Chapter XLV: Introduction: The object of the following essay is to give, as far as (1)

practicable in the limits of an encyclopædic article, an account of the eye symptoms which may be seen in the course of diseases of the general system and in connection with the pathological conditions of the various organs of the body. The eye has always been looked on as a valuable indicator of general systemic disturbance. Its expression has been noted as showing the general vigor or feebleness of the patient, as well as his varying mental moods, while paralysis of its external and internal muscles has in all times been regarded as a sign of disturbed intracranial action or disease. In order to judge of the state of the circulation the physician habitually looks at the lips, the tongue, and the nails, where the capillaries are covered by translucent material, to appreciate the state of the circulation. How much better are we enabled to do this when, by the use of the ophthalmoscope, we look at the interior of the eye and see the blood-columns in the veins and arteries of the head of the optic nerve and the retina laid bare to our view without any opaque covering whatever! Such an examination, besides showing the state of the circulation, will frequently reveal a neuritis which may be due to some intracranial disease, or show a degeneration of the optic nerve which may point to impaired power and tissue-change in the spinal cord or the brain; or there may be characteristic retinal changes associated, as, for instance, with disease of the kidneys, or extravasation of blood which may be dependent on general or local causes; these frequently serving as important indices of the state of the nerves and vascular tissues in other organs in the body.

In so vast a field, and in one so new as regards ophthalmoscopic appearances, there remains still much to be accomplished. Useful knowledge has accumulated slowly, but numerous enigmatical appearances have been referred to their true causes, while many which at first sight seemed important have been proved to be either anomalies of formation or to have no pathological import. A complete and accurate description of all the eye symptoms in all diseases is an herculean task, because it presupposes the careful study of vast numbers of cases in every department of medicine: it is therefore out of the question for any one man to complete such a description from his individual efforts, and he must either remain content with a mere sketch or collate the combined experiences of many observers in different fields in order that it may be in any way reasonably {738} perfect. To keep such an article within any moderate limits it has been necessary to condense much, and to consider only those points which the combined testimony of many observers shows to be important and of frequent occurrence. For similar reasons the writer has abstained from giving a complete list of all authorities treating of the subjects herein discussed, and has referred only to those which appeared to him to be some of the most important. Those readers who wish a more complete bibliography can readily obtain it by referring to the various monographs hereinafter quoted, and also by consulting the well-known essays of Foerster,[1] Robin,[2] and of Mauthner,[3] or the treatises of Albutt[4] and of Gowers.[5]

[Footnote 1: "Beziehungen der Allgemein-Leiden und Organ-Erkrankungen zu Veränderungen und Krankheiten des Sehorgans," in _Graefe und Saemisch's Handbuch der Augenheilkunde_, Bd. vii., 1877.]

[Footnote 2: _Des Troubles oculaires dans les Maladies de l'Encephale_, Paris, 1880.]

[Footnote 3: _Lehrbuch der Ophthalmoscopie_, Vienna, 1868, and _Gehirn und Auge_, Wiesbaden, 1881.]

[Footnote 4: _On the Use of the Ophthalmoscope_, London, 1871.]

[Footnote 5: _Medical Ophthalmoscopy_, London, 1879.]

Such an article is necessarily a chapter on symptomatology, giving the eye symptoms in various diseases and pathological conditions, and the reader will therefore look in vain in it for any directions as to the treatment of such maladies, or for formulæ showing advantageous modes of administering medicines. The writer has intended, by describing and grouping eye symptoms, to enable the practitioner more readily to diagnosticate the various pathological conditions of other parts of the economy. The reader should look for a description of treatment in the various articles of this work which are devoted to the discussion of such diseases and morbid states. Local diseases of the eye, except so far as they are manifestly related to or caused by general disease, have been avoided in this paper, these topics being appropriate to a treatise on the diseases of the eye.

Changes in the Eye-ground and its Appendages due to Diseases of the Circulatory Apparatus--Heart, Blood-vessels, and Blood.

The ophthalmoscope has laid bare to our view a living nerve of special sense, the highly-developed end-organ in which it terminates, and the blood-columns circulating in them. In no other part of the body has Nature vouchsafed to us so clear an insight into her mysteries. In a state of health the index of refraction of the walls of the retinal blood-vessels is so nearly coincident with that of the surrounding media that they either entirely escape our observation or are only slightly indicated, thus allowing us to see only the blood-columns which circulate within them. Owing to the distance from the heart and to the restraining influence of the intraocular pressure, as well as to the minute size of the vessels in question, the pulse-wave has so far died out as to be ordinarily invisible, even by the aid of the eye-lenses which Nature has so kindly placed as magnifying-glasses to assist us in the study of intraocular phenomena. Even where we avail ourselves of the upright image in examining the normal eye-ground, by which an amplifying power of seven to fifteen {739} diameters is obtained, we cannot usually detect any pulsation in the vessels, although exceptionally we may observe pulsation which is always venous and confined to the larger twigs of the venæ centrales as they pass over the disc and dip into the nerve-substance. By slight pressure on the eyeball with the finger venous pulse can always be produced. This phenomenon consists of an emptying of the vein from the optic pylorus toward the periphery, followed by a rush of return blood in an opposite direction, which takes place in eyes where the intravenous and intraocular pressures are nearly balanced. Under these circumstances the injection of a fresh quantity of arterial blood into the eye causes a temporary increase of intraocular pressure, which is transmitted through the vitreous to the main trunks of the veins, compressing them at the point nearest the heart (where the intravenous pressure is least) before the column of entering blood which has been hindered by the capillary resistance has had time to flow around to re-establish the current. Stronger pressure on the eye will produce an arterial pulsation by causing the intraocular pressure to become so high that the blood enters only during the systole of the heart and diastole of the arteries. This is not infrequently seen in glaucoma, where there is an augmentation of the intraocular pressure, but is never visible in the normal eye of a healthy individual. It should be kept in mind that the venous pulse often produces a slight change in the adjacent arteries which ought not be mistaken for arterial pulsation.[6] Wadsworth and Putnam[7] describe an intermittent variation in the size of the retinal veins independent of the pulsation produced by the heart's action, and having a period of about five respirations, analogous to the variation of arterial tension found in animals. Besides the arterial pulse already alluded to, produced by augmented intraocular tension, where the normal force of the circulation is not sufficient to drive the blood in a continuous stream into the tense eyeball, we have an analogous condition where the intraocular tension may be normal, but the arterial tension is diminished, and a full stream of blood can enter only during the diastole of the arteries or maximum of intravascular pressure. We may notice examples of this in _insufficiency of the aortic valves_, and in some very rare cases described by Quincke[8] and Becker,[9] who found it accompanied by an alternate flushing and pallor of the optic disc analogous to the capillary pulse which may at times be observed in the finger-nail under similar conditions of the general circulation. The arterial pulse may also accompany any cause which permanently or temporarily reduces the blood-pressure in the arterial system, such as pressure of a tumor on the ophthalmic artery or of a swollen nerve on the central retinal artery (as in neuritis): or, again, by feeble impulse of the heart, as in cases of fainting or in degeneration and dilatation of the walls of the blood-vessels.[10] Becker relates[11] a case of arterial pulsation in a left eye, supposed to be due to aneurism of the aorta at a point where the left carotid is given off, whilst {740} the other eye presented the usual appearance of healthy retinal circulation: an aneurism at the origin of the innominate might reverse this and give arterial pulsation in the right eye. Usually, the pulse-phenomena in the retina are confined to the vessels on the optic disc and its immediate vicinity, but both Jaeger[12] and Becker[13] give cases where it was visible over the entire eye-ground. In cases of _congenital malformation of the heart_ with cyanosis, such as defective closure of the foramen ovale or stenosis of the pulmonary artery, the retinal vessels show markedly the general distension of the veins and the change of color of the blood. Liebreich[14] gives a striking picture of such a case, and Leber[15] remarks that in two cases observed by him the dilatation affected the arteries as well as the veins. Knapp[16] describes a case of swelling of the discs, with a vast number of thickened arteries and veins which radiated from them, many twigs reaching the fovea centralis. The autopsy showed general enlargement and hypertrophy of the whole vascular system without disease of the heart. Arcus senilis is often an accompaniment of fatty heart and an indication of extensive fatty degeneration of other tissues of the body, such as the small arteries of the brain and the recti muscles of the eye.[17]

[Footnote 6: For a minute study of the phenomenon, vide Jaeger, _Med. Zeitschrift_, 1854. See also his _Ergebnisse des Untersuchung mit dem Augenspiegel, etc._, 1876, pp. 60, 61. See also Becker, _Arch. f. Oph._, vol. xviii., part 1, p. 270.]

[Footnote 7: Vide _Trans. of the Amer. Oph. Society_, 1878, pp. 435-439.]

[Footnote 8: H. Quincke, _Berl. klin. Wochenschrift_, No. 34, 1868.]

[Footnote 9: O. Becker, _Arch. f. Ophth._, vol. xviii., 1, pp. 207-296.]

[Footnote 10: Wordsworth, _R. L. O. II. Rep._, vol. iv. p. 111.]

[Footnote 11: _Loc. cit._, pp. 253-256.]

[Footnote 12: _Ophth. Hand Atlas_, p. 75, Fig. 52.]

[Footnote 13: _Loc. cit._, pp. 220, 221.]

[Footnote 14: _Liebreich's Atlas_, Tab. ix. Fig. 3.]

[Footnote 15: _Graefe und Saemisch_, vol. v. pp. 524-526.]

[Footnote 16: _Trans. Amer. Ophth. Soc._, 1870, p. 120.]

[Footnote 17: Canton, _The Arcus Senilis_, London, 1863.]

Since 1859, when Graefe[18] by means of the ophthalmoscope first diagnosticated this condition of the retina (which Schweigger[19] a year and a half later substantiated by anatomical proof, demonstrating a closure of the central artery by an embolus in it just behind the lamina cribrosa), embolism of the central artery of the retina has been a favorite explanation of all cases of sudden one-sided blindness. Since that date Sichel,[20] Nettleship,[21] Priestly Smith,[22] and Schmidt[23] have all published careful clinical studies of similar cases with autopsies. Embolism is less frequent in this situation than in many other parts of the body, and this, as has been pointed out by Foerster, is probably due to the fact that the ophthalmic artery is given off from the external carotid nearly at a right angle, and while it in turn again sends off its smallest branch--the central retinal artery--at nearly the same angle; consequently, emboli are more readily carried past their orifices into some other vascular area supplied by the main stem. Mauthner has suggested that the transitory but complete blindness which sometimes precedes embolism of the central artery may be due to the stoppage of the orifice of the artery (where it comes off from the ophthalmic artery) by a previous embolus which has been too large to enter the artery, and which, owing to the favorable position of the orifice, has been washed beyond into some of the other branches. In the majority of such cases the ophthalmoscope shows that the retinal arteries are diminished in size and partially filled with blood, while a white opacity of the fibre-layer of the retina extends centrifugally from the disc and between it and the macula lutea. When the opacity surrounds the latter, the fovea centralis (where the fibre-layer dies out) shows {741} by contrast as a reddish or at times a cherry-red spot. The state of the disc itself appears to differ in different cases: some authors have described it as unusually pallid, whilst others claim that it still retains more or less of its natural pinkish hue. In cases reported,[24] where the disc is said to be of normal color, this circumstance is probably due to collateral circulation which has been established with the ciliary vessels at the optic entrance. Where the obstruction of the artery is complete the blindness is permanent, and the disc and retina become atrophic. Embolism also occurs in the branches of the central retinal artery, and in such instances there is loss of a corresponding part of the field of vision. In some cases there is hemorrhagic infarction.[25] It is never present in embolism of the main stem of the central retinal artery. Inasmuch as this latter vessel is an end-artery, the absence of infarction and subsequent sphacelus is interesting. The intraocular pressure probably prevents the back current of venous blood into the obstructed area, while the nearness of the vessels of the chorio-capillaris allows the retina to obtain sufficient nutriment to prevent death without allowing it to carry on its functions. In the case of embolism of a branch, all the retinal blood being under the intraocular pressure, there would be no hindrance to the entrance of venous blood from the areas of the retina supplied by other arterial branches, although, as above mentioned, the infarction is not present in all such cases. _Thrombosis of the central retinal vein_ is also a rare affection, only recognized and diagnosticated of late years. Michel[26] reports 7 cases, with plates of the ophthalmoscopic appearances in 4 of them. The patients were all between fifty-one and eighty-one years of age, and all had rigidity of the peripheral arteries. The suddenness of the attack recalls the symptoms of embolism, but in thrombosis the blindness is said never to be absolute. The ophthalmoscopic appearances are described as consisting of a diffuse and intense reddish haze of the fibre-layer of the retina, hiding the outlines of the disc and usually extending one and a half disc-diameters from it. This area of haze shows numerous small hemorrhages, mostly linear, in the direction of the retinal fibres, and beyond it the arteries and veins of the retina again become visible. The veins are dilated, excessively tortuous, and carry dark blackish blood. In the periphery of the retina the hemorrhages are rounded and splotchy, whilst a dark rounded hemorrhage occupies the fovea centralis. There is no swelling or prominence of the disc. When the thrombosis has been complete, atrophy of the intraocular end of the optic nerve follows. Zehender[27] makes two classes of cases--the marasmic in old people, and the phlebitic in young--reporting an interesting case in a patient twenty-six years old. Leber[28] details a case of hemorrhagic retinitis with thrombosis of some of the venous trunks in the retina, which were swollen to two or three times their usual calibre, and filled with very dark, almost blackish, blood: as they approached the disc they rapidly diminished in size, and were almost thread-like as they dipped into it. Galezowski[29] {742} cites two instances--one in a case of injury to the ciliary region, and one after injury to the eye by steam. In the latter, the thrombosis affected the artery, and the subject was forty-nine years of age.

[Footnote 18: _A. f. O._, v. 1, S. 136.]

[Footnote 19: _Vorlesunqen über den Gebrauch des Augenspiegels_, S. 140.]

[Footnote 20: A. Sichel, _Archiv der Phys. Norm. et Path._, No. 1, pp. 83-89 and pp. 207-218 (quoted by Leber).]

[Footnote 21: _R. L. O. H. Rep._, vol. viii., pp. 9-20.]

[Footnote 22: _Brit. Med. Journ._, 1874, April, p. 452.]

[Footnote 23: H. Schmidt, _A. f. O._, xx., 2, pp. 287-307.]

[Footnote 24: Vide case by Schmidt, _Archiv f. Ophthalm._, xx., 2, p. 288.]

[Footnote 25: Knapp, _Archives of Ophthalmology and Otology_, vol. i. p. 84 (with plates), and Landesberg, in same journal, vol. iv. pp. 39, 40, have each given cases of embolism of a branch of the retinal artery, with infarction.]

[Footnote 26: _A. f. O._, xxiv., 2, pp. 37-70.]

[Footnote 27: In clinical lecture reported by Angelucci, _Klin. Monatsblätter f. Augenheilkunde_, 1880, p. 23.]

[Footnote 28: _Graefe und Saemisch_, vol. v. p. 531.]

[Footnote 29: _Gaz. méd. de Paris_, 1879, p. 217.]

Retinal hemorrhage is of frequent occurrence. It is often associated with inflammation in cachectic conditions of the system, as in the various forms of symptomatic retinitis, but is also found where there is not any demonstrable constitutional disease. Here, as in the other tissues of the body, apoplexies are favored by disease of the coats of the vessels, by alteration in the state of the blood, and by increased intravascular pressure. Anatomical examination has shown in the most common form of disease in the retinal vessels fatty degeneration of their walls, with calcareous deposits in them, and a condition (denominated sclerosis) in which the coats become thickened, homogeneous, and of a higher index of refraction. In this hardened tissue there is a condition similar to amyloid degeneration, but no reaction is to be obtained from iodine (Leber). No ruptures can be seen with the ophthalmoscope, but the vessels appear to pass on in contact with the hemorrhage without change of course or calibre. These circumstances have led Leber[30] to suppose that most retinal hemorrhages are due to diapedesis, and not to rhexis. When the blood escapes into the fibre-layer of the retina, it frequently diffuses itself along the course of the fibres and between them, and gives rise to linear and striated hemorrhages, while in the deeper layers its progress is barred by the connective-tissue elements--notably by the radiating fibres of Müller--and forms irregular masses which appear as more or less rounded clumps when looked at by the ophthalmoscope. Such extravasations of blood are frequently absorbed, or, again, they may leave black spots of pigment as the only marks of their presence. At other times they produce yellowish-white masses which disappear slowly, and often leave connective-tissue cicatrices behind them, dragging upon and displacing the retinal elements. When the hemorrhage is considerable, it may cause primary distortion of the images and impairment of vision by pressure on the rods and cones. At times it breaks through the limitans interna into the vitreous, giving rise to floating opacities, more rarely spreading itself out in a layer between the vitreous and the retina. The writer well remembers such an instance in the case of an apparently healthy woman about forty years of age, who, while sitting quietly in church, noticed that objects looked red and that a dense cloud came before the eye. Examination with the ophthalmoscope showed a large hemorrhage which covered the entire region of the macula and extended far beyond it, overlapping the temporal edge of the disc. This hemorrhage was slowly absorbed, and four years later the patient had a vision of 20/xx, and no trace of hemorrhage was visible in the entire eyeground. Liebreich[31] gives a good illustration of a similar case in a woman of forty-five years of age who, after suppression of the menses, had a similar state of affairs. Leber[32] has seen several such cases, in one of which the hemorrhage was changed into a brilliant white mass. This was entirely absorbed, leaving only a small pigmented stripe at its lower border as the sole trace of the previous large extravasation of blood. Occasionally retinal hemorrhage {743} ushers in glaucoma. Retinal apoplexies, like extravasations of blood in the conjunctiva of the eyeball, often come without apparent cause. In many cases they are finger-posts pointing to grave disease of the vessels in other parts of the body. The writer recalls a patient of seventy years of age who believed himself in perfect health until alarmed by a retinal hemorrhage, which a few months later was followed by a cerebral apoplexy which caused his death.

[Footnote 30: _Graefe und Saemisch_, vol. v. p. 554.]

[Footnote 31: _Atlas_, Table viii. Fig. 2 (1863 ed.).]

[Footnote 32: _Graefe und Saemisch_, v. p. 553.]

Aneurism of the central retinal artery is of excessively rare occurrence. Sous of Bordeaux quotes[33] the elder Graefe and Scultetus as having anatomically demonstrated the existence of the lesion, and Mackenzie refers[34] to a pathological specimen in the collection of Schmidler of Friburg where there was an aneurism of the central artery of each retina. Sous was the first who recognized it with the ophthalmoscope, and describes it as a red egg-shaped, pulsating dilatation of one of the main branches near the disc. Vision was so far destroyed that the patient was unable to recognize the largest letters. Martin describes[35] a similar case, while Magnus records what he supposed to be an arterio-venous aneurism following severe contusion of the eyeball, and Mannhardt a case of rupture of the choroid with a gray pulsating mass in the disc, which was also supposed to be aneurismal in nature. Schirmer has recorded[36] a case of widely-spread congenital telangiectasis of the face with a similar condition of the retinal veins of one eye. Liebreich[37] has pictured curious bead-like dilatations of the veins in a glaucomatous eye. Jacobi[38] gives three woodcuts of varix-like tortuosities of the retinal veins. Offsets extending from the retinal vessels forward into the vitreous have been observed during life and described by Coccius,[39] Becker,[40] Jaeger,[41] Samelsohn,[42] Jacobi,[43] and Norris.[44] They probably occur to some extent in many severe inflammations of the eye, and have been not unfrequently found and described in anatomical examinations of that organ; but their development is usually attended with so much cloudiness of the media as to prevent accurate ophthalmoscopic examination.

[Footnote 33: _Annales d'Oculistique_, 1865, pp. 241-243.]

[Footnote 34: _Practical Treatise on the Diseases of the Eye_, London, 1854, 4th ed., p. 1042.]

[Footnote 35: _Atlas d'Ophthalmoscopie_.]

[Footnote 36: _A. f. O._, vii., 1, pp. 119-121.]

[Footnote 37: _Atlas_ Plate xi. Fig. 1.]

[Footnote 38: _Klin. Monatsblätter_, 1874, pp. 253-260.]

[Footnote 39: _Glaucom._, 1859, p. 47.]

[Footnote 40: _Bericht der Wiener Auqenklinik_, 1866, pp. 65-74.]

[Footnote 41: _Ophth. Hand-Atlas_, Table xv. p. 72.]

[Footnote 42: _Klin. Monatsblätter_, 1873, pp. 216-218.]

[Footnote 43: _Klin. Monatsblätter_, 1874, pp. 252-260.]

[Footnote 44: _Trans. Amer. Oph. Soc._, 1879, p. 548.]

When carefully examining eyes with the ophthalmoscope, it is not a very unusual circumstance to see a small grayish tag arising from the lymph-sheath of the central retinal vessels and extending a short distance forward into the vitreous. These tags usually present slow, sinuous movements, following motions of the eyeball. It is, however, rare to have such obliterated vessels extend through the vitreous and show their previous distribution in the posterior capsule of the lens, as in the instances reported by Zehender,[45] Liebreich,[46] and Becker;[47] in Zehender's case the artery was patulous and blood-bearing. Little[48] has also depicted a case where the hyaloid artery was filled with blood. The central canal of the vitreous, which is occupied in the foetal eye by the artery in question, is readily demonstrated in pigs' eyes by allowing colored fluid to {744} flow into it from its central end. According to H. Müller,[49] atrophied remnants of the artery are always present in the eyes of oxen. Manz[50] gives an anatomical description and plate of a continuance of the lymph-sheath of the central artery through the vitreous forward to the capsule of the lens, the remnants of the artery being found only in its proximal portion: observation had been impossible during life on account of corneal opacities. The same writer describes a convolution of vessels as penetrating the posterior part of the vitreous from the retina in the eyes of some Australian reptiles (Trachyeaurus and Lygosoma), and regards it as a similar formation to the pecten of the bird's eye. According to Ammon, some forms of congenital cataract are connected with the too early obliteration of the hyaloid artery, which is so important in furnishing nutriment to the growing lens.

[Footnote 45: _Klin. Monatsblät. f. Augenheilkunde_, 1863, pp. 260-349.]

[Footnote 46: _Ibid._, p. 350.]

[Footnote 47: _Annales d'Oculistique_, 1865, p. 350.]

[Footnote 48: _Trans. Amer. Ophth. Soc._, 1881, pp. 211-213.]

[Footnote 49: _Gessamm. Schriften_, p. 365.]

[Footnote 50: _Graefe und Saemisch_, vol. ii. pp. 97-99.]

Von Graefe remarks, however, that this very unusual yet incomplete development of the retinal vessels is common in congenital amaurosis. He reports[51] an instance in a blind eye of a boy ten years of age, who also exhibited a convergent squint and nystagmus. Mooren[52] also gives a case of entire absence of the retinal blood-vessels in a child seven months old. Pathological conditions of the blood often give rise to visible changes in the eye-ground.

[Footnote 51: _Arch. f. Ophth._, vol. i., part 1, pp. 403, 404.]

[Footnote 52: _Ophthalmiatrische Beobachtungen_, 1867, p. 260.]

LEUCÆMIC RETINITIS.--Liebreich[53] was first to call attention to a retinitis which is due to leucæmia. In his _Atlas_ he gives an interesting picture of it, and states that he had then already had an opportunity of seeing six cases in the splenic variety of the disease. His plate shows a diffuse retinitis with scanty hemorrhages, with marked change in the color of the eye-ground and of the blood in the retinal veins and arteries. The blood-columns, especially in the veins, have acquired a slight rose tint, and have become less intense in color, whilst the hemorrhages appear slightly redder. He also describes white splotches like those of the retinitis of Bright's disease, differing from the latter only in the more peripheral situation. In one case these splotches were examined by Recklinghausen, and found to consist of patches of sclerotic degeneration of the nerve-fibres. Becker has pictured[54] two interesting cases, where, besides the diffuse retinitis with scanty hemorrhages, the main characteristics were the yellow color of the eye-ground and large white plaques with a red hemorrhagic border in the periphery. In the few cases, which the writer has had an opportunity of studying in the wards of his colleagues, the most striking change has been that of the color of the eye-ground and of the blood. In none of these were there either the white patches with red border or any extensive hemorrhage. We probably must not expect them in all cases and at all stages. In one of the patients, a negress, who was examined at the time of her admittance to the hospital, before any diagnosis had been made, the change in the color of the blood and fundus was so marked that he was able to call attention to it, as a probable case of leucæmia, and had the satisfaction of having the diagnosis confirmed by subsequent careful examination. Leber[55] states that the disease sometimes assumes the form of hemorrhagic {745} retinitis, such as is often seen in cases of disease of the heart and blood-vessels. Gowers[56] thinks that there is a much greater tendency to hemorrhage in leucocythæmia than in simple anæmia, and that the effused blood is of a pale chocolate color, while white or yellowish splotches, often edged by a halo of blood-extravasations, are commonly present. Immermann has seen the retinal affection occurring in mylogenic leucæmia, but in most of the instances above cited they accompanied the splenic form of the disease. In one of Becker's cases, in which Stricker examined the blood, the bulk of the white corpuscles exceeded that of the red ones, whilst some individual white corpuscles were so much increased in size that one white one might readily contain fifty red ones. Leber[57] describes a leucæmic tumor of the lids with exophthalmos, and marked leucæmic retinitis with hemorrhages, which affected both eyes of a patient who had enlargement of the liver and spleen. He quotes Chauvel as having recorded a somewhat similar case. In both of Leber's and Chauvel's patients there was also disease of the kidneys, as evidenced by the presence of albumen and casts in the urine. Another leucocythæmic tumor of the orbit has been described by Osterwald.[58]

[Footnote 53: _Atlas_, Plate x., 1863.]

[Footnote 54: _Archives of Ophthalmology_ (Knapp and Moos), vol. i., 1869, pp. 341-358, Tab. B. and C.]

[Footnote 55: _Graefe und Saemisch_, vol. v. p. 599.]

[Footnote 56: _Medical Ophthalmoscopy_, 1879, p. 192.]

[Footnote 57: _Arch. f. Ophth._, xxiv., 1, pp. 295-312.]

[Footnote 58: _Ibid._, xxvii., 3, pp. 202-224.]

PERNICIOUS ANÆMIA.--Biermer (1871) was the first to call attention to the retinal changes in this grave and rare disease. Since that date Horner[59] and Quincke[60] have given us the results of the careful study of a considerable number of cases. The former had seen 30 cases, and remarks that the color of the blood, the distension and tortuosity of the veins, and the numerous hemorrhages recall the cases of leucæmic retinitis: in all of his cases the discs were entirely white. The latter, in his latest paper on the subject, records 17 cases, and gives a careful chromo-lithographic picture of one of them. He describes the affection as an oedema of the retina with numerous hemorrhages, many of which have white or grayish centres, whilst others envelop the blood-vessels, and by irregularly distending their lymph-sheaths cause them to appear varicose. The oedematous condition of the retina produces an appearance as if a thin bluish-white film had been spread over the fundus oculi. The writer has had an opportunity of observing three cases of this rare affection: in each there was a diffuse retinitis, the veins were distended, the blood pallid, and the disc was dirty white with a faint greenish tint, whilst the eye-ground was decidedly yellow in hue. In one of them there were no other pathological appearances; in the second, only a few small hemorrhages into the lymph-sheath of some of the vessels near the macula; in the third, numerous irregularly round or ovoid hemorrhages with yellowish-white centres. It is evident, however, from the reports of Quincke, that any one case might in its various stages present all these phases. Horner considers[61] the colorless centre of the hemorrhages to be due to a commencing absorption of the blood, while Manz[62] holds that these yellowish-white spots are the dilated extremities of retinal capillaries.

[Footnote 59: _Klinische Monatsblätter für Augenheilkunde_, 1874, pp. 458, 459.]

[Footnote 60: _Deutsches Archiv f. klinische Medizin_, 1877, pp. 1-31 (with plate).]

[Footnote 61: Quoted by Quincke, _loc. cit._, p. 23.]

[Footnote 62: _Med. Centralblatt_, 1875, pp. 675-677.]

HEMORRHAGE.--Loss of blood may be the cause of impaired vision from transient anæmia of the retina or of the cerebral centres, but not {746} unfrequently, in some manner which we are not yet able satisfactorily to account for, it gives rise to permanent blindness. This failure of sight may come on immediately after the hemorrhage, but it is usually noticed at periods varying from two to fourteen days after the loss of blood. Fries[63] has written an admirable monograph on the subject, and gives 26 cases collected from various authors. According to his tables, 35½ per cent. of the cases are due to hemorrhage from the stomach or intestines; 25 per cent. to uterine hemorrhage; 25 per cent. to abstraction of blood; 7.3 per cent. to epistaxis; 52 per cent. to bleeding from wounds; and 1 per cent. each to hæmoptysis and urethral hemorrhage. Many of these cases are preopthalmoscopic, and consequently the exact pathological changes in the retina and optic nerve are necessarily matters of conjecture. Jaeger has given us two most interesting cases of blue degeneration of the optic nerve, with comparatively little change in the calibre of the main vessels of the disc and retina.[64] In both, the loss of blood occurred during labor; in the first, two births happened without accident; at the third and fourth labor there was severe hemorrhage, each followed by considerable and lasting impairment of vision, leaving ability to read Jaeg. No. iii. for a short time, and only by close approximation. In the other case there were four confinements, all accompanied by hemorrhage, each leaving the vision more and more impaired, until after the fourth labor there was no light-perception. At this time the ophthalmoscope showed only blue discoloration of the nerve, followed six years subsequently (after recurrent headaches from taking cold) by a more complete atrophy of the disc and retina, the former appearing of a dirty-green color and having acquired a saucer-like excavation, whilst the retinal vessels had undergone great diminution in their calibre. In most recorded cases no examination of the fundus has been made until long after failure of sight, and then there has generally been found some stage of atrophy; but when the ophthalmoscope has been used early in the case the eye-ground seems to have presented various appearances. Thus, Jaeger[65] says that soon after the hemorrhage the eye-ground presents a diminution in the calibre of the veins and arteries, with a light-blue discoloration of the optic disc, without any other demonstrable tissue-change. Graefe[66] saw slight diminution of the calibre of the retinal arteries and an increased pallor of the disc in a case where blood was vomited and passed by stool fourteen days after the occurrence of the blindness. On the other hand, Schweigger[67] (in two cases), Nagel,[68] Hirschberg,[69] Nägeli,[70] Horner,[71] and Landesberg[72] have all noted the occurrence of neuritis.

[Footnote 63: Sigmund Fries, "Diss. Inaug." in _Klin. Monatsblätter f. Augenheilkunde_, 1878.]

[Footnote 64: _Ergebnisse der Untersuchung mit dem Augenspiegel_, 1876, p. 87.]

[Footnote 65: _Loc. cit._, 1876, p. 87.]

[Footnote 66: _Arch. f. Ophth._, vol. vii., part 2, p. 146.]

[Footnote 67: _Handbuch der Augenheilkunde_, 1875 (3d ed.), p. 522.]

[Footnote 68: _Behandlung der Amaurose und Amblyopie mit Strychnine_, 1871, p. 51.]

[Footnote 69: _Bericht über die zehrite Vorsammlung der Ophth. Gessellschaft Heidelberg_, 1871, pp. 53-60.]

[Footnote 70: _Jahrbuch f. Ophthalmologie Literatur_, 1879, p. 253.]

[Footnote 71: _Klin. Monatsblätter f. Augenheilkunde_, 1877 (supplement), pp. 53-60.]

[Footnote 72: _Ibid._, 1875, pp. 98, 99.]

PROGNOSIS.--The prognosis is very unfavorable, and but few cases are recorded where there has been any improvement of sight.

PATHOLOGY.--The pathology of the affection is not well made out. Samelsohn,[73] who has reported a number of interesting cases, supposes {747} that where there is a great loss of blood the brain becomes anæmic and occupies less room in the skull, and serum exudes from the blood-vessels to fill the vacuum. As the patient regains strength and blood is re-formed, the increased intracranial pressure drives the fluid into the subvaginal space of the optic nerves and causes neuritis. In other cases a hemorrhage into the sheath of the nerve is assumed as the cause. For those very exceptional cases where, after slight loss of blood, there is sudden and complete blindness without marked changes in the optic nerves and retinæ (and prompt reaction of the pupils to light), we are obliged to assume some lesion of the optic centres. Samelsohn[74] attempts to explain it by comparison with the observations of Lussana, Brown-Séquard, Ebstein, and Schiff, who found that wounds of the brain involving the anterior prominences of the corpora quadrigemina and the thalamus opticus may cause hemorrhage into the mucous membrane of the stomach; consequently, he assumes a central lesion which produces simultaneously the blindness and the hemorrhage. All this is, however, but ingenious speculation, and the true pathology is still to be made out by careful autopsies.

[Footnote 73: _A. f. O._, xviii., 2, pp. 225-235.]

[Footnote 74: _A. f. O._, xxi., 1, pp. 150-178.]

The study of the eye-ground after death is difficult; for, apart from any hindrances due to the position of the body or to social customs, Nature soon interposes an efficient barrier to such examination by the rapidity with which cloudiness of the corneal epithelium and of the lens substance sets in. These optical hindrances advance sufficiently soon to make it impossible to focus accurately any object in the eye-ground. Poncet[75] asserts that this may be remedied to a certain extent by dropping water into the conjunctival sac, which will render the cloudy epithelium sufficiently transparent to permit examination from two to five hours after death. Most observers agree that in the human eye there is an immediate blanching of the disc and choroid, causing the latter to assume a pale-yellowish hue with a faint tint of rose, and that the arteries (by promptly emptying themselves) escape observation, while the veins retain for a time a considerable amount of their contents, the blood-columns often being discontinuous and broken. Later, these changes are followed by a gradually increasing haze of the retina, which gives the appearance of a bluish-white veil spread over the fundus. Schreiber[76] gives an instructive picture of the eye of a patient dying of phthisis, and another of the same eye five minutes after death. Gayat, who had the opportunity of studying this subject in the eyes of five individuals recently decapitated by the guillotine, describes the formation of a small red spot at the fovea centralis similar to that seen in embolism of the central artery.[77] On the other hand, Becker[78] thinks that the emptying of the vessels after death is rather the exception than the rule, basing his observations not on ophthalmoscopic examinations, but on the fact that in opening freshly enucleated glaucomatous eyes, and in the eyes of those who had been hung, he had observed all the vessels, arteries as well as veins, full of {748} blood. Weber[79] also, while admitting that the vessels both in men and animals usually empty themselves soon after death, describes as an exception a case in which there was no visible change in the blood-columns of the retinæ of the eyes of a patient with brain tumor, and a consequent optic neuritis, who was gradually dying of paralysis of the organs of respiration. This circumstance, in the opinion of the narrator, was very probably due to the obstruction to the escape of blood from the eye which would naturally be caused by the swollen and prominent optic nerve. Landolt and Nuel[80] assert that there is an increase in the refraction in rabbits' eyes after death, causing any existing hypermetropia to approach emmetropia. They call attention to the difficulty of such determinations, owing to rapidly-forming haze on the corneal epithelium and to more or less complete emptiness of the retinal vessels.

[Footnote 75: _Archives générales de Médecine_, Série 6, t. xv., 1870, pp. 408-424.]

[Footnote 76: Separat Abdruck aus dem _Deutschen Arch. f. klin. Med._, Bd. xxi. pp. 100, 101, Plates vii. and viii.]

[Footnote 77: _Annales d'Oculistique_, 1875, pp. 1-14.]

[Footnote 78: "Sitzungsbericht der Ophth. Gesellschaft," in _Klin. Monatsblätter f. Augenheilk._, 1871, p. 385.]

[Footnote 79: _Klin. Monats. f. Augenheilk._, pp. 383-385.]

[Footnote 80: _A. f. O._, xix. 3, pp. 303, 304.]

Diseases of the Organs of Respiration.

Diseases of the organs of respiration appear to have little direct influence upon the nutrition of the eye, except in so far as they cause venous stasis by obstruction of the circulation through the lungs. Jaeger was the first to call attention to this fact in cases of pneumonia and pleurisy. The stasis manifests itself by an increase in the calibre of the veins, with a broadening of the light-reflex from them and a marked change in the color of the blood, causing the venous columns to become dark bluish-red. The writer has often seen this condition well marked in cases where there was not sufficient interference with the oxidation of the blood to cause an appreciable cyanosis of the skin. A higher degree of impeded circulation in the lung doubtless gives rise to the retinal hemorrhages, which, according to Foerster, are not infrequent in emphysema. Schreiber[81] mentions that in the hectic fever of phthisis the dilatation of the retinal vessels causes a congested appearance of the eye-ground, in marked contrast with the anæmic pallor of the skin of the patients. In 1871, Horner[82] published 31 cases of herpes corneæ occurring either during the course of severe catarrhal affections of the respiratory organs or immediately following such attacks. The eruption, which first appeared upon the lips, and then upon the eyeball, usually took place after the culmination of the febrile symptoms. The progress of the affection is slow, the ulcers left by the bursting of the vesicles healing in a period varying from two to six weeks. The herpes was monolateral, except in one case of double pneumonia in a drunkard, where the eruption occupied the entire central area of both corneæ. In preophthalmoscopic times Sichel called attention to blindness after pneumonia and bronchial catarrh, which he thought was due to cerebral congestions occurring in the height of these diseases.[83] He considered these congestions harmless so long as the patients remained quiet under antiphlogistic treatment, but deemed them noxious in their influence upon the eye as soon as freedom was allowed. Seidel[84] relates {749} cases of amblyopia with contracted pupils and eyeballs which were painful on the slightest pressure. He says that coincident with croupous pneumonia on the fifth day there was color-blindness, followed two days later by a disappearance of the amblyopia, with a return of the pupils to their normal size.

[Footnote 81: _Veränderungen des Augenhinter-qrundes bei Internen Erkrankungen_, 1878, p. 87.]

[Footnote 82: "Bericht der Ophth. Gesellschaft," in _Klin. Monatsblätt._, 1871, pp. 326-328.]

[Footnote 83: Zehender, _Handbuch der Augenheilkunde_, vol. ii. pp. 188, 189.]

[Footnote 84: "Sehstörungen bei der Pneumonie," _Deutsches Klinik_, 1862, No. 27.]

Affections of the Eye caused by Diseases of the Digestive Organs.

TEETH.--Ophthalmic literature furnishes many instances of diseases of the eye said to be caused by affections of the teeth. These vary in severity from slight conjunctivitis and photophobia, or temporary failure of accommodation, to absolute amaurosis. It is natural to suppose that affections of the dental division of the trigeminus might readily give rise to reflex disorders in parts supplied by branches of the same main trunk. Although the writer has been on the lookout for such affections, he has seen very few cases of eye disease which could be logically attributed to disease of the teeth, and has known at least two sound teeth which were uselessly sacrificed to mistaken theories of pathology. Perhaps the most noteworthy effort to assign dental neuralgia as a cause of amaurosis is the well-known paper of Jonathan Hutchinson in the _Royal London Ophthalmic Hospital Reports_ for 1865. An attentive study of the interesting cases there recorded shows that but few of them can be considered as affording convincing evidence of the point which he desires to prove, and few are probably more keenly aware of this fact than the distinguished surgeon himself when he writes: "I am quite alive to some of the sources of mistake which attend the attempt to prove the occurrence of paralysis from reflex irritation consequent on a peripheral cause: chief among them we have, of course, the possibility that the neuralgia itself may have been due to central disease, and that the extension of the latter may have complicated other nerves."[85] That amaurosis does, however, sometimes follow dental irritation is proved by Hutchinson's first case in the above-quoted paper, where neuralgia of the eyeball with great intolerance of light was cured by extraction of a carious molar tooth. Perhaps the most striking case on record is that of Galezowski,[86] where a small fragment of wood which had entered the cavity of a carious tooth (probably from picking the teeth with a wooden toothpick), lodged at the extremity of one of the fangs, is said to have caused absolute blindness of the eye, with dilatation of the pupil on the same side. After a blindness of eleven months the tooth with the foreign body was extracted, causing the evacuation of a few drops of thin pus from the antrum; after which the patient improved and vision gradually returned, so that on the ninth day after the operation he could see with the affected eye as well as with the other. Schmidt, after an examination of 96 patients with carious teeth, formulates the following conclusions: "1. That we may have a more or less considerable limitation of the accommodation {750} in consequence of pathological irritation of the dental branches of the trigeminus. 2. This may occur on both sides. Where the affection is one-sided, it is always on the side of the affected tooth. 3. It is usually an affection of the young, very seldom or never occurring in old age. 4. That the diminution of the power of accommodation is due to increased intraocular pressure caused by reflected irritation of the vaso-motor nerves of the eye." These conclusions are interesting, but cannot be considered absolutely correct, in consequence of the fact that there are no recorded tests for astigmatism or insufficiency, and that accurate examination of the state of refraction was impossible through want of a mydriatic which may in measure have accounted for the existent diminution of accommodation. More extended and minute investigations of the subject are desirable.

[Footnote 85: "A Group of Cases illustrating the Occasional Connection between Neuralgia of the Dental Nerves and Amaurosis," by Jonathan Hutchinson, F.R.C.S., _R. L. O. H. Rep._, vol. iv. pp. 381-388.]

[Footnote 86: _Archives générales de Médecine_, t. xxiii. pp. 261-264.]

STOMACH, INTESTINES, AND LIVER.--Amblyopia and amaurosis with severe gastric symptoms are not very uncommon, but, although such cases are made much worse by the ingestion of indigestible substances, constipation, etc., it has nevertheless always appeared to the writer that the primary lesion lay in the nervous system. Galezowski, however, lays stress on this subject, and discriminates between a true and false locomotor ataxia; the latter being, according to this author, symptomatic of stomachic and intestinal lesions. Many of the older writers relate cases of amaurosis from worms in the intestines. Thus Laurence[87] gives an instance of sluggishness and partial dilatation of the pupils with dim vision which promptly disappeared after the evacuation of seat-worms consequent on an enema of turpentine. Hays calls attention[88] to a case recorded by Welsh of Massachusetts where complete amaurosis in a child instantly ceased on a worm being puked up. Many similar instances might be adduced which in modern books are either passed over in silence or looked at with a shrug of incredulity. Although the writer has had no personal experience with such cases, he can readily understand that in children the irritation of worms might easily give rise to enough reflex disorder of the spinal cord and brain as to cause impairment of the accommodation and partial dilatation of the pupils. (The effects of hæmatemesis and hemorrhage from the bowels have been already discussed.)

[Footnote 87: Amer. ed. by Hays, 1847, p. 554.]

[Footnote 88: _Ibid._, 1847, p. 555.]

That jaundice shows readily in the conjunctiva is well known to all practitioners, and yellow vision is described as an occasional symptom of severe icterus, Jaeger calls attention to a light-yellow color of the eye-ground and retinal vessels under these circumstances. Junge,[89] Stricker,[90] and Buchwald[91] have all recorded cases of retinal hemorrhage in cases of grave disease of the liver. Litten[92] says that for ten years he has examined every case of liver disease under his charge with the ophthalmoscope, and found retinal hemorrhages only in fifteen cases. These occur only when icterus is present, but are not due, as Traube assumes, to the action of the biliary acids on the blood-corpuscles. If they were so, we should have blood-stained lymphatic sheaths instead of corpuscular diapedesis and massing of the exuded blood. Of these 15 cases, 4 were cases of congestive jaundice, 4 of carcinoma, 1 each of acute fatty {751} degeneration and phosphorus-poisoning, 1 of abscess, 2 of cirrhosis, 1 of hydrops cystides filleæ. The hemorrhages were usually in the nuclear layers, and seldom presented white centres, as in leucocythæmia. In the case of phosphorus-poisoning there were large white plaques with marginal inflammation. Litten considers that the pigment-spots reported in the retina in cases of liver disease (his own cases and Landolt's) are due not to cirrhosis hepatis, but to a congenital or acquired disposition to connective-tissue hyperplasia [syphilis?]. Foerster[93] has called attention to a group of cases which he ascribes to hyperæmia of the liver and plethora abdominalis, where we find discomfort in the use of the eyes from the accompanying retinal hyperæmia and diminution of the range of accommodation, and where the ophthalmoscope frequently shows premature senile degeneration of the lens, manifested by striæ occurring in the extreme periphery. Every careful observer will doubtless agree to the accuracy of this description, and to the advantages of proper hygiene, exercise, and the alterative mineral waters (Karlsbad, Saratoga) in such cases.

[Footnote 89: _Heinrich Müller's Gesammelte Schriften_, pp. 331-335.]

[Footnote 90: _Berliner klin. Wochenschrift_.]

[Footnote 91: Foerster, _loc. cit._]

[Footnote 92: _Deutsche med. Wochenschrift_, 25 März, 1882, pp. 179-182.]

[Footnote 93: _G. u. S._, vol. vii. p. 74.]

SPLEEN.--The effect of disease of the spleen in causing disease of the eye has already been alluded to in the discussion of leucæmic retinitis.

Xanthopsia appears to be a very infrequent complication of liver disease. Moxon,[94] who records seven cases of fatal obstructive jaundice, has never seen it. He remarks that in these cases the vitreous and lens remained perfectly clear, while the blood-serum was saffron-yellow and the sclerotic deeply stained (yellow or olive-green). Rose[95] gives the only case with which the writer is familiar, in which it was carefully studied and demonstrated with the spectroscope. Here the violet end of the spectrum was shortened as in poisoning by santonin, and the blue blindness was so marked that a few days before his admission to the hospital the patient had excited the astonishment of his fellow-workmen by mistaking the color of a door which had been freshly painted blue. The autopsy showed here also that the vitreous and aqueous were colorless, but the cornea was clearly yellow. This Rose thinks insufficient to have caused the xanthopsia, and therefore attributes it to the effect of the jaundice in the nerve-centres.

[Footnote 94: "Clinical Remarks on Xanthopsia and the Distribution of Bile-Pigment in Jaundice," _Lancet_, Jan. 25, 1873. p. 130.]

[Footnote 95: "Die Gesichtsläuschungen im Icterus," _Virchow's Archiv_, vol. xxx. pp. 442-447.]

HEMERALOPIA.--The curious affection hemeralopia, which we well know to be a constant accompaniment of some forms of congenital nerve-atrophy (retinitis pigmentosa), and also to affect, at times, considerable numbers of persons exposed to the glare, overwork, and exposure of an active campaign, is probably always due to some form of malnutrition or disorder of the digestive apparatus, and in many cases it is associated with jaundice and disease of the liver. That glare of light is not necessary to its production is shown by its development in convalescent hospitals. Reymond of Turin reports it as developing in an individual affected by pellagra on whom he had operated for cataract, and who during the four weeks subsequent had never been out of his room. Cornillon[96] reports 5 cases of hemeralopia during jaundice, and of these 4 came under his observation {752} in a single winter in the hospital in Vichy. It never appeared early in the congestion of the liver, but always after jaundice had existed for some time, and disappeared without special treatment--often to recur when the disease of the liver became more marked. Parinaud[97] has reported 4 such cases in all, with jaundice, the conjunctiva being yellow, but the media not tinged. There were no ophthalmoscopic changes. One of these cases was malarial hepatitis, the other three probably cirrhosis. A curious change in the ocular conjunctiva has been noted in many of these cases of hemeralopia, and attention was first called to it by Bitot.[98] He observed 29 cases at the Hospice des Enfants Assistés at Bordeaux. The bulbar conjunctiva in the palpebral fissure, usually at the outside of the cornea, becomes dry and anæsthetic (epithelial xerosis), and a number of minute points form in it, and the little patch becomes like mother-of-pearl, iridescent and silvery. They become paler before they disappear, and come and go with the advent and cessation of the hemeralopia. Pressing on the conjunctiva over the spot by rubbing the lids over it often causes little fragments of the dry patch to crumble off. The adjoining conjunctiva is dry and less pliant, more like parchment. The extensive occurrence of hemeralopia during the severe Easter fasts of the Greek Church has been noted by Blessig. There is frequently diarrhoea associated with this condition. Teuscher also speaks of conjunctival xerosis and hypopyon keratitis in the young slave-children in the Brazilian coffee-plantations, associated with gastric catarrh and diarrhoea.

[Footnote 96: _Le Progrès médicale_, No. 9, Fèvrier 26, 1881, pp. 157-159.]

[Footnote 97: _Archives générales de Médecine_, April, 1881, pp. 403-414.]

[Footnote 98: _Gaz. méd. de Paris_, No. 27, 4 Juillet, 1863.]

Diseases of the Kidneys and Skin.