema, hemorrhagic spots, etc. The so called progressive or pernicious anernia, the most serious of all forms of anemia, is accompanied by slight edema of the retina, seen by the ophthalmoscope as a thin white veil, covering the fundus, and with numerous small hemorrhages in the course of the attenuated retinal vessels (see article on Apoplexy of the Retina). These hemorrhagic spots, as a rule, have a white centre, and in a short time disappear, to reappear in other parts of the retina. The indications for treatment are those furnished by the general state of health.

ART. II. Retinitis.

1. SEROUS RETINITIS EDEMA OF THE RETINA.

This disease can only be diagnosed by the ophthalmoscope, for the external appearance of the eye is not in the least changed, and the complaints of the patient are in no wise characteristic.

To the ophthalmoscope, there are two chief symptoms, but present in very variable degree. They are loss of transparency of the retina, and hyperemia of its vessels. The first of these symptoms, due to a serous exudation (serous retinitis), is especially well seen at the point where the membrane is thickest i. e., near the intraocular termination of the optic nerve. Thus, we find that the contour of the nerve loses its distinctness, or is completely masked by the retinal opacity.

When this opacity is situated in the deep layers of the membrane, we may find round the papilla exceedingly fine strie, which radiate in the direction of the nerve fibres (Fig. 88).

The serous exudation in the retina gives, moreover, a distinctly grayish tint to that membrane, especially round the nerve and along the course of the large vessels (Peripapillary retinitis), which tint gradually disappears as we approach the equator of the eye. At the yellow spot, the retina is much thinner than in the neighboring parts thus the brownish red color of the choroid shining through the retina, and in the midst of the surrounding gray, may simulate a hemorrhagic spot.

As to the hyperemia, it begins in the optic nerve, which becomes of an intense red, in consequence of the increase in number of its intimate vessels. The aspect of the veins is still more characteristic ; they not only increase in calibre, but also elongate, and, with the ophthalmoscope, are seen to be of a very deep color, and somewhat thick and tortuous. The flexuosities dip into the thickness of the retina, which, if it be opaque' hides the deep portions of the vessels, whilst the superficial portions are clearly seen and are of a bright red.' Thus the veins seem to have some solution of continuity.

The arteries generally preserve their volume and direction. Yet, when the transudation and consequent imbibition of the tissue extend to the lamina cribrosa, the increase in the volume of the optic nerve experiences a certain resistance at the sclerotic ring. Hence, there is some compression of the central arteries, and, simultaneously with the hyperemia of the veins, anemia of the arteries which appear to be diminished in calibre. The other parts of the eye do not at all participate in the disease; the external aspect of the eye is normal, and all symptoms of irritation, such as lachrymation and pericorneal injection, are completely absent.

The disturbance of vision accompanying the retinitis varies very much, and must be attributed as much to the serous exudation as to the compression of the nervous elements by the swelling of the cellular tissue.

In the early stages, the patients have the sensation as if there were, between their eyes and objects at which they are looking, a fog, which, gradually becoming denser, diminishes more and more the acuteness of their central vision, till by and by they can only distinguish large objects. Contemporaneously the periphery of the field of vision is contracted, vision is gradually diminished from the periphery towards the centre, and in the more serious cases the patients can only dis¬tinguish night from day. In other cases of retinitis, which show the same appearances to the ophthalmoscope, the visual disturbance is of quite another kind. The central visual acuteness is not diminished to any great extent, and the visual field remains almost entire. There appears, however, a slight cloud, as it were a veil before distant objects, and the patients suffer from a sensation of trembling in the air before the eyes. They also are greatly dazzled by ordinary daylight, and see much better in the evening (Nyctalopic retinitis, Arlt).

The perception of colors is, as a rule, normal, at least in ;light cases of this affection. When the acuteness of central vision is much diminished, we also find a greater difficulty in recognizing tints; but this quantitative dyschromatopsia is not characteristic, and is not of importance in the diagnosis of retinitis.

Progress. Serous retinitis may remain in the state which we have just described for a long time, and end in resolution, although leaving for a very prolonged period some perturbation of vision.

More frequently it is followed by important alterations of the retinal tissue, and assumes the character of parenchymatous, retinitis.

Our prognosis should always he very reserved, for we are never sure whether the disease which we see is not merely the first phase of a much more serious affection. It is more favorable if, after a somewhat long duration, the ophthalmoscopic symptoms do not change, and if the visual field at the same time preserves its normal limits.

Etiology. As the first phase of other retinal affections, serous retinitis may be due to various circumstances which we shall enumerate later.Serous retinitis, properly so called, frequently results from a chill, or may be the effect of too strong a light, or of excessive use of the eyes under bad conditions. In many cases the cause is very obscure.

Treatment. It chiefly consists in giving the eyes rest, which may be accomplished by slightly darkening the room and wearing bluish glasses when out of doors.

We may also use the artificial leech of Heurteloup with due precautions; derivation through the skin ; if necessary also mild laxatives. In general terms it may be said, that this disease requires a careful study of the general state of health, so that we may clearly realize the indications and contra indications of treatment.

Retinitis from Contusion. After contusion of the eyeball, ()edema of the retina has been observed in the form of large grayish stains in the neighborhood of tile papilla, upon which the vessels look prominent and darker. Strength of vision is weakened to one fourth or one third of the normal, and the sense of light suffers in the same way. There may be also spasms of accommodation, with myosis or mydriasis, and slight muddiness of the cornea and the aqueous humor. Sight is generally restored in about a week. Rest of the eyes and atropine act favorably.

Macular Retinitis by Direct Sunlight has been* noticed only on the occasions or solar eclipses, when it has been caused by observation with unprotected eyes. The patients complain of central scotoma and scintillation, and if this positive scotoma is Not absolute, we may notice quantitative diminution of the color sense. The oph. thalmoscope shows alteration of the macula as by hemorrhage, sometimes with a bright white spot in the middle. Experiments on rabbits prove a real burning of the retinal layers (Cerny). Improvement in vision takes place, but a slight central alternation in the field of vision persists for years. Darkness, cupping on the temple, and hypodermic injections of strychnia have been used in this affection.

2. PARENCHYMATOUS RETINITIS.

This form of retinal inflammation, apart from the symptoms of hyperemia and exudation already spoken of in connection with simple retinitis, presents also those of alteration of the tissue of the retina itself (hyperplasia and sclerosis).Theme alterations, which extend t It roughout t lie en t i re ret i till ( Diffuse renitis),generally begin in the cellular elements and in the diatin grem. From the compression of lite nervous elements by the altered cells, the nervous tissue becomes more or less atrophied This process may be localized, sometimes to the external retinal layers (affecting also the choroid), sometimes to the internal. In this last case the membrana limitans is disorganized, and condylomatous growths are produced (Iwanoff) which project into the vitreous and there become vascular.

This morbid condition is accompanied with change in the structure of the retinal vessels, their walls being thickened by the hypertrophy of their adventitious membrane. Much more rarely, the retinitis seems to begin in the walls of the vessels and in their immediate neighborhood (retinitis Perivascularis) ; it is localized to these structures, whilst the remainder of the cellular tissue is little altered, and the nervous elements are entirely preserved. In these exceptional cases, anatomical investigation has shown a considerable proliferation of cells in the adventitious membrane of the arteries, of the veins and of the capillaries, but in very various degrees (Iwanoff ).

Diagnosis. With the ophthalmoscope, we find in diffuse retinitis the signs of venous hyperemia and retinal edema (loss of transparency), which have already been mentioned in connection with simple retinitis. In addition, we also find whitish or yellowish, sometimes even greenish opacities on the retina, which may be in the form of isolated points, or of large irregular patches, in strie or narrow bands.

The vessels are partially covered with these yellowish exudations; they seem to dip into them on one side and to come out on the other. The large vessels are bounded on both sides by a whitish line which extends along their walls.


Round the macula, the retinal opacities are grouped in a peculiar manner, in very fine lines, and more rarely small strie, which radiate out from the fovea Centralis ; this star shaped figure may also be composed of very fine points. There are also sometimes more or less numerous ecchymoses, disseminated through the retina as small red spots, or as fine strie, or even as irregular red patches in the immediate neighborhood of the vessels of the retina. These will be fully described in the chapter on Retinal Hemorrhages.

In Perivascular retinitis, the arteries and their branches seem to be transformed into whitish threads, in the centre of which a red line is visible ; the larger veins are diminished and irregular in calibre ; at the periphery only, a few branches have the same appearance as the arteries. The retina at various points seems opaque, and in these situations it is covered with punctated ecchymoses.

On the optic nerve, the point of emergence of the vessels is covered with a brilliantly white prominent mass, with red spots and strie which come from the new vessels ; these may be made momentarily to disappear by compressing tile eyeball (Nagel). The external appearance of the eye is perfectly normal ; occasionally the tissue round the cornea is injected, sometimes the iris is slightly sluggish in its movements, and after a certain time the pupil becomes slightly dilated.

In the early stages, the patient feels as if there were a cloud before the eye, or a fog round the objects at which he is looking, which cloud grows thicker when an effort is made to distinguish these objects clearly ; the eyes are easily dazzled, and the patient complains of flashes of light. The central visual acuteness is considerably diminished ; the visual field is contracted, or may present small absolute deficiencies (scotomata), which vary in form and situation. This weakening of the visual acuteness is especially remarkable in a dim light. As to color perception, we need only repeat the statements Already made when speaking of serous retinitis.

Sometimes objects seem smaller than they really are (micropsia), sometimes larger (megaloopsia), or contorted (metamorphopsia). The presence of the phenomena may be easily ascertained by placing a prism before the eye with the base turned upwards or downwards. The patient can then compare the images coming from the two eyes.

In very pronounced cases vision is completely destroyed, the patients are scarcely able to distinguish night and day, and the eye is not dazzled even by a very bright light. The condition of the eye, as seen by the ophthalmoscope, does not correspond with the functional symptoms.

As a rule, patients do not experience pain, or at most they suffer from a feeling of pressure in the bottom of the orbit.

The progress of parenchymatous retinitis is usually very slow. Even when the characteristic symptoms of the disease are rapidly established, it becomes after a short time almost stationary, with alternating remissions and exacerbations.

If the morbid process is not intense ', if the exudations are insignificant, and if the disease is of short duration, we may perhaps expect complete recovery ; but, even in such cases, relapses are frequent. If the disease is of long duration, with a considerable amount of exudation, and if there are already secondary changes in the nerve elements, recovery is always imperfect. Vision remains more or less altered, according as the process is localized to the centre or periphery of the retina. Again, the disease often terminates in atrophy of the retinal tissue and definite abolition of vision.

The prognosis is therefore always very serious, and should be guided by such special circumstances as the duration of the disease, the intensity and extension of the process, and its localization. The prognosis becomes more grave with advancing years, with defects in the field of vision, with any tendency to vascular changes, and with the probability of an analogous cerebral affection. The more numerous the relapses, the greater is the danger of final atrophy.

Etiology. The cause of this affection, excepting where there is a syphilitic taint, is often unknown. It has been attributed to heredity, dysmenorrhea, the sudden effect of a dazzling light, and contusions of the eyeball. The disease may also extend to the retina from the choroid; again, it may be in connection with some atheromatous alterations of the brain.

Treatment. Complete rest to the eyes, keeping the patient for a long time in a room always at the same degree of darkness, and diet regulated to suit the general constitution are essentials ; any considerable hyperemia of the retina and congestion to the head demand repeated local depletion of blood, effected by applying a wet cuppingglass to the temple, cold compresses and mild purgatives. For the exudations we may give internally calomel, sublimate of mercury, and iodine preparations; externally inunction with mercurial and iodine ointment.

After there is an improvement in the condition, the patient should begin to use his sight only very gradually; he should avoid too bright

  • light, and for a length of time should use every precaution to prevent
  • relapse.
Retinitis punctata albescens and Retinitis striata. Some observations have been published of a peculiar retinal affection in which the ophthalmoscope shows great numbers of small white round dots, chiefly between the papilla and macula. They are supposed to be the result of hemorrhages, but they may be also of inflammatory origin. The defect of vision consists in the diminishing of central vision, the eccentric visual field remaining intact.

Much more frequently, extensive white strie are seen in the retina, covering part of the vessels and even passing through the papilla. They result probably from development of connective tissue after hemorrhagic or inflammatory processes. Vision is often but slightly affected. In both of these diseases treatment consisted in the application of Heurteloup's leech, iodide of potassium, small doses of sublimate, and care of the general health.

3. SYPHILITIC RETINITIS.

Constitutional syphilis becomes localized in the retina as in other portions of the eye, such as the iris and choroid. In the nervous membrane, it is characterized by a general opacity which gives the fundus of the eye on ophthalmoscopic examination a grayish or bluish reflection, in which the outline of the optic nerve is no longer visible. This opacity disappears near the periphery of the membrane. It is very visible along the large retinal vessels. The veins seem swollen and tortuous, but in a very variable degree; hemorrhage has occasionally been observed. The detection of these symptoms becomes very difficult when we have also opacities of the vitreous, which in the early stages are very thin, but become more apparent as the disease progresses.

When, in any case, ophthalmoscopic examination leaves us in doubt whether we have to do with opacity of the retina, or of the vitreous in the fundus of the eye, we must direct our attention to the periphery. In this situation, opacity of the retina becomes less and less and disappears, whilst opacities of the vitreous body are here much more pronounced than at the centre.

Another common complication is an alteration in the choroid. This, indeed, may be the starting point of the disease which has secondarily spread to the external layers of the retina (chorio retinitis).

The changes in the choroid, concealed at first by the loss of transparency in the subjacent membrane, are often invisible till the retinal affection has passed off.

In a rarer form of syphilitic retinitis, the opacity is very well marked at the fovea centralis, and gradually decreases round the macula The optic papilla and its neighborhood preserve their transparency (recurring central retinitis of von Graefe). This condition supervenes suddenly and is accompanied with great diminution in the acuteness of central vision, which may even amount to blindness if both eyes are affected. In a short time the disease disappears, but returns after a few weeks or months. The relapses may be very frequent, leaving after the first attacks a normal condition of the fundus and of vision. But later the vision is permanently injured, and the retinal affection remains constant.

In the ordinary variety of syphilitic retinitis, the functional disturbance consists in a diminution, at first of little moment, although sometimes very rapid, of the central visual acuteness, whilst the periphery of the field of vision in the majority of cases remains normal. The results of the examination vary considerably with the illumination (torpor retinae). Frequently, patients complain of the presence of immobile black spots (positive scotomata), of floating bodies (opacities of the vitreous humor), of luminous and colored apparitions (photopsia and chromopsia).

When the disease is in the form of chorio retinitis, we sometimes Mid, with the perimeter, defects in the visual field, which correspond ill form and situation 10 the disseminated foci On the fundus of the is eye; thus, if the morbid process occupies the periphery, the visual field is perceptibly contracted. Yet there is not always a direct relation between the alterations visible to the ophthalmoscope and the amount of functional disturbance. If the macula is affected, we find a central scotoma with dyschromatopsia throughout the entire scotoma; sometimes also patients see objects smaller than they are in reality (micropsia) and difformed (metamorphopsia).

The progress of the disease, besides being very slow, is very variable. It is often cured by active treatment in six or eight weeks, at other times it is very stubborn, and it is always apt to recur. When the relapses are very frequent, the arteries become thinner, with slow atrophy of the retina and optic nerve. In the last place, the pigmentary epithelium becomes diffusely discolored, and black spots make their appearance in the fundus of the eye. From their star like appearance and connection with the retinal vessels, the ophthalmoscopic appearance of this last stage of chorio retinitis resembles very closely that of pigmentary retinitis, and we may fall into an error of diagnosis if we do not take into careful consideration the antecedents.

The prognosis is, as a rule favorable in the early stages of the disease, and becomes more serious the longer it lasts, and the greater the number of relapses. The possibility of complete recovery depends on the density of the opacities, and on the alterations of the retinal tissue.

Etiology. Statistics as to the antecedents of patients affected with this disease show that the constitutional syphilis manifests itself in a large number of cases by retinal inflammation, with the ensemble of symptoms which we have described. If there is nothing in these symptoms absolutely pathognomonic, still they derive some value from the fact that they are much more frequently seen in syphilitic persons than in others affected with retinitis. I

Treatment. The treatment consists almost entirely of antisyphilitic medication, regular mercurial inunction, with confinement to bed in a dark room, the internal administration of mercurials and iodide of potassium. We may add to this treatment with advantage sudorifics, which should be given according to the general strength of the patient.

When there are acute symptoms, we may derive benefit by applying the artificial leech to the temple. The treatment should be continued for some time after the disease has disappeared, and should only be gradually and cautiously stopped, as relapses are apt to occur.

The torpor of the retina, which sometimes remains for .1 considerable period, is best treated by subcutaneous injections of strychnia in the temple.

4. RETINITIS ALBUMINURICA.

In addition to venous hyperemia, we find a grayish opacity of the retina, surrounding the optic papilla, obscuring its outline, and partially veiling the vessels. This opacity is condensed, and in it we find small hemorrhages of a round or striated form. At some distance from the papilla, there are developed a certain number of milk white points or small patches, which increase in size, become united to each other, and so form a large grayish white glittering ring around the nerve, sending offshoots towards the periphery of the eye, where we find a few isolated white patches. The vessels are to a large extent buried in the tumefied retinal tissue, on which we also find numerous apoplectic foci (Fig. 89).

Round the yellow spot, we observe a mass of small white spots, arranged in lines, radiating from the fovea centralis, which is of a deep red color. The peripheral parts of the eye do not undergo any alteration.

This appearance of the retina is due to a serous transudation in the neighborhood of the optic disc, with hypertrophy of the cellular tissue of the retina. We then have fatty degeneration of these structures, and, later, sclerosis of the nerve fibres and ganglion cells. As the radiating fibres III the region of III( macula radiate from the central spot, their special arrangement explains the peculiar appearance in this region that is to say, the star shaped arrangement of the white points and spots which indicate the fatty degeneration of the radiating fibres.

The walls of the vessels also are affected with analogous changes.

In a few cases the inflammatory process is concentrated on the optic nerve, and it becomes the seat of a considerable swelling, the ophthal image of which exactly resembles strangulated papilla. (See Diseases of the Optic Nerve.)

In this disease, the functional disturbance is very variable, and does. not bear any relation to the ophthalmoscopic alterations. Central vision always suffers more or less, but is rarely completely destroyed. In most cases the visual field remains entirely free, unless at a later stage the disease is complicated with separation of the retina. Perception of colors is normal. The disease generally affects both eyes, but in different degrees.

The progress of the disease is, as a rule, slow, being interrupted by stationary periods; at times there seems to be some improvement, and then again a sudden exacerbation.

Still, cases of complete recovery have been seen (in albuminuria, after scarlet fever, or in pregnancy), in which the retina and vision have returned to their normal state. In other cases traces of the retinal opacities remain, with the consequent disturbance of vision; or, again, the disease terminates in atrophic changes, or in separation of the retina. Often the progress of the general disease and the death of the patient put an end to the study of the development of the ocular affection.

Hemorrhages beneath the conjunctiva and into the vitreous body are common complications. They are important as indications of a general hemorrhagic condition, which may also manifest itself in epistaxis, purpura hemorrhagica, cerebral apoplexy.

The prognosis, although bad in itself, becomes more serious, in consequence of the danger to which the general disease exposes the life of the patient. If the general health be re established, the ocular affection may also pass off, and the vision improves, or even is restored to its normal state.

Etiology. This form of retinitis is closely connected with the appearance of albumen in the urine, especially if the albuminuria is chronic; consequently we have it in diseases of the kidneys (Bright's disease), in bad cases of intermittent fever, in chronic alcoholism, in the acute exanthemata, especially after scarlet fever, and during pregnancy. According to some authorities, the retinitis is due to a defi of the nutrition of the retinal tissue owing to the altered condition of the blood; according to others, it is due to the vascular tension of the arterial system, which increases with the disturbance of the general circulation (left ventricular hypertrophy) secondary to the disease of the kidneys. However, retinitis alburninurica is only observed in 8 or 10 per cent. of cases of Bright's disease, and if once established it may pursue a course perfectly independent of the general state.

Treatment. The general state of health seldom admits of bloodletting, which, however, when performed in suitable cases on the temple, seems to be beneficial in checking inflammatory symptoms; it may be replaced by dry cupping, administration of derivatives, etc. As far as the condition of the eyes is concerned, good results have been obtained by general treatment with iodide of potassium, iron preparations, tannin, digitalis, and the moderate use of diuretics and diaphoretics; a milk diet is generally of great benefit.

The majority of these patients cannot stand any reducing treatment; their general condition requires rather a strengthening and tonic course.

[We must take care not to confound the disease which we have just described with uramic amaurosis, which is also met with in Bright's disease, and which is not due to any alteration of the retina. It is characterized by sudden dimness of vision, which may amount to total blindness, coming on rapidly, and passing off after the attack (see further on Amblyopia from Intoxication)].

5. LEUKEMIC RETINITIS.

Leukemia must also be reckoned among the general affections which may give rise to retinitis.

On ophthalmoscopic examination we find the normal red color of the fundus changed into a pale lemon, which is due to an alteration in the color of the blood from the excess of leucocytes which it contains. This change of color is not, however, constant.

The neighborhood of the papilla is the seat of small, whitish, round opacities, which are often surrounded with hemorrhages, and the largest of which do not exceed the diameter of the papilla; they then seem to project beyond the level of the retina. These opacities are found an far as the equatorial region of the eye, and sometimes accompany the retinal vessels as white bands.

The anatomical cause of these opacities has been found in the collection of leuco (lymphatic corpuscles, Leber) which are analogous to the leukemic foci of other organs (Virehow), and of the choroid (Engel, reimers). In other cases, the opaci are duv to selerosis of the nerve fibres of the retina (Recklingbausen).

The functional disturbance is, as a rule, inconsiderable, at least when the disease is not complicated with hemorrhage in the neighborhood of the macula, or in the vitreous body. Apoplectic foci have also been seen in the choroid (Saemisch). This affection does not require any special treatment beyond that of the general disease.

ART. III. Retinitis Pigmentosa.

The first symptom of this disease, which is often present long before the characteristic alteration of the retina makes its appearance, is a marked diminution of the visual acuteness whenever the illumination is defective (hemeralopia). Hence, it happens that in the evening patients are not able to find their way, which symptom can be reproduced also in day time by examining them in a dimly lighted room. It thus appears that this phenomenon is due to torpor of the retina, which demands bright illumination to call forth its normal function.

For some time this hemeralopia is the only thing which annoys the patient ; but in time there supervenes a contraction of the visual field, at first only noticed when the light is insufficient, but after a time in any light.

This contraction follows an irregular concentric course, and slowly but continuously advances towards the point of fixation. Central vision may for a long time remain unaltered. Even when the field of vision is reduced to a few inches, patients may be able to read the smallest type, and yet be quite unable to move about alone (exactly as when a normal eye looks through a narrow tube). Again, in trying to see successively the objects which a normal eye includes in one picture, the eyes move about rapidly. This unsteady, uncertain and restless look may assume the character of nystagmus. Color perception is normal; the sense of light considerably weakened.

Gradually the insensibility also invades the central portion of the retina, and the disease ends in complete blindness.

To the ophthalmoscope, this disease is characterized by the appearance of pigmentary masses in the retina, in the neighborhood of the vessels and by a grayish or whitish discoloration of the optic papilla, which, however, never assumes a chalky whiteness, or resembles a tendinous reflection. There is also a more or less well marked diminution of the calibre of the vessels in the fundus of the eye (Fig. go).

The intensely black pigment, collected into denticulated and starshaped masses, as a rule, appears first of all near the periphery, and is inconsiderable ; after a time it increases in amount, and gradually encroaches on the posterior pole of the eye, often following the course of the vessels. The image of the fundus seems obscured by a slight veil.

The quantity of retinal pigment varies very much in this disease sometimes the entire fundus is covered with it, so that the contracted vessels can scarcely be traced among the masses of pigment; sometimes we find only a few isolated patches of pigment in the equatorial region of the fundus of the eye; finally, cases have been recorded which presented all the functional symptoms so characteristic of retinitis pigmentosa, and in which there was no trace of pigment in the retina.

Along with the pathological alterations which we have just described, we sometimes also find modifications in the choroid, which consist of an irregular discoloration of that membrane, due to the loss of pigment in its epithelial layer.

In cases of advanced retinitis pigmentosa, we also meet with partial opacity of the lens at its posterior pole, which only occasionally is the starting point of a complete cataract. rhe vitreous body is sometimes the seat of flaky or filamentous opacities (Mooren, Schweigger, Archive fur Ophthal. vol. a, p. 103).

Histological research tends to show that the choroidal pigment of the epithelial layer may be infiltrated into the retina. This process was first observed in chorio retinitis with exudation between the two membranes. In such cases the external layers of the retina are slowly destroyed, and the epithelial cells of the choroid with the pigment which they contain come forward to the internal layers of the retina; or again, these cells are disorganized, and their pigment alone penetrates the retina. In typical cases of retinitis pigmentosa, where there is no choroidal complication, we find a well. marked hyperplasia of the cellular tissue of the retina, more particularly in the neighborhood of the vessels, the walls of which have undergone a thickening, which causes contraction of the large vessels, and complete obliteration of the smaller. At the same time, the pigmented epithelium is altered. On the one hand, we find cells which have become atrophied; on the other, cells highly pigmented, which are infiltrated into the retina in the neighborhood of the vessels, Finally, the nerve elements are also atrophied (Leber). The retinal pigment sometimes seems to come from the pigmented epithelium of the ciliary body (Schweigger).

The progress of this disease is exceedingly slow; it generally begins with hemeralopia in early youth, rarely at an advanced period of life ; it attacks both eyes, and, ftt the age of forty or fifty, ends in complete blindness. Sometimes it may remain stationary for a long time.

The ultimate prognosis is thus absolutely bad.

The etiology of this disease is not known; it often appears in several members of the same family, as if it were hereditary, and sometimes is coincident with idiocy or deaf mutism. A certain number of children affected with the disease are the offspring of consanguineous marriages; others seem to be the subjects of hereditary syphilis. Pigmentation of the retina is also seen, as we have already said, in the last stage of chorio retinitis. It is likewise observed in some cases of atrophy of the optic nerve and retina.

Hitherto all treatment has been ineffectual. Local b