Volume 4 — MEDICAL OPHTHALMOLOGY. (continued 2)

¹⁴⁹ "An Essay on a Peculiar Inflammatory Disease of the Eye, and its Mode of Treatment," Trans. Med.-Chir. Soc. of London (read Dec. 11, 1827).

¹⁵⁰ "Post-febrile Ophthalmitis," Monthly Journ. Med. Sci., 1845, pp. 723-729.

¹⁵¹ Congrès internationale d'Ophthalmologie, Paris, 1868, pp. 114-117.

¹⁵² "Entzündung der Vorderen Abschnitten der Choroidea als Nachkrankheit der Febris Recurrens," A. f. O., Bd. xvi., 1, S. 352-363.

¹⁵³ Klinische Monatsblätter f. Augenheilkunde, 1878, pp. 487-497.

¹⁵⁴ A. f. O., xv. 2, pp. 108-143.

¹⁵⁵ Klin. Darstellung der Krankheiten des Auges, 1881, pp. 289-291.

¹⁵⁶ Vol. I. p. 399.

Exanthematous typhus fever is occasionally followed by the same train of symptoms as pointed out in discussing Larionow's statistics, who gives vitreous opacities as the most frequent forms of the eye affection. Out of a total of 57 fever patients with typhus exanthematicus, he found 1 case each of iritis, keratitis, and neuro-retinitis, 2 cases of contraction of the field of vision, 5 of subconjunctival ecchymosis, and 2 of conjunctival catarrh.

Abdominal Typhoid Fever.—Severe eye complications are less frequent in this disease than in either of the foregoing affections. During convalescence from this, as from all other exhausting diseases, there is usually feebleness of the accommodation, and occasionally the development of vitreous opacities, with or without the formation of cataract. The most common eye affections show as an optic neuritis or paralysis of some of the muscles supplied by the third pair of nerves, and are due to a complicating meningitis.

Yellow Fever.—In this disease most writers have called attention to the accompanying ocular symptoms—flushing and injection of the conjunctiva with increase of lachrymation, followed later by a change of the color of this membrane to a yellow hue, which precedes a similar change of the color of the skin of the face and other parts of the body. The first epidemic of the disease in Philadelphia occurred in 1762. Redman,¹⁵⁷ in describing it, says: "The patients were generally seized with a sudden and severe pain in the head and eyeballs, which were, I think, often, though not always, a little inflamed or had a reddish cast." Another severe epidemic of the disease visited the city in 1793, of which Rush¹⁵⁸ has given us a valuable account. Among the premonitory signs he enumerated "a dull-watery-brilliant, yellow or red eye, dim and imperfect vision;" and he defines his meaning by saying that the dull eye was found among the severe cases, and the brilliant one where the poison was less intense. Later in the disease there was "preternatural dilatation of the pupil," and in one case "a squinting which marks a high degree of morbid affection of the brain." There were hemorrhages, chiefly from the nose and uterus, and in but one case "a dropping of blood from the inner canthus." A dimness of sight was very common in the beginning of the disease, and many were affected with temporary blindness. In some there was a loss of sight in consequence of gutta serena or a total destruction of the substance of the eye. The eyes seldom escaped the yellow tinge. There were a number of cases of uncommon malignity without this symptom, but sometimes the yellow color appeared on the neck and breast before it invaded the eyes. Wood,¹⁵⁹ who witnessed a later epidemic (also in Philadelphia), says that even in the earliest period of the disease the white of the eye is often reddened and turbid, and in bad cases appears sometimes as if bloodshot. As before stated, in the course of the disease this redness yields to a yellow or orange color. Féraud,¹⁶⁰ in speaking of the symptoms of the second stage, lays great stress on the brilliancy of the eyes, their lachrymose condition, the fulness and nicety of the conjunctival injection, the dilatation of the pupil, and the presence of photophobia; adding that this congestion is diminished during the remission of the fever if the attack is not severe, but that if the conjunctiva darkens and assumes an icteric aspect, which becomes more and more intense, the case is undoubtedly severe. He adds that ocular hemorrhages occur in some grave cases during the second stage, producing subconjunctival suffusion and a flow of blood from the neighborhood of the commissure of the lids. Such "hemorrhages have frequently caused conjunctivitis, keratitis, and even such an accident as phlegmon." Fernandez¹⁶¹ gives three cases of delirium, suppression of urine, and loss of vision. One of these cases was examined with the ophthalmoscope, but no changes were found in the eye-ground. One case recovered, having entirely regained his eyesight; the other two died.

¹⁵⁷ "An Account of the Yellow Fever of 1762," by John Redman, M.D. (read before the College of Physicians of Philadelphia, Sept. 7, 1793).

¹⁵⁸ An Account of the Bilious Remitting Yellow Fever as it appeared in the City of Philadelphia in the Year 1793, by Benjamin Rush, M.D., Philada., 1794.

¹⁵⁹ G. B. Wood, Treatise on the Practice of Medicine, vol. i. p. 321, 1858.

¹⁶⁰ Béranger-Féraud, "La Fièvre jaune à la Martinique," quoted by Juan Santos Fernandez, Archiv. of Ophthalmology, x., 4, 1881, pp. 440-445.

¹⁶¹ Loc. cit.

Intermittent Fever.—Intermittent ophthalmia is but rarely encountered in countries where only a mild form of intermittent fever is present; in fact, it was so rare in Scotland that Mackenzie in the earlier editions of his work denied its existence, but a larger experience enabled him (in 1854) to give three cases. In 1828 and 1829 it was so infrequent in Marburg that Hueter devoted two papers to its study—one of a case of the quotidian type, and the second of the septan form of the ophthalmia. In countries where the malarial poison exists in more intense form, we have quite a different state of affairs; thus Levrier¹⁶² describes it as of common occurrence in the district of Landes in France, and says that its most frequent form is a periorbital and ocular neuralgia, accompanied by intense congestion of the conjunctiva, with increased flow of tears and a greater or less degree of photophobia, occurring in those who have had frequent attacks of intermittent fever. Wehle, whose observations were made in Hungary, describes an erysipelatous swelling of the lids with small hemorrhages in the palpebral conjunctiva, redness and swelling of the bulbar conjunctiva with intense photophobia, and occasional clouding of the cornea. Arlt¹⁶³ relates eight cases of chronic interstitial keratitis, all occurring in emaciated patients who had had severe malarial fevers, in Slavonia and Hungary. Only three of these stayed for prolonged treatment, which consisted of the use of Karlsbad water, followed by the preparations of quinine and iron; all of these recovered, and their eyes cleared, leaving only the faintest trace of corneal opacity. Galezowski¹⁶⁴ gives a case of malarial keratitis, and Griesinger,¹⁶⁵ after describing the usual symptoms of the disease (similar to that noted by Levrier), speaks of cases of long duration accompanied by clouding of the cornea and atrophy of the eyeball. He has also encountered an intermittent form of iritis. Mackenzie describes a case of it (one of those above referred to) which eventually ended in amaurosis. While affections of the retina and optic nerve from malarial fever would seem to be rare in temperate latitudes, Guéneau de Mussy,¹⁶⁶ however, relates a case of optic perineuritis with retinal apoplexies. Macnamara, observing in India, says the serous retinitis is not uncommon in malarial fever, and that in severe cases of this disease amaurosis is not infrequent. Galezowski and Kohn each reports a case of atrophy of the optic nerves after a severe attack of intermittent fever, but it is not quite evident from the clinical history whether the blindness might not be attributed to the large doses of sulphate of quinia which had been administered.

¹⁶² J. F. Levrier, Thèse de Paris, 1879, "Des Accidents oculaires dans les Fièvres intermittentes," p. 56.

¹⁶³ Klinische Darstellung der Krankheiten des Auges, 1881, pp. 121, 122.

¹⁶⁴ Quoted by Levrier, loc. cit., p. 39.

¹⁶⁵ Traité des Maladies infectueuses.

¹⁶⁶ Journal d'Ophthalmologie, p. 1, 1872.

ERYSIPELAS.—Erysipelas of the face and head frequently causes swelling of the lids and chemosis of the bulbar conjunctiva, and occasionally gives rise to an orbital cellulitis which by its effects on the optic nerve impairs or destroys sight. Beer¹⁶⁷ speaks of an idiopathic erysipelatous conjunctivitis which may not be accompanied by swelling of the lids. The conjunctiva is of a pale, somewhat livid-red hue, in which no distinct vessels are visible, there being numerous bright-red ecchymotic spots in the subconjunctival tissue. Vesicular prominences form around the cornea, and become so large as to project between the lids. The folds and interstices of this swollen membrane are covered with thin mucus, which often adheres so closely to the cornea as to make it look hazy, but which can be washed off, leaving the corneal surface as brilliant as in its normal state. The conjunctival swelling finally subsides, and the membrane again adheres to the sclerotic. Even after there is apparent absorption of the ecchymoses, the places where there were extravasations of blood are slow in adhering to the sclera, and often roll into folds with every motion of the eye. Mackenzie describes the conjunctiva as of a pale yellowish-red color: it rises in soft vesicles around the cornea, and these change in shape with every motion of the eye. There is slight photophobia and a pricking sensation, with a large quantity of white mucus, which is secreted by the conjunctiva and the Meibomian glands. Where a low grade of orbital cellulitis ensues we may have only slight prominence of the eye and some interference with its motions, in which a complete subsidence of the symptoms without any failure of eyesight may take place. We may encounter more severe cases, where the intense swelling and inflammation of the orbital tissues so impair the functions of the optic nerve and retina as to permanently destroy the eyesight, and at times destroy life by the extension of the inflammation to the meninges. The cellulitis may attack one or both orbits. Poland¹⁶⁸ has recorded a case of protrusion of both eyes where, after death, the ophthalmic veins and the cavernous sinuses were found full of pus; while Cohn¹⁶⁹ has reported another fatal case of double erysipelatous cellulitis, in which post-mortem showed purulent phlebitis of the orbit and brain with embolic infarcta in the lungs. All cases of double exophthalmos from erysipelas do not end as fatally: Jaeger has recorded two cases of recovery, where in each one eye remained permanently blind, while the other was restored to sight. He has given us accurate and beautiful ophthalmoscopic plates of the lesions in the blind eyes, these plates showing atrophy of the optic nerve, with great thickening of walls of the retinal vessels, which in some places totally hide their contents, while in others the blood-columns are still faintly visible. In one case the inflammation of the lids had been so severe that they had grown together in the middle of the palpebral fissure and had also formed an attachment to the eyeball. These cicatricial bands were divided with the knife, only to find a blind eye with dilated pupil. In one of Jaeger's cases there were pigment-masses in the choroid. Coggin¹⁷⁰ describes a case of double exophthalmos with blindness where the corneæ were so denuded of epithelium that no ophthalmoscopic examination was practicable. Three weeks later the media were clear and the discs atrophic, the vessels being visible as empty white cords. These effects be attributed to thrombosis. Knapp¹⁷¹ has recorded a most interesting case of erysipelas where there was severe fever with high temperature (104.8°) and marked protrusion of both eyes, in which he had an opportunity of observing the eye-grounds in all stages of the disease. On the ninth day ophthalmoscopic examination showed that the yellow spot and disc were both invisible, and that their localities could only be determined by the radiation of the tortuous veins, which were gorged with blood so dark as almost to be black, the retinal arteries being invisible. The posterior portion of the eye-ground was milky white, while the anterior was reddish white: numerous hemorrhages were scattered through the retina, more or less linear in shape in the posterior part and irregularly rounded in the anterior portion. Two days later the orbital swelling was less, and the arteries were visible, though much reduced in size, and the eye-ground was beginning to resume its normal color. About a month after seizure the patient was convalescent and he could go out. At this time the disc was atrophic, and there was a whitish cloud in the region of the yellow spot, with numerous hemorrhages: both arteries and veins presented isolated areas of perivasculitis, accompanied by snow-white patches of greater or less extent, which were of the same calibre as the adjacent dark-red blood-columns in each of them. Two months later, the disc was still atrophic, the hemorrhages had been absorbed, the blood-vessels were mostly visible as white cords—one of them presenting the usual appearance, while two showed blood-contents for a short distance surrounded by dense white walls. The white intercalary portions of the vessels seen in the examination two months after the onset of the disease are considered by Knapp to be thrombi. Arlt, Jr., reports a case of gangrenous erysipelas of the lids with loss of the eye, and mentions that his father had seen several similar cases.

¹⁶⁷ J. J. Beer, Lehre von den Augenkrankheiten, vol. i. 398, 399. (He also gives a colored plate of the appearance, Taf. 1, p. 3.)

¹⁶⁸ R. L. O. H. Rep., vol. i., pp. 26-31, 1857.

¹⁶⁹ Klinik der Embolischen Gefärskrankheiten, 1860, p. 196.

¹⁷⁰ D. Coggin, Trans. Amer. Oph. Soc., vol. ii. pp. 570-572 (session 1878).

¹⁷¹ Trans. Amer. Oph. Soc., 1883, and Arch. of Ophthalmology, 1884 (with plates and lithographs).

DISEASES OF THE NERVOUS SYSTEM.¹⁷²

¹⁷² In the foregoing sections the relationship between definite diseases and their concomitant eye symptoms have been dealt with; whereas in this division of the subject this has been found so impracticable that it had to be discarded in favor of an anatomical basis upon which to place the various affections. This change has necessitated the disuse of the representative headings of names of disease, and the substitution of absolute physical conditions with their hypothetical causes.

Symptoms of impaired function in the eyes and their appendages have always been regarded as valuable indices of disease of the nervous system; and when it is considered that six of the twelve pairs of cranial nerves send branches to these organs, and that the second, third, fourth, and sixth pairs are distributed exclusively to them, and that they are further supplied with twigs from the cervical and cerebral sympathetic nerves, it can be readily appreciated that a vast variety of nerve lesions, interfering with some of these connections either at their origins or in their course, may produce either impaired vision in the eye or loss of power in some of its appendages. Moreover, the retina and optic nerve originate as sprouts from the anterior cerebral vesicle, and retain respectively the structure of a ganglion and of a cerebral commissure. From these circumstances, as well as from the close connection of their blood and lymph circulations with those of the cerebrum, they frequently become delicate exponents of intracranial changes.

Affections of the Second Pair (Nervi Optici).

NEURITIS.—Five years after the discovery of the ophthalmoscope Graefe called attention to the fact that in many cases of intracranial disease the intraocular ends of the optic nerve presented marked changes. He had already discovered that when these changes were inflammatory in character they presented two main varieties—the one in which there was intense swelling of the intraocular end of the nerve (designated by him stasis papilla); and the other, in which there was a dull-red suffusion of the disc. In the first variety, which he attributed to increased intracranial pressure from tumor or other cause, the disc projected into the eye and formed a small tumor, often prominent to an extent equal to its own diameter, the oedematous and opaque nerve-fibre being permeated by tortuous, enlarged, and often newly-formed capillary vessels, which hide the arteries and allow only the projecting branches or lips of the tortuous and dilated retinal veins to be perceived as they slope down in the swollen papilla to regain their normal level in the retina; the other, which he thought was due to meningitis spreading along the nerve, was characterized by a slightly swollen disc of a dull-red color, with opacity of its nerve-fibre sufficient to completely hide its normal boundaries, associated with tortuous veins and arteries that were often diminished in size. Since that time volumes have been written on the subject, and it has given rise to most extended and searching discussion, causing researches to be instituted which have added much to the knowledge of the anatomy and pathology of the central connections, circulation, and lymph-supply of the optic nerves. To-day the first variety is usually designated as choked disc or papillitis, and the second as interstitial or descending neuritis. When typical cases are seen at the height of the disease, it is easy to make a distinction between the two varieties, but usually they shade off so imperceptibly, the one into the other, and the consecutive atrophies present so absolutely the same appearance, that no experienced observer would at all times claim an ability to distinguish between them. In the choked disc the intense swelling is limited to the intraocular end of the nerve, and therefore vision is little interfered with until the swelling becomes so great, or the contraction of the subsequent cicatrization so decided, that by pressure on the nerve-fibre they become atrophic and incapable of reporting the retinal image to the brain-centres, while in interstitial neuritis, owing to the primary interference with conduction, vision is impaired from the beginning. The choked disc usually develops slowly, requiring a period varying from a few days to two, three, or four weeks to attain its maximum, and it may exist unchanged for a long time before atrophy sets in. The writer once had an opportunity of observing a case in which the choking was produced by a cerebral gumma, and where for nearly a year the discs remained swollen and vision was still ⁶/8; and another of intense swelling, where the discs projected at least from one and a half dioptrics (one millimeter), in which for a period of three months vision was ⁶/6 and the field almost normal. Mauthner,¹⁷³ Blessig, and Schiess-Gemuseus¹⁷⁴ each record cases of marked choking of the discs lasting for some time, where the patients retained perfect central vision to the day of their death. Double choked discs are almost always a symptom of grave intracranial disease when all local causes in the eyes or orbits have been excluded. Even in the very exceptional cases where they form part of the symptoms of Bright's disease they are probably indicative of intracranial effusion. The lower grades of inflammation of the optic nerve are apt to be accompanied by marked proliferation of the connective tissue between the nerve-bundles. There are many cases of congestive atrophic change of the optic nerve where at first central vision is but little affected. In judging of the appearance of neuritis the observer should be sufficiently familiar with the changes in the eye-grounds of healthy individuals which occur from local causes not to allow himself to be led astray by the often very decided neuro-retinitis constantly encountered in hard-worked eyes with uncorrected astigmatism and slight degrees of ametropia; and not to mistake these changes, which are simply an expression of that local congestion which leads ultimately to softening and elongation of the eyeballs, for changes due to incipient cerebral disease, although each is accompanied by neuralgia. While, after careful study of the various forms of neuritis optici during the last few years, it is acknowledged that increased intracranial pressure is apt to cause choking of the disc, and that basilar meningitis frequently gives rise to interstitial neuritis, we are still far from having such a clear comprehension of the subject as to render the profession unanimous as regards its pathology; some observers claiming that choked disc is essentially a vaso-motor paralysis of the affected part, while others maintain that it is caused by infiltration of the disc and optic nerve with abnormal fluids which have been secreted within the cranium, and by increased intracranial pressure have been forced between the sheaths of the optic nerve and between it and its pial envelope. The ingenious explanation proposed by Graefe, that stasis papilla is produced by the damming up of the return blood in the cerebral sinuses, thus causing impeded circulation with increased blood-pressure in the ophthalmic vein and its branch (the central retinal vein), has generally been abandoned since the investigations of Sesemann and Merkel have demonstrated the free anastomosis between the facial and the orbital veins in whatever method the primary congestion may be brought about. The latter part of his explanation, in which he compared the rigid tissue of the lamina cribrosa to a multiplier, by its construction tending to augment any existing plethora in the head of the nerve, is still worthy of consideration. While the theory of vaso-motor paralysis is a most enticing one, it is, however, difficult to understand why paralysis of any of the fibres of the sympathetic should always be accompanied by such a limited local congestion without affecting the retinal tissue in their peripheral parts or without any branch leading to the iris, ciliary body, or choroid. Granting that there is some special filament of the carotid plexus distributed to this region of the nerve, it is hard to comprehend how it can be acted upon by tumors of almost any size or consistence situated in the most varied parts of the brain, and also why pressure on the various portions of the intracranial nerve, chiasm, and optic tracts (which so frequently cause hemianopia and partial atrophies) should not be associated with choking of the disc.

¹⁷³ Ophthalmoscopie, p. 293, 1868.

¹⁷⁴ Klinische Monatsblätter f. Augenheilkunde, 1870, p. 100.

THE LYMPH-SPACE THEORY—Since the anatomical researches of Schwalbe and of Retzius have given us a clear understanding of the lymphatic circulation in the eye, the effusions into the sheaths of the optic nerve that have been found in many cases of choked disc that have been examined post-mortem have been shown to be due to the effects of blocking up of the lymph-channels and of the effusion of cerebral fluids (lymph-pus and blood) in the intervaginal space of the nerve or between it and its pital sheath. In support of this, Manz in 1870 showed that injection of fluid into the cranial cavity of rabbits would produce a marked neuritis which was readily demonstrable by the ophthalmoscope; while Schmidt proved that the spaces of the lamina cribrosa of the optic nerves of the calf could be distended by fluid thus injected. In experiments on the human cadaver the writer has repeatedly seen that colored fluids could be readily driven between the sheaths of the optic nerve by injections from the subarachnoid and subdural spaces, and also that when high pressure was used and the injection made directly into the intravaginal space of the nerve, the fluid found its way from the subdural into the perichoroidal space. He once obtained traces of the colored fluid in the lamina cribrosa of the nerve. Since this mode of communication between the cavity of the cranium and the eye has been duly appreciated, a large number of autopsies have shown that choking of the disc has been accompanied by dilatation of the outer sheath of the nerve by lymph-pus or blood which has found its way down from the cranial cavity. It has also been demonstrated that proliferation of the intravaginal (arachnoid) tissue, and the formation of tumors (psammoma and tubercle) at the distal end of the nerve will produce choking of the disc by causing local accumulations of fluid. On the other hand, there are cases where this distension of the sheaths has been carefully looked for and not found; and those who hold the vaso-motor theory consider that it is in any case an accompanying accident, and not the cause, of the choking of the disc. The experiments of Rumpf and Kuhnt, however, add to its probability, by which the deleterious influence of lymph on the axis-cylinder of nerves adds to the probability of the above theory; moreover, even if it is granted that this accumulation of lymph or other fluid within the sheaths of the optic nerve is the cause of choking of the disc, it seems very unreasonable to the writer to expect to find it in all stages of the complaint. It is everywhere admitted that a cerebral tumor may exist for a long time without causing papillitis, and also that inflammation of the discs may exist for months or years, until they have become entirely atrophic, before the brain disease shall have caused death. Choking of the disc is essentially a temporary symptom. Although severe cerebral irritation may cause a great transient increase of cerebro-spinal fluids, which in their turn may produce the most intense inflammation of the intraocular end of the nerve, yet when the atrophied nerve comes to be examined months or years later they leave no traces sufficiently lasting to positively prove their previous existence. Whatever theory may be adopted as to the mode of production of optic neuritis, its clinical importance is admitted by all. Where it exists on both sides, and is accompanied by other cerebral symptoms, it usually points to increased intracranial pressure.

Since the earliest times, impaired vision and other ocular symptoms have been recognized as accompaniments of diseases of the brain. In more recent, but still preophthalmoscopic, times the statistics showing the percentage of blindness in brain tumor are most interesting: thus, Abercrombie noted failure of vision in 17 (38 ⁵/10 per cent.) out of 44 cases, while Ladame, in a study of 331 cases, estimated that there is disturbance of vision in about 50 per cent. This percentage represents the cases of atrophy consequent upon neuritis only. It must be remembered, however, that many die of the brain disease while the disc is still choked, and that this state of the eye-nerve may exist for a long time without any appreciable failure of vision, making it evident that should we look for choked disc with the ophthalmoscope while there are as yet no symptoms of failing sight, the above percentages would still be higher. In support of this we find that there is a rise of double optic neuritis to 93 per cent. in a series of 88 cases of brain tumor, 43 of which have been recorded by Annuske¹⁷⁵ and 45 by Reich,¹⁷⁶ these being here adduced because in all of them there was a careful ophthalmoscopic examination. Gowers thinks that this is an over-estimate, but admits that optic neuritis occurs in four-fifths (or 80 per cent.) of all cases of cerebral tumor. In considering this question we cannot too carefully keep in view the facts so well stated by Hughlings-Jackson,¹⁷⁷ that optic neuritis is essentially a transient symptom, and that, although it often occurs early in the disease, it may in some cases be developed only in the latter stages of the complaint. Jackson states that he frequently examined a case with the ophthalmoscope in which there was no appearance of choked disc till six weeks before the patient's death, when marked papillitis developed, the autopsy showing a tumor in the left cerebral hemisphere. In fact, where the tumor does not occupy the cortical sight-centres, the intercalary ganglia, or press on the tractus opticus or chiasm, it may exist a long time without producing any affection of the optic nerve or deterioration of vision. No neuritis will take place by increase of intracranial pressure so long as the growth of the tumor is slow and there is a corresponding absorption of brain-substance; but should the growth of the tumor be rapid, or any other cause exist by which increased pressure, with consequent irritation and effusion, would take place, infiltration of the nerve and its sheaths with lymph or inflammatory products would ensue, and give rise to swelling and increased growth of connective tissue. In cases of cerebral tumor, however, and where the growth presses on the intracranial portion of the optic nerves, or where the chiasm is compressed and atrophied by the protuberant and bulging floor of the third ventricle, as in the two cases recorded by Foerster,¹⁷⁸ optic atrophy may be produced without the occurrence of previous choked disc.

¹⁷⁵ A. f. O., xix., 3, pp. 165, 300.

¹⁷⁶ Klin. Monatsblätter f. Augenheilkunde, 1874, pp. 274, 275.

¹⁷⁷ Med. Times and Gazette, Sept. 4, 1875.

¹⁷⁸ G. u. S., vol. vii. p. 141.

HEMIANOPIA (HEMIOPIA, HEMIANOPSIA).—We may, however, have serious affections of the sense of sight without any marked alteration in the retina or optic nerve. Careful study of the various forms of hemianopia and other symmetrical defects in the field of vision will often surprise us by the extent of the defect which it reveals, and sometimes serve as a guide to the localization of the cerebral lesion which produces the defect. Hemianopia (or the not-seeing of half an object) is usually of the homonymous lateral variety, in which, if the centre of any object be fixed by the macula lutea of each eye, then either all parts of the object lying to the right-hand side of the points of fixation or else all parts lying to the left of that point become invisible. There may also be temporal hemianopia (hemianopia heteronymous lateralis),¹⁷⁹ in which the nasal side of each retina is blind, and the temporal field of each eye consequently abolished. In such case the right eye sees nothing to the right of the fixation-point, and the left eye nothing to the left of it. The external half of each retina may be blind, in which case there is loss of the nasal field of each eye and of the entire binocular field of vision. In all of these cases the dividing-line between the blind and seeing parts of the retina is a more or less vertical one, but there are also cases where the dividing-line is horizontal, and we thus have an upper or lower hemianopia. From a clinical standpoint the first-named variety (homonymous lateral hemianopia) is markedly distinguished from the others by its usual more rapid development, and by the absolutely sharp dividing-line which runs vertically through the retina at the macula; this field of vision retaining its form without subsequent development of zigzags or other irregularities. All other varieties of hemianopia develop more slowly, and their boundaries—which are usually not perfectly vertical or horizontal, and do not generally extend to the fixation-point—may vary from time to time. The homonymous lateral variety is of far more frequent occurrence than the other forms: out of 30 cases carefully observed by Foerster, where perimetric measurements of the fields were taken, 23 were of this variety, while the remaining 7 presented the heteronymous temporal form. The subject of homonymous lateral hemianopia is so important clinically, and so interesting as regards the probable course of the fibres in the optic nerves, chiasm, and cerebral centres, that it appears desirable to state briefly a few of the most decisive facts in regard to it which have been substantiated by careful autopsies.

¹⁷⁹ If we retain the word hemiopia (half-seeing), then this variety is termed medial hemiopia, because the lateral halves of the retina are still intact and vision is practicable in the median or nasal field of each eye.

1. In 1875, Hirschberg¹⁸⁰ published a case of right-sided homonymous hemianopia with perfect central vision. At first there was no paralysis of sensation or motion, but subsequently aphasia and right hemiplegia set in. The autopsy showed a large sarcomatous tumor which had caused atrophy of the left tractus opticus.

¹⁸⁰ Virch. Arch., Bd. lxv.

2. Hughlings-Jackson and Gowers¹⁸¹ (1875) relate a case of left homonymous hemianopia with hemianæsthesia and hemiplegia of the same side. The autopsy showed softening of the posterior part of the right thalamus opticus without other lesion.

¹⁸¹ R. L. O. H. Rep., vol. viii. p. 330.

3. Curschmann¹⁸² (1879) gives the case of a patient who drank sulphuric acid, which corroded the oesophagus and affected the aorta, causing embolus of the right brachial artery. On the day following there was complete left hemianopia. The autopsy showed a large area of cerebral softening in the right occipital lobe without other lesions. In the discussion of this case at the session of the Berlin Society of Psychiatry and Nerve Diseases, Westphal¹⁸³ related a case of unilateral convulsions without loss of consciousness where there was homonymous hemianopia, and in which the autopsy showed a large area of softening in the white substance of the occipital lobe in the side opposite to the defect in the field of vision.

¹⁸² Centralblatt f. Augenheilkunde, 1879, p. 256.

¹⁸³ Loc. cit., p. 181.

These cases might be multiplied, but the writer has selected them because they were made by careful and competent observers, and the lesions were so marked and limited in character as not to allow of any other interpretation than that given. If we admit the validity of the evidence, we have proved conclusively that, from a clinical and a pathological standpoint, binocular homonymous lateral hemianopia may be produced by lesions of the optic tract, of the posterior part of the thalamus opticus, and of the occipital lobe of the brain of the side opposite to the defect in the field of vision; and that, therefore, there must be a partial, and not a total, crossing of the fibres of the optic tracts at the chiasm. Moreover, as Foerster has most pertinently remarked, such a state of affairs does not violate the physiological law of the total crossing of other nerves, because in the binocular field of vision the partial crossing causes all objects to the right of the point of fixation to be seen by the left hemisphere, while those to the left of it are seen with the right hemisphere. While this problem appears sufficiently plain, and the view above advocated is adopted by the majority of writers of the present day, it is by no means equally satisfactory when looked at from a purely anatomical or physiological standpoint. Newton¹⁸⁴ in 1704 had already appreciated the importance and difficulty of the subject, and in the hope that others might further investigate it asked the question whether the fibres from the right sides of both retinæ do not so unite at the chiasm as to go together to the right side of the brain, those from the left side of each retina pursuing a similar course to the left hemisphere. He further remarks that "if he is correctly informed that the optic nerves of such animals as have a binocular field of vision join at the chiasm, while those of the animals who have no binocular vision, such as the chameleon and some fishes, do not so join."¹⁸⁵ Since his day the majority of authors have adhered to this view, until Biesiadecki,¹⁸⁶ by careful anatomical studies and lectures, attempted to prove that in both men and lower animals there is a total crossing of the fibres at the chiasm. Twelve years later Mandelstamm,¹⁸⁷ by clinical observations of nasal hemiopia and dissections of the chiasm, maintained the same view. In the same year Michel¹⁸⁸ supported the same doctrine, and since then Schwalbe¹⁸⁹ and Scheel¹⁹⁰ have each advanced the same view. However, Von Gudden,¹⁹¹ also basing his opinions upon dissections, takes the opposite ground, and has since endeavored by a series of experiments, in which he enucleated one eye of young rabbits and dogs, to prove¹⁹² that if the animals were allowed to live until central atrophy set in there is a partial atrophy of both optic tracts, more marked on the side opposite to that of the enucleated eye, because the crossed bundle is by far larger than the direct.

¹⁸⁴ Optiks, London, 1704, p. 136.

¹⁸⁵ Loc. cit.

¹⁸⁶ "Chiasma Nervorum Opticorum der Menschen und der Thiere," Sitzungsberichte der Wiener Akadamie.

¹⁸⁷ A. f. O., xix., 2, pp. 39-58.

¹⁸⁸ Ibid., xix., 2, pp. 59-84.

¹⁸⁹ G. u. S., vol. ii. p. 324.

¹⁹⁰ Klin. Monatsblätter f. Augenheilkunde (extra number 2), 1874.

¹⁹¹ Arch. f. Psychiatrie, vol. ii. p. 21.

¹⁹² A. f. O., xx., 2, p. 226, and also Ibid., xxv., 1, p. 1, 1879.

From similar experiments on rabbits, Mandelstamm¹⁹³ maintains that there is a total crossing at the chiasm, and Michel,¹⁹⁴ who repeated Von Gudden's experiments, arrived at the same conclusion. Brown-Séquard¹⁹⁵ asserted that a medial cut of the chiasm in rabbits produces amaurosis of both eyes, which would indicate that there is total crossing, while Nicati¹⁹⁶ a year later showed that a median section of the chiasma in young cats did not produce blindness of each eye, the animal following with the eye and the head the movements of a light held at a considerable distance from the eyes.¹⁹⁷ The condition of the optic nerve and brain obtained from the human subject, where by accident or by disease one of the eyes has been destroyed long before death, seems in the main to speak for partial decussation. Thus, Biesiadecki, while maintaining total decussation, could only conclude from such specimens of degenerated nerves and tracts that the greater part of the fibres of the atrophic nerve went to the tract of the opposite side. Woinow¹⁹⁸ demonstrated preparations to the Ophthalmic Society at Heidelberg where the left eye had been blind for forty years, and the atrophy, which had travelled up the left nerve, was plainly visible in both optic tracts. Schmidt-Rimpler¹⁹⁹ also showed atrophy of both tracts more marked in that of the opposite side, and Manz²⁰⁰ found atrophy of both tracts after atrophy of the nerve of one side; Plink²⁰¹ reports a similar state of affairs; while Popp²⁰² and Michel²⁰³ from analogous specimens draw conclusions favorable to the total crossing.

¹⁹³ Ibid., xix., 2, p. 47.

¹⁹⁴ Ibid., xxiii., 2, p. 227.

¹⁹⁵ Archiv de Physiologie, 1872, p. 261, and 1877, p. 656.

¹⁹⁶ Ibid., 1878, p. 658.

¹⁹⁷ Cats have a larger binocular field of vision, and are better subjects for experiments than rabbits.

¹⁹⁸ Klin. Monatsblätter f. Augenheilkunde, 1875, p. 425.

¹⁹⁹ Ibid., 1877, "Bericht der Ophth. Gesellschaft," pp. 44-48.

²⁰⁰ Klin. Monatsblätter f. Augenheilkunde, 1877, "Bericht der Gesellschaft," pp. 49, 50.

²⁰¹ Arch. f. Augenh. und Ohrenheilkunde, vol. v.

²⁰² Inaug. Diss., Embolie der Art. Centralis, Regensberg, 1875, p. 20.

²⁰³ A. f. O., xxiii., 2, p. 243.

The above cases are amongst the most decisive which have been reported, and are quite sufficient to show how great the conflict of opinions is among good observers. The observations and experiments on the subject of sight-centres in the cortex cerebri are also conflicting: thus, while Ferrier places the cortical sight-centre in the angular gyrus, and maintains that its destruction will produce blindness, Luciani and Tamburini agree as to the locality of the sight-centre, but maintain that its destruction produces hemianopia; while Munk places the sight-centre in the occipital lobe, and asserts that its loss causes hemianopia and not contra-lateral blindness. In the case of hemianopia reported by Keen and Thomson,²⁰⁴ where a bullet wound of the left occipital lobe produced right hemianopia without other apparent lesion, the writer has had an opportunity of personally examining it and of confirming their conclusions. The conclusions which he arrived at, associated with the knowledge which he obtained in Stricker's laboratory by witnessing experiments upon dogs and apes, where portions of the occipital lobes were destroyed, have convinced him that cortical lesions of the occipital lobes produce hemianopia. On the other hand, chiefly on clinical grounds and from the study of hystero-epilepsy, Charcot concludes that the band of uncrossed fibres in the chiasm bends again somewhere in the region of the geniculate bodies to join the crossed bundle once more in the cortical centre. According to this theory, destruction of the cortical centre should produce total amaurosis of the opposite eye, and lesions between the chiasm and geniculate bodies would produce homonymous hemianopia, while pressure in the crossing-point of those fibres (which in the chiasma are uncovered and run from the geniculate bodies to the opposite cortical centre) would give paralysis of the temporal halves of both retinæ.

²⁰⁴ Trans. A. O. Soc., 1871.

As regards pure crossed amblyopia, the scheme of Charcot is scarcely borne out by his clinical facts. The latest theories of those cases which were investigated by Landolt and himself showed, as they reported, marked amblyopia on the opposite side from the lesion, but associated with contraction of the field of vision in the eye of the same side. The question, however, is so vast, and so much remains to be learned concerning the brain-centres and their communications with the optic tracts, that it can scarcely be considered sufficiently ripe for an exhaustive discussion in a paper like the present.

According to Foerster, temporal hemianopia always develops slowly without any concomitant paralytic symptoms: it does not have constant boundaries, and is now progressive and again retrogressive. He cites cases which he has observed for years where at first small negative scotoma appeared just outside of the fixation-point, and increased till there was a total loss of the temporal fields. The line of division between the blind and seeing sides of the field of vision is not sharply defined and not accurately vertical. In some cases there is a gradual invasion of the sound side. Although it is usually assumed that some pressure in the anterior or in the posterior angle of the chiasm is the cause, yet the writer does not know of any post-mortem examination of a case. Mauthner²⁰⁵ gives short histories of 23 cases of temporal hemianopia, besides 11 cases relating to nasal hemianopia (or, according to his classification, hemianopia heteronyma medialis) from various authors, in most of which the ophthalmoscope showed either the presence of a neuritis or an atrophy of the nerve. There were two autopsies in the cases of nasal hemianopia related by Mauthner—those of Schule and Knapp—one of which showed an enlargement of the third ventricle and infundibulum, with atrophy of the nerves, and the other a high degree of ætheromatous degeneration of arteries at the base of the brain. Any cause which would produce simultaneous pressure on the outer angles of the commissure would give rise to nasal hemianopia. Little is known regarding hemianopia above or below the horizontal line: both Mackenzie and Graefe mention its occurrence, and Knapp, Schoen, and Mauthner give interesting cases. The writer has seen a case in a woman of fifty-five years otherwise apparently in good health. The upper part of each field was wanting, and the line of division ran slightly above the fixation-point, it being nearly horizontal. The optic nerves did not present any marked departure from their normal appearance, and central vision was fair (²⁰/x1). The only autopsy of a case of superior hemianopia with which the writer is familiar is that reported by Russell,²⁰⁶ in which there was a tumor involving the bones of the base of the cranium. The patient had upper hemianopia, confined to the right eye, followed by total blindness, coming on first in the right and then in the left eye. Genuine binocular hemianopia of the superior or inferior variety is probably produced by some symmetrical affection of the optic nerves between the chiasm and the eyes.

²⁰⁵ Gehirn und Auge, 1881, pp. 373-381.

²⁰⁶ Med. Times and Gazette, No. 47, 1873 (rep. Nagel's Jahresbericht, 1873, p. 361.)

In apparently healthy individuals transient hemianopia is not an unfrequent occurrence, and may either develop with or without other cerebral symptoms. It is usually followed or accompanied by headache, or more rarely by vertigo, tinnitus aurium, difficulty of speech, etc. Even in intelligent patients, who have not been drilled by their medical adviser to carefully analyze their symptoms, it is not recognized as half-vision, but here, as in the permanent variety of the affection, it is described as a dimness or blindness of the eye on the side in which the field of vision is defective. Some cases of transient hemianopia are accompanied by peculiar zigzag flickerings of light in the defective portions of the field of vision, which have given it the name of scotoma scintillans. We are fortunate in having an accurate description of this form of the affection by so competent an observer as Foerster, who has frequently experienced it in his own person. In his case the phenomena last from fifteen to twenty-five minutes, and commence with the appearance of dimness in both eyes, which gradually increases to a defect of the field of vision lying to one side of the fixation-point. This is soon followed by a flickering which commences in a zone around the scotoma, and increases centrifugally until it assumes the form of an arc with the convexity outward, the flickering rarely extending beyond the vertical line which separates the two halves of the field of vision. When it has reached the outer limits of the field, it generally diminishes and fades away. From a consideration of the celebrated case of Wollaston, it is probable that transient hemianopia may be caused by some temporary congestion of a brain tumor, but in the majority of instances it is certainly allied to functional disorders like migraine. Transient hemianopia has been observed in several members of the family of one of the writer's patients, all of whom are subjects of consecutive neuralgic headaches. Leber has observed the same thing. Brewster and Quaglino have attributed it to a retinal anæmia, but a careful ophthalmoscopic examination in two well-marked cases (that of Foerster and one related by Mauthner) failed to show any retinal changes. In some cases the well-marked hemianopic character of the attack speaks for its intracranial origin, which may be temporary derangement of the circulation, possibly in the optic tracts. Dianoux tells us that in his case the attack could be cut short by keeping the head down between the legs. In some of the cases which the writer has seen it may be cut short by a liberal dose of whiskey.

Affections of the Third Pair.

While a few words on the pathology of the third and sixth nerves tend to throw light on our knowledge of cerebral localization, they will also spare a good deal of needless repetition in the detailed discussion of the eye symptoms which accompany many well-marked diseases. Complete paralysis of the third nerve may be caused by pressure on its filaments at the base of the brain without other symptoms. Where it occurs with hemiplegia of the opposite side of the body and other cerebral symptoms, it is usually due to pressure on the nerve where it runs beneath the cerebral peduncle: according to Nothnagel,²⁰⁷ this localization of the disease is still more certain when paralysis of the facial and hypoglossal nerves exists on the same side as the hemiplegia (that is, on the side opposite to the third-pair paralysis). Hughlings-Jackson²⁰⁸ remarks that the symptoms are only positively diagnostic of a lesion in the neighborhood of the peduncle when they appear simultaneously, but when they are concentric to each other they may be due to an affection of the cranium. Ollivier and Little²⁰⁹ have each related a case where this group of symptoms has not originated in any lesion in the peduncle, but has been caused by an abscess of the middle and posterior lobes, which secondarily involved these parts.

²⁰⁷ Topische Diagnostik der Gehirnkrankheiten, p. 198, 1879.

²⁰⁸ In Russell Reynolds's System of Medicine, vol. ii., 1872.

²⁰⁹ Robin, Des Troubles oculaires dans les Maladies de l'Encephale, p. 95.

DOUBLE THIRD-PAIR PARALYSIS.—Double third-pair paralysis is rare, but might be produced by any cause acting on both peduncles. Kohts gives a case where such paralysis was caused by a tumor of the size of a cherrystone limited exactly to the posterior tubercles of the quadrigeminal body. Nothnagel remarks that paralysis of corresponding branches of the third pair point to the corpora quadrigemina as the seat of lesion. On the other hand, Panas²¹⁰ relates a case of absolute immobility of the eyes where the only demonstrable lesion at the autopsy was a meningo-encephalitis in the lower part of the cerebellum. Robin describes a case of double third-pair paralysis where there were ptosis and dilatation of the pupils, with a loss of all power to move the eyes except downward and outward. The diagnosis was that of an interpeduncular syphilitic gumma: there was complete recovery. In the above case it is interesting to note that while the paralysis of the left eye occurred previous to that of the right, the eye last attacked was the first to regain its motions.

²¹⁰ Cited by Robin, loc. cit., p. 74.

PTOSIS.—Paralysis of the branch of the third pair which supplies the levator palpebræ, when it exists without any lesion of the other branches or where it is coincident with hemiplegia of the opposite side, is frequently held to indicate a cerebral lesion, which may be either cortical or have its seat in the nucleus of the nerve. According to Grasset,²¹¹ when the lesion is cortical it is situated in the parietal lobe in advance of the angular gyrus. The localization is by no means well made out. Coignt²¹² has shown that it is not always crossed, for in 5 out of 20 cases mentioned by him it existed on the same side as the paralysis. Steffen²¹³ gives a case of double ptosis with sluggish pupils where there was complete control over the muscles moving the globe, the autopsy showing a tubercle in the tubercular quadrigemina which had entirely effaced their normal structure.

²¹¹ Robin, p. 104.

²¹² Thèse de Paris.

²¹³ Berliner klin. Wochenschrift, No. 20, 1884.

OPHTHALMOPLEGIA INTERNA.—In those cases where affection of the orbital ophthalmic ganglia can be excluded, paralysis of the pupillary and ciliary branches of the third pair is, according to Jonathan Hutchinson, due to an affection of the twig which runs through the lenticular nucleus in the striated body. It is frequently associated with paralysis of the internal rectus, and may be accompanied by paralysis of the ciliary muscle. After diphtheritis there is often paralysis of the ciliary muscle, with prompt reaction of the iris. The writer is not aware of any recorded instance of apoplexy or other sudden onset of disease which would enable us to localize exactly the centre for pupillary contraction. According to Hughlings-Jackson, we may have in apoplexy the most varied states of the pupil (normal, dilated, or contracted) independent of the seat of lesion: he further states that upon calling loudly to the patient there will sometimes be a transient pupillary dilatation. When we look at the state of the pupils as part of general symptomatology, we find a most perplexing confusion and contradiction: in fact, notwithstanding the quantity of material both in ancient and modern literature, we are far from having any satisfactory account of the subject. This is partly due to our imperfect knowledge of the anatomy of the brain and to the great difficulty of estimating exactly pupillary changes, and partly carelessness and want of a proper system of observation. The data have for the most part been hastily compiled, without a minute statement of concomitant symptoms or the stage of the disease in which they are developed. Usually, they have been made without any proper means for illuminating the pupil or apparatus for correctly magnifying and observing its motions. In most cases the want of knowledge of the more common sources of error, such as a difference in the size of the pupils owing to difference in the refraction of the eyes, posterior synechiæ, or other intraocular changes, has invalidated the results.

ASSOCIATED MOVEMENTS OF THE HEAD AND EYES.—In many central lesions, associated movements of the head and eyes are present, and, although the exact channels through which they are propagated are for the most part unknown, yet certain groups of these clinical symptoms are of so frequent occurrence as to be recognized and admitted by almost all observers. Vulpian and Prévost were the first to enter into a minute study of these movements. Vulpian in his lessons on the physiology of the nervous system (1866) states that "in cases of unilateral cerebral lesion, whether it be situated in the cerebral hemispheres, the striated bodies, the thalami optici, the cerebellum, or in the different parts of the isthmus cerebri, whether the lesion be softening or hemorrhage, there is often, immediately after the attack, a deviation of the eyes at the time of development of the hemiplegia. The deviation is in general transient, and may last either a few minutes or hours or several days. The eyes are usually turned in a direction opposed to that of the hemiplegia; thus, if the right side is paralyzed, both eyes are turned toward the left. On regaining consciousness the patient, if he tries to turn his eyes to the right, may either be entirely unable to move them, or, what is more usual, may succeed in bringing them to the middle of the palpebral aperture without being able to turn them farther in that direction. Does this phenomenon depend on a paralysis of the muscles which cause conjugate motion of the eyes, or on a spasmodic contraction of their opponents, over which they are unable to triumph?" He further states: "I incline strongly to the latter view, as it is in accordance with what we observe in animals. The analogy of the phenomena goes still farther: often the head of the patient has made a more or less marked movement of rotation on the neck—a movement as the result of which the face is turned toward the non-paralyzed shoulder, and in the cases where we cannot observe a deviation by turning back the head into its normal position, an action which can often be only brought about by considerable effort."

Prévost²¹⁴ has since formulated the following laws for cases of hemiplegia: "I. When the hemiplegic looks toward his lesion and away from his paralyzed side, the lesion is hemispherical. II. If he looks toward his paralyzed side, the latter is situated in the mesencephalon." This statement coincides with the facts reported by Hughlings-Jackson, Charcot, and many other observers. Nothnagel²¹⁵ admits that this is the rule, but quotes as an exception to it a case of his own where, with right hemiplegia and head turned to the right, the eyes were turned to the left, the autopsy showing an extensive patch of softening in the left hemisphere which involved the frontal convolutions, the central convolution, and the adjacent white substance. In addition, he cites Bernhardt as giving other exceptional cases which, in his own judgment, "considerably diminishes the diagnostic value of the phenomenon." Landouzy and Coignt²¹⁶ have attempted to define still more clearly the diagnostic value of the associated movements of the head and eyes, and, while they admit the correctness of these laws of hemiplegic paralysis, they add that in convulsive cases in which there are symptoms of irritative lesions the above rules are reversed. To explain such cases they lay down the following rules: first, that if the patient looks toward his convulsed side the lesion is situated in the hemisphere of the opposite side; and second, if he looks away from his convulsed side (or toward the lesion) there is an irritant lesion of the mesencephalon.

²¹⁴ Thèse de Paris.

²¹⁵ Topische Diagnostik der Gehirnkrankheiten, p. 580, 1879.

²¹⁶ Thèse de Paris, 1878.

NYSTAGMUS.—This is a term applied to a periodic type of involuntary oscillatory or rotatory movements of the eyeballs. The oscillatory are due to rapid alternate contraction of the straight muscles, while the rotatory indicate either similar actions of the oblique muscles alone or in conjunction with the straight. The oscillatory motions are usually horizontal, but instances of vertical nystagmus occur, as in the case recorded by Soelberg Wells.²¹⁷ Nystagmus may be either congenital or acquired; the latter variety being much the more frequent form of the affection. Congenital nystagmus is usually associated either with cataract or imperfect development of the optic nerve and retina. It is a very frequent accompaniment of albinism and pigmentary retinitis. We often see the acquired form arise during the first few months of life, when the child in its effort to see is hindered by corneal or lenticular opacities resulting from ophthalmia neonatorum. One of the most interesting of the acquired forms is that which occurs amongst coal-miners, rendering a considerable number of those thus affected unfit for work. At first the symptoms are that the lights in the mines and the objects on which the patients endeavor to fix their attention begin to dance, this being accompanied by a sensation of dizziness and discomfort. In the first part of the attack they disappear when work is stopped, and the miners come up into the daylight; but if work be persisted in they become permanent and exaggerated. When the nystagmic motions have ceased, they may often be called into activity by placing the patient in a dark room and getting him to direct his eyes to a candle held above the horizontal line of the field of vision. The motions are usually lateral, or in some cases the centre of the cornea describes an ellipse or circle which causes the patient to see a ring of light. It has been observed to occur much more frequently in those working in shafts where there is a good deal of fire-damp; which has caused some writers to assert that the nystagmus has been dependent upon the action of the gas. This view would seem to receive some support from an instance reported by Bright of nystagmus, in a case of suffocation from the fumes of burning coals, which he attributed to cerebral pressure. In these cases it is more probably due to fatigue of the eye and its nerve-centres in the endeavor to see in the dim light and strained position which the miner is often obliged to maintain, which is intensified by the enfeeblement of the nerve-centres due to the action of the gas: these, associated with the diminution of the light caused by the wire gauze of the safety-lamp, would further increase the strain in those obliged to work in the shafts pervaded with fire-damp. The statements of Dransart,²¹⁸ founded on the examination of a large number of miners, probably give a correct idea as to the frequency of the affection. He states that among 12,000 workmen employed by one company, there were 30 under treatment for nystagmus, which would give about two and a half patients per thousand. In any form of nystagmus the motions of the eyes usually become more rapid when they are used for near work. According to Nagel,²¹⁹ excessive convergence will at times cause a temporary cessation of all nystagmic motion; and he further proved this by putting extra strain on the interni by means of prisms with their base out. The true pathology of the various forms of nystagmus is still imperfectly known. Arlt²²⁰ supposes that there is a rapid repetition of reflex movements in the endeavor to attain distinct vision in those forms which develop on account of corneal and lenticular opacities. He explains this by the supposition that the retinal impression is strengthened by the same retinal areas being rapidly and repeatedly subjected to the action of the rays of light from the same object, while a longer period of fixation would cause retinal fatigue and blur; showing the same principle by reminding us that our perceptive powers for a test object, upon first being brought into view at the periphery of the field of vision, are much stronger when the object is shaken than when it is brought quietly toward the fixation-point. Some forms of the affection, however, are manifestly due to fatigue of the nerve-centres, and have been by some authors placed in the same category as writers' cramp. For its causation we would naturally look for the anatomical changes either in the cortical centres for the eye-muscles or in the nuclei of the third and sixth pairs. Vulpian²²¹ states that wounds of the medulla in dogs cause nystagmus, and Schiff asserts that wounds of the white substance of the cerebellum near the peduncles give rise to the same phenomenon; while Ferrier has produced it by the influence of electricity on the cerebellum of apes. Cohn²²² records a case of gunshot wound of the right parietal bone (near the angular gyrus) which produced nystagmus. Merkel's case, occurring in a patient with embolism of the artery of the fissure of Sylvius, would also point to lesion near the angular gyrus. Stintzing²²³ gives a case where there was thrombosis of the basilar and Sylvian arteries. Oglesby²²⁴ relates two cases where nystagmus came on suddenly with dilatation of the pupils, the autopsies showing a clot which pressed on the medulla. Fienzal²²⁵ also gives a case where there was a tumor in the left peduncle of the brain. It is often seen during epileptic convulsions. According to Raehlmann,²²⁶ the motions of both eyes are under the control of psychic centres which regulate them according to the necessities of vision: for Willbrand²²⁷ it is a sign of weakness of the voluntary cortical centres which fail to regulate the reflex activity of the middle brain and cerebellum. The latter author shows that the extent of the field of vision is increased in the direction of the oscillations in those cases where direct vision is not much impaired, while there is marked contraction of the field in cases where the direct visual acuity is much diminished. He also states that there is contraction of the field in the nystagmus of miners, which is greater during the intervals of the paroxysm than during their occurrence, and, further, that the contraction is greater where the case is one of long standing.

²¹⁷ Lancet, 1871, p. 662.

²¹⁸ Annales d'Oculistique, 7, 82, p. 177.

²¹⁹ Graefe u. Saemisch, vol. vi. p. 226.

²²⁰ Krankheiten des Auges, Bd. iii. p. 335.

²²¹ Comptes Rendus de la Société de Biologie, 1861 (quoted by Robin, p. 157).

²²² Schussvorletzungen des Auges, p. 19.

²²³ Jahresbericht f. Ophth., vol. xiv. p. 306.

²²⁴ Brain, vol. iii., 1880.

²²⁵ Trans. Internat. Congress, at Milan, 1881, p. 126.

²²⁶ "Nystagmus und seine Aetiologie," A. f. O., xxiv., 4, p. 237 (1878).

²²⁷ Klin. Monatsblätter f. Augenheilkunde, vol. xvii., 1879, pp. 419-438 and 461-480.

In some rare cases nystagmus may be produced at will. Raehlmann,²²⁸ Lawson,²²⁹ Benson,²³⁰ all report cases of the voluntary type. In one of those given by Lawson the patient (a gentleman in good health) "first made his eyes steady, and then set both into rapid lateral motion—so rapid that the outline of the cornea was completely lost to view." Zehender²³¹ observed it in a case of a twelve-year-old boy, where he was able to produce it by the instillation of a strong solution of eserine. Charcot states that ordinary nystagmus is a valuable symptom of disseminate sclerosis, and that it is present in about half of these cases, while it is exceptional in locomotor ataxy. "In some patients the look is vague until the eyes are made to fix some object, when the nystagmus develops."

²²⁸ Loc. cit.

²²⁹ R. L. O. H. Reports, vol. x. p. 203.

²³⁰ Ibid., vol. v. p. 343.

²³¹ Klin. Monatsblätter f. Augenheilkunde, vol. xviii., 1879, p. 127 (note).

According to Hammond, in disseminate sclerosis, nystagmus may be the only symptom for the period of a year before other symptoms develop. Moos²³² speaks of oscillatory movements of the eyes in Menière's disease, and Schwalbach²³³ describes them in a case of purulent catarrh of the middle ear where they could be produced either by syringing or by pressure on the mastoid process.

²³² Arch. f. Augenheilkunde und Ohrenheilkunde, vii. 2, p. 508.

²³³ Deutsches Zeitschrift f. prakt. Med., No. 2, 1878.

Affections of the Fifth Pair.

HERPES FACIALIS.—Herpes facialis frequently appears on the lips and angles of the mouth, and occasionally in the eye and its appendages. When upon the conjunctiva or cornea, it commences as clear watery vesicles, usually in groups, which soon burst and leave open ulcers looking very much like abrasions or scratches of this membrane. They usually occur in successive crops after fevers, especially pneumonia, although at times they may appear without any assignable cause. They are also slow to heal, but are not dangerous to the eyesight, except where they give rise to purulent infiltration leading to hypopyon.

HERPES ZOSTER OPHTHALMICUS.—Herpes zoster ophthalmicus is a far more formidable affection. The eruption, as is well known, follows the distribution of the divisions of the ophthalmic branch of the trigeminus, and when the eyeball is affected the sight is always threatened. Clear watery blisters form on the cornea, which soon burst, the exposed tissue taking on purulent infiltration, while pus is not infrequently deposited in the anterior chamber. These ulcers are slow to heal under the most careful treatment, which, as a rule, consists in washing with disinfecting solutions and applying a bandage, etc. There is almost always iritis, as evidenced by the sluggish pupil and at times by marked synechiæ.

The burning and pricking pain at the seat of eruption is marked, and there is severe neuralgia in the temple, forehead, and side of the nose. The intensity of the iritis varies considerably in different cases, and, although some terminate favorably, having had but few and slight symptoms, yet the one case reported by Noyes, where it led to cyclitis, followed by shrinking of the eyeball, which ultimately gave rise to sympathetic irritation of the fellow-eye, shows how serious its consequences may be. Permanent opacities of the cornea are not infrequent. The disease is, fortunately, a rare one. It usually comes on either in middle or declining life, although Wadsworth has reported a case in a child four years old. The cornea becomes anæsthetic, both in the ulcers and over the rest of its surface, a long time often elapsing before any of its sensibility is regained. Horner²³⁴ was the first to demonstrate that the corneal ulcers originated in vesicles, and the very great diminution of intraocular pressure in the affected eyeball, and also to show the marked difference in the temperature of the skin of the two sides. The temperature on the affected side is usually one and a half to two degrees higher than on the other side, while the cutaneous sensibility is markedly diminished; as, for instance, the æsthesiometer might give twelve lines on the healthy forehead as against twenty-two lines on the diseased side, and the superciliary ridges and the upper eyelid on the normal side might give respectively nine and five lines as against seventeen and seven lines on the affected side. In the cases which the writer has had an opportunity of studying he has found similar variations in intraocular tension, temperature, and sensibility. Hutchinson²³⁵ thinks that the affection of the nasal branch is always accompanied by inflammation of the eyeball, and says: "Thus far, I have never seen inflammation of the whole side of the nose without witnessing inflammation of the eye;" while Bowman²³⁶ says that he has "not found affections of the eyeball to occur, especially in those cases of ophthalmic zoster in which the eruption followed the course of the nasal branch." Wadsworth²³⁷ gives a case where the entire side of the nose was involved, the eyeball and conjunctivæ not being affected. He suggests that possibly the explanation in these cases is an anomaly of distribution described by Turner, where the side of the nose is supplied by a long, slender infratrochlear branch. Bowman,²³⁸ although realizing that peripheral excitement of sensory nerves may originate in a central or reflected source, and induce tenderness and redness in the parts supplied by them, yet nevertheless holds that ophthalmic zoster is a peripheral disease, having its primary seat in the branches of common sensation, the nerves probably becoming inflamed in the more superficial portions of their trunks, as the eruption succeeding as an extension of vascular excitement to the cutaneous tissue: he thus explains the tenderness of the skin before it reddens and the often lasting alteration of sensibility. In reference to whether the neuritis causing the eruption is an ascending or descending one, the only two careful autopsies that give answer with which the writer is familiar are those of Wyss and of Weidner, where both show extensive changes in the nerve-centres. The latter, made five years after the attack, showed cicatricial shrinking of the ganglion of Gasser and of the root of the nerve between it and the medulla; while that of Wyss, made within two weeks of the outbreak of the affection, showed that the entire ophthalmic branch of the trigeminus was thickened, reddened, softened, and surrounded by extravasation of blood from the entrance of the orbit up to the ganglion of Gasser; while the other branches of the trigeminus were normal in size and appearance. The Gasserian ganglion itself was enlarged and bright red, while that of the other side of the head was yellowish-white. As is well known, zoster in other parts of the body not infrequently affects the two sides simultaneously; and there are recorded cases where it has twice attacked the same locality, but the writer is not familiar with any such facts as regards ophthalmic zoster.

²³⁴ Klinische Monatsblätter f. Augenheilkunde, 1871, p. 321.

²³⁵ R. L. O. H. Rep., 1866, pp. 191-215.

²³⁶ Ibid., 1867.

²³⁷ Trans. of Amer. Oph. Soc., 1874.

²³⁸ Loc. cit.

NEURO-PARALYTIC OPHTHALMIA.—In 1822, Herbert Mayo²³⁹ showed that section of the fifth nerve within the cranium produces insensibility of the eye; and Charles Bell²⁴⁰ in 1830, while recognizing this fact, maintained that "when that sensibility is destroyed, although the motions of the eyelids remain, they are not made to close the eye, to wash and clear it, and consequently inflammation and destruction of that organ follow." Since that time the subject has been a favorite theme with both clinicians and physiologists, but opinions as to its cause have been a good deal divided. While, perhaps, a majority, with Bell,²⁴¹ Snellen,²⁴² Kondracki,²⁴³ Gudden,²⁴⁴ Senftleben,²⁴⁵ and others, hold that the inflammation of the cornea is of traumatic origin, many writers—amongst whom may be mentioned Longet,²⁴⁶ Graefe,²⁴⁷ Meissner,²⁴⁸ Schiff,²⁴⁹ and Eckhard²⁵⁰—assert that it is caused by the impaired action of the trophic fibres of the nerve; and again others, such as Ferrier,²⁵¹ Balogh,²⁵² and Buchmann,²⁵³ maintain that the inflammation is peripheral, consequent upon the drying of parts of the cornea. Clinically, soon after the occurrence of complete palsy of the trigeminus, there is an interstitial punctate keratitis, which makes the cornea so cloudy that the motions of the iris are with difficulty observed, this being accompanied by conjunctival and ciliary injection. The symptoms, especially where the paralysis is incomplete, are often much alleviated by maintenance of careful closure of the lids and repeated washing of the eye, which protects the enfeebled tissue from the action of foreign bodies. Success is not, however, always obtainable, for occasionally, even with the most complete protection of the eye, eventual sloughing of the cornea cannot be prevented. This is not a usually-accepted doctrine, but the writer is convinced²⁵⁴ of its truth by a case seen within a week of the commencement of the disease, in which the cornea was not yet ulcerated, where the most sedulous care in cleansing the eye and protecting it from external irritants did not prevent the necrosis and perforation of the central part of the cornea. Since then other cases of similar import have been published. Quaglino²⁵⁵ gives an instance where complete ptosis shielded the eye from all gross insults, but where, nevertheless, a central slough of the cornea formed. Laqueur²⁵⁶ also found that the cornea sloughed in spite of the most careful protection. In all other cases where the cornea is exposed to air and external irritants, as in lagophthalmos or excessive exophthalmos, the case is quite different, the consequent inflammation being much better borne. While this is a fact more or less familiar to all clinicians, it is nowhere better shown than in the case of Horner,²⁵⁷ where there was caries of the petrous portion of the temporal bone and complete paralysis of the facial nerve. Two years later the trigeminus was attacked, and then for the first time ulceration occurred in the hitherto sound cornea. Hirschberg²⁵⁸ describes neuroparalytic keratitis and panophthalmitis consequent upon a neurectomy of the infraorbital nerve, and quotes Langenbeck as relating a similar case after section of the supraorbital nerve.

²³⁹ Anat. and Physiol. Commentaries, London, 1822, No. 2, p. 5.

²⁴⁰ Nervous System of the Human Body, London, 1830, p. 207.

²⁴¹ Loc. cit.

²⁴² Virchow's Archiv, Bd. xiii. S. 107, 1850.

²⁴³ Nagel's Jahresbericht (Lit. 1873), p. 266.

²⁴⁴ Idem.

²⁴⁵ Virchow's Archiv, Bd. lxv. Heft. 1, pp. 69-99.

²⁴⁶ Anatomie et Physiologie du Système nerveux, t. ii. p. 161, Paris, 1842.

²⁴⁷ Arch. f. Ophthalmologie, Bd. i. Abth. i. S. 306-315.

²⁴⁸ Henle und Pfeuffer's Zeitschrift (3), xxix. p. 96 (quoted by Soelberg Wells).

²⁴⁹ Ibid., p. 217 (also quoted by Wells).

²⁵⁰ Centralblatt f. Med. Wiss. (cited by Nagel, Literature, 1873).

²⁵¹ Nagel's Jahresbericht, (Lit. 1876), p. 51.

²⁵² Ibid.

²⁵³ Ibid., 1883, p. 153.

²⁵⁴ Norris, "Case of Paralysis of the Trigeminus, followed by Sloughing of the Cornea," Trans. Amer. Ophth. Soc., 1871, pp. 138-141.

²⁵⁵ Nagel's Jahresbericht (Lit. 1874), p. 26.

²⁵⁶ Klinische Monatsblätter f. Augenheilkunde, 1877, p. 228.

²⁵⁷ Nagel's Jahresbericht (Lit. 1873), p. 267.

²⁵⁸ Berliner klinische Wochenschrift, 1880, S. 169; Sitzung der Gesell. f. Psych. und Nervenkrankheiten, 10 März, 1879.

INJURIES OF THE FIFTH PAIR.—Although daily clinical experience shows us how promptly irritation of the sensitive branches of the trigeminus are followed by symptoms of reflex action in the eye—as, for instance, a cinder in the conjunctiva will cause contraction of the pupil, or a sharp pinch of the temple will at times cause pupillary dilatation—nevertheless, instances of impairment of the eyesight due to injury of the branches of the infraorbital or supraorbital nerves, and to this alone, are of rare occurrence. Sympathetic ophthalmia is the exception in which we too frequently see inflammation of one eye cause severe and often irreparable damage to its fellow. Scattered through ancient and modern surgical works there are many interesting and well-attested cases of impaired vision, some of which should be excluded on account of the want of proper evidence, which is now obtained from testing of the acuity and field of vision and ophthalmoscopic examination. Erichsen²⁵⁹ cites cases from Hippocrates, Fabricius Hildanus, and La Motte where amaurosis was produced by a wound of the brow. Chelius²⁶⁰ gives a case from similar injury, while Wardrop²⁶¹ narrates three instances—one of wound of forehead, one from a blow on it with a ramrod, and one from an injury by a fragment of shell. The same author calls attention to the fact that amaurosis is more readily caused by wounds and injuries of the supraorbital and infraorbital nerves than from complete division of them. The various neurotomies and neurectomies performed upon the supraorbital branch since his day bear witness to the accuracy of his deduction. The same author quotes Morgagni as saying that Valsalva has seen amaurosis follow a wound of the lower lid which has been inflicted by the spur of a cock. Morgagni relates a similar case where the injury was inflicted by the broken glass from the windows of an upset carriage; and Beer reports a similar case of amaurosis from wound of the cheek. Guthrie²⁶² remarks that "when the eye becomes amaurotic from a lesion of the first branch of the fifth pair of nerves, the pupil does not become dilated; the iris retains its usual action, although the retina may be insensible and the vision destroyed." More recently, Rondeau²⁶³ gives two cases, one of which caused lachrymation, photophobia, and eventual atrophy of the eye on the affected side, followed, fifteen years later, by loss of the fellow-eye from sympathetic ophthalmia, which had been produced by degenerative changes taking place in the shrunken bulb; and a second, in which a wound of the left brow became painful eight days after the receipt of the injury, and where pains became more severe as the wound cicatrized: in this latter case the left eye became foggy in three weeks, and soon sight was entirely lost, whilst six weeks after the accident there was dull pain in the right eye, with a sensation of cloudiness and a gradual development of photophobia in it. By local bloodletting, which caused the photophobia to rapidly yield, and a derivative and alterant treatment, the patient's right eye was so far improved that fifteen days later he could find his way about with the left eye, and could see to read with the right. Ophthalmoscopic examination showed in the left eye a serous swelling of the retina which entirely obscured the margin of the discs and gave the whole fundus a grayish tint, the veins being much enlarged and very tortuous. The right eye showed similar changes, though less developed.

²⁵⁹ Loc. cit., pp. 233-261.

²⁶⁰ South's translation of Chelius's System of Surgery, vol. i. p. 430.

²⁶¹ Morbid Anatomy of the Human Eye, vol. ii. pp. 180, 181, London, 1818.

²⁶² Quoted by White-Cooper, Injuries of the Eyes, London, 1859, p. 92.

²⁶³ Des Affections oculaires Reflexes, Paris, 1866, pp. 53, 54.

Affections of the Sixth Pair.

The extremely limited distribution of the sixth pair of cranial nerves renders the clinical study of their pathology comparatively simple. The eye supplied by the paralyzed muscle turns inward to an extent corresponding to the degree of loss of power in the paretic muscle plus the energy of its opponent rectus internus. The image of the object fixed by it falls, therefore, to the inner side of the macula lutea, and, being projected outward, causes a double vision, in which the image of the deviated eye appears to be in the temporal field of the affected eye (homonymous diplopia). When the healthy eye is covered and the patient endeavors to fix any near object with the paralyzed eye, it will be found that (as in all other cases of peripheral paralysis affecting any of the extra-ocular muscles) the secondary deviation of the sound eye is considerably greater than the primary deviation of the affected one; this being accounted for by the fact that the amount of consentaneous innervation which is sufficient to cause a small motion in the paretic muscle will produce a marked effect in the sound one.

Paralysis of the external rectus is quite common, and is either transient or permanent. The former variety is often put down as rheumatic, when it is really a symptom of tabes dorsalis. The permanent paralysis is frequently an accompaniment of the affections of the base of the brain: when these are located in the middle fossa of the skull it is often associated with paralysis of the facial. If hemiplegia be present, the lesion is usually situated farther back toward the exit of the nerve from the pons. Graux²⁶⁴ and Ferréol have called attention to a form of paresis which results from disease of the nucleus of the sixth pair. In this form, owing to the affection of the filament which the nucleus of the sixth nerve gives to the nucleus of the third nerve, which is distributed to the internal rectus of the other side, the amount of the secondary deviation is much diminished, and there is more or less the appearance of an ordinary concomitant convergent squint (where, as is well known, the excursions of the two eyes are nearly equal). In one case, where the autopsy showed that a small tubercle had been developed at the junction of the medulla and pons, just beneath the surface of the fourth ventricle, there was no other symptom than this conjugate deviation of the eyes. In another case, in which there was hemiplegia (hemiplégie alterne), a tubercle was found higher up in the pons, bulging into the fourth ventricle. In addition to the conjugate deviation of the eyes already mentioned, Graux and Ferréol believe that this central form of paralysis is distinguished by its gradual access, slow development, and persistence. They say that in pure cases of lesion of the nucleus it is characterized by the absence of all other symptoms, and still further assert that in those cases in which it is but partially involved the accompanying symptoms are either complete facial paralysis or alternate hemiplegia.

²⁶⁴ Thèse de Paris.

Affections of the Seventh Pair.

Loss of power in the orbicularis palpebrarum, and consequent lagophthalmos, is frequently encountered as part of paralysis of the facial nerve. Where the paralysis is complete, it prevents closure of the eyelids. Variation in the size of the palpebral fissure is, however, by no means abolished, for, owing to relaxation of the levator palpebrarum, the fissure diminishes when the patient looks down, but is increased by the activity of this muscle when he looks up.

BLEPHAROSPASM.—Spasmodic closure of the lids is frequent in phlyctenular conjunctivitis and in many corneal and conjunctival affections. It is evidently reflex in its origin, and often entirely out of proportion to the amount of conjunctival or corneal disease. A foreign body under the lids will frequently give rise to a similar state of reflex spasm. We also encounter a greater or less degree of twitching of the lids as part of general or local chorea.

Affections of the Twelfth Pair.

BULBAR PARALYSIS, LABIO-GLOSSAL LARYNGEAL PARALYSIS.—Affections of the eye and its appendages are rather exceptional in this form of disease. In one case Galezowski describes unilateral atrophy of the optic nerve, and Dianoux²⁶⁵ bilateral atrophy in another. In the latter the atrophy came on after partial paralysis of the lips and of the muscles of deglutition, it being preceded by paralysis of the right external rectus. Hallopeau²⁶⁶ quotes a case from Wachsmuth where there was partial paralysis of the facial which rendered the face immobile and effaced its wrinkles, allowing the lower lid to fall. He cites also a case of Hérard in which there was amblyopia and partial ptosis. He justly remarks that such phenomena indicate an extension of the lesion from the nucleus of the twelfth pair to other parts of the central nervous system. The pupils are sometimes described as contracted, more rarely as dilated. Leeser quotes Leube²⁶⁷ to the effect that "paralytic myosis, when it occurs in bulbar paralysis, is generally a sign that it is complicated either by progressive muscular atrophy or with sclerosis of the brain and spinal cord."

²⁶⁵ Quoted by Robin, Troubles oculaires dans les Maladies de l'Encephale, p. 335.

²⁶⁶ Des Paralysies bulbaires, Paris, 1875, p. 41.

²⁶⁷ Deutsches Archiv f. klin. Med., Bd. viii. pp. 1-19, quoted by Leeser, p. 94.

Mental Affections.

It is admitted by all observers that affections of the pupillary branch of the third pair, such as mydriasis, myosis, and inequality of the pupils, are of comparatively frequent occurrence among all classes of the insane. There is the widest difference of opinion as to the percentage of cases in which it occurs: thus, Nasse out of 229 cases found 146 (64 per cent.) with difference in the size of the pupils, while Wernicke found 24 per cent. in the Leubus Asylum, and only 13 per cent. in the Breslau Institute. The latter author has attempted to classify the pupillary lesions into three groups:

I. Mydriasis, with loss of accommodation, where the pupil does not react to light nor with increased convergence of the eyes.

II. Where the pupillary difference is slight and the irides less prompt than normal in reaction to light, all difference of the pupils disappearing upon convergence of the eyes.

III. In which the irregularity is still less, the narrower pupil being absolutely insensitive to light, but prompt in responding to convergence, while the more dilated pupil acts promptly in obedience to both light and convergence.

In the first group there is some lesion in the course of the third pair; in the second, some lesion of the sympathetic either in the cilio-spinal centre or in its unknown intracranial distribution; whilst in the third, which is not so readily explained, there is possibly an affection of those fibres which pass from the third pair to the optic nerve. Foerster²⁶⁸ states that he has frequently seen cases where at different times the same pupil under similar circumstances showed different diameters; also asserting that variation in the relative sizes of the two pupils sometimes occurred within a few days or weeks. He also maintains that in many cases the occurrence of inequality in the pupils precedes and presages the occurrence of insanity; and as a marked example of it he quotes the case of a friend and colleague who observed this phenomenon in himself. This person was well aware of the theories on the subject, and while yet of sound mind jokingly remarked that on account of this inequality of pupils having set in, he thought of taking up his quarters in an insane hospital. A few years later he actually died insane in the Leubus Asylum. Myosis is said to be frequent in states of mental exaltation. Seifert asserts that when it is accompanied by acute mania general paralysis will sooner or later ensue. Griesinger asserts that the same thing occurs in chronic mania. As regards the changes in the optic discs in the insane, we find usually recorded either a low grade of neuritis or of atrophy: according to Leber²⁶⁹ this atrophy is histologically similar to that occurring in gray degeneration of the nerves. The outer strands are usually those most affected. Indeed, as far as these obscure diseases are at present understood, there is no good reason why any changes should be found in the optic nerves except the congestion which accompanies acute or subacute mental disease and the nerve-degeneration of various grades which might be expected to be found in all worn-out lunatics. Illusions and hallucinations referable to the sense of sight are not uncommon in the insane, and are perhaps due to degenerative changes in the visual centres. In classifying such cases for study of the intraocular changes most writers place them under the following heads—viz.: general paralysis, dementia, mania, and melancholia,²⁷⁰ the account of the changes in the eye-ground and the proportion of cases in which they occur being found to vary greatly.

²⁶⁸ G. u. S., vol. vii. p. 227.

²⁶⁹ A. f. O., xiv., 2, p. 203.

²⁷⁰ Noyes, "Ophthalmoscopic Examination of Sixty Insane Patients in the State Asylum at Utica," pp. 6 (extra copy from Amer. Journ. of Insanity, Jan., 1872).

GENERAL PARALYSIS.—Almost all agree that in this form of the disease we frequently have gray degeneration of the optic nerve, with pupillary symptoms which strongly resemble those found in tabes dorsalis, in some instances the autopsy showing the same location of spinal changes which characterizes the changes seen in locomotor ataxia.

DEMENTIA.—In chronic dementia Albutt found either hyperæmic or atrophic changes in the disc in 23 out of 38 cases. Noyes²⁷¹ found hyperæmia in 18 cases, and infiltration of the optic nerve and retina in 12. Jehn and Klein were unable to find changes in the discs of any of the cases which they examined.

²⁷¹ Idem.

MANIA.—Albutt found the discs hyperæmic except in one case examined during a paroxysm, in which they were pale. Out of 20 cases of acute mania, Noyes²⁷² found 14 which showed hyperæmia of the discs; the discs of the remaining 6 were either anæmic or normal, these latter cases all being of short duration (less than three months); the 6 cases of chronic mania had eye-grounds which showed no lesion, while the other 3 exhibited hyperæmic or inflammatory changes.

²⁷² Loc. cit.

MELANCHOLIA.—In Noyes's examination 4 out of 5 cases had healthy eye-ground, and 1 moderate hyperæmia and striation. Jehn found hyperæmia in every one of 40 cases examined, 2 of these having decided neuritis, which he supposed to be due to meningeal change.

Spinal Cord.

INJURIES TO THE SPINE.—Physiologists have frequently shown that pupillary and other eye-symptoms may be produced by experimental injury to the spinal cord of animals, which would lead us to naturally expect analogous results in man in cases of spinal fracture and injury. This subject has received great attention in England, where spinal injury from railway accidents appears unusually frequent. Albutt²⁷³ tells us that it is tolerably certain that disturbance of the optic nerve and its neighborhood is seen to follow disturbance of the spine with sufficient frequency and uniformity to establish the probability of a causal relation between the two events. Erichsen,²⁷⁴ who has collected his large clinical experience into a book on Concussion of the Spine, after citing Plutarch to show how Alexander the Great was in danger of losing his eyesight from the blow of a heavy stone on the back of the neck, gives 53 cases (not tabulated with this view by the author), of which 49 were apparently undoubted cases of spinal injuries: of these, 13 (36 per cent.) showed decided eye-symptoms. Erichsen says: "My experience accords fully with that of Albutt. I found that in the vast majority of cases of spinal concussion unattended by fracture or dislocation of the vertebral column there occurred within a few weeks distinct evidence of impairment of vision." As enumerated by this author, these symptoms consist of difficulty of seeing in dim light, blurring and running together of the letters, and at times (in the early stages) slight diplopia. Later, there is photophobia, with contraction of the brow, which gives a peculiar frown, and at times an injection of the conjunctiva; these symptoms often being accompanied by muscæ volitantes and photopsia. He agrees with Albutt in attributing these to an ascending meningitis, while Wharton Jones considers that the eye symptoms are better accounted for by the action of the cilio-spinal centre and the sympathetic filaments springing from the dorsal and cervical cord. Wharton Jones²⁷⁵ lays stress upon the undue retention of after-images and upon the small amount of comfort which a positive (convex) glass gives the patients, and "to the pain extending from the bottom of the orbit to the occiput, which is always a symptom belonging to deep-seated disturbance in the circulation of the optic apparatus." Rondeau²⁷⁶ gives an interesting example of severe affection of the eyesight from apparently slight injury to the spine. The patient, seventeen years old, fell on the staircase, striking the neck and shoulders. There was complete loss of sight. Light-perception returned in a month, and four years after he could distinguish large objects in front of him, but vision remained stationary at that point. Albutt informs us that the percentage of visual affections is greater in proportion to the height of the seat of the injury in the spine.

²⁷³ Use of the Ophthalmoscope, London, 1871.

²⁷⁴ Concussion of the Spine, by John Eric Erichsen, London, 1875.

²⁷⁵ Failure of Sight after Railway and Other Injuries of the Spine and Head, London, 1869.

²⁷⁶ Affections oculaires Reflexes, Paris, 1866.

TABES DORSALIS.—That affections of the eye are common in this grave malady is admitted by all writers, but as to their frequency and nature at the different stages of the disease, there is wide diversity of opinion: this is probably in part due to the fact that from the chronic nature of the disease, which extends usually over a period of several years, it is rare that the case remains from beginning to end under care of the same observer. The symptoms are of three varieties—viz. firstly, transient paralyses of the external muscles of the eye; secondly, changes in the iris and ciliary body; and, thirdly, affections of the optic nerve. The first-named symptoms are frequent in the early stages of the disease. Sometimes they affect the external muscles supplied by the third pair, and at others the rectus externus. Their transient character and frequency, while admitted by all observers, have as yet received no adequate explanation, it being indeed difficult to see why transient affections of the motor nerves should be so common in a disease which has its seat in the posterior sensory columns of the spinal cord, and which presents such formidable and irreparable lesions. The pupillary symptoms are, as a rule, those of myosis, sometimes mydriasis, and at times the so-called Argyll-Robertson symptom (viz. a moderate myosis, with diminished reaction to light, but prompt response to convergence and accommodation). The last symptom is by no means present in all cases and at all stages of the complaint; but where it exists there is a remarkable resistance to the action of mydriatics. Trousseau was probably the first to call attention to this state of affairs. The writer has repeatedly seen cases where a strong solution of sulphate of atropia failed to produce any more than one-third of the usual dilatation produced by the same amount of the drug. Trousseau and Duchenne have both observed that during attacks of violent pain the pupils of ataxic patients will sometimes undergo temporary dilatation. Atrophy of the optic nerve (either partial or complete) is a frequent, and often an early, symptom of tabes dorsalis, and even may precede by many years the development of spinal symptoms. Foerster relates a case where complete optic atrophy preceded the development of all other symptoms by a period of three years, he having seen a number of other instances when atrophy preceded the other symptoms for a less period. Charcot records a case where the interval was ten years, and states that sooner or later locomotor ataxia develops in the majority of cases of optic atrophy in his wards in the Salpêtrière. Gowers gives two interesting cases, in one of which blindness came on fifteen years before the development of the other symptoms, the interval in the second being twenty years. Buzzard²⁷⁷ also has recorded an observation where blindness and lightning pains manifested themselves fifteen years before the development of the other ataxic symptoms. If we were to estimate the frequency of optic atrophy as a symptom of early development of tabes dorsalis by the cases seen at ophthalmic hospitals, we should probably much overrate its proportion, inasmuch as those cases in which atrophy is a more marked and early symptom alone resort to such places. Leber found that 13 (26 per cent.) out of 87 cases at his clinic had spinal symptoms, while Gowers gives 20 per cent. as a relation existing between degeneration of the optic nerves and tabes. The latter author thinks that the ratio should really be stated as 15 per cent., because 5 per cent. was due to cases which had been sent to him for examination by his colleagues. Nettleship classifies 76 cases of optic atrophy as follows: 38 as presenting undoubted symptoms of locomotor ataxia; 11 as showing mixed spinal and cerebral symptoms (as in general paralysis of the insane); 9 with other forms of spinal degeneration without brain lesions, these associated with reflex iridoplegia without other symptoms of spinal or cerebral disease; and 15 only in which there was no manifest disorder of other parts of the nervous system. In the earlier stages of degeneration of the optic nerve in tabes dorsalis the discs are usually of a dull reddish-gray tint, and, while they are still capillary superficially, their deeper layers next to the lamina cribrosa have a decidedly diminished blood-circulation, and appear of a marked and more neutral gray color. The surface of the discs often looks more or less fluffy, there being enough haze of the retinal fibres to veil, and at times to hide, the scleral ring. Later, the superficial capillarity disappears and the discs assume a pallid, filled-in aspect, being surrounded by a scleral ring which is everywhere too broad: at this stage the main stems of the retinal arteries and veins exhibit no marked change in calibre, but later on we find them shrinking, and the surface of the disc becomes excavated, the nerve itself often assuming a greenish tint. The earlier stages of such degenerations often exist for a long time, and are demonstrable by the ophthalmoscope before the sight is sufficiently impaired to prevent the patient from executing any ordinary work; this being dependent upon the facts that at first there is only a concentric diminution of the field for form and colors, while central vision remains for a long time unaffected. According to Foerster, this contraction of the field commences at the outer part. In advanced cases there are often irregular sector-like defects. This state of affairs makes it probable that while the number of cases in which total blindness precedes the development of tabetic symptoms is probably rated much too high, from the natural gathering of such cases at ophthalmic hospitals, yet, nevertheless, the frequency of incomplete gray degeneration of the optic nerves in the early stages of the complaint is probably, as a rule, much underrated.