Letter C (part 3 of 3)

Letter C (part 3 of 3)

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

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

[Footnote 97: Archives générales de Médecine, April, 1881, pp. 403-414.]

[Footnote 98: Gaz. méd. de Paris, No. 27, 4 Juillet, 1863.]

Diseases of the Kidneys and Skin.

DISEASES OF THE KIDNEYS.--As has been abundantly proved by careful autopsies, inflammation of the retina may be developed during any form of Bright's disease, either with the enlarged mottled kidney of acute parenchymatous nephritis, the large white kidney, the amyloid kidney, or the cirrhotic kidney of chronic disease. In the vast majority of cases the retinal inflammation appears during the later stages of the last-named form of disease, and seems to be in some way dependent upon blood-poisoning, which has been caused by the degenerating kidney.

The retinitis presents various aspects, not only in different cases, but also in the different stages of its development in the same case, and distinguishes itself mainly from other forms of inflammation of the retina by its marked tendency to fatty degeneration. As seen at an eye hospital the disease usually presents a type quite different to that which predominates in the wards of a general hospital. In the former class of cases the blood-poisoning seems to fall with peculiar intensity on the nervous system, and the patients come complaining of headache, dizziness, and dim vision, these being the only marked symptoms of the malady, while the anæmia, dropsy, and other symptoms are either absent or present in so slight a degree that the patients have not supposed themselves to be suffering from any constitutional malady or to need any medical advice. In the walking cases the retinal changes are usually very extensive (and those in the cerebrum would possibly be found equally developed if we {753} had only as accurate a method of investigating them), whilst among hospital inmates we often see only a few white splotches in the retina, either with or without hemorrhages, and occasionally only a slight atrophy of the optic disc due to a previous retinitis. In the wards of a general hospital we have a much better opportunity to study the early development of the retinitis, and it is there most frequently encountered among those suffering from dropsy and dyspnoea--patients whose waxy skin and general appearance indicate at a glance how seriously their nutrition has been impaired by the ravages of the disease. When the individual lives and is not markedly relieved by the rest and treatment adopted, we frequently have an opportunity of seeing the development to a greater or less degree of the typical form of the affection.

In typical cases the retinal changes commence with slight oedema of the disc and surrounding retina, associated with a few irregular white splotches and striated hemorrhages in the fibre-layer. These white patches multiply and extend, but are usually confined within an area of two or three disc-diameters from the optic entrance. In high grades of the affection they coalesce and form a broad zone around the disc, which is itself swollen and prominent, its outlines being hidden by the opaque nerve-fibres which diverge from it. From time to time fresh hemorrhages occur, which are striated when in the fibre-layer, and of irregularly rounded outline when they invade the deeper portions of the retina. These were formerly supposed to be absolutely characteristic of the disease, but it is now asserted by several good observers that similar appearances have been seen in the neuro-retinitis caused by brain tumor or by basilar meningitis where there was no accompanying disease of the kidney. Graefe,[99] Schmidt and Wegner,[100] Magnus,[101] Leber,[102] Carter,[103] and Eales[104] have each reported such cases. The hemorrhages are usually either entirely absorbed or leave behind them a fatty clot, which adds an additional white patch to the splotches already existing in the retina. In many cases occurring in the last stages of the disease, a remarkably yellowish tint of the fundus is observed, together with decided alteration in the color of the blood-columns in the retinal blood-vessels, the blood in the arteries being too yellow, and that in the veins presenting too little of its usually pronounced red-purple tint. In short, there is a state of affairs approximating in some degree to that which we find in cases of pernicious anæmia.

[Footnote 99: A f. O., xii. 2.]

[Footnote 100: Ibid., xv. 3.]

[Footnote 101: Ophth. Atlas, Taf. vi. Fig. 2.]

[Footnote 102: Graefe und Saemisch, Bd. v. p. 581.]

[Footnote 103: Diseases of the Eye (Am. ed.), p. 382.]

[Footnote 104: H. Eales, Birmingham Med. Review, Jan., 1880, p. 47.]

Exceptional forms of albuminuric retinitis have been recorded where the only change seen in the fundus oculi was a pronounced choking of the disc similar to that with which we are familiar in cases of brain tumor. The writer has seen cases which at the start could not be diagnosticated by the ophthalmoscope from cases of retinal hemorrhage due to other causes. Magnus has published similar cases.

In the course of Bright's disease uræmic amaurosis is much more rarely encountered than albuminuric retinitis. It is, however, occasionally developed in cases in which albuminuric retinitis already exists. It is rapid in its development, and in its subsidence is without retinal changes, the blindness being evidently due to some transient affection of the cerebral centres.

{754} DISEASES OF THE SKIN.--The eczema of the lower lid, nose, angle of the mouth, and external meatus of the ear which so frequently accompanies the phlyctenular conjunctivitis of scrofulous children is probably the most common example of coincident skin and eye disease. Lepra is a frequent cause of severe affections of the eye in localities where it is endemic. Bull and Hansen[105] assert that the cornea is frequently attacked. They divide the manifestations of the disease upon this membrane into two varieties--the one in which there is a diffuse infiltration of the tissue, and the other where there is a formation of tubers. The first variety is a gray opacity limited to the border of the cornea, not separated from its circumference by any such clear area as is found in arcus senilis. This opacity becomes vascularized, and may remain quiet for years till another attack of hyperæmia occurs, which, also in time receding, leaves the tissue more opaque than before. In the second there are nodes which appear to start at the margin of the cornea and to accompany either its superficial or its deep layer of vessel-loops: this latter form is more dangerous to vision. The paralysis of the orbicularis muscle which is a frequent attendant upon the smooth form of the disease allows an exposure of the membrane to irritants which often produce a third form of inflammation. The iris also exhibits the smooth and the tuberous forms of the disease. Iritis occurring in lepra is, however, by no means pathognomonic; 50 per cent. of all cases exhibiting synechiæ are the result of extensions of corneal inflammations due to orbicular paralysis. The superciliæ and the eyelashes are said to be frequent seats of leprous tubercules. In the lids the first symptom is the falling of the eyelashes, which is dependent upon the formation of the tubers before they become manifest to sight and touch. Mooren[106] maintains that chronic skin eruptions favor the development of cataract by causing creeping inflammatory processes which alter the character of the exudations into the vitreous humor, and moreover claims that when such skin eruptions have their seat in the scalp they favor the occurrence of retinitis by maintaining a constant hyperæmia of the meninges. He further cites a case where he observed a decrease in the acuity of vision corresponding with the breaking out of a skin eruption, and an increase in the power of vision coincident with the disappearance of the eruption. Foerster[107] agrees with Mooren in the statement that cataract may be formed in cases where chronic skin affections favor the development of marasmus. Rothmund[108] reports a noteworthy curiosity to the effect that cataract followed a peculiar degeneration of the skin in three families living in separate villages in the Urarlberg. The skin of these patients showed a fatty degeneration of the rete Malpighii and of the papillæ, with consecutive thinning and atrophy of the epidermis: this was most marked on the cheeks, chin, and the outer surfaces of the arms and legs. In the individuals thus affected the skin disease commenced between the third and sixth months of life, whilst the cataract appeared in both eyes between the third and sixth years. Rothmund thinks that the same congenital predisposition to disease exists in both organs, because the lens is developed out of an unfolding of the external skin.

[Footnote 105: The Leprous Diseases of the Eye, Christiana, 1873.]

[Footnote 106: Ophthalmologische Mittheilungen, 1874, p. 93.]

[Footnote 107: Graefe und Saemisch's Handb., vol. vii. p. 152.]

[Footnote 108: A. f. O., xiv., 1, p. 159.]

{755} Disturbances of Vision caused by Disease of the Sexual Organs.

The eyes and their appendages frequently exhibit the effects of perverted function or diseased conditions of the sexual organs. As might be expected, these ocular effects are most marked in the female, whose generative apparatus is so much more complex and extensive. While it is true that there are thousands of women with grave disease or derangement of these organs who are free from any uncomfortable eye symptoms, still, clinical experience shows that there are crowds of others who present eye lesions due entirely to such causes. Still more frequently do we see some slight optical defect (previously scarcely noticed) become so unbearable that the patient is unfitted for any useful employment. In fact, at most eye hospitals, and still more markedly in private practice, we find an excess of female over male patients. This excess becomes more palpable when we throw out of consideration the large number of male patients who are under treatment for injuries of all sorts the result of mechanical occupations not pursued by females, and the inflammations due to direct exposure to storm, cold, and intense heat.

MENSTRUATION.--When menstruation is profuse its effects are with difficulty distinguished from those of anæmia and loss of blood, but where it is retarded, irregular, or scanty the effects are more readily traced. All surgeons of experience are agreed that it is undesirable to perform operations for cataract or to make iridectomy at the menstrual period, and it is well known that eyes which have been progressing favorably after operations become congested and irritable during the monthly period. In trachomatous eyes retardation of the catamenia often causes the eruption of a fresh crop of granules, while in cases of phlyctenular and interstitial keratitis there are still more frequently relapse and exacerbation of the disease. Vaso-motor disturbances connected with the period of puberty and with that of cessation of the menses are of daily occurrence: we constantly see cases at these epochs where some slight astigmatism or hypermetropia, which has previously given no practical annoyance to the patient, becomes absolutely unbearable. The eyes become watery and sensitive to light; there is marked congestion of the retina with tortuosity of its veins, together with serous infiltration and swelling often sufficient to obscure the margins of the disc. These symptoms frequently entirely disappear when the menses have either become established or have permanently ceased. In some rare cases the symptoms are anomalous and striking: thus the writer has seen vicarious menstruation from the lachrymal caruncle, and a case of pemphigus of the upper lid occurring regularly at each menstrual period for some months. In another patient menstruation came on during the thirteenth year with intense headache, epistaxis, and photophobia, and for a long time afterward there was utter inability to use the eyes for school-work even during the catamenial interval. At almost every menstrual epoch during a period of eight years there has been a recurrence of these symptoms, although they subside sufficiently in the interval to allow the patient to use her eyes for a very limited amount of near work. At the first examination the ophthalmoscope showed that the retinal fibres were swollen and oedematous, hiding the outlines of the discs, while the lymph-sheaths of the retinal vessels at {756} their point of emergence from the disc presented an almost snow-white appearance. The discs and the retinæ have never quite resumed a normal appearance.

Disturbances in the circulation of the eye and its appendages are frequently associated with the menopause. The writer recalls a case where for years there was headache with intense congestion of the palpebral and bulbar conjunctiva, with a fulness and pressure on the orbits at each menstrual period, all these symptoms disappearing with the cessation of the menses. The most striking examples of the influence of the menses on the eyesight are those where the flow has been suddenly checked. Rejecting examples from the older authors, where the want of exact helps to diagnosis might leave room for a different interpretation of the symptoms, we will content ourselves with two examples where the testing of the eyesight and the ophthalmoscopic examination were made by skilled observers. Thus, Mooren--to whom we are indebted for a careful discussion of the relations between uterine disease and disturbances of sight--recites[109] the case of a peasant-woman aged twenty-three years who had complete stoppage of the menstrual flow from exposure to wet during the catamenial period: this was accompanied by high fever and delirium, with pain in the region of the right ovary. When these symptoms subsided, she noticed that there was absolute loss of sight in the right eye, and so great a diminution of it on the left that she could only distinguish movements of the hand. The ophthalmoscope showed in the right side a multiple detachment of the retina, and on the left an intense neuro-retinitis. Rest in bed, inunctions of mercurial ointment, and cataplasms over the region of the ovaries, with leeches to the septum of the nose and the neck of the uterus, gradually brought about amelioration of the symptoms, with restoration of the eyesight in the left eye. As might be expected, the retinal detachment and consequent loss of vision in the right eye remained permanent. In confirmation of this case, but in contrast with it as regards the retinal symptoms, is the one related by Samelsohn.[110] The patient (a peasant-girl) by standing in a cold running brook while at work had her menses suddenly stopped. There was no marked uterine or abdominal pain. The patient complained of a feeling of pressure on the orbits, and experienced a gradual failure of sight with contraction of the field of vision. In five days there was absolute amaurosis of both eyes (no sensation of light and no phosphenes to be obtained by pressure). The sight gradually returned in each eye, this being preceded by a copious flow of tears, so that in sixteen days the patient could read small print fluently. In seven weeks the menses returned. There were no ophthalmoscopic symptoms: each eye, both during the attack and subsequent to it, showed only striation of the retina and tortuosity of its veins, the calibre of the retinal arteries being unchanged. Unfortunately, any pupillary changes that might have been recognized were annihilated by previous instillation of atropine into the eye. In the first case there was every probability in favor of a serous effusion into the subarachnoidal and the intravaginal spaces. The latter case is more difficult to explain: if it were due to orbital or intracranial neuritis, why should there not have been some ophthalmoscopic changes during the {757} time that the patient was under observation? If to effusion within the cranium or to local circulatory disturbances in either the corpora quadrigemina or the occipital lobes, why were there not other symptoms of intracranial disturbance?

[Footnote 109: Arch. f. Augenheilkunde, Bd. x., 1881.]

[Footnote 110: Berliner klin. Wochenschrift, Jan., 1878, pp. 27-30.]

In further illustration of the effects of a stoppage of menstruation, Mooren[111] cites the case of a peasant-woman aged thirty-one who had complete suppression of the menses after the birth of her fourth child, and where subsequently an almost continuous headache, dimness of vision, and eventually epileptiform attacks, followed. The ophthalmoscope showed a double neuritis so intense as to lead to the supposition of a possible cerebral tumor. Mercurial inunctions with seton to the back of the neck were resorted to without result. Emmenagogues also failed to give relief. An examination of the uterus was now made, which showed great enlargement and hyperplasia, especially of its mouth and neck, for which scarifications and sitz-baths were employed with good result. The headache and epileptoid attacks disappeared, and the vision improved so far that the patient (who when admitted to the hospital could only decipher Jaeger No. xviii.) could read fluently Jaeger No. iii.

[Footnote 111: Loc. cit., p. 551.]

DISPLACEMENTS OF THE UTERUS.--Anteflexion and retroversion of the uterus are frequent causes of retinal hyperæsthesia. In this connection we may quote from the same author two cases, as showing how slight mechanical irritations of the uterus may cause eye disturbance--one where a patient had an episcleritis and a chronic metritis with malposition of the uterus, in whom there was an exacerbation of the ciliary neuralgia and of the local eye inflammation every time that the ulcerated os uteri was cauterized or a pessary introduced; and a second with an adhesive kolpitis, in whom the introduction of a pessary caused unpleasant feelings about the head and oppression in the cardiac region, accompanied on two separate occasions by capillary hemorrhages into the retina, all of these symptoms disappearing rapidly after the removal of the pessary. Mooren[112] has also seen a double neuro-retinitis caused by retroversion of the uterus. The sight was so much impaired that the patient could with difficulty decipher Jr. No. xx.; but it was entirely regained within a few months after the uterus had been replaced in its proper position. No other treatment was employed.

[Footnote 112: Ophthalmologische Mittheilungen, 1878, p. 97.]

PELVIC CELLULITIS.--Still more frequently are the reflex eye disturbances caused by parametritis and the various forms of pelvic cellulitis. Every practitioner has had abundant opportunity of studying the easy fatigue of the eye, the burning and stinging conjunctival sensations, the orbital and periorbital pains, the retinal hyperæsthesia and sensitiveness to artificial light, which characterize the early stages of the affection, accompanied later on by symptoms of retinal anæsthesia. Inasmuch as the cause of these symptoms is irremediable, we find in the majority of cases that it is impossible to relieve the sufferings of the patient; this cause consisting in the cicatricial shrinking of the parametrium and the pelvic connective tissue. Sleep gives relief only so long as it lasts, and the patients upon awakening, instead of feeling rested, often experience their greatest pain and discomfort. Foerster[113] and Freund, who were the first to demonstrate this {758} form of parametritis, call special attention to the fact that the patients have their good and bad days entirely independent of any use of the eyes. In many of the milder cases, however, we find that the sufferings of the patients are enhanced and aggravated by the presence of some defect, such as astigmatism, hypermetropia, or insufficiency. Although the careful correction of such defects will give considerable relief and enable the patients to use their eyes for near work for a much longer period, nevertheless the pain and discomfort are out of all proportion to the amount of error. Of course, we are very far from having converted such eyes into useful instruments for every-day work or for long-continued labor, but we have removed an appreciable source of irritation from an oversensitive nervous system, and done much to relieve the toedium vitæ in cases which perhaps for months previously have been unable to amuse or occupy themselves by the use of their eyes in either reading, writing, or sewing.

[Footnote 113: "Allgemein-Leiden und Veränderungen des Sehorgans," in Graefe und Saemisch, vol. vii. pp. 88-96.]

MASTURBATION is also an occasional cause of reflex eye disturbances. Mooren[114] relates two aggravated cases in women who for years had been excessively addicted to the vice. In both of these there were accommodative asthenopia and tenderness in the ciliary region, dread even of moderate illumination, which increased from year to year. In both cases there were attacks of dyspnoea and other disturbance of innervation of the pneumogastric nerve. Cohn has also published a number of cases of eye disease in the male sex due to the same cause. The main symptoms were a feeling of pressure on the eyes, bright dots moving before them, and a sensation as if the air between the patient and the object looked at was wavy and trembling. In some of the individuals a discontinuance of onanism and a moderate indulgence in sexual intercourse effected a complete cure. Travers[115] gives a case of loss of sight from excessive venery, and another from masturbation. Mackenzie[116] quotes Dupuytren as relating the case of a man who lost his sight on the day after his wedding, but where it was promptly restored by the use of a cold bath with stimulants and the application of counter-irritation to the skin of the lumbar region. Foerster[117] has recorded a case of kopiopia hysterica in a man where, from the eye symptoms alone, he diagnosticated disease of the genital organs, and where it was afterward proved that there was inability to copulate, the patient having extremely small testicles and there being a thin whey-like discharge from the urethra.

[Footnote 114: Loc. cit.]

[Footnote 115: Synopsis of Diseases of the Eye, 1820, p. 145.]

[Footnote 116: Diseases of the Eye, 1854, p. 1075.]

[Footnote 117: G. u. S. Handb., vol. vii. p. 95.]

CONGESTION AND INFLAMMATION OF THE OVARIES.--Disease of the ovaries is frequently associated with retinal oedema and hyperæsthesia. In women complaining of weak and painful eyes pressure in the ovarian region often causes pain. Where only one ovary is tender to the touch, we often notice that the patient complains more of the corresponding eye, although there may be no difference or abnormality in the ophthalmoscopic appearance of the two eyes. Under this head may be appropriately mentioned the eye symptoms of patients affected with hystero-epilepsy, a disease which is always associated with ovarian trouble, of which Charcot has given us so graphic a picture. He says that previous to the attack the patient experiences an aura which starts from the abdomen. The convulsion is ushered in by a loud cry, which {759} is accompanied by pallor of the face and loss of consciousness. These symptoms are succeeded by twitching and rigidity of the face-muscles, with foaming at the mouth, followed by contortions of the muscles of the trunk, abdomen, and lower limbs, the paroxysm terminating with sobbing, weeping, and laughing. Landolt has given us a careful description of the eye symptoms in such cases, and groups them into four stages. In the first, the outer and inner tunics of the eye appear healthy and the acuity of vision is normal, but there is a contraction of the form- and color-folds, always more marked on the affected side. In the second group the acuity of vision begins to fail, and the symptoms become more marked on the hitherto sound side. In the third with the more affected eye fingers can scarcely be counted, while the field of vision is limited to a few degrees from the fixation point; at this stage the ophthalmoscope shows a serous swelling of the retina, with fulness and tortuosity of its veins. In the fourth stage there is a partial atrophy of the optic nerve on both sides.

PREGNANCY.--Cases of amaurosis occurring during pregnancy, in which the vision was impaired after delivery, are recorded by Beer, Ramsbotham,[118] and other writers of the preophthalmoscopic period. Some of them, at least, may probably be accounted for by the occurrence of albuminuric retinitis in the puerperal state, but no such interpretation can be put on the more recent cases reported by Lawson[119] and Eastlake,[120] which in their main features strongly recall the amaurosis after loss of blood, although there is no history of any similar hemorrhages. In Lawson's case, we have an amaurosis which commenced during the gestation of the eighth child, and recurred during the ninth and tenth pregnancies. After the eighth labor the patient recovered sufficient sight to be able to sew; the amount of vision being gradually lessened after each gestation until finally complete atrophy of the optic nerve ensued. In Eastlake's case, the patient (æt. thirty-four) had borne nine children at full time. The labors were normal in character, and the amount of blood lost was not excessive. On the second or third days after the second and each subsequent delivery, sudden loss of vision occurred, and the woman became insensible. On recovering her consciousness, her sight did not at once return, the amaurosis remaining from three to five weeks. After the last labor there was complete and permanent loss of sight in both eyes: Z. Laurence examined this case with the ophthalmoscope, and reports only a slight contraction of the retinal arteries, without other positive lesion. Zehender,[121] in treating of the subject, remarks that "almost every busy eye-surgeon has encountered similar sad cases."

[Footnote 118: Med. Times and Gazette, March 7, 1834.]

[Footnote 119: R. L. O. Hos. Rep., vol. iv. pp. 65, 66.]

[Footnote 120: Obstet. Trans., vol. v. p. 79 (1864).]

[Footnote 121: Handbuch der Augenheilkunde, vol. ii. p. 180.]

PUERPERAL PHLEBITIC OPHTHALMITIS.--According to Mackenzie, this dread malady, which, as a rule, causes the death of the patient, may develop at any time from the third to the thirtieth day after delivery. It frequently attacks both eyes, and in those cases which do not terminate fatally eyesight is usually lost. Hall and Higginsbottom,[122] Mackenzie,[123] Fischer,[124] {760} Arlt,[125] and Hirschberg[126] have all given good clinical descriptions of the disease, with careful autopsies. As in other forms of metastasis, it is ushered in with a chill. Soon after, transient darting pains are felt in the eye, which are sometimes associated with photopsies and followed by serous infiltration of the conjunctiva bulbi. Later, owing to effusion in the capsule of Tenon and to the swelling of the orbital tissues, the eye projects forward and its motility is impaired, these symptoms being accompanied by a clouding of the cornea and the formation of pus in the anterior chamber. If the patient lives, we may have either discharge of pus through the cornea or sclera, or its gradual absorption: in either case, the eyeball shrinks to a small stump. Anatomical examination shows that the starting-point of these symptoms is a septic embolism of either the choroidal or central retinal blood-vessels. According to Hirschberg, "In other pyæmic affections in which the eye is attacked with septic embolism life is dangerously threatened, but there is a larger percentage of recovery with permanent blindness (single or double) than in the puerperal form."

[Footnote 122: Medico-Chirurgical Transactions, 1829, vol. xv. p. 120.]

[Footnote 123: Treatise on Diseases of the Eye, London, 1854.]

[Footnote 124: Lehrbuch der Entzündungen und Organischen Krankheiten des Menschlichen Auges, 1866, p. 285.]

[Footnote 125: Die Krankheiten des Auges, 1863, Bd. ii. pp. 167, 269.]

[Footnote 126: Archives of Ophthalmology, 1880, vol. ix. p. 177.]

Influence of Lactation.--The asthenopia, feeble accommodation, photophobia, and obstinate phlyctenular inflammations of the conjunctiva and cornea which occur during prolonged lactation are subjects of daily observation to every ophthalmic surgeon. They unfrequently fail to yield to appropriate remedies so long as the patients continue to nurse their children. Besides these symptoms, Critchett[127] has called attention to the sudden unilateral affection of sight which occurs during lactation, and is due to hemorrhage situated either in or behind the retina. This author has frequently seen such cases coming on without pain.

[Footnote 127: Medical Times and Gazette, 1858, p. 118.]

PATHOLOGY.--As regards the pathology of these affections we are still very much in the dark. Mooren in his elaborate paper (previously quoted) considers that the reflex disturbances of the retina and optic nerve may either be transmitted directly, or may cause primarily a spinal myelitis, which in its turn affects the eyes. He points out that the subperitoneal connective tissue of the pelvis and the uterus is so rich in blood-vessels, lymphatics, and nerves that Rouget has likened it to cavernous tissue. He asserts that the uterine and pelvic nerves re-enter the lumbar cord, while the veins anastomose freely with the veins of the spinal column; and quotes Röhrig to show that electric stimulation of the ovary causes a rise in the general blood-pressure and a diminution of the heart's action--effects which he attributes to irritation of the vagus. He further maintains that any long-standing or often-repeated congestion of the visual centres, of the optic nerve, or of the retina would cause increase of connective tissue and a subsequent tendency to contraction, while the lymph which is poured out, acting on the cylinder axis of the nerves, causes them first to swell, and finally to absorb (Rumpf,[128] Kuhnt[129]).

[Footnote 128: Untersuchungen am d. Physiol. Institut. d. Univ. Heidelberg, Bd. ii. Heft 2.]

[Footnote 129: Ueber Erkrankung der Sehnerven bei Gehirnleiden, 1879.]

{761} Febrile and Post-febrile Ophthalmitis.

VARIOLA.--Various affections of the eye which at times impair its functions, and at others destroy vision, frequently arise during the course as well as during the subsidence of smallpox. When pocks form in the skin of the eyelids, they cause the lids to swell to such an extent as to completely close the eye: many patients so affected relate how, after being blind for a week or ten days, they again recovered their eyesight. The cicatricial processes which ensue often produce falling of the eyelashes with incurvation of the tarsus, which changes the direction of the ciliæ and causes the lashes to rub against the eyeball. During the first stage of the disease there is always flushing and congestion of the conjunctiva, frequently associated with increased flow of tears and sensitiveness to strong light. In some cases we find small elevated yellowish spots, often in groups of two or three, surmounted by an area of vascularization on the edges of the lids and in the tarsal conjunctiva. Similar efflorescences are at times seen in the conjunctiva bulbi and on the limbus corneæ. These coincide in the time of their appearance with the eruption on the skin, and are probably of the same nature, although from the difference in the anatomical structures they do not present the same appearance as the pocks in the skin. Hebra, who has observed and analyzed twelve thousand cases, says that 1 per cent. of the total number presented efflorescences in the conjunctiva. Neumann, Knecht, Schely, Buck, and other German authorities describe them; and Adler in his able monograph (On Eye Diseases during and after Variola) gives an accurate account of them. In opposition to the above statement it should be mentioned that Gregory maintains that no mucous membranes except those of the fauces, larynx, and trachea are capable of taking on variolous inflammation. Marson[130] also, who from his position at the London Smallpox Hospital had unusual opportunities for witnessing the disease, maintains "that pustules never form on the conjunctiva;" Coccius[131] is also of the same opinion. These authors call attention to the fact that the well-known abscesses of the cornea which occur during the drying and desquamation of the eruption, and which have frequently been described as pocks by the older authors, cannot in any sense be considered as pocks. Beer, however, while calling these formations pocks, distinctly states[132] that they occur during the suppurative or drying stage. There seems to be no good reason why the above-described conjunctival efflorescences, which come on simultaneously with the skin, should not be considered as analogous in their natures, although from the absence of the corium in the conjunctiva they cannot assume the well-known form of the skin eruption. At times the conjunctivitis becomes catarrhal, and even purulent, leaving in some cases an acute dacryo-cystitis (Adler), and more frequently a low grade of blenorrhoea of the lachrymal duct. Beer states that "those authorities may be right who suppose that there is a real eruption of pocks in the mucous membrane of the tear-sac, because no other sort of inflammation of it is so apt to cause complete closure in its entire length."[133] The cornea may present either diffuse or interstitial keratitis. Malacia or abscesses are more {762} frequent in the severe cases, where there are evidences of metastases to other organs. They usually form in the outer quadrant of the cornea, and are accompanied by marked ciliary injection, the patients complaining of stitches in the ball with frontal and temporal neuralgia. Prolapse of the iris and often the formation of a staphyloma are produced by the perforation of resultant ulcers; sometimes the entire cornea is swept away. Marson declares that he has seen this last condition occur within forty-eight hours from the time of the commencement of the corneal affection. Iritis is a less frequent complication. It is of the seroplastic variety, and, according to Adler, comes on only after the twelfth day and in cases where the progress of the disease is slow and insidious. It is always accompanied by some degree of cyclitis and by vitreous opacities. Four cases of glaucoma are on record as occurring during variola; and one (that of Adler) is noteworthy from the fact that the prodroma of glaucoma coincided with those of the smallpox. It was successfully operated on, notwithstanding the fact that the incision was made difficult by the necessity of avoiding a pock on the limbus of the cornea. Fortunately, the present generation has rarely an opportunity of seeing great numbers of eye affections from smallpox, and when they do occur, the partial protection from previous vaccination often modifies their severity. In these days of antivaccination societies, it is interesting to turn back to the accounts of the disease given by those who were in active practice at the time of Jenner's great discovery, and to see how serious the matter appeared when viewed through their spectacles. Thus, Andreæ says, "No disease is so dangerous to the eyesight as the smallpox, and before the introduction of vaccination it caused as much blindness as all other eye inflammations put together."[134] Benedict[135] also bears testimony to the great diminution in the intensity of variolous ophthalmia after the introduction of vaccination.

[Footnote 130: London Med. Gazette, 1838-39, pp. 204-207.]

[Footnote 131: De Morbis Oculi humani que e Variolis exedi, etc., Leipzig, 1871.]

[Footnote 132: Lehre von den Augenkrankheiten, vol. i. p. 527.]

[Footnote 133: Op. cit., p. 525.]

[Footnote 134: August Andreæ, Grundriss der Gesammten Augenheilkunde, vol. ii. p. 260.]

[Footnote 135: P. W. G. Benedict, De Morbis Oculi humani inflammatorii, lib. iii. p. 367.]

Writing later, Himly[136] says: "Smallpox, formerly a rich source of all eye diseases by which the doctor was most busied, is at present only feebly represented by the varioloids (i.e. smallpox modified by cowpox)." Mackenzie[137] states that "in former times smallpox proved but too often the cause of serious injury to the eyes, and even of entire loss of sight. It was by far the most frequent cause of partial and total staphyloma." Dumont in his work on blindness, the result of his own observations at the Hospice des Quinze-Vingts at Paris, and from its extensive statistics in previous years, records that out of a total of 2056 blind, 262 were blind from variola (or 12.64 per cent.); and, further, that the old records of the hospice showed 17.9 per cent., whilst at present (1856) it was 12 per cent. amongst the older inmates, and but 7 per cent. amongst the more recently admitted. He quotes Carron du Villars as giving the ratio before Jenner at 35 per cent. From immunity we become careless, so that when an epidemic breaks out (as that in Mayence in 1871) we have a state of suffering which forcibly brings back our remembrance of old times. Thus, Manz asserts that "the pestilences of the last (Franco-German) war have revived the remembrance of a disease which in the {763} beginning of this century was a terror to humanity, but which in the last decade was so rare that many now living physicians know it only by the writings of the older authors: the late epidemics, however, have enlarged their experience, and added a new contingent to the almost extinct army of the smallpox-scarred blind."[138]

[Footnote 136: Krankheiten u. Missbildungen des Auges, Berlin, 1843, p. 481.]

[Footnote 137: Diseases of the Eye, p. 500.]

[Footnote 138: Jahresbericht f. Ophth., 1873, pp. 178-183.]

RUBEOLA.--Preceding the outbreak of the skin eruption, or coincident with it, every case of measles presents a greater or less degree of catarrhal conjunctivitis, often accompanied by lachrymation, itching, and burning of the lids, slight pain, and photophobia. In from two to three weeks the catarrh usually disappears of itself, but in many cases leaves behind it an asthenopia and sensitiveness to light which often lasts for months. In some fortunately rare cases the catarrh increases, and we have a severe muco-purulent inflammation of the eyes, causing partial or total sloughing of the cornea, and thus leading either to the formation of a staphyloma or to the total loss of the eye. Moreover, we often have the development of phlyctenular keratitis as one of the sequelæ, especially among the weak and badly nourished. Some authors (Rilliet and Barthez, Mason, Schmidt-Rempler, De Schweinitz, etc.) relate cases where diphtheritic conjunctivitis, with all of its well-known symptoms--yellow, ropy-like secretion, great bulbar chemosis, and hard board-like infiltration of the lids--set in during the course of the disease. Kerato-malacia (a rapid sloughing of the cornea with marked anæsthesia of the ball, without swelling of the lids) was probably first observed as a consequence of measles by Fischer.[139] He had seen three cases, each accompanied by suppression of the skin eruption, severe fever, and delirium. The corneæ were entirely destroyed in twenty-four to forty-eight hours, and the children died soon after the development of the eye affection. Beger and Begold (Leber) have each reported similar cases. Sometimes in the course of this disease, amaurosis, either permanent or transient, is doubtful. Graefe[140] gives a case where failure of sight came on during convalescence, and where for a week there was absolute loss of perception of light, without any other ophthalmoscopic appearances than a slight neuritis, the patient gradually recovering his eyesight. In an epidemic of measles with severe cerebral symptoms, Nagel[141] records a case of a child where on the third day sopor, convulsions, opisthotonos, and dilatation of the pupils set in. The patient remained soporose for ten days, and then, on regaining consciousness, was found to be entirely blind. On the twenty-fifth day from the setting in of the convulsions, perception of light was dubious, and the pupils, which remained insensitive to the reflection from the ophthalmoscopic mirror, contracted slightly on exposure to the full glare of daylight. There was eventually complete recovery both of health and eyesight, the return of the latter being apparently hastened by the use of strychnia. The same author relates two other cases, in one of which the ophthalmoscope showed neuritis. One of them was fatal, the other terminated in recovery, and in neither was there any return of eyesight. In some cases of measles where Bright's disease of the kidneys is pre-existent or sets in during the {764} attack, there may be the development of the characteristic form of retinitis albuminuria.

[Footnote 139: J. N. Fischer, Lehrbuch der Entzündungen und Organischen Krankheiten des Menschlichen Auges, Prag, 1846, p. 275.]

[Footnote 140: A. f. O., xii., 2, p. 138.]

[Footnote 141: Behandlung der Amaurosen, pp. 24-30.]

SCARLATINA.--In scarlatina we have usually a hyperæmia of the conjunctiva coincident with the skin eruption. Inflammatory affections of this membrane and of the cornea are much less frequent than in measles. Martini[142] remarks that only in one case in twenty is there any inflammation of the eye. Beer[143] informs us that the tears are more irritating than in morbillous ophthalmia, and that the photophobia is more persistent. When ichorous ulcers form, they attack not only the cornea, but also the white of the eye, and spread much more rapidly in this situation than in the conjunctival leaflet of the cornea. Kerato-malacia occurs more frequently than in rubeola. Bonman[144] relates that in a severe epidemic of scarlet fever five boys in one family were taken sick, and that two of them lost their sight from sloughing of the cornea within a week of their seizure. Of these, one died, and the other was brought to him with a shrunken globe and without light-perception. The eyes of the other three children were not affected. Arlt in the first volume of his work on diseases of the eye[145] has given us a clinical description of this form of kerato-malacia. The patient, a boy of four and a half years, was first seen by him on the eighth day of the disease. The child was very pallid, with a burning-hot skin, hoarse voice, slight diarrhoea, and flat abdomen. The right cornea was evenly clouded throughout, swollen, and softened, while the left had lost its brilliancy and was slightly clouded, presenting the appearance of an eye thirty-six hours after death. The conjunctivæ of both eyes were white, with a few vessels and ecchymotic spots in their lower parts. On the tenth day, the right cornea was converted into a mass as soft as schmeer-käse, and was beginning to be thrown off on the centre, where there was a hernia of the hitherto unaffected membrane of Descemet. Both eyes eventually had the cornea completely destroyed, and the patient died on the seventeenth day. Iritis is more frequent than after measles.

[Footnote 142: Von dem Einflusse des Secretions Flussigkeiten, vol. ii. pp. 267, 268.]

[Footnote 143: Lehre von dem Augenkrankheiten, Bd. i. pp. 536, 537.]

[Footnote 144: Lectures on the Parts concerned in the Operations in the Eye, London, 1870, p. 110.]

[Footnote 145: Krankheiten des Auges, vol. i. pp. 211-213.]

Considering the frequency of acute nephritis in this disease, the retinal lesions are comparatively rare. Schreiber[146] gives two interesting plates of chorio-retinitis after scarlatina. Ebert[147] at a meeting of the Berlin Medical Society in 1867 called attention to some cases of transient blindness in the course of scarlatina without ophthalmoscopic changes; and Graefe, who presided at the meeting, remarked that in all these cases of absolute blindness there was still reaction of the pupil to the light, and that therefore there could be no neuritis or decided lesion between the corpora quadrigemina. He considered the prognosis favorable so long as there was pupillary reaction, and not necessarily bad where it was wanting. Although this is the rule, the prognosis is certainly more favorable when the pupil reacts promptly and to moderate light. Hirschberg[148] has recorded a case of blindness following meningitis, where light-perception failed to return, although the pupillary reaction lasted several weeks.

[Footnote 146: Veränderungen des Augenhinter-grundes, Plates iii. and iv., Figs. 7 and 8.]

[Footnote 147: Berliner klin. Wochenschrift, Jan. 15, 1868, pp. 21-23.]

[Footnote 148: Ibid., 1869, p. 387.]

{765} Relapsing typhus fever is frequently followed by amblyopia and inflammation of one or both eyes. Considerable variety in the intensity and in the symptoms of the disease has been manifested in different epidemics, and the ratio of the percentage of eye cases has greatly varied. In most outbreaks of relapsing typhus fever amblyopia is followed by inflammation. This was the sequence of the symptoms in the epidemic in Dublin in 1826, in Glasgow in 1845, and in Finland in 1865, although in the last-mentioned the inflammatory symptoms were less prominent and severe than in the first two. The eye symptoms rarely develop during the first attack of the fever, but usually occur after a second or third attack or during convalescence. The earliest careful study of the eye symptoms in a severe epidemic is that of Wallace,[149] who tells us that "there is often that haggard and worn aspect, that sickly, mottled, pallid hue of skin, that sleepy, exhausted, and oppressed appearance of the eye, which is more easily observed than described. The patient only half opens the lids of the affected organ. They are of a purplish-red color and humid. Their subcutaneous vessels are preternaturally enlarged. The vascularity of the sclerotic and conjunctiva is greatly increased. The vessels of the former describe a reticulated zone round the cornea, and those of the latter run in a direction more or less straight to the edge of this membrane, and sometimes appear to pass on the edge. The hue of the redness is peculiar; it is a dark brick-red. The pupil is generally much contracted, and its edge thickened and irregular. The iris is altered in color, generally greenish, and incapable of motion. There exists dimness of the cornea, which may be compared to the appearance glass assumes when it has been breathed upon. There is often a turbidness of the aqueous humor, and a pearly appearance of the parts behind the iris may be observed by looking through the pupil. There is great intolerance of light, and a copious, hot lachrymal discharge. The vision will be found for the most part so extremely imperfect that the patient can merely distinguish light from darkness, and he is often tormented by flashes of light which shoot across his eye, and these occur more particularly in dark places; or he is troubled by brilliant spectres or by the constant presence of muscæ volitantes. There is very considerable pain, which returns in paroxysms, and these are almost always more severe at night. The pain is sometimes referred to the ball of the eye, sometimes to one of the lids, sometimes to the temple or to the circumference of the orbit." Mackenzie agrees in the main with the foregoing description: his cases were also accompanied by severe inflammation, with hypopyon and copious precipitates in the membrane of Descemet and on the anterior capsule of the lens. He also called attention to the diminution of the intraocular tension and the consequent flabbiness of the eyeball, and states that out of 1877 cases of fever admitted to the Glasgow Infirmary during the epidemic of 1843, 261 (one-seventh) were attacked by the disease of the eye. Anderson,[150] who describes the same epidemic later in the course, takes exception to Wallace's statement that there is always an amaurotic stage at the outset of the disease. He computes these cases at two-thirds of the entire number, and tabulates five cases of inflammation without {766} amaurosis. He also describes and gives plates which show opacities of the vitreous, posterior synechia, pigment on the anterior capsule, posterior polar cataract, and other forms of lenticular degeneration; these conditions ensuing not only in this disease, but in all other affections where the circulation in the ciliary body and the constitution of the vitreous are profoundly involved. Schweigger, in describing an epidemic in Berlin, says that in one-third of the cases of ophthalmia there was simple unilateral iritis, and that in a second third there was diffuse punctiform or flocculent vitreous opacities without any trace of iritis or external symptoms of disease; while in the remaining third there was iritis with vitreous opacities in common: when it ensues in its usual form the effects of annular synechiæ or detachment of the retina; rarely from suppuration of the corneæ. Although of late years the Russian writers have materially added to our knowledge of the affection, nevertheless in most essentials their observations agree with those above quoted. Thus, Blessig[151] gives an account of an epidemic in St. Petersburg, while Logetschnikow[152] describes an epidemic in Moscow in which he encountered over 700 cases of this form of ophthalmia. Larionow[153] relates the history of a mild epidemic in the Russian army of the Caucasus, and tabulates 767 cases of the fever, in which are also included a number of cases of exanthematic typhus and a few cases of typhoid fever. Exclusive of the ischæmia of the retina and feebleness of the accommodation which were present in every case during convalescence, there were 3 cases of serous retinitis, 2 of hemeralopia, and only 3 of iritis; while in 10 per cent. of these there were vitreous opacities. He did not see a single case of genuine irido-choroiditis in the entire number. Estlander[154] has given a masterly description of two epidemics which he observed at Helsingfors in Finland, both of which occurred after a failure of the crops and consequent famine. In the first of these epidemics, which was of a mild type, only 3 out of 222 patients died, and the concomitant eye affections were few in number; while in the latter, 18 out of 242 patients died, and extensive vitreous opacities with severe inflammation of the eyes were frequent. He agrees with Mackenzie that the fever attacks few children under ten years of age, and says that although the disease is much more liable to attack people between twenty and thirty years of age, here it is less frequent than it is in patients between ten and twenty years of age, where it exists in one half of the cases. Arlt[155] agrees with this, and says that it is due to the fact that hunger and malnutrition are in general much worse borne by adolescents than by adults. As regards the period of the disease at which the eye symptoms come on, Estlander says that out of 28 carefully observed cases it developed 6 times during the fever or a week after its cessation, 11 times between the second and fourth week, 5 times in the second month, and 6 times from the third to the fifth month. These figures agree well with those given by Mackenzie, and show that there is both a feeble state of constitution and a prolonged convalescence from {767} this severe fever. Pepper,[156] in a previous volume of this work, has given an interesting account of an epidemic in this city in which he states that eye affections were of rare occurrence.

[Footnote 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).]

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

[Footnote 151: Congrès internationale d'Ophthalmologie, Paris, 1868, pp. 114-117.]

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

[Footnote 153: Klinische Monatsblätter f. Augenheilkunde, 1878, pp. 487-497.]

[Footnote 154: A. f. O., xv. 2, pp. 108-143.]

[Footnote 155: Klin. Darstellung der Krankheiten des Auges, 1881, pp. 289-291.]

[Footnote 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 Rush[158] 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 {768} 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." Fernandez[161] 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.

[Footnote 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).]

[Footnote 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.]

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

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

[Footnote 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 Levrier[162] 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. Arlt[163] 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. Galezowski[164] 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 {769} 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.

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

[Footnote 163: Klinische Darstellung der Krankheiten des Auges, 1881, pp. 121, 122.]

[Footnote 164: Quoted by Levrier, loc. cit., p. 39.]

[Footnote 165: Traité des Maladies infectueuses.]

[Footnote 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. Beer[167] 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. Poland[168] 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 Cohn[169] 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 {770} 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. Coggin[170] 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. Knapp[171] 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.

[Footnote 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.)]

[Footnote 168: R. L. O. H. Rep., vol. i., pp. 26-31, 1857.]

[Footnote 169: Klinik der Embolischen Gefärskrankheiten, 1860, p. 196.]

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

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

* * * * *

{771} DISEASES OF THE NERVOUS SYSTEM.[172]

[Footnote 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 {772} 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-Gemuseus[174] 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 {773} 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.

[Footnote 173: Ophthalmoscopie, p. 293, 1868.]

[Footnote 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 {774} 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 Annuske[175] 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 {775} 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.

[Footnote 175: A. f. O., xix., 3, pp. 165, 300.]

[Footnote 176: Klin. Monatsblätter f. Augenheilkunde, 1874, pp. 274, 275.]

[Footnote 177: Med. Times and Gazette, Sept. 4, 1875.]

[Footnote 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 {776} 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.

[Footnote 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, Hirschberg[180] 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.

[Footnote 180: Virch. Arch., Bd. lxv.]

2. Hughlings-Jackson and Gowers[181] (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.

[Footnote 181: R. L. O. H. Rep., vol. viii. p. 330.]

3. Curschmann[182] (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, Westphal[183] 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.

[Footnote 182: Centralblatt f. Augenheilkunde, 1879, p. 256.]

[Footnote 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. Newton[184] in 1704 had already appreciated the importance and difficulty of the subject, and in {777} 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 Michel[188] supported the same doctrine, and since then Schwalbe[189] and Scheel[190] 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 prove[192] 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.

[Footnote 184: Optiks, London, 1704, p. 136.]

[Footnote 185: Loc. cit.]

[Footnote 186: "Chiasma Nervorum Opticorum der Menschen und der Thiere," Sitzungsberichte der Wiener Akadamie.]

[Footnote 187: A. f. O., xix., 2, pp. 39-58.]

[Footnote 188: Ibid., xix., 2, pp. 59-84.]

[Footnote 189: G. u. S., vol. ii. p. 324.]

[Footnote 190: Klin. Monatsblätter f. Augenheilkunde (extra number 2), 1874.]

[Footnote 191: Arch. f. Psychiatrie, vol. ii. p. 21.]

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

From similar experiments on rabbits, Mandelstamm[193] 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-Séquard[195] asserted that a medial cut of the chiasm in rabbits produces amaurosis of both eyes, which would indicate that there is total crossing, while Nicati[196] 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. Woinow[198] 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-Rimpler[199] also showed atrophy of both tracts {778} more marked in that of the opposite side, and Manz[200] found atrophy of both tracts after atrophy of the nerve of one side; Plink[201] reports a similar state of affairs; while Popp[202] and Michel[203] from analogous specimens draw conclusions favorable to the total crossing.

[Footnote 193: Ibid., xix., 2, p. 47.]

[Footnote 194: Ibid., xxiii., 2, p. 227.]

[Footnote 195: Archiv de Physiologie, 1872, p. 261, and 1877, p. 656.]

[Footnote 196: Ibid., 1878, p. 658.]

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

[Footnote 198: Klin. Monatsblätter f. Augenheilkunde, 1875, p. 425.]

[Footnote 199: Ibid., 1877, "Bericht der Ophth. Gesellschaft," pp. 44-48.]

[Footnote 200: Klin. Monatsblätter f. Augenheilkunde, 1877, "Bericht der Gesellschaft," pp. 49, 50.]

[Footnote 201: Arch. f. Augenh. und Ohrenheilkunde, vol. v.]

[Footnote 202: Inaug. Diss., Embolie der Art. Centralis, Regensberg, 1875, p. 20.]

[Footnote 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.

[Footnote 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 {779} 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. Mauthner[205] 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.

[Footnote 205: Gehirn und Auge, 1881, pp. 373-381.]

[Footnote 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, {780} 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-Jackson[208] 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 Little[209] 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.

[Footnote 207: Topische Diagnostik der Gehirnkrankheiten, p. 198, 1879.]

[Footnote 208: In Russell Reynolds's System of Medicine, vol. ii., 1872.]

[Footnote 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, Panas[210] relates a case of absolute {781} 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.

[Footnote 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. Coignt[212] 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. Steffen[213] 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.

[Footnote 211: Robin, p. 104.]

[Footnote 212: Thèse de Paris.]

[Footnote 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 {782} 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."

Prévost[214] 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. Nothnagel[215] 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 Coignt[216] 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 {783} 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.

[Footnote 214: Thèse de Paris.]

[Footnote 215: Topische Diagnostik der Gehirnkrankheiten, p. 580, 1879.]

[Footnote 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 {784} 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. Arlt[220] 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. Vulpian[221] 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. Cohn[222] 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. Stintzing[223] gives a case where there was thrombosis of the basilar and Sylvian arteries. Oglesby[224] relates two cases where nystagmus came on suddenly with dilatation of the pupils, the autopsies showing a clot which pressed on the medulla. Fienzal[225] 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 Willbrand[227] 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.

[Footnote 217: Lancet, 1871, p. 662.]

[Footnote 218: Annales d'Oculistique, 7, 82, p. 177.]

[Footnote 219: Graefe u. Saemisch, vol. vi. p. 226.]

[Footnote 220: Krankheiten des Auges, Bd. iii. p. 335.]

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

[Footnote 222: Schussvorletzungen des Auges, p. 19.]

[Footnote 223: Jahresbericht f. Ophth., vol. xiv. p. 306.]

[Footnote 224: Brain, vol. iii., 1880.]

[Footnote 225: Trans. Internat. Congress, at Milan, 1881, p. 126.]

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

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

{785} 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." Zehender[231] 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."

[Footnote 228: Loc. cit.]

[Footnote 229: R. L. O. H. Reports, vol. x. p. 203.]

[Footnote 230: Ibid., vol. v. p. 343.]

[Footnote 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. Moos[232] speaks of oscillatory movements of the eyes in Menière's disease, and Schwalbach[233] 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.

[Footnote 232: Arch. f. Augenheilkunde und Ohrenheilkunde, vii. 2, p. 508.]

[Footnote 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 {786} 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. Horner[234] 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. Hutchinson[235] 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 Bowman[236] 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." Wadsworth[237] 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 {787} 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.

[Footnote 234: Klinische Monatsblätter f. Augenheilkunde, 1871, p. 321.]

[Footnote 235: R. L. O. H. Rep., 1866, pp. 191-215.]

[Footnote 236: Ibid., 1867.]

[Footnote 237: Trans. of Amer. Oph. Soc., 1874.]

[Footnote 238: Loc. cit.]

NEURO-PARALYTIC OPHTHALMIA.--In 1822, Herbert Mayo[239] showed that section of the fifth nerve within the cranium produces insensibility of the eye; and Charles Bell[240] 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 Eckhard[250]--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 convinced[254] 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. Quaglino[255] gives an instance where complete ptosis shielded the eye from all gross insults, but where, nevertheless, a central slough of the cornea formed. Laqueur[256] also found {788} 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. Hirschberg[258] 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.

[Footnote 239: Anat. and Physiol. Commentaries, London, 1822, No. 2, p. 5.]

[Footnote 240: Nervous System of the Human Body, London, 1830, p. 207.]

[Footnote 241: Loc. cit.]

[Footnote 242: Virchow's Archiv, Bd. xiii. S. 107, 1850.]

[Footnote 243: Nagel's Jahresbericht (Lit. 1873), p. 266.]

[Footnote 244: Idem.]

[Footnote 245: Virchow's Archiv, Bd. lxv. Heft. 1, pp. 69-99.]

[Footnote 246: Anatomie et Physiologie du Système nerveux, t. ii. p. 161, Paris, 1842.]

[Footnote 247: Arch. f. Ophthalmologie, Bd. i. Abth. i. S. 306-315.]

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

[Footnote 249: Ibid., p. 217 (also quoted by Wells).]

[Footnote 250: Centralblatt f. Med. Wiss. (cited by Nagel, Literature, 1873).]

[Footnote 251: Nagel's Jahresbericht, (Lit. 1876), p. 51.]

[Footnote 252: Ibid.]

[Footnote 253: Ibid., 1883, p. 153.]

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

[Footnote 255: Nagel's Jahresbericht (Lit. 1874), p. 26.]

[Footnote 256: Klinische Monatsblätter f. Augenheilkunde, 1877, p. 228.]

[Footnote 257: Nagel's Jahresbericht (Lit. 1873), p. 267.]

[Footnote 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. Erichsen[259] cites cases from Hippocrates, Fabricius Hildanus, and La Motte where amaurosis was produced by a wound of the brow. Chelius[260] gives a case from similar injury, while Wardrop[261] 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. Guthrie[262] 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, Rondeau[263] {789} 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.

[Footnote 259: Loc. cit., pp. 233-261.]

[Footnote 260: South's translation of Chelius's System of Surgery, vol. i. p. 430.]

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

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

[Footnote 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. Graux[264] 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 {790} 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.

[Footnote 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 Dianoux[265] 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. Hallopeau[266] 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. {791} The pupils are sometimes described as contracted, more rarely as dilated. Leeser quotes Leube[267] 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."

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

[Footnote 266: Des Paralysies bulbaires, Paris, 1875, p. 41.]

[Footnote 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. Foerster[268] 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 Leber[269] this atrophy is histologically similar to that occurring in gray degeneration of the nerves. The outer strands are {792} 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.

[Footnote 268: G. u. S., vol. vii. p. 227.]

[Footnote 269: A. f. O., xiv., 2, p. 203.]

[Footnote 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. Noyes[271] 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.

[Footnote 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, Noyes[272] 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.

[Footnote 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. Albutt[273] 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 {793} 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 Jones[275] 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." Rondeau[276] 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.

[Footnote 273: Use of the Ophthalmoscope, London, 1871.]

[Footnote 274: Concussion of the Spine, by John Eric Erichsen, London, 1875.]

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

[Footnote 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 {794} 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. Buzzard[277] 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 {795} 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.

[Footnote 277: Brain, ii. 1878, p. 168.]

Foerster has most justly called attention to the remarkable mental cheerfulness of persons laboring under this malady, and states that he has frequently seen cases where the patients would insist that they were improving, while examination of the acuity and of the field of vision showed steady failure of the eyesight. The writer's personal experience has on several occasions substantiated this statement. According to Cyon,[278] tabes presents three varieties: First, tabes dorsalis. This variety commences with paralyses of the eye-muscles and amblyopia. The pupils are not contracted. The amblyopia progresses. Cramp-like disturbances of innervation are always present, with a want of co-ordination of movements and anæsthesia of the upper extremities, while mental disturbances are often demonstrable. Second, tabes cervicalis. Myosis, with intense boring pains in the extremities and impotence, are its chief characteristics. Ataxia is rare, and disturbances of vision develop only late in the course of the disease. Third, a class which he considers the true form of tabes dorsalis, in which there are marked anæsthesia, formication, bladder and rectal symptoms, associated with motor disturbances which often end in paralysis. In such cases there are no eye symptoms except occasional dilatation of the pupil. The same writer has collected 203 cases reported by various authors, and gives the following tables as showing the relative frequency of eye symptoms:

Amblyopia . . . . . . . . . . . . . . . . . . . . . . . . 33 times. Paralysis of eye-muscles . . . . . . . . . . . . . . . . 30 " Mydriasis . . . . . . . . . . . . . . . . . . . . . . . . 3 " Myosis . . . . . . . . . . . . . . . . . . . . . . . . . 9 " -- 75

Amaurosis with affections of eye-muscles . . . . . . . . 16 times. Amaurosis with mydriasis . . . . . . . . . . . . . . . . 8 " " " myosis . . . . . . . . . . . . . . . . . . 1 " Affections of the eye-muscles with mydriasis . . . . . . 4 " Amaurosis with mydriasis and affection of the eye-muscles 2 "

He remarks[279] that the number of reported cases of mydriasis is probably excessive, and says that dilatation has been improperly noted, as, for instance, where one pupil is normal and the other contracted. As regards the frequency of the Argyll-Robertson symptoms, Vincent[280] found it {796} present in 40 cases out of 51, in which there were 7 cases of amaurosis with immobile pupils, 5 being marked exceptions to the rule. Out of 51 cases of tabes, the same author found myosis in 27. The statements of Vincent (as will be seen) differ materially from those of Cyon. Erb[281] found that in 56 cases, there were only 7 in which the optic nerves were affected (12½ per cent.), while in 17 there were affections of the eye-muscles (30-3/10 per cent.). He considers myosis a frequent symptom, but thinks that the stage at which it develops is not yet determined. The anatomical cause of the want of sensitiveness of the pupils to light, while they retain their movements of convergence and accommodation, has not been well made out. Vincent[282] attributes it to a paralysis of the excito-motor filaments which supply the iris, and which he locates at the upper portion of the spine; while Wernicke thinks it due to degeneration of the filaments which go from the third pair to the optic nerve. Hughlings-Jackson[283] tells us that the pupils which fail to react to light often act but slightly with convergence, and in a note gives two cases of absolutely immobile pupils where the accommodation was nearly normal for the age. In fact, much remains to be accomplished in the study of the innervation of the iris and ciliary muscle in tabes. The proportion of cases in which cycloplegia occurs, and what relation it bears in point of time and frequency to the presence of iridoplegia, are far from being well made out. Jackson also insists that tabes does not necessarily follow in all cases of long-standing optic atrophy. On a basis of 72 cases Gowers says that some formal ophthalmoplegia interna was present in 92 per cent. He groups these cases into three stages: No. 1, where there is loss of knee-jerks, lightning pains, difficulty of standing with toes out and heels together, there being a want of ataxic gait; 2, where there is an ataxic gait, but the patient can still walk by the aid of a stick; 3, where the patient cannot walk without the assistance of another person. In 23 of his cases in the first stage (84 per cent.) symptoms of palsy of some of the intraocular muscles were found; in the second stage, 29 cases (93 per cent.); in the third stage, 18 cases (100 per cent.). Erb has called attention to the fact that reflex dilatation of the pupil from sharp stimulation of the skin of the temple is usually absent where we have the Argyll-Robertson pupil. Gowers admits that this is the rule, but has seen several cases where, although there was no attempt at myosis on exposure to light, yet there was marked dilatation on stimulating the skin.

[Footnote 278: Tabes Dorsalis Berlin, 1866, p. 43.]

[Footnote 279: Loc. cit., p. 71.]

[Footnote 280: Thèse de Paris, cited by Robin, p. 20.]

[Footnote 281: Nagel's Jahresbericht der Ophthalmologie, 1872, p. 150.]

[Footnote 282: Thèse de Paris.]

[Footnote 283: Transactions of the Ophthalmological Society of the United Kingdom, vol. i. pp. 139-154.]

Unclassified Nerve Diseases.

DIABETES.[283]

[Footnote 283: This affection has been placed here for convenience of classification, and because there is a form of the disease which is of neurotic origin.]

DIABETES MELLITUS.--This disease, which affects so profoundly all tissues of the body, necessarily manifests its influence on the tissues of the eyes. It frequently impairs the nutrition of the vitreous and causes the formation of cataract. The presence of grape-sugar is readily detected in such lenses by chemical examination. Mitchell and other {797} experimenters have produced cataract in frogs by placing them in a solution of sugar. In such instances the lens tissue is said to become transparent when the animal is removed from its sugar bath and placed for a time in water; therefore, it is probable that the cataract has been developed by the simple abstraction of water. Diabetic cataracts are often extracted successfully, and the wound usually heals well; but we occasionally have intraocular hemorrhage during the course of healing. At times the nutrition of the patients is so impaired that a slight accident is dangerous, such as happened in a patient of the writer, where the striking of the hand against an iron bedstead caused gangrene and death. Nettleship[285] has recorded an analogous case, where accidental injury during convalescence caused death from gangrene. At times marked retinitis and hemorrhages with clear media have been encountered; thus, Jaeger in 1855 gave us an admirable picture of such a case, in which there was retinal swelling so great as to hide the outlines of the nerve, it being accompanied by numerous hemorrhages and yellow splotches. In his description of the case he also states that there was a marked central scotoma (a denser inside of a lighter one) in the field, while the periphery of the retina was so little affected that the patient could still decipher large letters (No. 18 of Jaeger's test-types). We might perhaps think that the scotomata are accidental and due to the location of the retinal changes in the given case, but later researches seem to show that we may have them in diabetes without retinal changes, Nettleship and Edmunds describing two such cases. In one of these cases there seems to be some doubt whether it was not a tobacco amblyopia which had been developed in a diabetic subject; but in the other case there was no such complication. The retinal changes which have been recorded in some cases have much resembled those due to albuminuria, but these alterations in the eye-ground have been seen in a number of cases where no albumen in the urine could be obtained.

[Footnote 285: Transactions of the Ophthalmological Society of the United Kingdom.]

Diabetes also may, by impairing the nutrition, diminish the power of accommodation in the young and cause a rapid increase of presbyopia in old persons (Graefe, Nagel, Foerster). Horner[286] proved that a hypermetropia of 1/14 in a patient of fifty-five years of age rapidly diminished to H. = 1/48, and the amount of presbyopia remained unaltered, while the general health had improved and the quantity of sugar had diminished. He attributes this rapid increase and subsequent diminution of the hypermetropia to a change in the amount of the fluid contents of the eye. Were this reporter any less careful an observer, one might be inclined to suspect swelling of the lens; but he specially mentions that there was no trace of cataract formation.

[Footnote 286: Klin. Monatsbl. f. Augenheilkunde, 1873, p. 490.]

EPILEPSY.

IDIOPATHIC EPILEPSY.--In idiopathic epilepsy--that is, in those cases where no gross changes in the brain can be demonstrated by autopsy--the eye symptoms are numerous and interesting. Wecker[287] tells us that at the commencement of the spasm there is contraction of the pupils. Usually, soon after the tonic spasm sets in or coincident with it, we have marked dilatation of the pupil and an abolition of the eye-reflexes, this {798} being shown by the want of contraction of the orbicularis or of the pupil when the conjunctiva is touched. Reynolds, Echeverria, Clouston, and Hammond have called attention to a development of hippus (an alternate contraction and dilatation of the pupil) at the end of the convulsive paroxysms; but this is exceptional. The last author considers a state of alternate contraction and dilatation of the pupils, or a contraction of one pupil with dilatation of its fellow, to be characteristic of the convulsive stage. When the convulsions are unilateral the head and eyes are often turned toward the convulsed side. Although ophthalmoscopic examination is favored by dilatation of the pupil, yet the convulsions make it so difficult that we have quite conflicting accounts of the state of the disc and retina during the paroxysm. Six cases have been accurately examined by Albutt during the convulsion, in three of which there was congestion of the disc, and pallor in the remainder. Jackson also reports cases of pallor during the convulsion. More lately, Schreiber[288] has examined three cases in which he found pallor in the convulsive stage, this being very marked in one case, where the convulsion was violent. Gowers, on the other hand, maintains that in convulsions which commence locally without initial pallor of the face he was unable to perceive any alteration of the calibre of an artery which he kept continuously in view during the convulsion. The same author tells us that during the stage of cyanosis the veins of the retina become distended and dark, and that once in the status epilepticus he has seen a congestion of the discs with oedema, which subsequently disappeared. He does not consider that there is any abnormal appearance of the discs in the intervals between the attacks, while both Albutt and Bouchut hold that they are congested. In several of the chronic cases which the writer has had an opportunity of examining there has been a low grade of atrophy of the discs with concentric limitation of the field of vision. That this, at least, is common in advanced cases is well shown by the observations of Michel,[289] who in 1867 published careful examination of the eye-ground, acuity, and field of vision of 58 epileptics. In 15 of these cases there were no visible changes; in 10, hyperæmia; in 1, hyperæmia with oedema; 1 of hyperæmia passing into atrophy; 10 of unilateral atrophy (9 of the right nerve and 1 of the left); 13 cases of atrophy of both optic nerves; the remaining cases showing changes in the eye-ground which were probably attributable to other causes. Auræ which affect the special senses have been recorded, and have been usually described as flashes of light or balls of fire. Maisonneuve (quoted by Robin) gives an instance where the auræ consisted in convulsions of the eyelids. Gowers gives 119 cases of auræ which affected the special senses, 84 of these being of the sense of sight. He divides the latter into five classes: I. Sensation in the eyeball; II. Diplopia; III. Apparent increase or diminution in the size of objects; IV. Loss of eyesight; V. Distinct visual sensations, consisting sometimes of flashes of light, colored spectra, and rarely some more specialized sensation, such as an apparition. The only one of these cases in which there was an autopsy appears to have been one of symptomatic rather than idiopathic character, as there was found a tumor of the occipital lobe which had extended as far forward as the angular gyrus.

[Footnote 287: G. u. S., Bd. iv. p. 565.]

[Footnote 288: Ueber Voränderungen des Augenhintergrundes, etc., 1878 (S. 42).]

[Footnote 289: Inaug. Diss., von Dr. Julius Michel, Würzburg, 1867.]

{799} HYSTERO-EPILEPSY.--The remarkable co-ordinated convulsions which are associated with hemianæsthesia, and which have been so minutely described by Charcot as characteristic of this disease, are constantly accompanied by subjective or objective disorders of the visual apparatus. Visions of animals, such as rats, vipers, crows, cats, etc., frequently precede the convulsive seizure, followed by a transient loss of sight; a return of the illusions (sometimes pleasant and gay, at others erotic in their nature, or again sad or terror-striking) coming on in a later stage. It is said that processions of animals are often seen, which usually come and go on the hemianæsthetic side as the attack passes off and the patient becomes quiet. The objective symptoms have been carefully studied by Landolt in Charcot's wards. They were found by him to consist in a diminution of the acuity of vision and a concentric limitation of the field for form and color. All these symptoms are bilateral, and much more marked on the anæsthetic side, they occurring before any ophthalmoscopic changes are visible. These are followed later by alterations in the eye-ground, which consist at first of slight congestion and oedema of the discs, followed by partial atrophy. The difference in the affection of the two eyes was so marked that Charcot at first described it as a crossed amblyopia, but he admits that the lesion is bilateral, as above described.[290]

[Footnote 290: Leçons sur les Localisations dans les Mal. du Cerveau, vol. i. p. 119 (foot-note), Paris, 1876.]

EXOPHTHALMIC GOITRE.

GRAVE'S DISEASE; BASEDOW'S DISEASE.--The most prominent characteristics of this affection are an irritability of the heart with increased frequency of the pulse, and enlargement of the thyroid gland and a swelling of the tissues of the orbit, which cause the eyeballs to become prominent. The size of the goitre and the amount of protrusion of the eyeball vary very much in different cases. Frequently there is a symptom to which Graefe was the first to call attention--namely, a disturbance of the usual consensual movements of the eyeball and upper eyelid. When the patient looks downward below the horizontal line, the lid no longer accompanies the eyeball in its motion, but halts in its course. This derangement in the action of the lid is supposed to depend upon some defect in the innervation of the orbicularis, as it is not present in cases of equal prominence of the eyeball from other causes. The amount of secretion from the tear-glands and from the conjunctival surface is also at times much diminished. Owing to the prominence of the eyes and the relaxation of the orbicularis, the fissure of the lids is wider open than usual, and the eye has a peculiar stare. At times, when the prominence of the eyes is very great, the lids fail to cover the balls during sleep, and the cornea becomes inflamed and ulcerated from exposure to air and dust. The disease rarely develops till after puberty, and is more frequent in females than in males: in the former it often develops after childbirth. It is so frequently accompanied by disease of the reproductive organs that Foerster, in his paper on the "Relation of Eye Diseases to General Disease,"[291] places it in the section devoted to eye symptoms from diseases of the sexual organs. Ophthalmoscopic examination usually shows a slight thickening of the fibre-layer of the retina in and around the disc, with dilatation and tortuosity of the veins--a state of affairs which may often {800} be fairly attributed to venous stasis caused by the swelling tissues. In addition to these symptoms there is sometimes, as Becker has pointed out, a dilatation of the arteries, which may almost equal the veins in calibre. At times there is an arterial pulse. As found by autopsies, the anatomical changes are usually enlargement and dilatation of the heart, hypertrophy and various degenerative changes in the thyroid glands, and a state of hyperæmia at times associated with hypertrophy of the fat tissue of both orbits.

[Footnote 291: Graefe und Saemisch, vol. vii. p. 97.]

Affections of the General System.

CHOLERA.--In this disease the eyelids are said to show an early development of cyanosis, which becomes more marked as this symptom develops in other parts of the body. The contents of the orbits shrink and the eyes are drawn back in their sockets, there being an imperfect closure of the lids, which leads at times to necrosis of the exposed lower part of the cornea. There is a marked diminution in the secretion of tears, and often a dilatation of the veins of the exposed part of the conjunctiva bulbi, which are turgid with the black blood, this state being at times accompanied by subconjunctival hemorrhages. The pupils are usually contracted. The retinal arteries are much diminished in size, and the veins although not dilated, are filled with blackish blood. Owing to the great feebleness of the circulation, the slightest pressure with the finger on the eyeball produces arterial pulse; Graefe[292] in some cases describes a pulsating movement of interrupted blood-columns in the veins, such as is sometimes seen in incomplete embolism of the arteria centralis.

[Footnote 292: A. f. O., xii. 2, p. 210.]

RHEUMATISM AND GOUT.--In the older books on diseases of the eye we constantly meet references to rheumatic and arthritic forms of inflammation of that organ. In the later works on the subject the list has been greatly reduced, partly because an anatomical classification has been attempted, and partly because many such affections have been attributed to other causes, such as syphilis, etc. Catarrho-rheumatic ophthalmia, rheumatic iritis, rheumatic paralysis of the eye-muscles, etc. have been so classified, not on account of their occurrence in the course of attacks of acute rheumatism, but because the writers have been unable to attribute them to any other source than that designated as having taken cold. That recurrent attacks of iritis are frequent in some individuals who have recurrent attacks of chronic inflammation of the joints is a fact familiar to many practitioners, amply attested by the cases published by Hutchinson[293] and by Foerster.[294] As regards gout, the direct proofs of its relations to eye disease are still less manifest, and most cases supposed to be attributed to this cause by both the older and more modern writers are to be classed as primary or secondary glaucoma.

[Footnote 293: "A Report on the Forms of Eye Disease which occur in connection with Rheumatism and Gout," by Jonathan Hutchinson (R. L. O. H. Reps., vol. vii. pp. 287-332; also vol. viii. pp. 191-216).]

[Footnote 294: "Beziehungen der Allgemein-Leiden, etc., zu Veränderungen des Sehorgans," Graefe u. Saemisch, vol. vii. pp. 155-160.]

SYPHILIS.--All the tissues of the eyeball and eyelids may at times manifest the signs of this dread and searching dyscrasia, although it is {801} rarely so marked in its character as to be distinguished with certainty from other forms of eye disease by its appearance alone. Primary syphilis of the lid is rare, but when it occurs it is liable to be mistaken for epithelioma, where there is absence of a distinct history of infection. In the eyeball itself the uveal tract (iris, ciliary body, and choroid) is the favorite seat of disease. Iritis is said by Fournier[295] to be developed in from 3 to 4 per cent. of all cases of syphilis, and, according to Coccius, 11-6/10 per cent. out of 7898 cases of eye disease in Leipzig were due to this cause. Syphilitic iritis certainly constitutes a large proportion of the cases of inflammation of the iris seen in hospital practice: Coccius places the percentage at 46-6/10 per cent., while Wecker puts it at 50 to 60 per cent. It usually develops during the subsidence of the secondary skin affections, and is often to be distinguished by its insidious course and the amount of plastic exudation which accompanies it. There is ciliary injection and sluggishness of the pupil, with the formation of synechiæ, before there is any very decided pain or photophobia, this latter being usually strongly developed at a later period. The formation of gummata in the iris, which are generally seen in the smaller circle, is much rarer, generally developing in the tertiary stage of the disease; occasionally they are developed in the ciliary body. In the former situation they usually disappear under active treatment, leaving fair vision in the eye, but when situated in the latter place they usually lead to shrinking and atrophy of the eyeball, even under the most vigorous treatment. When iritis occurs in infants it is generally specific in origin. When they are born with posterior synechiæ and complicate cataract, similar occurrences during intra-uterine life may be suspected. Syphilitic choroiditis is frequent, but its frequency is probably overrated on account of a disposition to assume syphilis as a cause of cases of choroiditis in which the pathology is not evident. Foerster has very properly pointed out that a majority of the cases of disseminate choroiditis are not due to this cause, and that the changes are developed slowly, and remain stable for a long time even when not treated; while the usual form of specific choroiditis shows rapid progress, with failure of the sight, photopsies, vitreous opacities, hemeralopia, and zonular defects in the field of vision. Opinion, however, is divided on this point: Wecker thinks that two-thirds of the cases of disseminate choroiditis are due to syphilis. In many of the chronic cases of syphilitic choroiditis there is a wandering of the pigment out of the cells of the choroidal epithelium, and a distribution of it into the lymph-sheaths of the retinal vessels and capillaries, these changes producing ophthalmoscopic appearances which closely resemble those of typical pigmentary degeneration of the retina. Affections of the head of the optic nerve and superficial layers of the retina, such as are represented by Liebreich,[296] are much more rare, but the writer has repeatedly seen them both at Liebreich's Paris clinic and in our own hospitals. They are characteristic, and usually accompany the tertiary symptoms. There is a dense haze which seems to lie partly in front of the retina, and to extend around the disc for a space of one and a half to two disc-diameters, generally including the macula lutea, and rapidly diminishing as it approaches the equator. Vision is usually much reduced, and even under persistent {802} antisyphilitic treatment it is slow to clear up. Hereditary syphilis frequently manifests itself in an interstitial keratitis, which begins with small irregularly-rounded dots near the centre of the cornea. They gradually become more numerous, and coalesce, until the membrane appears as if a thin layer of ground glass had been imbedded in its tissue, leaving the epithelium clear and bright. Although there is no ulceration, yet there is a great tendency to the formation of new blood-vessels, which often goes on until the entire cornea is permeated by them and becomes of a dull venous blood-like red color. These vessels are continuous with superficial and deeper shoots which pass in from the two layers, normally forming loops in the corneal periphery. This form of keratitis is usually accompanied by marked photophobia, pain, ciliary injection, and low grades of iritis. The pathological processes which take place in the cornea during the disease generally leave it more or less clouded, and often much misshapen by softening and alteration of its curvature.

[Footnote 295: Quoted by Foerster, Graefe und Saemisch, vol. vii. p. 189.]

[Footnote 296: Plate 10, Fig. 2, ed. 1863.]

TUBERCULOSIS.--Except in children, the eyeball is rarely the seat of a deposit of tubercles, and even then it is much more likely to give evidence of their seat in the membranes of the brain by its secondary affection than to be itself directly affected by them. When they form in the eye, they may affect the choroid, the intraocular end of the optic nerve, the retina, or the iris. Jaeger was the first to call attention to their ophthalmoscopic appearances. Their favorite seat, as is well shown in one of Jaeger's plates, is the macular region and its vicinity. They develop in the stroma of the choroid, and appear as whitish-yellow spots varying from one-eighth the diameter of the optic disc to the size of the disc itself, and by aggregation may form even larger masses. They are usually seen in cases of well-marked acute miliary tuberculosis, although doubtless they are often overlooked, on account of not giving rise to any symptoms; besides, thorough ophthalmoscopic examination of such sick and restless children is difficult, and the general diagnosis is usually well made out from other symptoms. They may, however, precede all other symptoms, as in the cases reported by Steffen[297] and Fraenkel.[298] Development of tubercular masses in the intraocular end of the opticus has been described by Chiari,[299] Michel,[300] and Gowers.[301] In the case cited by the last author the growth extended from the disc to the ora serrata, which during life gave rise to the peculiar reflection from the eye so often seen in intraocular tumor. According to Cohnheim,[302] tubercle is to be found in the choroid in all cases of acute miliary tuberculosis. Other observers, however, have not been able to support him in this assertion: Albutt,[303] who repeatedly searched for them both in living and dead subjects, failed to find them; Garlick[304] during two years' experience at a children's hospital found them but once; Heinzel[305] in ten cases of general tuberculosis in children was at the autopsies unable to find any tubercles of the choroid. According to Stricker, they may at times develop very rapidly, coming on in from twelve to twenty-four hours. Tubercles have been {803} found in the retina in the cases of papillary tuberculosis already referred to, and also with cases of tubercle in the iris (Perls, Manfredi). At times, tubercles in the iris occur in scrofulous and feeble children, appearing as growths in all respects closely resembling syphilitic gummata. As in the latter case, they are accompanied by severe iritis, and at times with hypopyon. Tuberculosis of the conjunctiva is a very rare affection. It is described as commencing with swelling of the lids, and when these are everted exuberant granulations of the conjunctiva are seen which are most frequently situated in the retrotarsal folds. These granulations are at first of a grayish-red color, but when they have existed for some time, superficial erosion of their surface occurs, and uneven yellowish-red ulcers are formed. The disease usually occurs in young people, and generally affects but one eye. Haab[306] has given a description of six cases of it, with reference to a few instances described by other authors.

[Footnote 297: Jahresbericht f. Kinderheilkunde, 1870 (Gowers).]

[Footnote 298: Berliner klinisches Wochenschrift, 1872, pp. 4-6 (Foerster).]

[Footnote 299: Wien. Med. Jahrbucher, 1877, p. 559.]

[Footnote 300: Archiv der Heilkunde, 1873.]

[Footnote 301: Medical Ophthalmoscopy, 1879, p. 250.]

[Footnote 302: Virch. Arch., 1867, Bd. xxxix. p. 49 (Foerster).]

[Footnote 303: Quoted by Gowers, p. 203.]

[Footnote 304: Quoted by Gowers, Med. Ophth., p. 200.]

[Footnote 305: Quoted by Foerster, p. 99, Jahrbuch der Kinderheilkunde, Neue Folge, viii., 3, p. 331.]

[Footnote 306: "Die Tuberculose des Auges," A. f. O., xxv., 4, p. 163.]

Toxic Amblyopiæ.

TOBACCO AND ALCOHOL.--These two lesions strongly resemble each other, and it is impossible to differentiate them when we find them in persons who are addicted to the abuse of both of these drugs; consequently, for a time, in Germany, there was a disposition to underrate the potent destructive agency of the latter drug, but every practitioner of experience in eye disease must have seen cases of tobacco amblyopia in which there has been no abuse of alcohol. The best proof of the deleterious influences of tobacco on the eyesight is the improvement which results by simple abstinence from its use where the vision has been seriously affected by its influence. In the earlier stages of both forms of amblyopia there is a contracted pupil and a slight dimness of vision, the patients claiming that they see better in feeble light and twilight. The ophthalmoscope shows a slight oedema of the disc with tortuosity of the veins, the rest of the eye-ground appearing normal. Later, the usual appearances of blue-gray atrophy set in. In the earlier stage there are often color scotomata, which are usually ovoid in form and lie between the disc and the macula lutea. Unless carefully looked for with color squares of one to two millimeters in diameter, they are apt to be overlooked. Later, there is a marked reduction of central vision. When the atrophy has progressed farther, there is decided contraction of the field.

LEAD-POISONING.--The deleterious effects of lead on the eyesight are undoubted, although rare in proportion to the cases of colic and wrist-drop produced by this metal. When amaurosis develops, it is usually either in acute lead-poisoning or after a gradual saturation of the system, as is shown by repeated attacks of lead colic. In either case the amaurosis is usually accompanied by dilatation of the pupils, delirium, and convulsions. The amaurosis generally passes off, and the pupils contract with the return of vision, although it may remain permanent, and leaves the patient with atrophic nerves, as in a case observed by Trousseau, where the patient was subsequently transferred to the Salpêtrière. The only two cases which the writer has had an opportunity of witnessing showed {804} marked choking of the discs and severe cerebral symptoms. One of these cases died and one recovered: both were results of the use of white lead as a cosmetic. Rognetta[307] quotes Vater as reporting a case of hemianopia produced by lead-poisoning, which recovered when the lead colic was cured. Trousseau[308] quotes Andral as giving a case of diplopia due to the same cause, and disappearing as the patient recovered.

[Footnote 307: Recherches sur la Cause et la Siège d'Amaurose.]

[Footnote 308: Thèse de Concours.]

QUININE.--Over-doses of quinine seriously impair the eyesight, and in some cases have produced temporary but absolute blindness. The usual symptoms are a deterioration of central vision and a contraction of the field. The ophthalmoscopic examination reveals a pallid disc with marked diminution in the size of the retinal arteries and veins. In many of the reported cases it is difficult to decide positively how much of the amaurosis is due to the quinine and how much to the disease for which the patient is under treatment. This is especially true where the patient has been suffering from severe intermittent fever or from exhausting hemorrhages complicating uterine disease, which are well known frequently to produce more or less complete atrophy, with shrinking of the vessels. There are, however, a sufficient number of well-observed cases on record to satisfactorily establish the lesion. One of the most striking is a case of poisoning recorded by Giacomini, where the patient took at one dose three drachms of sulphate of quinia by mistake for cream of tartar. This was followed by severe headache, pain in the stomach, dizziness, unconsciousness, with slow and scarcely perceptible pulse and infrequent respiration. The pupils were widely dilated. On regaining consciousness the patient found that he was almost blind, the weakness of sight lasting a long time. As the poisoning occurred in the preophthalmoscopic era, there is of course no description of the eye-ground. In all recorded cases, while central vision has been either partially or entirely regained, the field of vision has remained permanently contracted.

SANTONIN.--In very large doses santonin produces dilatation of the pupil, amblyopia, and complete color-blindness. Smaller doses produce a shortening of the violet end of the spectrum and cause yellow vision. The disturbance of vision usually lasts only a few hours. The poison seems to be eliminated by the urine, as the sight is said to become normal while traces of the drug can still be seen in the secretion of the kidneys. Rose has given us a most careful study of this subject in his papers entitled "Color-Blindness from Santonin"[309] and "Hallucinations in Santonin Intoxication."[310]

[Footnote 309: Virch. Arch., Bd. xx., 1860 (Separat Abdruck, S. 48).]

[Footnote 310: Ibid., Bd. xxviii., 1863 (Separat Abdruck, S. 12).]

SALICYLATE OF SODIUM.--Gatti[311] reports a case of transient amblyopia, due to the ingestion of one hundred and twenty grains of salicylate of sodium, in a sixteen-year-old peasant-girl who had acute articular rheumatism. There were no changes in the eye-ground except a fulness of the veins, which persisted after the eyesight had returned. There was mydriasis. No phosphenes could be produced. As the urine did not present any traces of salicylate of sodium, it would seem to show that it was not eliminated by the usual emunctories.

[Footnote 311: Gaz. d. Ospital Milano, p. 129, 1880; Nagel's Jahresbericht, 1882 (Lit. 1880), p. 245.]

{805}

MEDICAL OTOLOGY.

{806}

{807}

MEDICAL OTOLOGY.

BY GEORGE STRAWBRIDGE, M.D.

In this article on Medical Otology it is proposed to include those diseases of the ear that are frequently seen by the general practitioner, and especially those that exist as sequelæ to some general disease, and where the ear complication would be treated in connection with the general disorder.

Examination of a Patient.

As nearly all ear patients are afflicted with varying degrees of deafness, one of the first points of inquiry will be as to their hearing power. There are three tests commonly employed for this purpose: the ticking of a watch, the human voice, and the tuning-fork.

1st. The Watch.--By this method of examination the patient is placed with closed eyelids, so as to exclude the visual power as a factor in the examination, as it is a curious fact that many people are apparently unable to distinguish between seeing a watch and hearing its tick, and therefore so long as they can see the watch they will imagine that they can hear it ticking. Bring the watch (held by the physician) from a distance toward the patient until the tick is heard, and note the distance in inches. The plan of holding the watch close to the ear, and then slowly removing it until the extreme limit of hearing is attained, gives an incorrect result as regards the distance that the watch can be heard, due to the fact that the impressions produced on the terminal endings of the auditory nerve by the watch-tick continue a sensible time after the watch-tick has passed out of the nerve-limit, and therefore the watch-tick can still be noted. Prout has prepared a convenient method for recording the hearing power. Note the number of inches that the watch-tick can be heard by a normal ear, and let this serve as a denominator of a fraction, the numerator of which is the number of inches that the same watch-tick can be heard by the ear of the person under examination. For instance: a normal ear can distinguish my watch-tick at a distance of twenty inches; if, now, the patient's ear can perceive the same sound at only five inches, the hearing power would be noted as 5/20. By this it is not meant that the hearing power is one-fourth of normal hearing, as it would be only one-sixteenth of normal hearing, as the volume of sound is inversely in proportion to the square of the distance.

2d. The human voice tells more about the hearing power for practical purposes than does the watch. There are many persons who can readily {808} hear the watch-tick at several inches, and yet who hear very imperfectly ordinary conversation, and also many who hear very well the human voice and very badly the watch-tick. The method of examination is to speak ordinary words in a tone that can be heard by the average ear a given number of feet, and to note the distance in feet that the ear under observation can detect the words that are spoken. In this way can be noted the hearing power of the human voice, the numerator of the fraction being the distance that the word can be heard by the observed ear, the denominator being the distance that the word can be distinguished by the normal ear.

The patient should always be examined with closed eyelids, as deaf people quickly learn by watching the movements of the lips of the speaker to know the words that are being spoken. Another precaution is to have the ear to be tested directly opposite the mouth of the observer, the other ear being firmly closed.

3d. The Tuning-Fork.--Bone-conduction of sound is used by this method. The great use of the tuning-fork is in determining diseased conditions of the auditory nerve and internal ear, and it enables one to make a differential diagnosis as to whether deafness is due to a diseased condition of the sound-conducting apparatus or whether the nerve portion of the ear is at fault. For instance: a patient complains of deafness. This may be due to some obstruction in the external auditory canal, such as impacted cerumen, or it may be due to a diseased middle ear, with thickening of its membranes, or it may be due to a diseased internal ear. The watch and human voice would only show the ear to be defective in its hearing power, and it may be from any of the above-mentioned causes. The tuning-fork, in vibration, placed on an incisor tooth or on the frontal bone, would bring out the fact that if the deafness was due to a diseased middle ear or obstruction in the external auditory canal, the tuning-fork would be heard best by the defective ear; but if due to a disease of the internal ear, it would be heard the least distinctly by the defective-hearing ear. Mack explains this by the supposition that the sound-waves are prevented from freely escaping through the sound-conducting apparatus, and are reflected back on the auditory nerve-elements, and thus make a double impression. Tuning-forks having the note C are best adapted for this examination.

EXAMINATION OF THE EXTERNAL CANAL AND TYMPANIC MEMBRANE.--This can be done by direct or by reflected light, better by the latter. A mirror and speculum are needed. The mirror should be concave, with a focal distance of from 5"-7" and a diameter of 2½"-3", with a ball-and-socket-joint and head-band, so as to allow of the two hands being free, the head holding the mirror in the required position. The mirror should have a central perforation of 2'''-3''', with a brass back, rendering it less liable to break. As a light-source can be used the light from an argand burner, but preferably sunlight reflected from a cloud or white wall.

The Ear Speculum.--The Wilde or Gruber speculum answers equally well. The Wilde speculum is cone-shaped, and best of German silver: it is easily cleansed and has four sizes. The Gruber speculum has a larger mouth and gives a large visual field. It has a parabolic curve, for the purpose of admitting more light; there are also four sizes. The {809} speculum should be warm when in use, and is to be held in position in the canal by the thumb and forefinger of the left hand. Often in the examination of an external canal an angular-toothed forceps is needed to remove foreign substances.

The cotton-holder is a most important instrument, furnishing a means of thoroughly drying the external canal of any fluid with the least possible amount of irritation--much less than that caused by the use of the ear-syringe. It is a slender steel rod 6" long, having a number of serrations at one end to more easily allow cotton to be wrapped around it; the other end has a convenient handle. In using this instrument a small tuft of well-cleansed cotton is wrapped around the holder, so that one half of the length of the cotton tuft projects beyond the end of the instrument. By slight adaptation with the fingers the cotton roll can be made soft or quite firm, and large or small in proportion to the amount of cotton used. The cotton-holder should always be used under the light from the head-mirror.

The curette is of the same length as the cotton-holder, but is made of heavier steel, and terminates at one end in a small ring of a diameter of from 2-3 mm. It is useful in removing scabs, etc. from the external canal, also in loosening impacted cerumen.

Probes are also needful. A good middle-ear probe is made of a single piece of silver, of the same length as the cotton-holder, and tapering down to a slender shank with a small knob-like ending.

The ear syringe, a most excellent instrument, is now made of rubber, holding two ounces of fluid, and has a bulbar extremity, so as to avoid injuring the external canal or tympanic membrane. The syringe has a finger-rest, with the piston ending in a ring, so as to admit of its use with one hand. In using a syringe warm water should be always employed, and at a temperature that the finger would indicate as being quite warm. Also at first force the water very gently into the meatus, so that the patient shall not be startled; also it is well to bear in mind that many patients become very giddy under its use, necessitating either very gentle use or its being abandoned for the time.

EXAMINATION OF THE EUSTACHIAN TUBE.--The main point is as to whether the tube permits the free passage of air up to the middle ear. This can be ascertained by three methods: 1. Valsalva's method; 2. Politzer's method; 3. Catheterization of the tube.

Valsalva's method consists in forcing air through the tube by a forced expiration, the mouth and nasal passages being at the same time firmly closed. The patient can distinctly feel the air pressing against the tympanic membrane, causing it to bulge outwardly, provided the tube is open. This proceeding has certain disadvantages, sometimes causing head congestions and giddiness.

Politzer's Method.--In this proceeding a gum air-bag is used as the means of forcing air into the tube. In the act of swallowing the soft palate is drawn against the posterior wall of the pharynx, and at the same time the pharyngeal mouth of the tube is well opened, so that air forced through the nasal passages at such a moment, being prevented from passing downward by the up-drawn palate, is forced up through the Eustachian tube into the middle ear. The success of this procedure depends entirely upon the inflation being made at the same moment that {810} the soft palate is drawn up against the pharyngeal wall; otherwise the air would naturally pass by the widest passage, in this case downward into the stomach. The usual plan of inflating at the moment that the patient is told to swallow fails, from the fact that patients differ so materially in the quickness with which they respond to an order. Many in their anxiety will swallow before the word is given, others will allow an appreciable time to pass before swallowing, so that the inflation will fail. For this reason I have adopted the following plan: It is well known that in the act of swallowing the larynx is drawn forcibly upward, and also that the moment of the extreme elevation is nearly coincident with the moment that the soft palate is drawn against the wall of the pharynx. The prominence of the thyroid cartilage (the so-called pomus Adami) enables one to easily watch until the maximum elevation of the larynx is reached, and then quickly, by a forcible contraction of the air-bag, to thoroughly inflate the middle ear. The Politzer method so thoroughly accomplishes the object, and with the least possible irritation, that the use of the catheter in the majority of cases is no longer indicated. The method of Politzer is as follows: The patient takes some water in the mouth; the air-bag has attached to it a short piece of gum tubing ending in a nose-piece in shape like an olive, or sometimes a small gum catheter is attached to it. This is placed in the lower nasal passage and the nose held firmly closed over it with one hand, the second hand grasping the air-bag. The patient is then told to swallow, so as to cause elevation of the soft palate (this can also be accomplished by the patient speaking quickly some word like hoc), and the air-bag is forcibly pressed. In this way the air is quickly driven, viâ the nasal passage and Eustachian tube, into the middle ear. In little children it is sufficient to quickly inflate, as the crying of the child elevates the soft palate to a certain degree, and so cuts off the downward passage into the stomach.

External Ear Diseases of the Auricle.

ECZEMA.--This disease occurs very frequently in infants during dentition, where irritation of the dental branches of the fifth pair of nerves causes irritation in other branches of the same nerve, including those distributed to the skin of the face and auricle, causing acute attacks of the disease. It is also frequently observed that successive teeth penetrating the periosteum will cause fresh attacks of this skin irritation, so that as long as the teething process continues, so long is the eczema apt to continue, and treatment will probably prove only palliative. Eczema occurs also in both the male and female approaching the period of adolescence, a time when other forms of skin disease are especially common.

The aged do not escape this annoying malady, where it is apt to occur in the chronic form, and is due to want of nerve-force in the skin branches of the nerves distributed to this part--a wise provision of nature allowing nerve-power to fail first in the nerves distributed to parts where the harm done is a minimum one, rather than in the nerve-centres, where disease fatal to life would result. The treatment in this class of cases would be radically different from the preceding divisions, where nerve-irritation is the cause.

{811} DIAGNOSIS.--The acute form shows the same diagnostic appearance as does eczema occurring elsewhere--the same redness and swelling of skin, followed by the vesicular eruption with serous oozing and loss of epithelium. In the chronic variety there is marked thickening of the skin, and the auricle is often covered with crusts, but here and there a deep fissure in the skin, from some one of which pus will exude.

Marked itching and burning and a sensation of fulness occur, both in the acute and chronic forms.

COURSE.--The acute variety may last only a few days, but as a rule tends to recur at frequent intervals. The chronic variety can last almost any length of time, and will often prove to be most obstinate.

TREATMENT.--Acute Variety.--The first indication is to relieve the burning and itching. This is often best done by the use of some mild anodyne powder which protects the part from the air and tends to relieve the existing skin irritation. Finely-powdered starch dusted over the part is a good remedy. One of the best anodyne powders is that of McCall Anderson:

Rx. Pulv. camphoræ, drachm iss; Pulv. zinci oxid. ounce ss; Pulv. amyli, ounce j.

To be dusted over the inflamed surface.

Often there will be difficulty in preventing the powder from falling off. When this is the case a very thin coating of the skin with the oxide-of-zinc ointment furnishes an excellent ground for the powder to adhere to. The oxide-of-zinc ointment alone is also an excellent application.

In the chronic variety a more stimulating application is needful, and some preparation of tar will prove valuable, such as--

Rx. Ungt. picis liquidæ, drachm j-drachm iij; Ungt. zinci oxid. ounce j.

The crusts that collect on the auricle are best removed by a poultice of bread and milk, or a cotton pad moistened with olive oil can be bound over it for a few hours, and will serve to cleanse the part. In the very chronic cases, where points of suppuration are found, a caustic application like nitrate of silver is needed. Careful regulation of the diet and habits of the patient is indicated; an outdoor life, abstinence from alcohol and tobacco, nutritious food, will greatly aid. Iron, quinine, cod-liver oil can be used frequently with good results, while in teething children incising of the gums will sometimes give temporary relief.

Diseases of the External Auditory Canal.

IMPACTED CERUMEN.--This disease occurs very frequently, and, as a rule, is considered a matter of very little moment by the profession at large, whereas, in fact, it is often a symptom of grave disorders of the middle ear. Roosa mentions that in 1448 cases observed by him in private practice, only 101 were cases of inspissated cerumen alone, the great majority showing in addition serious disorders of other parts of the organ of hearing. The ceruminous glands are found chiefly in the cartilaginous portion of the external canal, and, according to Kessel, resemble the sweat-glands not only in the time and manner of their development, {812} but also in their external form and minute histology. This is also true of the contents of the ceruminous glands, as far as the microscope allows us to judge, the only difference being that in cerumen masses of very fine corpuscles of coloring matter are found.[1] The ceruminous glands secrete but slowly, and the cerumen tends to harden and become dark in color as it grows older. The removal of the secretion is probably effected by several factors. Numerous experiments prove that the epithelial lining of the external canal has a constant motion from within outward; necessarily any substance resting on it will move with it. Cerumen could in this way be constantly extruded from the external canal; and the cerumen, becoming dry and hard by exposure to the air, would tend to separate from the skin by curling itself into small rolls, and so drop out from the external meatus. The question naturally arises, Why does the cerumen form such impacted masses as are met with? We submit the following explanation:

In many of these cases the secretion is largely above the normal, and catarrh of the naso-pharynx is found associated with it. Pomeroy first noticed this connection, and suggested the probability that the ceruminous function is greatly affected in catarrhal disease, on the theory that the earlier stages of catarrh would result in hyperæmia, and consequently augmented function, of the ceruminous glands, which if continued may result in atrophy with abolition of function, precisely as results in inflammation of the mucous membrane lining the fauces.[2]

[Footnote 1: Vide Stricher, Textbook, p. 951.]

[Footnote 2: American Otological Soc. Trans., 1872.]

The pneumogastric nerve by its pharyngeal branch is connected with the pharynx, and by its auricular branch with the external auditory canal, so that irritation of the pharyngeal branches of the nerve, as would occur in pharyngeal catarrh, could readily excite reflex irritation in the auricular branch, with increase of function of the parts to which it is distributed, causing increase of the ceruminous secretion. Conversely, atrophy of the nerve would be followed by atrophy of function of correlated parts. The external canal often presents a sharp angle in its course near the meatus, and this also would tend to cause an accumulation of cerumen.

It is a well-established clinical fact that the great majority of cases of impacted cerumen are found to be associated with serious diseased conditions of the middle ear especially, and probably the diseased middle ear is often an important factor in causing impaction to take place; so that it frequently happens that the patient will experience no increase of hearing after removal of such an impacted mass, owing to the diseased middle ear that may be present. I remember one case where the hearing was absolutely lessened after removal of a ceruminous plug; doubtless in this case the solid conduction through such a mass was better than through an air-filled auditory canal.

SYMPTOMS.--Sudden loss of hearing: this is due to the fact that the mass grows slowly from the periphery toward the centre, and as long as a small central opening remains the hearing power will remain good. Some sudden jolt or misstep, or some quick-acting force, will cause occlusion of this narrow passage, with consequent sudden loss of hearing. The tuning-fork, placed on the incisor teeth, will be best heard on the affected side by reason of vibrations being impeded by the mass in their passage through the external canal.

{813} Tinnitus aurium and vertigo are often present, both being due to the mass pressing inward the tympanic membrane, with consequent increase of pressure on the labyrinthine fluid by the chain of small bones pressing on the membrane of the foramen ovale. These symptoms are sometimes alarming to the patient, as in his judgment indicative of serious brain lesion.

DIAGNOSIS.--Examination of the external canal with the speculum and reflected light reveals a dark amber-colored mass lying in the external canal, which can be very hard, the result of exposure to the air for a length of time, as well as the union with it of epithelial débris of the skin of the canal; or it may be soft, like syrup, in its consistence.

The PROGNOSIS is to be guarded until the condition of the middle ear is known.

TREATMENT.--If the mass is hard in its character, its removal is best effected by the forceps or curette or blunt hook, it being understood that the external canal is well illuminated, so that the course of the instrument can be carefully watched. The curette or blunt hook will loosen the attachments of the mass to the sides of the canal, and then it can be readily removed by the forceps, care being taken not to injure the tympanic membrane. In such a way a hard plug can be removed at one sitting that otherwise would require repeated efforts to accomplish the same purpose.

If these instruments are not at hand, the next best method is to effect the removal with the syringe and warm water. A caution is to be given in the use of the syringe. There are a great number of people who are not able to have the external ear syringed, even though gently, without becoming giddy, and if the syringing is then continued the vertigo will end in a fainting attack. My rule is to caution the patient of the above fact, and always promptly stop at the first symptom of vertigo. Sometimes a short rest will allow the operator to proceed, but often it is necessary to postpone any further attempt at removal until a succeeding day. Always use quite warm water. If in a fair trial with the syringe it is found that the mass does not soften and break up, it is better to make an application of olive oil to it, and at a subsequent time repeat the attempt at removal. Soft masses of cerumen are best removed by the use of warm water and the syringe.

In some few cases inflammation of the external auditory canal will complicate the treatment, and the question will come up as to whether it is best under such circumstances to attempt the removal of the impacted mass. As a rule, the removal of the mass is the best means of combating such an inflammation, and therefore an attempt at removal should be made unless the inflammation is very acute, when treatment of this complication would be in order, and the removal of the plug deferred for the moment. In all cases the condition of the middle ear and hard pharynx should be noted after the removal of the impacted mass, and these parts often will need treatment.

Furuncle of External Auditory Canal (Acute Circumscribed Inflammation).

ETIOLOGY AND PATHOLOGY.--In a great number of cases furuncle is to be regarded as an evidence of general bodily debility. For example, {814} in the richer classes it is often a result of over-dissipation, while in the poorer classes insufficient food, bad clothing, and such like are important factors. Local irritations of the external canal may cause the disease, such as rubbing the canal with a hairpin or toothpick to relieve itching. The use of alum and nitrate-of-silver washes in the canal will cause a furuncle in some cases. Furuncle occurs in the outer third of the canal as a rule, and often develops around a ceruminous gland, and will generally be followed by a number of others.

SYMPTOMS.--Pain is the most marked one--in the beginning of the attack of an intermittent character, with a tendency to increase toward and in the night; but as the attack advances pain becomes more marked, and may extend over the entire temporal region well down into the neck. The jaw movement also becomes very painful. The furuncle will rupture at any time, from the third day up to the tenth day, according to its location. The more deeply seated it is, the slower will be its progress toward maturity. The pain quickly disappears after the rupture, and then a short interval of rest is followed too often by the recurrence of the same disease. A varying degree of deafness is usually present, due to partial closure of the canal by the swollen soft tissues, and also it may be in rare cases through involvement of the tympanic cavity in the inflammation. Fever is often present. The great objective symptom will be the circumscribed swelling found in the cartilaginous portion of the canal and often along its anterior wall, and will show great increase of pain by but slight pressure. The swelling as it matures becomes more circumscribed, and will end in a pus collection and subsequent rupture.

DIAGNOSIS.--The disease most likely to be confounded with it would be an acute middle-ear inflammation, with involvement of the periosteum of the osseous part of the canal; but the history of the case would clear up this point.

The PROGNOSIS is favorable as to hearing, but with great probability of successive crops of the same disease.

TREATMENT.--The local application of heat and moisture is a remedy of great value, and a good method of application is to bend the head into a horizontal position, as by resting the side of the head on a table, and then fill up the external canal with water as warm as the ear will allow without causing pain; then quickly place over the auricle towels that have been dipped in very warm water and wrung dry by being twisted in a second towel, and over this a large pad of warm flannel or some similar covering. The heat and moisture will be retained for quite a time, and then the procedure can be repeated until relief from pain is obtained. In the interval the auricle is to be covered with a pad of cotton. A steam atomizer furnishes a convenient way of applying heat and moisture. Dry heat is sometimes preferred: a flannel bag filled with bran or hops and well warmed in a hot oven would carry out this indication; also a hop pillow moistened by hot whiskey is a good application.

An application of leeches affords great relief from pain. The best point to place a leech (which should be a Swedish leech) is just in front of the tragus. Two or three leeches can be applied at this place, and by encouraging the after-bleeding by warm applications any desired amount of blood can be taken. The after-bleeding can be readily controlled by the use of styptic cotton.

{815} Incision of the Furuncle.--It is a mooted question as to whether an incision is capable of giving relief, and when it should be done. My own experience has been that the application of a leech has given greater relief than the use of a knife in those cases when the furuncle has been deep seated. Later on, when the swelling has become circumscribed and shows evidence of pus, the incision is clearly indicated.

General treatment is to be of a tonic character, and during the acute stage, when the pain is severe, anodynes are indicated.

Foreign Bodies in the External Auditory Canal.

1. VEGETABLE PARASITES.--Aspergillus flavescens and Aspergillus nigricans are found on the inner part of the canal and over the external surface of the tympanic membrane. This growth largely depends for its development upon a diseased condition of the epithelial layer of the skin lining the external canal, such as is found in cases of chronic middle-ear suppuration and in eczema of the skin of the external canal, by furnishing a moist nidus for its development.

SYMPTOMS.--Intense itching in the external canal, with a sense of fulness; also sometimes pain, with tinnitus and difficulty of hearing. The growth is found in the inner part of the canal, or over the surface of the tympanic membrane in the form of yellow or black flakes according to the variety. It may be found in spots or may form a complete covering to the canal-walls, so that when removed it forms a mould of the canal, leaving a raw skin surface, on which the growth rapidly reproduces itself. The disease is found in an acute and a chronic form, and in a few days can attain full development; also there exists a marked tendency to relapse as long as any portion remains undestroyed.

PROGNOSIS.--Favorable.

TREATMENT.--The main point is to thoroughly remove the parasite. This is best effected by the use of warm water and the syringe, carefully picking off any small portion that may remain by the forceps or curette. My practice is then to fill up the external canal with alcohol, allowing it to remain a few moments, and then to carefully dry the canal by the aid of styptic cotton. This procedure may have to be repeated every second day for a number of times until the growth is entirely destroyed. Wreden recommends the use of the hypochlorate of lime in the strength of one or two grains to the ounce of water, the salt to be freshly dissolved in water at each application. The condition of the middle ear and the integument of the external canal is to be considered after the removal of this growth, and treated as indicated by the state of the case.

2. INSECTS IN THE EXTERNAL AUDITORY CANAL.--Cases of this character occur frequently during the summer season to persons who by lying on the ground give insects an opportunity to crawl into the external canal. The common house-fly also affects an entrance into the canal quite often; also during the summer it is not uncommon to find grubs or larvæ in the canals of patients suffering from suppurative inflammation of the middle ear resulting from the deposit by insects of their eggs in the moist coverings of the canal. The movements of insects in the sensitive {816} external ear cause great pain to the patient, and their removal is sometimes difficult. For instance, the grub is provided with two hooks, by means of which it adheres tenaciously to the skin, so that it may be necessary to remove each one separately with the forceps. The quickest method of removal, as a rule, is to wash out the insect by the use of warm water and a syringe; and if this is not at hand the insect can be drowned by filling the canal with water, olive oil, or some demulcent liquid.

OTHER VARIETIES OF FOREIGN BODIES, such as grains of corn, beans, peas, cherry-stones, beads, buttons, pieces of slate-pencil, are found in the external canal, and the symptoms that are present arise partly from the presence of the body, but more frequently from the irritation produced by attempts at removal.

SUBJECTIVE SYMPTOMS.--Difficulty of hearing, often due to the foreign body filling up the external canal and thus excluding all sound-vibrations. Tinnitus aurium and vertigo are often present, and caused by pressure of the body on the tympanic membrane with resulting abnormal labyrinthine pressure; also a variety of reflex conditions are noted as a result of the presence of a foreign body in the external canal, such as coughing and vomiting, partial paralysis, etc.

OBJECTIVE SYMPTOMS.--The appearance of the external canal will depend greatly upon the amount of pressure that the foreign body has exerted. For instance, a body loosely lying in the canal will irritate but little; on the contrary, a hard body like a cherry-stone firmly impacted in the canal will quickly cause a severe inflammation.

DIAGNOSIS.--As a rule, the foreign body can be readily seen with the aid of the mirror and speculum, unless the canal has become swollen to such an extent as to hide the body from sight. Probing and such-like procedures are not advisable.

TREATMENT.--The question comes up if it is good practice to make an attempt at immediate removal of a foreign body if the external canal is in a condition of acute inflammation. Unless grave head symptoms are present it is often good practice to delay, and reduce the inflammation by proper treatment, and then remove the foreign body. In other words, there is more risk by a forcible removal during a stage of acute inflammation than to permit the foreign body to remain until the inflammatory stage is past. Numbers of cases are on record where foreign bodies have remained for years in the external canal without causing serious sequelæ. Also, be sure a foreign body really exists in the canal, as it is not uncommon for patients to come with the statement that such is the case, and yet no foreign body has been discovered.

The majority of foreign bodies can be removed by the use of the syringe and warm water. The impacted bodies--and particularly those having a hard, smooth surface--present the greatest difficulties. A good plan is to try first the syringe and warm water, and if not successful try with a toothed angular forceps to grasp the body. If, as is often the case, it is found that the forceps slips off the body, then the curved blunt hook is to be used. This can be passed by the body and then turned on its axis, so that the hook is firmly placed behind it, and then a slow upward movement will often dislodge the body. On some occasions I have used two hooks, holding the body between them, and thus dragging it out. It is also better to desist after a fair trial until a succeeding day, rather {817} than make excessive efforts at removal, which will often cause violent inflammation to follow. After the body is dislodged examine the condition of the tympanic membrane, as this is often found to be perforated by the foreign body.

Diseases of the Middle Ear.

ANATOMY.--The cavity of the middle ear is of small dimensions: antero-posterior diameter, 13 mm.; vertical diameter at the anterior part, 5.8 mm.; vertical diameter at the posterior part, 15 mm.; transverse diameter at the anterior part, 3-4.5 mm.; transverse diameter at the opposite drumhead, 2 mm. (Von Tröltsch). It is situated in the petrous portion of the temporal bone and surrounded by bony walls, with the exception of the opening covered by tympanic membrane and the opening of the Eustachian tube, having a mucous periosteal covering, very thin, transparent, and colorless. This membrane covers not only the tympanic cavity, but is reflected over the chain of small bones and tendons of the tensor tympani and stapedius muscles. It is essentially a mucous membrane, and may be considered a continuation of the naso-pharyngeal mucous membrane reflected through the Eustachian tube to the middle-ear cavity; also subject to the same pathological changes as other mucous membranes.

The tympanic cavity normally is an air-filled cavity, and allows of free vibration of the tympanic membrane and its ossicles, as well as the membrane covering the oval and round foramina; and it is readily understood that any interference with the vibration of this sound-conducting apparatus will at once affect the hearing.

Its arterial blood is supplied from the middle meningeal, stylo-mastoid, ascendant pharyngeal, posterior auricular, tympanic, and internal carotid arteries. These freely anastomose with each other. The veins pass internally through minute openings of the petrosal squamous fissure to the veins of the dura mater, and thence into the superior petrosal sinus, and also externally into the venous ring surrounding the tympanic membrane, and also to the veins of the meatus (Schwartze). This is important to bear in mind, as furnishing an easy passage for the extension of middle-ear inflammation to the brain membranes.

The nerves forming the tympanic plexus are as follows: The mucous membrane is supplied by the tympanic plexus, formed from the tympanic branch of the petrous ganglion of the glosso-pharyngeal nerve--from the branch of the superficial petrosal and branches of the sympathetic nerve. The otic ganglion receives fibres from the inferior maxillary nerve, from the auriculo-temporal nerve, and from the sympathetic plexus, and it is distributed to the tensor tympani and tensor palati muscles.

The mastoid cells lead directly from the tympanum. They consist of one large opening, the antrum, and the lower mastoid cells. These cells consist of a large number of varying-sized cavities, and are enclosed by a dense layer of bone. The mucous membrane lining these cells is a direct extension of the tympanic membrane, and liable to the same pathological conditions as that mucous membrane.

{818} The Eustachian tube connects the cavity of the tympanum with that of the naso-pharynx, and is mainly intended for the introduction of air into the tympanic cavity. It has a length of 35 mm., partly bone (11 mm. in length), partly cartilaginous (24 mm. in length). The pharyngeal opening is 8 mm. high and 5 mm. wide; the tympanic orifice, 5 mm. high and 3 mm. wide (Schwartze). The mucous membrane lining this canal is a continuation of that of the naso-pharynx, and affords an easy way for the transmission of disease from the naso-pharynx to the middle ear. The Eustachian tube at rest is probably closed, although this is a matter still discussed; but it is essential for normal hearing that the air-pressure exerted on the tympanic membrane through the external auditory canal should be equalized by that exerted through the Eustachian tube. This necessitates the opening of the tube from time to time for free admission of air into the tympanic cavity. This is accomplished by the action of the musculus dilator tubæ, the tensor veli palatini, and the salpino-pharyngeus muscle. In the act of swallowing the tube opens; also, if the nostrils are closed and the act of swallowing is performed, air will be pumped out of the middle ear; on the contrary, if the nostrils are open air will be forced into the middle ear.

Diseases of the middle ear can involve the superficial layers of the middle-ear mucous membrane only, and may be of a catarrhal character. Hyperæmia and swelling of the epithelial cells, with increased mucous secretion, will be found. Later on, if the inflammation assumes a higher degree, a serous fluid will be profusely poured out, with lessening of the mucous secretion. When the deeper epithelial cells are involved, then pus-cells often appear, and a suppurative process becomes established, with frequent destruction of the soft tissues of the middle ear.

These different grades of inflammation are seldom found distinct, but run one into another. A case can start as a pure catarrhal inflammation; this, after attaining its acme, may end in recovery or degenerate into a chronic catarrh; or, on the contrary, it may advance into an acute purulent inflammation with a subsequent chronic stage.

CAUSES OF INFLAMMATION OF THE MIDDLE EAR.--Change of temperature, causing a sudden cooling of the body, is a frequent cause of this disease; for instance, exposure to wind from a partly-open window, a sudden rush of cold water into the external canal, as in surf-bathing, etc. Irritating foreign bodies in the external auditory canal may also cause this disease.

But inflammation of the middle ear occurs most frequently as a sequela of diseases affecting the general body. Among these may be mentioned, in order of their relative importance--

1. Scarlet Fever.--This disease is apt to cause the purulent form of middle-ear inflammation, and often of a very grave character. The ear complication can occur during the existence of the rash or immediately after its cessation (Thomas), and may run a rapid course, causing destruction of the tympanic membrane and middle-ear ossicles. Destruction of the facial nerve in its passage through its bony canal is not infrequent. Wendt has noticed in severe cases that the periosteum of the mastoid process, also that of the squamous and petrous portions, may participate in the purulent process, and end in subsequent caries of the bone. The severity of the ear complication will largely depend upon the condition {819} of the naso-pharyngeal mucous membrane. Light attacks of scarlet fever with slight throat symptoms would most probably cause slight irritation of the middle-ear mucous membrane, while the anginose variety would cause most violent inflammatory sequelæ.

2. Measles is apt to cause the catarrhal variety of middle-ear inflammation rather than the purulent form. It occurs during and immediately after this eruption, and is a direct continuation of the naso-pharyngeal inflammation viâ the Eustachian tube. Hearing, as a rule, is diminished, due to the swollen mucous membrane of the Eustachian tube and middle ear, and also to fluid accumulations that often exist in the middle ear. Wendt[3] draws attention to the fact that chronic affections of the auditory apparatus, such as formation of adhesions between the ossicles or between the tympanic membrane and wall of the tympanum, may arise while the soft parts are in a swollen condition, and often chronic catarrhal sequelæ may be traced to this cause.

[Footnote 3: Ziemssen, ii. 112.]

3. Tuberculosis is often associated with the catarrhal and purulent varieties of middle-ear inflammation, having, as a rule, a subacute course, the patient's attention sometimes only being drawn to his ear by the escape of pus from the middle ear into the external canal, the medium of communication being the mucous membrane of the pharynx viâ the Eustachian tube. Wendt[4] states that as yet the presence of tubercles has not been authenticated, although the clinical observations of rapid destruction, especially of the tympanic membrane, would seem to indicate it.

[Footnote 4: Ibid., vii. 77.]

4. Retro-nasal catarrh is a frequent cause of middle-ear inflammation, the disease being communicated along the mucous membrane of the Eustachian tube. All degrees of inflammation are found, the catarrhal variety being the most frequent, while acute nasal catarrh is a cause of a large number of ear complications. Chronic retro-nasal catarrh is apt to cause a chronic middle-ear catarrh, that progresses insidiously, and almost unnoticed by the patient until the deafness begins to interfere with the ordinary affairs of life.

5. Scrofulosis causes most frequently the catarrhal form of middle-ear inflammation; and this is a direct continuation of the catarrhal affections of the naso-pharyngeal mucous membrane viâ the Eustachian tube. Birch-Hirschfeld[5] asserts that scrofulosis is the cause of the largest number of those cases in which weakening or destruction of the function of hearing has occurred during childhood; also, that the large number of scrofulous individuals found in deaf-and-dumb asylums is explained in this way; and that after the scrofulosis is cured the deafness remains as a result of permanent pathological middle-ear changes produced by the former disease.

[Footnote 5: Ibid., xvi. 794.]

6. Smallpox may cause several varieties of middle-ear hyperæmia, and frequently also a hemorrhagic catarrhal process is met with. Not seldom is found a suppurative inflammation, with extensive destruction of the soft tissues and ossicles, with permanent subsequent deafness. There is probably no reason to doubt that a pustule itself can develop in the middle-ear mucous membrane, just as is found in the cornea, and cause an acute inflammatory process; but, as a rule, the middle-ear mucous membrane is secondarily involved as a consequence of inflammatory process existing in the naso-pharyngeal mucous membrane.

{820} 7. Diphtheria is a cause of middle-ear inflammation. Wendt[6] states that in a fifth of the entire number of cases of croup and diphtheria; and in two-fifths of those cases in which the naso-pharyngeal space participated, but in no case without immediate connection with the corresponding affections of this space, he found an extension of the specific process into the middle ear. In some cases the tubal prominences were covered with membrane terminating at their orifices; in other cases a membranous cast of the cartilaginous portion of the tube was found. As a rule, the pathological changes noted were hyperæmia of the mucous membrane of the middle ear and catarrhal and purulent inflammation.

[Footnote 6: Ziemssen, vii. 71.]

8. Syphilis causes most frequently the catarrhal variety of middle-ear inflammation; the purulent variety is also met with, but much less frequently, the disease of the naso-pharyngeal mucous membrane determining largely the grade of inflammation. Hereditary syphilis may cause this complication, as well as the primary disease, but not so frequently. Hutchinson has observed some cases of deafness in which the disease was situated either in the labyrinth or auditory nerve, the middle ear being healthy. Also, deafness may be caused by syphilitic affections of the external auditory canal, causing obstructions to sound-vibrations passing through it.

9. Typhoid fever may cause either the catarrhal or purulent form of middle-ear inflammation. For instance, Hoffmann[7] found fourteen cases of deep-seated disturbance of the faucial mucous membrane; he also met with perforation of the tympanic membrane four times--twice in connection with caries of the mastoid process.

[Footnote 7: Ibid., i. p. 159.]

It is easy to understand why middle-ear complications should complicate such a disease as typhoid fever, where the mucous membranes generally are the favorite seat of inflammation. Disease of the internal ear and auditory nerve are not uncommon after typhoid fever.

10. Bright's disease is a cause of hemorrhage into the middle ear. Schwartze reports in the year 1869 the case[8] of a young man who suffered from albuminuria with retinal hemorrhages; also, enlargement of the liver and spleen existed. He suddenly complained of pain in the right ear. The tympanic membrane was of a red color and devoid of concavity. Three days later an abundant serous discharge existed, with a small blood-coagulum, the patient dying a few days later of the kidney disease. Examination showed a hemorrhagic inflammation of the mucous membrane of the right tympanic cavity, which was also found filled with a bloody purulent fluid. The left tympanic cavity also was found filled with a similar fluid. A number of other similar cases are reported.

[Footnote 8: Archiv für Ohren Heilkunde, Bd. iv. p. 12.]

11. Whooping cough has been noted in several cases to have caused hemorrhage into the middle ear, with perforation of the tympanic membrane, with subsequent partial deafness.

The two principal types of acute middle-ear inflammation are the catarrhal and purulent; and these up to a certain stage have similar symptoms, but when pus has formed it gives rise to conditions that must be described as peculiar to purulent inflammation alone.

{821} Acute Catarrh of the Middle Ear.

This may be described as acute catarrh of the mucous membrane lining the middle-ear cavity. The prominent symptoms are as follows:

1. Pain.--This is, as a rule, of the most violent character. It is described as a boring or tearing pain situated in the ear itself, and often extending over the entire temporal region: any muscular exertion like swallowing or sneezing causes increase of it. The external ear becomes swollen, and so exquisitely tender to the touch that the least pressure over the tragus causes the patient to flinch very markedly. The pain tends to increase during the night up to the early morning hours, and to lessen during the day. The immediate effect of a middle-ear inflammation is to render the entire region of that side of the face tender, so that any movement of the jaws or neck becomes painful. It is also not uncommon to find the sympathetic glands of the neck becoming enlarged and tender, and they may go on to suppuration. The adult will complain most vigorously of the pain, so that there will be no difficulty in locating it; but in the infant or young child the greatest difficulty may be experienced in determining its precise seat, owing to its inability to express in language its suffering. Two points may be mentioned as aids in the diagnosis: (a) the cry of a young child suffering from an acute inflammation of the middle ear has a peculiar shrill, continuous character, an intermission sufficient only to inspire being noticed; (b) pressure over the tragus of an inflamed middle ear will cause a quick shrinking away of the little sufferer, thus showing the seat of the disease.

2. Loss of Hearing Power.--This depends partly on a lessening of the vibratory power of the conducting apparatus, partly due to a thickened tympanic membrane, and also to the fact that the mucous membrane covering the middle ear and chain of small bones becomes swollen, and so clogs their movements. Again, the tympanum may be filled with a mucous or muco-serous fluid, instead of being an air-chamber, as in the normal condition, so that vibrations of the conducting apparatus may cease entirely, while at the same time increase of intra-labyrinthine pressure takes place. A tuning-fork placed on the incisor teeth or on the forehead is heard more distinctly on the deaf side, due to the sound-vibrations being retarded in their outward passage through the diseased middle ear; also, the voice of the patient is heard by himself with increased resonance, due to the same cause (retarded sound-vibrations), and the patient unconsciously lowers the voice below its normal tone.

3. Giddiness is not uncommon, due partly to increase of labyrinthine pressure, and in some cases to a sympathetic irritation and congestion of the vessels of the basilar brain membrane. Fever is always to be looked for in acute middle-ear disease.

4. Noises in the ear (tinnitus aurium), resembling the noise produced by the escape of steam or the singing of crickets, etc., are common, and are due to a variety of causes. For instance, a large number of these noises (according to Theobold's theory) depend upon muscle and blood-vessel movements, causing vibrations that in a normal condition pass out through the external auditory canal without being noticed; but if their outward passage is impeded by obstructions existing in the middle ear, like thickened tissue or the existence of fluids, as mucus or pus, or by {822} obstructions in the external auditory canal itself, such as impacted cerumen, etc., then these vibrations are thrown back and impress for a second time the auditory nerve-endings, and thus become noticeable sounds. (A familiar example is to shut the external auditory canal by closing the meatus: a tidal noise is at once noticed.) A crackling noise is often caused by air entering the middle ear and bubbling up through the confined fluids.

OBJECTIVE SYMPTOMS.--The tympanic membrane is at first slightly injected, particularly along the manubrium and the anterior and posterior folds; but as the inflammation advances the entire membrane becomes intensely injected and red. The cone of light is either very small or may be entirely absent, due to the membrane having lost its high reflective power. At this stage exudations into the middle ear frequently show themselves, and if of sufficient quantity may cause an outward bulging of the membrane: frequently the tympanic membrane at its lower third becomes less transparent, and in some cases fluid collections show a dark border-line stretching across the tympanic membrane, and movable by change of position of the head.

DIAGNOSIS.--This disease can be hardly mistaken: the only difficulty that can arise is whether the case is one of simple acute catarrh or is one of commencing purulent inflammation, as the symptoms are identical in each up to the formation and escape of pus, when no doubt can arise.

TREATMENT.--This must be directed against the acute inflammation that exists, then as quickly as possible to restore the mucous membrane to its normal condition and return to the sound-conducting apparatus its normal vibrating power.

Local bleeding is to be considered among the most important remedies, and therefore is taken first. This is best done by the use of the Swedish leech, applied to the tragus, as at this point the blood is most easily drawn from the tympanic cavity, in number from one to three; and if the taking of a larger quantity of blood is desired, this can be accomplished by encouraging the after-bleeding by hot fomentations. When great pain exists, when the auricle is tender and pressure on the tragus produces marked increase of pain, the application of a leech is indicated. In children it is best to refrain from the use of leeches.

The use of heat and moisture is most valuable. An effective method of application is as follows: Place the head of the patient in a horizontal position, with the affected ear turned upward, and fill the external auditory canal with water at the temperature, say, of 100° Fahr. Place quickly over the auricle towels that have been dipped in very hot water and wrung out as dry as possible, and over these a large flannel pad. This makes an excellent dressing, and one retaining the heat and moisture for a length of time. When it cools repeat the same proceeding until relief is obtained, when a large dry cotton pad can take the place of the previous dressing. Patients suffering from acute catarrh of the middle ear should be confined to the house, and, still better, to bed. All physical exercise aggravates this disease, and a suitable anodyne may be given to procure sleep if it be found necessary. Paracentesis of the tympanic membrane is sometimes indicated in those cases where the membrane shows distinct bulging and perforation is clearly close at hand; also in some cases where, notwithstanding previous treatment, the pain still {823} continues with great severity. This operation is best done by incising the posterior half of the membrane by means of a broad paracentesis needle. The incision should be made at a point midway between the periphery of the membrane and the handle of the hammer, and on the dividing-line of the upper and lower posterior quadrants, the cut to be made downward. Paracentesis of the membrane is to be done while the head of the patient is well supported and the membrane illuminated by means of a light reflected from the head-mirror. Immediately after the operation wet hot flannels should be applied to the ear to relieve the pain.

The condition of the pharyngeal and nasal mucous membrane should be thoroughly attended to, as from this source a large number of cases of acute middle-ear catarrh have their origin. Nitrate-of-silver solutions are often of great service as a local application to the naso-pharynx. Tannic acid makes a good astringent gargle, and is more particularly adapted to those cases where a pure astringent effect is needed. Chlorate of potash is an excellent gargle, and often proves of great service. It may not be out of place to state that the use of alcohol and tobacco tends to keep up an irritated condition of the naso-pharyngeal mucous membrane, and they should be dispensed with. As part of the treatment inflations of the middle ear are used to aid in the removal of abnormal secretions from the tympanic cavity and to restore the sound-conducting apparatus to its normal condition. This can be thoroughly carried out by the Politzer proceeding. This consists in forcing air (by compressing a rubber hand-bag, Politzer's air-bag, so called) through the lower nasal passage up the Eustachian tube, and so into the middle ear. The patient holds a small quantity of water in the mouth. The nasal end of the tubing connected with the air-bag is placed in one of the lower nasal passages, and the nose tightly closed over it. The patient is then told to swallow, and at the same moment the air-bag is forcibly compressed, and the air is thus compelled to travel along the nasal passage and up the Eustachian tube into the middle ear. The act of swallowing causes the soft palate to be forcibly pressed up against the posterior pharyngeal wall, and at the same time causes the Eustachian tube orifice to open widely. A column of air thus used will expel large accumulations of mucus from the Eustachian tube, and to some extent from the middle-ear cavity, and at the same time the thorough distension of this cavity throws into motion the tympanic membrane and chain of small bones--a most desirable proceeding. In acute conditions the inflation should be made only after all pain has ceased, and then at first very gently; but in a short time a thorough inflation two or three times repeated, say every two or three days, is most beneficial. The inflation of the middle ear by the use of the Eustachian catheter is a more irritating procedure, and does not accomplish the purpose any more completely than the Politzer method. Therefore the latter is to be preferred in adults, while in children it is the only available method that can be used.

Chronic Catarrh of the Middle Ear.

Various classifications of this disease have been made by different authors: I prefer the division that Buck has used in his textbook. The following summary will give an idea of it:

{824} Chronic catarrh is a name that has been given to a class of cases where deafness and tinnitus are prominent symptoms, and where no suppurative action in the middle ear has existed at any previous time, and where the internal ear is supposed to be in a healthy condition. In some of these cases there will be found a marked hypertrophy of the mucous membrane, and sometimes of the submucous connective tissue, accompanied with excess of secretion, with the same condition existing in the naso-pharyngeal membrane. The tympanic membrane often becomes sunken, and therefore strongly concave outwardly. The short process of the malleus is very prominent, and the handle of the malleus, by being drawn forcibly backward, becomes apparently shortened (foreshortening of the malleus handle, so called).

The membrane loses its vibratory power to some extent, and the cone of light is either very small or is entirely absent. The color of the membrane changes to a more or less opaque white, with often a line of vascularity along the manubrium, or it may assume the color of ground glass; white calcareous deposits are not seldom met with; marked evidences of catarrhal inflammation exist in the naso-pharynx, such as increase of mucoid secretion, with enlargements of the tonsils, and often granular pharyngitis may be found. The mucous membrane of the Eustachian tube is often involved in the process: marked swelling of its mucoid tissue, with the tube filled with secretions, prevents free entrance of air into the middle-ear cavity. In the nasal mucous membrane, beyond the ordinary catarrhal conditions, polypoid formations are common; also thickening of the mucoid and submucoid tissues prevents the free passage of air.

In another class of cases coming under the head of chronic catarrh of the middle ear a very different set of symptoms from the class first described are noticeable. In these cases perhaps catarrhal symptoms have at one time existed, but have completely passed away, and the mucous membrane not only of the tympanic cavity, but also of the pharynx and Eustachian tube, has undergone a fibroid degeneration, causing destruction of the glandular elements and ending in an atrophied mucous membrane (the so-called proliferous degeneration of some authors). The tympanic membrane in these cases is abnormally thin and very transparent, sometimes much sunken, no doubt due to connective-tissue adhesions in the middle-ear cavity. The external auditory canal is devoid of cerumen and hair; also the same change in the mucous membrane of the naso-pharynx and Eustachian tube gives a smooth, transparent appearance to their surface. In this class of cases in post-mortem examinations there have been found the stapes firmly ankylosed to the margin of the fenestra ovalis; the chain of small bones firmly ankylosed; fibroid adhesions in the mastoid cells; and adhesions between the tympanic membrane and the labyrinthine wall.

CAUSES.--A percentage of cases result from a previous acute middle-ear catarrh. Others apparently originate as a chronic condition and slowly advance. Beyond all doubt, a large percentage are inherited, as the same disease can be traced back through several generations, where signs of the disease were noted in early youth, with slow advance as years go on. It is also a matter of interest to note that these cases are apt to show sensible advance in women at the birth of a child.

{825} PROGNOSIS, as a rule, bad, both as to the possibility of preventing increase of deafness and of doing away with tinnitus--a most annoying factor.

TREATMENT is successful in proportion to the catarrhal symptoms that exist, and which are to be treated on the general plan laid down for catarrhal inflammation. A great number of these cases call for a tonic plan of treatment, such as iron tonics, cod-liver oil, etc.

Local treatment consists in inflations of the middle ear by the Politzer method. In those cases where a thin, sunken membrane exists care should be observed not to use undue pressure, lest a rupture of the membrane result. In those cases where tinnitus aurium is a prominent factor a few drops of ether placed in the Politzer bag cause a more stimulating effect from the inflation than the use of pure air, and is sometimes of service in lessening this annoyance. It is an important part of the treatment that the general health should be in the most vigorous possible condition.

Acute Purulent Inflammation of the Middle Ear.

The disease proceeds very frequently from some inflammation in the naso-pharyngeal cavity, the mucous membrane of the Eustachian tube furnishing a ready way of communication between the pharynx and middle ear.

The exanthematous diseases furnish a large proportion of these cases. Scarlet fever stands first on the list, as causing the largest number of these cases, and also those of the most serious character. Measles, smallpox, diphtheria, the different forms of fever, such as typhus and typhoid, cerebro-spinal meningitis, pneumonia, bronchitis, etc., are complicated by this form of inflammation, and the ear disease represents simply a continuation of the naso-pharyngeal inflammation which occurs so frequently in the above-mentioned diseases. Another set of causes come under the head of change of temperature, such as exposure to draughts of air and sea-bathing, where the cold water entering the external auditory canal acts directly upon the tympanic membrane. Some few cases occur as the result of injury, such as blows upon the ear or direct injuries to the tympanic membrane.

COURSE.--The same pathological conditions are to be noted here as in the acute catarrhal attack, with the difference that the inflammation goes on to a higher grade--namely, pus-formation. In this form of disease there exists marked hyperæmia and swelling, not only of the superficial but also of the deep-seated tissue, with pus-formation, and generally perforation of the tympanic membrane, with occasional ulceration and destruction of other parts of the middle ear. The neighboring cavities of the antrum and mastoid cells participate more or less, while blood-vessels penetrating the superior wall of the middle ear furnish a ready means of communication between the inflamed middle-ear tissues and the brain-membrane, so that the wonder is not that brain complications result, but that they occur so seldom.

The changes in the tympanic membrane in the first stage are marked hyperæmia and swelling of the tissue, so that it often assumes a uniform red appearance, without a trace of the malleus or cone of light. {826} Pus-formation in the middle ear is quickly followed by bulging of the tympanic membrane, due to increase of middle-ear pressure; and this in the great majority of cases is followed by perforation of the tympanic membrane, due not only to increase of pressure, but also to a destructive ulcerative process in the membrane itself. The latter process is seen in those cases of great destruction of the tympanic membrane that occurs in scarlet fever, where almost entire destruction of the membrane is often found. Perforation may occur at any part of the membrane.

SYMPTOMS AND COURSE.--These are very much the same, up to a certain point, pus-formation, as have been described under the head of Acute Catarrh--namely, the great pain, deafness, tinnitus, headache, tenderness on pressure over the tragus, increase of pain by movement of the jaw, followed often by quick relief by perforation of the membrane and escape of pus through the external auditory canal, with a subsequent subsidence of inflammation and restoration of the tympanic membrane. A moderate attack may run a course of from two to six weeks, and end in entire recovery, or it may end in a chronic suppuration with its sequelæ.

DIAGNOSIS.--It often will be difficult at the outset to know if the case is one of acute catarrh or whether it will advance to a purulent inflammation; but as the disease goes on to pus-development and subsequent drum-perforation, no doubt can exist as to its true character. The perforation can often be seen, and air may be forced through it with a whistling sound by a forcible expiration of the patient. In regard to whether complications exist, such as mastoid or brain involvement, several points can be given as aids in the diagnosis. When mastoid involvement exists, the soft tissues over it become swollen, very tender on pressure, with pain in that part of the bone; also, often swelling of the posterior upper wall of the external auditory canal, a part adjacent to the mastoid process.

In those cases where the inflammation tends toward the cranial cavity, the pain spreads over the entire side of the head, and often becomes marked in the occipital and frontal regions, and is of a peculiar lancinating character. Vertigo is also present, even if the head is in a quiet horizontal position, but greatly increased by movement of the head. The body-temperature in acute purulent inflammation in adults is not altered as a rule, but in children it is raised.

PROGNOSIS.--An uncomplicated case if properly treated will generally result in a good recovery, and often with but slight impairment of the hearing power. If allowed to run its course, it may cause serious and permanent changes in the middle ear destructive to hearing, and may end either in a chronic purulent inflammation with bone destruction or in involvement of brain membranes or brain tissue proper.

TREATMENT.--In the early stages absolutely the same treatment as recommended for acute catarrh is indicated--the use of leeches, hot-water applications, rest in bed, anodynes, etc. When pus has formed and the tympanic membrane is bulging, paracentesis is indicated (method of operation, vide p. 917), to be quickly followed by the use of hot water to relieve the pain of the operation; the gentle use of the syringe and warm water will keep the canal free of pus during the suppurative process; also the external ear is to be kept covered by a cotton pad or some other like application as long as pain and tenderness exist.

{827} In young children suffering from scarlet fever it is of the utmost importance to cleanse frequently the pharynx of its muco-purulent secretions. This can be done by means of a probang or cotton wrapped on a curved end of whalebone, and afterward some detergent wash can be used, such as a strong decoction of green tea containing alum or a solution of common salt. The muriated tincture of iron, one part to five parts of water, is an excellent local application to be applied with a camel's-hair brush. Chlorate of potash makes a valuable gargle. In young children Meigs suggests the use of a powder containing one part of chlorate of potash to six parts of sugar, and a pinch of this placed on the tongue and allowed to dissolve.

By such a plan of treatment an acute purulent case will be best carried over the acute stage, and in many instances will end in entire recovery without the necessity of local treatment; but in some cases the purulent discharge from the middle ear will continue, and it remains to consider the best local remedies for checking this discharge and when they are to be used. It is with me an absolute rule that no remedy is to be used with a view of checking a purulent discharge until absolutely all pain has passed away and no pain is caused by pressure on the tragus or over the mastoid. During the interval the local treatment will consist of cleansing the external canal from the contained pus by the use of the syringe and warm water, the canal being afterward dried by cotton on a cotton-holder. If the discharge is small in quantity, the use of cotton on a cotton-holder will be sufficient to cleanse the canal, and causes less irritation than the syringe and warm water. The frequency with which the ear is to be cleansed will depend upon the amount of the discharge, as it should be done as little as is consistent with keeping the external canal free from pus. It is also useful for the patient by the Valsalva method of self-inflation to cleanse the middle ear from the therein-contained pus just before the time of using the syringe. If this is not feasible, the Politzer method of inflation answers the same purpose. When all pain has passed away, and if the discharge still continues, it will be proper to make a local application. My favorite one is insufflation of a small quantity of finely-powdered boracic acid (a convenient rubber blower is made for this purpose). This application answers well also in chronic purulent middle-ear affections. In applying this powder a very small portion only is to be used, so that there can be no danger of blocking the discharge by the powder obstructing its passage through the middle-ear cavity. A small portion is to be placed in an insufflator and blown in, the application to be repeated every few days. I would also mention the great importance of keeping the external canal closed by a wad of absorbent cotton, which not only absorbs the pus as it slowly escapes, but also prevents the immediate contact of air with the middle-ear cavity--a most desirable aid in the cure.

Chronic Purulent Inflammation of the Middle Ear.

Urbantschitsch[9] calls attention to two distinct pathological conditions that are to be noted in this disease--the one a swelling and hypertrophy, {828} the other a thinning, of the mucous and submucous tissues. The thickening consists in an infiltration, with subsequent connective-tissue development, either in the submucous or over the free surface of the mucous membrane, causing in the first case a diffuse tissue hypertrophy; in the latter case forming a circumscribed connective-tissue formation, papillary excrescences, and nodes. The condition accompanied with thinning of the tissue is to be considered a higher grade of purulent inflammation, by which it results that a portion of the normally existing tissue disappears, and is not again reproduced, while the newly-developed inflammatory products do not advance to organization, but are thrown off in the purulent discharge. In this way can be explained why at one time, by examination through the external canal and perforated tympanic membrane, there is found a swollen connective tissue, while at another time the bone can be seen through the thinned membrane.

[Footnote 9: Vide Textbook, p. 351.]

CAUSES.--As a rule, it is a sequela of a previous acute attack. And it is also safe to say that a large number of chronic purulent cases are the result of bad treatment or non-treatment of the acute attack. To mention the causes of chronic suppuration is to repeat those causing the acute variety, such as diseases of the naso-pharynx resulting from scarlatina, variola, measles, typhus, tuberculosis, bronchitis, syphilis, etc.; also the external irritating causes, effect of change of temperature, as by draughts of air, cold water entering the external auditory canal, etc.

SUBJECTIVE SYMPTOMS.--Difficulty of hearing is always present. This is often caused by masses of granulations or collections of pus, filling up largely the tympanic cavity. These with a hypertrophied mucous membrane could sensibly interrupt sound-vibrations; and it will not be out of place to remark that the recovery of hearing will depend largely on what amount of change can be effected in these different conditions. Tinnitus aurium is not a constant factor; a few patients suffer from discomfort caused by pus passing down the pharynx, causing nausea.

OBJECTIVE SYMPTOMS.--More or less swelling of the external canal, while the constant passage of purulent fluids over the skin results in exfoliation of its epithelial layer and a subsequent weeping from the skin tissue. The secretion varies from an abundant discharge to a minimum of a few drops per day. It may be watery or muco-purulent, or of a thick, creamy, tenacious consistence. Odor is common, and if the bone is involved of a most disagreeable character. The perforation in the tympanic membrane may vary in size from that of a pin-head to a loss of the greater part of the entire membrane; also, the membrane is found thickened, with an occasional calcareous deposit in its fibrous layer. Granulations and polypoid growths are found in the external canal and middle-ear cavity. The mucous membrane of the naso-pharynx will show the various changes that are found associated with the different diseases that cause this complication.

DIAGNOSIS.--This is without difficulty as a rule. The discharge, the perforation that often can be seen, the whistling caused by the air being forced through the middle ear and the perforation in the tympanic membrane by the Valsalva or Politzer method of inflation, are very significant of middle-ear suppuration. The pulsation often noticed at the bottom of the external auditory canal, and which has been considered indicative of perforation, is caused by a thin surface of fluid in contact with a {829} pulsating blood-vessel, and therefore is not necessarily a sign of perforation of the tympanic membrane, as fluids are found in the external auditory canal from inflammation of its coats, and in such a case pulsation might occur; but this is but seldom the case, and the removal of the fluid would remove any doubt as to whether the fluid was a result of external-ear inflammation or caused by purulent middle-ear disease.

The course of a chronic purulent inflammation is very variable. In many cases under proper treatment healing and restoration of tissue go on rapidly. The secretion grows daily less and of a thicker consistence, and the mucous membrane of the middle ear rapidly returns to a normal condition. The perforation in the tympanic membrane becomes smaller, and often entirely closes, so that in a young person the restoration may be so complete that it is difficult to know where the seat of perforation has been. In one case in my practice in a child of ten years, where the membrane had been destroyed to at least three-fourths of its extent, a full restoration took place. In another class of cases the course is not so favorable. The tympanic membrane is largely destroyed, and is not regenerated. The chain of small bones may be either partly or entirely lost. Granulations form in the mucous membrane of the middle ear, and the bony walls of the tympanum undergo partial necrosis, the pus appearing as an acrid, irritating fluid with more or less odor. The graver complications of purulent inflammation are apt to occur in those cases of chronic purulent inflammation where there has been a stoppage of the free discharge of pus from the middle ear, causing it to collect in the antrum and mastoid cells.

TREATMENT.--The first indication is to cleanse as thoroughly as possible the middle-ear cavity of the muco-purulent fluid that may have collected. This is best accomplished by forcing air up the Eustachian tube and through the middle ear by either the Politzer or Valsalva method of inflation. The fluids thus forced out into the external canal can be removed by the use either of warm water and the syringe if large in amount, or by cotton on a cotton-holder if small in quantity: the latter plan is less irritating, and also completely dries the external canal. No local application ought to be made as long as any pain exists.

The local applications that my experience has shown to give the best results consist of boracic acid and iodoform. (The latter is objectionable on account of its odor.) The powder-insufflator furnishes a convenient method of applying these powders, and only small quantities should be used, so that no possible plugging of the middle ear can take place. Some authorities prefer fluid applications instead of powder. Weak solutions of sulphate of zinc, from one to four grains to the ounce, are frequently used: a few drops, warmed, are poured into the external canal and allowed to remain a short time, and then removed by a twisted tuft of cotton on a cotton-holder. Nitrate-of-silver solutions are to be used on a cotton-holder; and if a very strong solution is used it should be neutralized with salt and water.

The frequency of application of any remedy will depend upon the amount of discharge; but as the discharge lessens, so should the remedy be less frequently applied. The same rule applies to the cleansing of the ear, as I have no doubt that excessive use of the syringe often tends to re-establish and increase the discharge. In some cases, where the discharge has {830} become very small in quantity, a thick scab will form over the tympanic perforation, and restoration of the tympanic membrane will rapidly advance under such a covering, showing that it is good practice not to remove such a scab, provided pus is not thereby prevented from escaping. A cotton plug should always be worn in the external canal of a purulent ear, as it acts as an absorbent of the purulent secretions, as well as protects the middle ear from the irritating contact of the air.

The naso-pharyngeal cavities are to be considered and appropriately treated; also, a general tonic treatment is often indicated.

SEQUELÆ OF PURULENT INFLAMMATION.--I. Brain involvement, either of the meninges or its substance proper: a, purulent meningitis; b, abscess of the brain; c, phlebitis with thrombosis of the sinuses. II. Mastoid disease.

I. Brain Involvement.

It will be proper for a clear understanding of the subject to briefly consider the anatomy of the middle-ear cavity with reference to this complication. The middle-ear cavity is practically surrounded by bony walls, with the exception of the foramen closed by the tympanic membrane and the opening of the Eustachian tube. The roof of the middle ear is of varying thickness, and is perforated by a number of canals for the passage of blood-vessels, forming a direct communication between the circulation of the middle ear and the meninges of the brain; also, the petro-squamous suture in the earlier years of life before complete ossification has set in provides a way for spreading of the inflammatory process from the tympanum to the brain tissue; also, cases are recorded where caries has formed actual openings in this bony roof, through which pus has entered into the brain cavity. The floor of the tympanic cavity is very thin, and forms a fossa in which lies the jugular vein, so that involvement of this vein in the inflammatory process could occur by the close apposition of these parts. The anterior wall is formed in part by the carotid canal, and cases are noted where defects in this bony wall are found. Under such circumstances the coats of the artery would lie in direct contact with the middle-ear membranes. Also, it is to be noted that small twigs from the carotid artery pass through its bony canal and anastomose with vessels of the middle ear, furnishing a way for the spread of inflammation from the middle ear to the carotid artery that may result in thickening of its walls.

The superior and posterior surfaces of the petrous bone are in direct contact with the brain membranes. The posterior wail contains the passage into the mastoid cells by way of the antrum, through which middle-ear inflammations spread and involve the mastoid cell cavities, and may result in some cases in thrombosis of the transverse sinus.

The inner wall presents two weak points--the one the round foramen, covered with membrane; the other, the oval foramen, covered with the stirrup and the annular ligament. Inflammation can cause destruction of these coverings and give free access of pus through their foramina into the labyrinth, and thence through the internal auditory canal into the brain cavity. It is not difficult, therefore, with so many ways of {831} communication between the middle ear and brain cavity to have easy spread of inflammation between these two regions.

(a) PURULENT MENINGITIS may arise from continuance of the inflammation along the veins which penetrate the roof of the tympanic cavity in their passage from the middle ear to anastomose with the blood-vessels of the meninges, or may in rare instances be caused by pus entering the brain cavity by way of the internal ear, or it can result from caries of the petrous portion of the temporal bone.

SYMPTOMS.--Fever will be present; distressing headache; vertigo, a most significant symptom, and often present even when the head is quiet and in a horizontal position, but greatly increased by the vertical position and motion; pain of a lancinating character, shooting over the entire affected side and even down the neck; the occiput and vertex are favorite points for pain to locate. Nausea and hiccough are present. Abdomen depressed; pupils reacting to light but feebly; slow pulse; and in some cases paralytic symptoms are prominent. Post-mortem appearance: meninges congested, and lymph and pus often found at various points. Dura mater over the diseased petrous bone will be found thick, congested, and pus may be found between it and the bone. Caries of the petrous bone also is found in some cases.

(b) ABSCESS OF THE BRAIN.--With the exception of wounds and injuries, chronic purulent middle-ear inflammation is the most frequent cause of brain abscess. Meyer, in a collection of 89 cases of brain abscess tabulates the causes as follows: Typhus, 1; intercranial tumor, 2; disease of nasal mucous membrane, 3; disease of the blood-vessels, 5; inflammation of neighboring parts of the brain, 5; unknown causes, 11; suppuration of distant organs, especially the lungs, 19; caries of the petrous bone, 20; injuries, 21. Lebert collected 80 cases of brain abscess, and found that one-fourth were caused by purulent middle-ear inflammation, caries of the petrous bone being frequently present; in one-seventh of the cases the brain abscess appeared before puberty, in the remaining cases mostly between the sixteenth and thirtieth years; also, that in some cases the abscess developed in the part of the brain lying over the bony roof of the middle ear; in other cases it was found in a distant part of the brain or the cerebellum, probably developing as a metastatic abscess. Toynbee considered the retention of purulent products in the middle ear or mastoid cells as the chief cause of brain complications from ear sources: he also endeavored to show that an inflammation of the external auditory canal will tend to implicate the cerebellum and lateral sinus--that inflammation of the middle-ear cavity would extend to the cerebrum, and that of the labyrinth to the medulla oblongata. But, practically, such a rule will not hold good, and Gull has modified Toynbee's law as follows: The cerebellum and lateral sinus may suffer from mastoid disease, while the cerebrum is threatened by caries of the roof of the tympanic cavity.

Brain abscess is generally located in the medullary substance, very rarely in the cortex. The middle portion of the brain hemisphere is the most frequent seat of abscess, and very often in that part adjacent to the diseased ear. The abscess may be located directly over the diseased bone, so that the dura mater forms its covering on one side and the brain tissue on the other, or it may be located in the brain parenchyma with perfectly healthy brain tissue between it and the diseased bone. Meyer traces the {832} origin of a brain abscess from ear disease in this manner: A chronic catarrh of the middle-ear mucous membrane results in an hypertrophy of the mucosa on one side and a chronic inflammation of the neighboring bone on the other side. Caries of the petrous bone, so caused, produces inflammation and adhesion of the dura mater, and from here as a starting-point the inflammation spreads into the brain tissue. In rare cases the brain abscess has been found connected by a fistulous tract with the diseased bone.

SYMPTOMS.--Headache is generally present in varying degree, often of a lancinating character. Vertigo frequently present. Fever generally present, with or without chill. Convulsions frequent, with loss of consciousness and unsteadiness of gait, and often paralysis of different parts of the body. The pupils are often contracted, and not unfrequently this disease may closely resemble typhus fever. Lebert noticed in his cases that failure of the intellect was not the rule, but paralysis of sensibility occurred in two-thirds of them. It is also to be noted that cases occur where all these symptoms are absent. This disease can run an acute or chronic course. In the acute condition a fatal termination is caused by the great destruction of brain tissue involved in the suppurative process. In the chronic cases the abscess becomes encapsulated, but finally terminates by rupture of the abscess and escape of pus into the ventricles or over the surface of the brain. In Lebert's cases the fatal termination occurred in half of them during the first month, in one-third of the remainder toward the end of the second month, and in the remaining cases in a varying time between the third and eighth months.

(c) PHLEBITIS WITH THROMBOSIS.--This sequela of middle-ear suppuration is not infrequent. Von Dusch in 32 cases of phlebitis with thrombosis found that purulent middle-ear disease was the cause of 20 of them. It is frequently found in the venous sinuses in proximity to the petrous portion of the temporal bone, especially in the lateral and petrosal sinuses, and often caused by caries of the petrous bone.

Phlebitis with thrombosis of the lateral sinus is characterized by a swelling of the mastoid region which extends downward into the neck, due to an extension of the phlebitis from the lateral sinus along the veins leading from that sinus through the mastoid process to the exterior of the skull. Giddiness and unsteady gait are often present. If the inflammation involves also the superior longitudinal sinus, it will cause symptoms such as epileptic convulsions and violent hemorrhage from the nose. Wreden considers that the epileptic seizure is due to a capillary hemorrhage in the cortical substance of the posterior cerebral lobes, caused by obstruction of the veins passing over the brain substance. The nose-bleeding is due to the fact that a part of the blood circulating through the veins of the nasal passages, and then through the superior longitudinal sinus, is hindered by the sinus obstruction and accumulates in the veins of the nasal passages, and finally causes a rupture in some part.

Phlebitis with Thrombosis of the Cavernous Sinus.--Urbantschitsch gives the following summary of this complication:[10] A thrombosis of the cavernous sinus can be caused by a thrombus in the internal jugular or facial veins or by a clot passing from the superior petrosal sinus into the {833} cavernous sinus, or, finally, by inflammation and thrombosis in the venous circulation of the carotid canals.

[Footnote 10: Vide Textbook, p. 367.]

PROMINENT SYMPTOMS.--Retro-bulbar oedema and exophthalmos, caused by stoppage of the blood from passing from the orbit into the cavernous sinus. This may result in a mechanical compression of the retinal vessels and temporary blindness; also, occasionally swellings appear about the eyelids and nose. Compression of the oculo-motor and abducens nerves as they pass along the outer wall of this sinus may cause paralysis of these nerves, and consequent inward turning of the eye, with ptosis of the eyelids; also, pressure on a branch of the fifth pair of nerves as it passes along the outer wall of the sinus may cause neuralgia in the parts supplied by the branch, or neuralgia in the supraorbital region.

Phlebitis with thrombosis of the internal jugular vein is marked by a well-defined swelling extending from the angle of the jaw downward along the line of the sterno-cleido-mastoid muscle, painful on pressure, with marked distension of the veins of the face and neck, especially the external jugular vein. Later on, when the collateral circulation is established, the superficial veins are apt to return to their former calibre. If the inflammation extends downward, it can involve the vena cava; and if upward, the facial veins, causing a swelling of the cheeks and eyelids. The process can also extend from the facial to the orbital veins, and thence into the cavernous sinus. Pressure of the thromboid mass on the internal jugular vein, on the glosso-pharyngeal hypoglossus and pneumo-gastric nerves at the opening of the jugular foramen, will cause nervous symptoms corresponding to the nerve involved.

PROGNOSIS of a phlebitis with thrombosis, as a rule, is unfavorable. Chronic middle-ear suppuration can also form a starting-point of metastatic abscess, also of tubercular formations in the lungs and other organs of the body. I have also been much impressed with the frequent occurrence of kidney complications, such as granular nephritis, in this disease. A gradual absorption of pus will develop a general bodily weakness, and it is a fairly well established fact that, as a rule, patients suffering from chronic middle-ear suppuration are not apt to be long lived: many life insurance companies now order that this disease will prevent the case from being considered a first-class risk.

II. Mastoid Disease.

The mastoid process of the temporal bone presents an outer convex with an inner concave surface. On the upper and posterior borders of the bone are found several canals, through which the external vessels form a union with those of the dura mater; also, by which the outer cranial veins form a union with the transverse sinus. There is also an important suture--the petro-squamous suture, which admits of the passage of blood- and lymph-vessels. These vessels furnish a channel for the spread of inflammation from the antrum outwardly, involving the tissues of the neck, and inwardly to the brain membranes and brain tissue proper; phlebitis with thrombosis of the lateral sinus can also occur. The interior of the mastoid process contains one large opening, the antrum, with numerous communicating air-cells, and all lined with {834} an extension of the tympanic mucous membrane. Inflammation of the mastoid process, as a rule, is an extension of inflammation from the middle ear. The cause will be found in an obstruction to the free escape of the purulent products from the antrum out through the middle ear. It is also found that in a great number of cases of purulent middle-ear inflammation the air-cells are closed by a process of sclerosis. There are two forms of mastoid disease--1, periostitis of the bone; 2, inflammation of the mucous membrane of the mastoid cells.

1. Periostitis of the Mastoid Bone is caused either by external injuries, or more frequently by inflammation extending from the mastoid cells outwardly to the periosteum.

SYMPTOMS.--Pain, severe in character, also fever. Redness over the mastoid and great sensibility to the touch, followed by marked swelling, which may extend far down the neck, involving the lymphatic glands. Later, pus will be found between the periosteum and bone, and in a few cases caries of the bone.

2. Inflammation of the Mucous Membrane of the Mastoid Cells is caused generally by extension of inflammation from the middle-ear cavity, either of a catarrhal or purulent character, causing the cell-cavities to quickly fill up with the inflammatory products which escape through the antrum and middle-ear cavity into the external canal. If this way is closed, the fluids accumulate in the mastoid cells and form conditions favorable to involvement of the internal organs.

SYMPTOMS.--Severe pain, tenderness, and redness of skin over mastoid, but not the marked swelling that is found in periostitis. During such an inflammation facial paralysis may develop, showing that the inflammation has extended into the bone itself. Delirium is occasionally met with, probably due to a more or less circumscribed meningitis; coma is also occasionally noted, caused by effusion into the lateral ventricles. In many cases of antrum inflammation there is a marked swelling of the upper and posterior cutaneous covering of the osseous part of the external canal, making it a valuable symptom in determining the degree of the inflammatory action.

Caries and necrosis of the mastoid bone are resultants of the above-described conditions, and are especially found in early childhood, and generally caused by retention of pus in the mastoid cells and breaking down of their walls. This process can be limited to the cell portion of the bone or can also involve the cortex, with formation of an external fistulous opening.

TREATMENT.--Use of heat and moisture, either by hot-water fomentations or warm poultices, like flaxseed, over the entire temporal region of the head on which the diseased mastoid is located. The flaxseed poultice is to be covered with oil silk and changed as often as needful to keep it warm. The use of leeches to the mastoid is indicated by tenderness of the part to the touch, with heat and swelling of the tissue covering the bone. Two or three foreign leeches can be used, and if the abstraction of more blood is desired the after-bleeding is to be encouraged by warm moist applications. If the disease advances notwithstanding this treatment, an opening down to the bone is indicated. The incision is usually described as the Wilde incision. The length of the cut is to be from a half to one inch, down to the bone, the point of the knife entering the {835} skin on a level with the upper wall of the auditory canal, about half an inch behind the auricle. Occasionally the posterior auricular artery is cut, but hemorrhage is readily controlled by pressure over the artery. During the entire treatment the external auditory canal is to be cleansed from time to time of the purulent secretions, so as to facilitate the discharge of pent-up fluids from the middle ear and antrum. Also, the condition of the pharynx is to be noted, and treated if needful. Finally, if all these measures fail to relieve, and the patient shows signs of meningeal or brain involvement, together with marked redness, tenderness, and swelling over the mastoid bone, showing that pus is being retained in the mastoid cells, there only remains the making of an opening into the mastoid process and antrum by means of a bone-drill or gouge. This is best done by a free vertical incision through the skin and periosteum covering the mastoid process. Examine then the bone, and a fistulous opening may be found which can be enlarged by a probe, and so allow the free escape of pus. If such does not exist, apply a drill to the bone at a point a quarter of an inch posterior to the external canal and just below a horizontal line drawn tangent to its upper wall. The instrument is to have a direction inward, upward, and slightly forward. The depth to which it should penetrate varies: usually cell-structure is reached at a slight depth, when the drill should be withdrawn. If sclerosis of bone exists, it will be necessary to go deeper, but never more than three-quarters of an inch, or about 20 millimeters. This is Buck's rule. Schwarze says, never go deeper than 25 millimeters, otherwise there is risk of plunging the drill into the labyrinth. Also, during the drilling process Buck recommends keeping the fore finger of the operating hand constantly pressed against the neighboring bone, so as by counter-pressure to reduce to a minimum the risk of wounding the lateral sinus if it should lie in an abnormal position in the path of the drill. After-treatment consists in keeping the canal open by gentle washing. The use of a bone-gouge is preferred by some to the drill, as being a less dangerous instrument.

Diseases of the Internal Ear.

ANATOMY.--The internal ear consists of a central cavity, from one end of which arise the semicircular canals, and from the other the cochlea. The interior of these contains the membranous portion and fluids of the internal ear. The cochlea contains the most important part--namely, the terminal endings of the auditory nerve. Sound-vibrations pass through the external canal and strike against the tympanic membrane, throwing it into vibration. The vibrations of this membrane are carried across the middle ear by the chain of small bones to the membrane closing the foramen ovale of the internal ear, throwing this and the labyrinthine fluid also into vibration, and these latter vibrations, impinging on the terminal endings of the auditory nerve in a way as yet unknown, produce sound.

Vessels of the Labyrinth.--The labyrinth obtains its blood partly from the arteria auditiva interna, a branch from the basilar artery which comes from the vertebral, and partly through vessels communicating with the middle ear viâ the round and oval windows, and through others passing {836} through the long walls themselves. The arteria auditiva interna divides in the internal meatus into a vestibular and cochlear branch. The former is distributed to the soft structures of the vestibule and semicircular canals. The cochlear branch is distributed to the modiolus and layers of the lamina spiralis. The venæ auditivæ internæ empty into the inferior petrosal sinus or the lateral sinus; other branches empty into the superior petrosal sinus.

The auditory nerve or portio mollis of the seventh nerve arises by two roots in the medulla oblongata. One ganglionic nucleus of origin is in the floor of the fourth ventricle, the other is in the crus cerebelli ad medullam (Stieda). The nerve winds around the restiform body, and passes into the meatus auditorius internus, and finally divides into a vestibular and cochlear branch. The vestibular branch divides into three branches: the superior is distributed to the utricle and ampullæ of the superior vertical and horizontal semicircular canals; the middle to the sacculis, and the inferior to the ampulla of the inferior vertical semicircular canal. The cochlear branch enters the modiolus and breaks up into smaller branches, which radiate fan-shaped into the lamina spiralis, and are then distributed between the two plates of the lamina spiralis through all its turns.

TINNITUS AURIUM.--It may be assumed that the normal ear is filled with continuous sound. The blood flowing through the large arteries and veins in close proximity to it (such as the carotid arteries and jugular vein), as well as the blood flowing through the vessels of the internal ear, will give rise to sound by throwing into vibration the soft tissues surrounding them, including also the walls of the vessels themselves. This motion is sufficient to excite the auditory nerve-elements by causing vibrations of the intra-labyrinthine fluids, and so produce sound; which, being a normal condition, and one to which the ear is accustomed, will remain unnoticed.[11]

[Footnote 11: To Theobald we are indebted for the vascular theory of sound.]

The arterial system of the body throws the neighboring tissue into vibration, but this is not recognized unless our attention is particularly directed to it; or, in other words, the entire body is filled with movement as a normal condition, and therefore attracts no attention. But let this movement be increased--for instance, by violent muscular exertion, increasing the arterial action--or lessened, as in syncope, and at once an abnormal condition draws our attention to it.

In the same way the ear is filled with continuous sound as a normal condition, and therefore it is not perceived, these sound-vibrations escaping out through the middle ear and external canal. This can be readily proved. Let the external auditory canal be obstructed artificially, either by the finger or by a cork. At once a tidal tinnitus, so called, is produced, this being caused by the normal sound-vibrations being impeded in their outward passage and being thrown back again to impress the nerve-elements for a second time. This, being an abnormal condition, is at once recognized.

Different Varieties of Tinnitus Aurium.--I. Tinnitus caused by obstruction of the normal sound-vibrations in their outward passage through the middle ear and external canal; tidal tinnitus, so called from a resemblance to the noise of the ocean. Such obstructions may exist in the middle-ear {837} cavity, as thickening of the soft tissues of the middle ear, exudations and adhesions, as found in chronic catarrh, or in the external canal, as impacted cerumen, a swollen canal, etc. The effect of such obstruction would be to interrupt the normal sound-vibrations and cause them to be reflected back again to impress for a second time the auditory nerve-elements, causing an abnormal and therefore recognized condition. This is the most frequent variety of tinnitus, and for the reason that it is produced by the more ordinary ear diseases.

II. Tinnitus caused by abnormal sound-vibrations produced either by increase or by decrease of intra-labyrinthine pressure. In a normal condition the auditory nerve-elements are subjected to a given intra-labyrinthine pressure; now, if this pressure be altered (either by being increased or diminished) an abnormal condition ensues, and is noted as such.

a. Tinnitus produced by increased intra-labyrinthine pressure may be caused by increase of the intra-labyrinthine fluids (by effusions, hemorrhages, etc., as in Menière's disease), or can be caused by increase in the amount of blood flowing through the arteries and veins of the internal ear. In either case there will result an increase of pressure that is exerted on the auditory nerve-elements. Also, another result of such increase of pressure on the arteries of the labyrinth would be to throw them into more active pulsation, and so cause greater movement on the intra-labyrinthine fluids. These abnormal vibrations impinging on the auditory nerve-endings would be noticed as such, and give rise to tinnitus of a pulsating character corresponding to the movements of the pulsating vessels. Such a condition is noticed in an eyeball afflicted by glaucoma, or can be artificially produced by finger-pressure on a normal eye. The veins of the retina will be first thrown into movement, and as the pressure increases the arteries will show marked pulsation. Why should not a similar set of conditions in the internal ear produce similar results?

b. Tinnitus produced by a lessened intra-labyrinthine pressure may be caused either by loss of intra-labyrinthine fluid or by a lessened blood-supply to the internal ear. The latter cause being the most frequent, a familiar example of this would be the tinnitus experienced by a fainting person, a common sensation being a swimming head accompanied with strange whizzing noises in the ears. The tinnitus of anæmia is of this class, and frequently of the pulsating variety. Another explanation might be given: an anæmic heart murmur might be conveyed along the blood-vessels as through a speaking-tube, and in that way impress the auditory nerve. In this variety of tinnitus it is supposed that the sound-conducting apparatus of the middle and external ear is normal; if any obstruction exists, it would cause increase of tinnitus of this variety.

III. Tinnitus caused by a diseased condition of the auditory nerve, either in the part lying between the internal ear and brain or in the brain-centre itself--pure subjective tinnitus. Here we enter upon a subject obscure from the fact that so little pathological research has been made in this direction; but, reasoning from analogy, why cannot the auditory nerve be subject to as many diseased conditions as the optic nerve, where the ophthalmoscope has clearly shown the existence of neuritis, atrophy, and many other pathological changes, caused, it may {838} be, by disease of the retina, or it may exist as an inflammation of the nerve itself exterior to the eyeball, or it may be due to a brain tumor pressing on the optic nerve or optic tracts, also basilar meningitis? Gummata, osseous growths, etc. have in turn caused optic neuritis; finally, lesions at the optic nerve-endings in the brain itself have caused well-defined pathological changes in the optic nerve, which by the aid of the ophthalmoscope are recognized. Now, if these changes exist in the optic nerve, why may not the same conditions be present in connection with the auditory nerve, although from its anatomical location they are not capable of demonstration, as in the case of the optic nerve? And, as in the latter phosphene symptoms are common, due to nerve-irritation, so in irritation of the auditory nerve tinnitus would be developed, but of a subjective character. (In this connection it is not out of place to remark that in obscure internal ear disease examination of the optic nerve will often give valuable information toward clearing up the ear complication.) This variety of tinnitus may in some cases be due to a reflex nerve-irritation.

Finally, tinnitus may be noticed in cases of inflammation of the middle ear where fluid has collected, and is caused by the bursting of air-bubbles in their passage through this fluid, the air gaining access to the middle ear by way of the Eustachian tube. Tinnitus so produced resembles a bubbling or crackling sound. Hinton draws attention to certain cases where the tympanic membrane has lost its normal elasticity and become stiff, any movement of such a membrane causing a crackling sound. Also, there are some cases of tinnitus produced by foreign bodies being deposited on the tympanic membrane, such as cerumen, pieces of hair, etc., making a rustling or rasping noise.

Tinnitus produced by abnormal contractions of the tensor tympani or stapedius muscles has been thought to exist. Tinnitus may be intermittent or continuous. It also has an endless variety of sound, from one almost unrecognizable to a roar so loud as to render the patient nearly distracted.

Location of the Tinnitus.--Those varieties due to a diseased external or middle ear locate the sound, as a rule, in the ear itself. Subjective tinnitus is often located in the frontal and occipital regions; often also in the ear itself. It is also to be noted that marked tinnitus may be associated with a low degree of deafness, and the converse is true: slight tinnitus may be associated with a high degree of deafness.

PROGNOSIS.--The removal of tinnitus depends entirely upon the cause of it and the possibility of its removal. Continuous tinnitus is always to be regarded as a more pronounced symptom than the intermittent form.

The TREATMENT will be directed to the removal of the cause. If the disease is located in the external canal or middle ear, or in a diseased condition of the naso-pharynx, these irritating causes should be removed by treatment already laid down in previous pages. The treatment of subjective tinnitus will be guided by the same principles. Determine the cause and seek for its removal. As to whether any particular drugs exist peculiarly adapted to the removal of tinnitus, I would say that in tinnitus of a subjective character or due to nerve-irritation the bromides are indicated in appropriate doses. Inflation of the middle ear with air impregnated with ether (a few drops of ether dropped into a Politzer air-bag {839} and the inflation made by the Politzer method), at intervals of three or four days, in some cases proves of benefit.

Deafness after Cerebro-Spinal Meningitis, Scarlet Fever, Mumps, etc.

This opens up a chapter in which our knowledge derived from post-mortem examination is very limited. In a given number of such cases the inflammation probably extends from the brain to the labyrinth; in others the changes that are found exist chiefly in the middle ear, so that it must be supposed that the inflammation in such cases has originated in the middle ear, and has secondarily invaded the labyrinth. In some cases, such as deafness after mumps, Toynbee is of the opinion that the peculiar poison of that disease affects the nervous apparatus of the ear, as the deafness comes on suddenly, and is usually complete, without evidence of disease in any other part of the ear. In this class of cases the prominent symptoms are deafness--which is total--and staggering gait, with vertigo. This symptom may last many weeks, and then cease. As a rule, examination of the tympanic membrane is negative, and the seat of disease is to be sought for in the labyrinth, whether it may be an inflammation of the soft structures or an effusion, causing increased intra-labyrinthine pressure. In many cases the suddenness of the attack would point to an effusion as the more probable cause.

Brunner in a comparison of five cases of deafness after mumps[12] gives the following symptoms and course of the disease: 1. The nervous deafness after mumps can be one-sided or double-sided, the former being more frequent. 2. It is complete, and, according to past experience, incurable. 3. It develops rapidly, with vertigo and subjective noises, the later symptom lasting a long time. 4. There is little or no fever. 5. Pain is never or very seldom present. 6. Consciousness is not lost; excessive vertigo a prominent symptom. 7. It happens both in children and adults.

[Footnote 12: Archiv Otology, vol. xi., No. 2, p. 103.]

Menière's Disease.

A. Guye of Amsterdam has published a very full summary of the history of this disease.[13] The following is extracted from it: Under the head of Menière's disease is included those cases of inflammatory processes in the semicircular canals or in the middle ear producing vertigo, which is either continuous, or caused by normal movements of the head, or appearing only at intervals of weeks or months; also, that this disease is of a secondary nature, and is due to inflammatory processes in the tympanum or antrum. In typical cases the vertigo is accompanied by sensations of rotation: first a sense of rotation about a vertical axis and toward the affected side; this is followed by a sensation of rotation about a transverse axis forward and backward. The vertigo then becomes complete, and is followed by fainting, with or without loss of consciousness and vomiting. The attack in some cases may last for a few minutes to a half hour; in others every movement will tend to produce vertigo for {840} several days. In chronic cases the feeling of vertigo to a slight degree persists between the attacks. Guye considers the causes of middle-ear catarrh as the factors most likely to cause Menière's disease. Syphilis is also noted in some cases.

[Footnote 13: Ibid., vol. ix., No. 3.]

TREATMENT.--In some cases an alterative treatment is most serviceable, such as iodide of potassium, also the bromide of potassium; quinine is also by some recommended. The use of alcohol and tobacco is to be forbidden.

The disease known as boiler-makers' deafness, because generally found among men laboring in machine-shops, where they are subjected to loud noises connected with the work they are engaged on, is thought to be due to a paralysis of the terminal endings of the auditory nerve due to concussion. The middle ear sometimes shows some thickening of the tympanic membrane. Treatment is without avail.

In internal-ear diseases a few common symptoms can be noted. All cases show deafness, and in most of them of an absolute degree. And here is where the tuning-fork proves a valuable aid in diagnosis of deafness due to middle-ear disease, in which cases the tuning-fork is heard best on the deaf side, and to deafness due to internal-ear disease, where the tuning-fork is heard the least on the deaf side. Vertigo and a staggering gait are quite common symptoms, probably due to irritation of the semicircular canals. Prognosis as a rule is bad, as far as recovery is concerned, and an alterative treatment is often indicated. Electricity, I would state, in my experience has not proved to be of any avail.

Deaf-Mutism

may be either congenital or acquired. Two-thirds of all cases will come under the first class, and often depend upon a mal-development of some part of the central nervous system or the ear itself, or may be due to intra-uterine disease of the ear. There is a strong tendency for this disease to be inherited, and particularly in children where there exists a blood-relationship between the parents. The acquired cases may arise from defects in the central nervous system or in the internal ear, or may be due to diseases affecting the middle ear, such as purulent inflammation; and this latter cause is to be noted, as no doubt proper treatment of the middle-ear disease in many cases would have prevented such a result.

All deaf cases become mute, unless the disease has occurred in adult life, when the patient has already acquired the power of language. A deaf-mute does not speak, because he cannot hear, and therefore speech is an unknown quantity.

The TREATMENT would consist in treating any middle-ear disease that might exist, such as the sequelæ of purulent inflammation, and the instruction of the patient in acquiring the power of intercommunication either by the methods long employed of finger-reading, or, much better, by the lip method, so called, where the power of speech is given to the patient. Such cases should attend schools where such instruction is given, commencing at five years of age, and many cases now attest the value of the latter method of instruction.

DIFFERENT METHODS OF DETECTING FEIGNED DEAFNESS.--The {841} Moos Method.--Stop the external canal of the sound ear with a cork; place a vibrating tuning-fork on the head. If the person under examination declares that he does not hear the fork with either ear, he is feigning deafness, as it would be heard well by the sound ear.

The Urbantschitsch method makes use of the human voice. First determine that good hearing power exists in the sound ear; then shut the external canal of this ear with a cork and address the individual with a few loudly-spoken words. If he denies hearing at all, he is feigning, as a good hearing ear, by simple closure of the external canal, will be still able to hear loudly-spoken words.

Another method is to determine the distance at which the person can hear certain words and repeat them correctly. Then have the patient close the eyes and let the examiner try by lengthening and shortening the distance, and note the result. Often he will hear and repeat words spoken at long distances, and apparently not be able to repeat words spoken at short distances.

Müller's Method.--Speak into the sound ear through a tube or paper roll different words as softly and quickly as the examined person can repeat; then let a second examiner repeat the same in the deaf ear. Of course nothing will be heard by the person feigning. Then let the first examiner repeat his performance; the feigner will quickly repeat after him. Suddenly begins the second examiner to softly and quickly speak in the deaf ear, but choosing different words from the first examiner. A really one-sided deaf person will repeat the words spoken into the sound ear only, while the feigner will be in doubt, and will not be able to separate the words heard by both ears, so as only to repeat the words heard by the sound ear.

{842}

{843}

INDEX TO VOLUME IV.

A.

ABORTION, 467 Changes in maternal system, 474 Changes in uterus and pelvic viscera, 475 Classification, 467 Criminal, causes of, 493 Course of, 497 Diagnosis, 505 Duration, 503 Hemorrhage, 516 Morbid anatomy of, 494 Pain, 516 Pathology of, 494 Preliminary symptoms, 499 Prognosis, 508 Symptomatology, 497 Symptoms of, 500 Termination, 504 Treatment of, 509 Abortion which is thoroughly inaugurated, 516 After-treatment, 523 Anæsthetics, 514 Antiseptics in, 510 by tampons, 517 Dressing-forceps, use of, 513 in cases of retention of ovum, 519 Instruments, 512 Medication, 512 Preparations for, 509 Preventive, 515 Definition of, 467 Development of ovum, 477 Etiology, 479 Amnion, the, 491 Chorion, 490 Decidua, 488 Exciting causes, 481 Hemorrhage, 490 Local causes, 488 Ovum, the, 489 Placenta, the, 490 Predisposing causes, 480 Umbilical, the, 491 Uterine mucosa, 488 Frequency, 468 History, 470 Importance, 468 Physiology of early pregnancy, 474 Synonyms, 467 Uterine mucosa, 476

Abscess of the brain as a sequel of chronic inflammation of middle ear, 832

Absence of one kidney, 21 of pain in fibroma of skin, 686

Acanthia lectularia, 733

Accidents and complications of ovariotomy, 336

Acne, 641 rosacea, 647

Aconite in the treatment of parametritis, 221

Acquired anteflexion of uterus, 177

Actual cautery in the treatment of the pedicle after ovariotomy, 326

Acute catarrh of middle ear, 821 cystitis, 126 diffuse nephritis, 82 nephritis of scarlatina, 84 endocarditis in pregnancy, 430 endometritis, 460 infectious diseases of pregnancy, 424, 425 lobar pneumonia in pregnancy, 430 metritis, 447 ovaritis, 283 parenchymatous nephritis, 78 pleuritis in pregnancy, 431 purulent inflammation of middle ear, 825 urethritis in women, 353 vaginitis in prolapse of uterus, 158

Affections of the eye caused by diseases of the digestive system, 749 of fifth pair of cranial nerves, 785 of second pair of cranial nerves, 771 of seventh pair of cranial nerves, 790 of third pair of cranial nerves, 780 of twelfth pair of cranial nerves, 790

After-treatment in anterior elytrorrhaphy for prolapse of uterus, 163 of abortion, 523

Age in epithelioma, 709 in progressive muscular atrophy, 542 of menstruation, 182

Albinismus, 676

Albumen in the urine as a symptom of acute diffuse nephritis, 82 of chronic parenchymatous nephritis, 81

Albuminoids in albuminuria, 35

Albuminuria, 34 as a symptom of congestion of kidney, 70 in Bright's disease of kidneys, 73, 75 in calculous pyelitis, 47 in chronic diffuse nephritis, 96 of nervous affections, 40 of pregnancy, 40

Alcohol as a cause of toxic amblyopia, 803 effects of, on the eye, 803

Aleppo bouton as a variety of furunculus, 606

Alimentary canal, disorders of, during the menopause, 440 in pregnancy, 408

Alkalies in treatment of acute cystitis, 127 of chronic cystitis, 131

Alopecia, 678 areata, 680

Alterations in condition of blood as a disorder of pregnancy, 405 in nutrition during menopause, 437 in secretion of kidneys during menopause, 437 of functions of skin during menopause, 435

Alteratives in local treatment of chronic metritis, 459

Alum in the treatment of dilatation of the urethra in women, 359

Amenorrhoea, 183 atrophy of uterus in, 186 chlorosis in, 186

Ammonia hydrochlorate in the treatment of fibrous tumors of the uterus, 259

Amnion, the, as a local cause of abortion, 491

Anidrosis as a disorder of secretion in diseases of skin, 584

Anæmia, pernicious, as a disorder of pregnancy, 406

Anatomical characteristics of seminal incontinence, 141

Anatomy, course, pathology, and termination of parametritis, 210 of internal ear, 835 of middle ear, 817 of syphiloderma bullosum, 705 of vagina, 367 of vulva, 388 pathological, of progressive muscular atrophy, 543

Anæsthetics in treatment of abortion, 512

Aneurism, retinal, 743

Angioma of the skin, 688

Anodynes in acute cystitis, 127

Anomalies of kidneys, 19

Anteflexion of uterus, 176, 177

Ante-locations of uterus, 153

Anterior elytrorrhaphy for prolapse of uterus, 161

Anteversion of uterus, 174

Antiseptics in treatment of abortion, 510

Apiol in treatment of amenorrhoea, 190

Applications in treatment of seborrhoea, 589

Arrangement of tables in ovariotomy, 320

Arsenic as a cause of dermatitis medicamentosa, 602 in the constitutional treatment of eczema, 632 in the treatment of lichen ruber, 624

Articles needed for operation of ovariotomy, 318

Ascites in the diagnosis of cystic tumors of ovary, 305

Aspiration in the treatment of ovarian cysts, 308 of pelvic abscess, 225

Assistants in ovariotomy, 320

Associated movements of head and eyes in affections of third pair of cranial nerves, 782

Astringents in treatment of albuminuria, 42

Atony of bladder, 133

Atresia, 373 hymenalis, 374 vaginal, 376 vulvæ, 373

Atrophia cutis, 683 pilorum propria, 682 unguis, 683

Atrophied tubules in congestion of kidney, 69

Atrophies of skin, 676

Atrophy of bladder in women, 348 of uterus in amenorrhoea, 186 progressive muscular, 540

Atropia as a cause of dermatitis medicamentosa, 602 in polyuria, 34 in treatment of seminal incontinence, 146

Autopsies in nystagmus, 784 of cases of pseudo-hypertrophic paralysis, 558

Axis of arteries, 148

B.

Baldness in tinea tonsurans, 720

Basedow's disease in medical ophthalmology, 799

Baths in the treatment of lichen ruber, 624

Battey's operation, 290

Bearing-down feeling in prolapse of uterus, 158 in retroversion of uterus, 166

Belladonna as a cause of dermatitis medicamentosa, 602 in acute cystitis, 127

Bimanual replacement of retroflexed uterus, 170 of retroverted uterus, 170

Biskra bouton as a variety of furunculus, 606

BLADDER, DISEASES OF, 123 Atony, 133 Causes of, 133 Treatment of, 134 Catheterization, 134 Electricity, 134 Strychnia, 134 Catarrh, 128 Catarrh of, in prolapse of uterus, 157 Cystitis, acute, 126 Causes of, 126 Prognosis of, 127 Symptoms of, 126 Epididymitis as a symptom, 127 Treatment of, 127 Alkalies in, 127 Anodynes in, 127 Belladonna in, 127 Hyoscyamus, 127 Opium, 127 Sitz-baths in, 127 Cystitis, chronic, 128 Causes of, 128 Pathology of, 130 Prognosis, 130 Symptoms, 129 Degrees of, 129 Severe pain in, 129 Treatment of, 131 Alkalies in, 131 Clothing in, 131 Emptying bladder, 132 Hemorrhage from, 134 Diagnosis of, 135 Treatment of, 135 Gallic acid, 135 Ice, 135 Iron, 135 Nitrate of silver, 135 Opium, 135 Tannic acid, 135 Inflammation, 123 Pathology of, 124 Symptoms of, 124 Treatment of, 125 Marriage as a, 125 Ointments in, 125 Passing sound as, 125 Varieties of, 123 New growths of, 136 Neurosis of, 132 Prognosis, 133 Treatment of, 133 Organic diseases of, in wound, 339 Paralysis of (see Atony of), 133

Blepharospasm, 790

Blindness after pneumonia, 748

Blistering in the treatment of parametritis, 222

Blisters in the treatment of chronic perimetritis, 236

Blood in Bright's disease of kidneys, 77

Bloody urine as a symptom of acute diffuse nephritis, 82

Boil or evil as a variety of furunculus, 606

Boric acid in treatment of chronic purulent inflammation of middle ear, 829

Boracic acid in the treatment of pyelitis, 55

Borax and water in the treatment of cystitis in women, 346

Bougies in the treatment of seminal incontinence, 144

Brain abscesses as a sequel of chronic purulent inflammation of middle ear, 832

Bright's disease of the kidneys, 72 as a cause of inflammation of middle ear, 820

Bromides as a cause of dermatitis medicamentosa, 602 of potash in the treatment of seminal incontinence, 145

Bromidrosis as a disorder of secretion in diseases of skin, 584

Bulbar paralysis, 790 in medical ophthalmology, 790

C.

Caffeine in treatment of chronic congestion of kidneys, 72

Callositas, 662

Calorica, 601

Canal of Nuck, cysts of, 397

Cancer of the vagina, 382 of the vulva, 402

Canities, 678

Cannabis as a cause of dermatitis medicamentosa, 602

Cantharidal collodion in treatment of seminal incontinence, 145

Carbolic acid for instruments, 321 in the treatment of pyelitis, 55 spray in ovariotomy, 320

Carbunculus, 606

Carcinoma of the uterus, 274

Cardiac disease in congestion of kidney, 71 diseases in pregnancy, 429

Caruncle, urethral, 403

Cases of hemianopia, 776 of parametritis, 217

Castration for the cure of chronic metritis, 459

Casts as a symptom of congestion of kidney, 70 in calculous pyelitis, 451 in urine in chronic diffuse nephritis, 96

Catarrh of bladder, 128 in prolapse of uterus, 157 of middle ear, acute, 821

Cathartics in the treatment of diseases of kidneys in pregnancy, 419

Catheterization in the treatment of atony of bladder, 134

Cause of elephantiasis, 674 of scabies, 726 of tinea versicolor, 725

Causes of abortion, exciting, 481 local, 488 predisposing, 480 of acute cystitis, 126 of alopecia areata, 681 of albuminuria, 39 of amenorrhoea, 183 of atony of bladder, 133 of carbunculus, 607 of chloasma, 659 of chronic catarrh of middle ear, 824 of chronic cystitis, 128 of chronic purulent inflammation of middle ear, 828 of criminal abortion, 493 of death after ovariotomy, 314 of foetus in pregnancy, 424, 425 of dermatitis medicamentosa, 602 of ecthyma, 653 of erythema nodosum, 596 of herpes zoster, 610 of hypertrichosis, 670 of inflammation of middle ear, 818 of impacted cerumen in the external auditory canal, 812 of impetigo contagiosa, 652 of inversion of urethral mucous membrane in women, 362 of keratosis pilaris, 660 of lupus erythematosus, 690 of menorrhagia, 201 of molluscum epitheliale, 661 of myalgia, exciting, 530 of myalgia, predisposing, 530 of ophthalmitis, febrile, 761 of pelvic hæmatocele, 241 of progressive muscular atrophy, 541 of pruritus, 712 of pyelitis, 53 of pyelo-nephritis, 99 of scleroderma, 672 of sudamen as a disease of the skin, 586

Caustic potash in the treatment of lupus vulgaris, 696

Caustics in treatment of angioma of the skin, 688 of hypertrichosis, 670 of verruca, 664

Cauterization in the treatment of angioma of the skin, 688

Cautery, actual, in the treatment of pedicle after ovariotomy, 326

Cephalodynia as a symptom of myalgia, 531

Cerebral hyperæmia during the menopause, 443 symptoms of acute diffuse nephritis, 82

Cerebro-spinal meningitis, deafness after, 839

Cerumen, impacted, in the external auditory canal, 812

Cervix, enlargement of, in prolapse of uterus, 157 erosion of, in prolapse of uterus, 157

Cessation of menstruation, date of, 432

Change in quantity of urine as a symptom of nephritis, 81 in specific gravity of urine as a symptom of nephritis, 81

Changes in dermatitis herpetiformis, 613 in eye-ground and its appendages due to diseases of circulatory apparatus--heart, blood-vessels, and blood, 738 in maternal system in early pregnancy, 474 in uterus and pelvic viscera in early pregnancy, 475

Chloasma, 659

Chloral as a cause of dermatitis medicamentosa, 602 in the treatment of vaginitis, acute, 372

Chlorosis as a cause of amenorrhoea, 185 and hydræmia as a disorder of pregnancy, 405

Choked disc, 772

Cholera, effects of, in medical ophthalmology, 800 in pregnancy, 428 in relation to diseases of the eye, 800

Chorea in pregnancy, 422

Chorion as a local cause of abortion, 490

Chromidrosis as a disorder of secretion in diseases of skin, 585

Chronic catarrhal endometritis, 462 catarrh of middle ear, 823 congestion of kidney, 69 cystitis, 128 diffuse nephritis, 84 endometritis, 461 heart disease in pregnancy, 430 metritis, 450 ovaritis, 284 parenchymatous nephritis, 80 purulent inflammation of middle ear, 827

Cicatrices, 380

Circulatory disturbances in pregnancy, 407

Circumscribed urethritis in women, 355

Clamp in treatment of pedicle after ovariotomy, 325

Classification of abortion, 467 of seminal incontinence, 137

Clavus, 663

Climacteric neuroses during the menopause, 442

Clinical history of epithelioma of uterus, 279 of fibrous tumors of uterus, 250 of seminal incontinence, 138

Clothing in treatment of chronic cystitis, 131

COLIC, RENAL, 42 Diagnosis, 44 Prognosis, 45 Symptoms of, 43 Treatment of, 45

Coma as a symptom of chronic congestion of kidney, 70

Comedo as a disorder of secretion in diseases of skin, 589

Complications of chronic diffuse nephritis, 94 of myalgia, 534 of ovariotomy, 336 of parametritis, 210 of pelvic hæmatocele, 243 of progressive muscular atrophy, 552 of vaginismus, 384

Congestion and inflammation of ovaries as a cause of disturbed vision, 758 of kidney, 69

Connective tissue in pathological anatomy of pseudo-hypertrophic paralysis, 571

Constipation during menopause, 440 in amenorrhoea, 189 in pregnancy, 413 in retroversion of uterus, 166

Constituents of urine in chyluria, 115

Constitutional treatment of eczema, 632

Contraindications for ovariotomy, 316

Convallaria in treatment of chronic congestion of kidney, 72

Convulsions as a symptom of diseases of kidneys in pregnancy, 418

Copaiba as a cause of dermatitis medicamentosa, 602

Cornu cutaneum, 663

Corrosive sublimate in the treatment of lupus vulgaris, 696

Course and prognosis of pseudo-hypertrophic paralysis, 568 and symptoms of chorea in pregnancy, 422 of acute purulent inflammation of middle ear, 825 of angioma of the skin, 688 of congestion of kidney, 71 of criminal abortion, 497 of eczema erythematosum, 626 of the auricle, 811 of myalgia, 533 of pelvic hæmatocele, 243 of perimetritis, 229 of pityriasis rosea, 621 rubra, 622 of polyuria, 30 of prolapse of uterus, 158 of pruritus vulvæ, 393 of retroversion of uterus, 166 of tinea circinata, 717 of vaginismus, 384 of vomiting of pregnancy, 409 of vulvitis, 389

Criminal abortion, course of, 497

Cubebs as a cause of dermatitis medicamentosa, 603

Culex, 733

Culex lectularius, 733

Cupping, dry, in retroflexion of uterus, 168

Cups, dry, in treatment of nephritis, 83

Curative treatment of chronic endometritis, 465

Curette, use of, in treatment of epithelioma, 710 of lupus erythematosus, 692

Cystic tumors of ovary, 301 of vagina, 381

Cysticercus cellulosæ, 732

Cystitis, acute, 126 chronic, 128 in pyelo-nephritis, 100 in women, 341

Cystocele in prolapse of uterus, 158 vaginalis, 377

Cysto-vaginal hernia, 377

Cysts of canal of Nuck, 397 of kidney, 63 of parovarium, 293 of terminal vesicle of oviduct, 296

D.

Date of cessation of menstruation, 432

Deaf-mutism, 840

Deafness after mumps, 839 scarlet fever, 839 in acute catarrh of middle ear 821 of cerebro-spinal meningitis, scarlet fever, and mumps, 839

Decidua as the local cause of abortion, 488

Decubitus in treatment of vaginitis, 371

Definition and synonyms of parametritis, 209 of pelvic hæmatocele, 240 of abortion, 467 of acne, 641 of acne rosacea, 647 of albinismus, 676 of albuminuria, 34 of angioma of the skin, 688 of atresia, 373 of atrophia cutis, 683 of atrophia pilorum propria, 682 of callositas, 662 of carbunculus, 606 of chloasma, 659 of chronic diffuse nephritis, 85 metritis, 450 parenchymatous nephritis, 80 of chyluria, 114 of clavus, 663 of cornu cutaneum, 663 of cysts of canal of Nuck, 397 of dermatitis herpetiformis, 611 of dermatolysis, 675 of displacements of uterus, 150 of ecthyma, 653 of eczema vesiculosum, 627 of elephantiasis, 674 of the vulva, 399 of erythema nodosum, 596 of fibroma of the skin, 686 of functional disorders in connection with the menopause, 432 of furuncles of labia, 392 of furunculus, 604 of hæmatoma, 401 of herpes iris, 609 simplex, 607 zoster, 610 of hypertrichosis, 669 of impetigo, 651 contagiosa, 652 of keloid, 685 of keratosis pilaris, 660 of lentigo, 658 of lichen ruber, 623 of lupus erythematosus, 689 vulgaris, 693 of miliaria, 654 of morphoea, 672 of myalgia, 529 of nævus pigmentosus, 666 of nystagmus, 783 of onychauxis, 669 of ovariotomy, 313 of pemphigus, 656 of perimetritis, 227 of phlegmonous inflammation of the labia majora, 391 of pityriasis rosea, 621 rubra, 622 of pompholyx, 655 of progressive muscular atrophy, 540 of prolapsus vaginæ, 376 of prurigo, 639 of pruritus, 711 hiemalis, 714 vulvæ, 392 of psoriasis, 614 of pseudo-hypertrophic paralysis, 557 of pudendal hernia, 398 of sarcoma of the skin, 710 of scabies, 726 of sclerema neonatorum, 671 of scleroderma, 671 of scrofuloderma, 698 of seborrhoea, 586 of seminal incontinence, 134 of sycosis, 649 of syphilis cutanea, 699 of tinea circinata, 717 favosa, 715 sycosis, 723 tonsurans, 720 tricophytina, 717 versicolor, 724 of urethral caruncle, 403 of urticaria, 597 of vaginitis, 368 of verruca, 664 of vitiligo, 677 of vulvitis, 389

Degrees of prolapse of uterus, 154

Delhi boil as a variety of furunculus, 606

Dementia in ophthalmology, 792

Demodex folliculorum, 732

Depletion in the treatment of chronic metritis, 458

Dermatalgia, 711

Dermatitis, 600 exfoliativa, 623 gangrenosa, 604 herpetiformis, 611 traumatica, 600 venenata, 600

Dermatolysis, 675

Dermoid cysts of ovary, 299

Descent of uterus, 154

Description of alopecia areata, 680 of cystic tumors of ovary, 301 of dilatation of the uterus in women, 355 of dislocation of the urethra in women, 360 of erythema multiforme, 595 of inflammation of urethral glands in women, 354 of kidneys, 19 of milium as a disease of skin, 592 of ovaries and oviducts, 282

Development of the ovum, 477

Diabetes insipidus (see Polyuria), 27 mellitus, effects of, in medical ophthalmology, 796 in pregnancy, 416 in relation to diseases of the eye, 796

Diagnosis of abortion, 505 of acne, 642 of acne rosacea, 647 of acute catarrh of middle ear, 822 endometritis, 461 metritis, 449 purulent inflammation of middle ear, 826 urethritis in women, 353 of alopecia areata, 681 of anteflexion of uterus (acquired), 177 of anteversion of uterus (pathological), 175 of atrophia pilorum propria, 683 of atrophia unguis, 683 of calculous pyelitis, 49 of cancer of the vagina, 383 of carcinoma of the uterus, 276 of chronic endometritis, 464 metritis, 456 purulent inflammation of middle ear, 828 of cystic tumors of the ovary, 304 of cystitis in wound, 344 of cysts of parovarium, 295 of dermatitis herpetiformis, 612 of dilatation of urethra in women, 358 of dislocations of the urethra in women, 361 of disorders of function of uterus, 186 of displacements of uterus, 151 of dysmenorrhoea, 194, 195 of ecthyma, 653 of eczema, 629 of eczema of auricle, 811 of epilepsy in pregnancy, 423 of epithelioma of the uterus, 279 of fibroid tumors of the ovary, 297 of fibrous tumors of the uterus, 252 of floating kidney, 24 of foreign bodies in the external ear, 816 of furuncle of the external auditory canal, 814 of furunculus, 605 of hæmatoma, 401 of hemorrhage from bladder, 135 of herpes iris, 609 zoster, 611 of hyperæmia of bladder in women, 339 of hypertrophy of the bladder in women, 348 of impacted cerumen in the external auditory canal, 813 of imperforate hymen, 374 of impetigo contagiosa, 652 of lichen ruber, 624 scrofulosus, 625 of lupus erythematosus, 690 vulgaris, 694 of malformations of ovaries and oviducts, 283 miliaria, 654 of malignant icterus in pregnancy, 415 tumors of the ovary, 298 of molluscum epitheliale, 662 of morphoea, 673 of myalgia, 537 of parametritis, 215 of pemphigus, 657 of perimetritis, 231 of phlegmonous inflammation of the labia majora, 391 of pityriasis rosea, 621 of polyuria, 31 of progressive muscular atrophy, 552 of prolapse of ovary, 288 of uterus, 159 of prurigo, 640 of pruritus, 712 of pseudo-hypertrophic paralysis, 578 of psoriasis, 616 of pyelitis, 84 of renal colic, 44 of retroversion of uterus, 166 of sarcoma of the skin, 710 of sarcomatous tumors of the uterus, 272 of the vagina, 382 of scabies, 727 of seminal incontinence, 141 of stricture of the urethra in women, 364 of sycosis, 650 of syphiloderma erythematosus, 700 of tinea circinata, 718 favosa, 716 tonsurans, 721 versicolor, 725 of tuberculosis of kidney, 65 of urethral caruncle, 403 of vaginismus, 385 of vaginitis, 371 of verruca, 665 of the vomiting of pregnancy, 410

Diarrhoea during the menopause, 439, 440 in pregnancy, 414

Diet in hygienic treatment of vomiting of pregnancy, 410 in preparation of the patient for ovariotomy, 317

Differential diagnosis of parametritis, 215

Difficulties in diagnosis of floating kidney, 25

Digital uterine examinations, 152 touch in retroflexion of uterus, 168

Digitalis as a cause of dermatitis medicamentosa, 603 in treatment of chronic congestion of kidney, 72

Dilatation of the urethra in women, 355

Dilators in the treatment of vaginismus, 386

Diphtheria as a cause of inflammation of middle ear, 819

Diseases of bladder, 123 in women, organic, 339 of digestive system, effects on eye, 749 of ear, see Otology. of eye, see Ophthalmology. of external auditory canal, 811 of internal ear, 835 of kidneys and skin, affecting eyes, 752 in pregnancy, 416 of liver in pregnancy, 414 of lungs in pregnancy, 430 of middle ear, 817 of nervous system, affecting eye, 771 of organs of respiration, effects of, on eye, 748 of ovaries and oviducts, 282 of parenchyma of uterus, 447 of skin, 583 in pregnancy, 420 of uterus, 67 of urinary organs in women, 339 of vagina and vulva, 367 of vulva, 388

Dislocations of the urethra in women, 360

Disorders of alimentary canal during menopause, 440 in pregnancy, 408 of function during menopause, 432

Disordered functions of uterus, 182

Disorders of liver during menopause, 441 of secretion, 583 of special senses in pregnancy, 423

Displacements of uterus, 150 as a cause of disturbed vision, 757

Distribution, geographical, of chyluria, 115

Disturbances in circulation in pregnancy, 408 of vision caused by diseases of sexual organs, 755

Diuretics in treatment of calculous pyelitis, 51 in medical treatment of diseases of kidneys in pregnancy, 449

Diurnal pollutions in sexual incontinence, 138

Dividing cervix for anteflexion, 179

Dorsodynia as a symptom of myalgia, 532

Double vagina, 380

Douches, vaginal, in retroflexion of uterus, 168

Dover's powder in the treatment of wounds, 346

Dragging sensation in pathological anteversion of uterus, 175

Drainage-tubes after ovariotomy, 332

Dressing-forceps in treatment of abortion, 513 of wound after ovariotomy, 331

Dressings in treatment of carbunculus, 607

Dropsy as a symptom of acute diffuse nephritis, 82 of chronic congestion of kidney, 70 of nephritis, 81 of scarlatina, 84 time of occurrence, 84 Fallopian, 295 in calculous pyelitis, 51

Drugs in preparation of the patient for ovariotomy, 317 in treatment of pruritus, 712

Dry cupping in retroflexion of uterus, 168

Duration of abortion, 503 of acute parenchymatous nephritis, 79 of chronic parenchymatous nephritis, 81 of congestion of kidney, 72 of myalgia, 533 of pelvic hæmatocele, 243 of psoriasis, 614 of vaginismus, 384 of vulvitis, 389

Dysmenorrhoea, 192 membranacea in chronic endometritis, 463

Dyspnoea as a symptom of chronic congestion of kidney, 70 of nephritis, 81 in congestion of kidney, 71

E.

Ear, diseases of, deaf-mutism, 840 Treatment, 840 Examination of, 807 External, diseases of, 810 Eczema, 810 Course, 811 Diagnosis, 811 Treatment, 811 Foreign bodies in, 815 Insects, 815 Other varieties of, 816 Diagnosis, 816 Objective symptoms, 816 Subjective symptoms, 816 Treatment, 816 Vegetable parasites, 815 Prognosis, 815 Symptoms, 815 Treatment, 815 Furuncle, 813 Diagnosis, 814 Etiology and pathology, 813 Prognosis, 814 Symptoms, 814 Treatment, 814 Impacted cerumen, 811 Diagnosis, 813 Prognosis, 813 Symptoms, 812 Treatment, 813 Feigned deafness, methods of detecting, 840 Internal, anatomy of, 835 Diseases of, 835 Tinnitus, 836 Varieties, 836-838 Location, 838 Prognosis, 838 Treatment, 838 Post-febrile deafness, 839 Menière's disease, 839 Middle, anatomy of, 817 Diseases of, 818 Acute catarrh, 821 Diagnosis, 822 Symptoms, 821 Giddiness, 821 Loss of hearing-power, 821 Noises in, 821 Objective, 822 Pain, 821 Treatment, 822 Acute purulent inflammation, 825 Course, 825 Diagnosis, 826 Prognosis, 826 Symptoms, 826 Treatment, 826 Chronic catarrh, 823 Causes, 824 Classification, 823 Prognosis, 825 Treatment, 825 Chronic purulent inflammation, 827 Causes, 828 Diagnosis, 828 Symptoms, objective, 828 Subjective, 828 Treatment, 829 Sequelæ, 830 Brain involvement, 830 Abscess of brain, 831 Symptoms, 832 Phlebitis with thrombosis, 832 Prognosis, 833 Symptoms, 833 Purulent meningitis, 830 Symptoms, 831 Mastoid diseases, 833 Periostitis, 834 Symptoms, 834 Inflammation of mucous membrane of mastoid cells, 834 Symptoms, 834 Treatment, 834 Inflammation, causes of, 820 Bright's disease, 820 Diphtheria, 820 Measles, 819 Retro-nasal catarrh, 819 Scarlet fever, 818 Scrofulosis, 819 Smallpox, 819 Syphilis, 820 Tuberculosis, 819 Typhoid fever, 820 Whooping cough, 820

Ecthyma, 653

Eczema, 625 erythematosum, 626 of auricle, 810 papulosum, 627 pustulosum, 627 squamosum, 628 vesiculosum, 627

Effects of high temperature on foetus in acute infectious diseases of pregnancy, 424 of oöphorectomy, 293 of hemorrhage on eye, 745

Electrical reactions as a symptom of pseudo-hypertrophic paralysis, 560

Electricity in treatment of amenorrhoea, 191 of atony of bladder, 134 of paralysis of bladder in women, 351 of progressive muscular atrophy, 551 of pseudo-hypertrophic paralysis, 579

Electrolysis in radical treatment of ovarian cysts, 313 in the treatment of angioma of skin, 689

Elephantiasis, 399, 674

Elytrorrhaphy anterior, 161

Emptying the bladder in chronic cystitis, 132

Endocarditis, acute, in pregnancy, 430

Endometritis, 447, 460, 461 acute, 460 chronic, 461

Enterocele vaginalis, 378

Entero-vaginal hernia, 378

Epididymitis as a symptom of acute cystitis, 127

Epilepsy during menopause, 445 effects of, in medical ophthalmology, 797 in pregnancy, 423 in relation to diseases of the eye, 797

Epithelioma, 707 of the uterus, 278

Ergot in polyuria, 34 in treatment of chronic metritis, 460 in treatment of fibrous tumors of uterus, 259

Erosion of the cervix in prolapse of uterus, 157

Erysipelas as a cause of ophthalmitis, 769

Erythema intertrigo, 594 multiforme, 595 nodosum, 596 simplex, 593

Ether in treatment of chronic congestion of kidney, 72

Etiology and pathology of diseases of kidneys in pregnancy, 418 of furuncle of external auditory canal, 813 of malignant uterus in pregnancy, 415 of abortion, 479 of acute diffuse nephritis, 82 of acute endometritis, 460 of acute parenchymatous nephritis, 79 of chronic diffuse nephritis, 87 endometritis, 462 metritis, 450 parenchymatous nephritis, 81 of chlorosis and hydræmia as a disorder of pregnancy, 406 of chorea in pregnancy, 422 of chyluria, 116 of congestion of kidney, 69 of cystitis in women, 341 of dilatation of urethra in women, 357 of dislocation of urethra in women, 361 of eczema, 629 of elephantiasis of vulva, 399 of fibrous tumors of uterus, 250 of hæmatoma, 401 of hyperæmia of bladder in women, 339 of hypertrophy of bladder in women, 348 of lichen ruber, 624 of medullary cancer of uterus, 274 of metritis, acute, 447 of myalgia, 530 of parametritis, 209 of pathological anteflexion of uterus, 176 of pathological anteversion of uterus, 174 of perimetritis, 228 of perinephritis, 102 of pityriasis rubra, 622 of progressive muscular atrophy, 541 of prolapse of uterus, 154 of prolapsus vaginæ, 377 of pruritus vulvæ, 392 of pudendal hernia, 398 of pyelo-nephritis, 100 of retroflexion of the uterus, 166 of retroversion of the uterus, 166 of seminal incontinence, 140 of simple icterus in pregnancy, 414 of urethral caruncle, 403 of vaginismus, 384 of vaginitis, 368 of verruca, 665 of vulvitis, 389

Estimation of albumen in albuminuria, 38

Eustachian tube, examination of, 809

Examination in medical otology, 807 by tuning-fork, 808 by voice, 807 by watch, 807 of Eustachian tube, 809 of external auditory canal and tympanic membrane, 807 of urine in calculous pyelitis, 49

Examinations of uterus, 151

Excision in treatment of dilatation of the urethra in women, 359

Exciting causes of abortion, 481 of myalgia, 530

Exophthalmic goitre in relation to diseases of the eye, 799

Explorations of uterus, 152

Exposure as a cause of amenorrhoea, 187

External auditory canal, examination of, 807 treatment of alopecia areata, 681 of eczema, 634 of psoriasis, 617 of urticaria, 599

Eye, 737 Affections of, from diseases of the digestive organs, 749 from diseases of intestines, 750 of liver, 750 of spleen, 751 of stomach, 750 of teeth, 749 Hemeralopia, 751 Affections of the fifth pair, 785 Herpes facialis, 785 zoster ophthalmicus, 787 Injuries of, 788 Neuro-paralytic ophthalmia, 787 Symptoms, 787 Affections of, from diseases of the general system, 800 from cholera, 800 from gout, 800 from rheumatism, 800 from syphilis, 800 from tuberculosis, 802 Affections of, from diseases of respiratory organs, 748 Affections of the second pair, 771 Choked disc, 772 Hemianopia, 775 Cases of, 775 Symptoms of, 778 Neuritis, 771 The lymph-space theory, 773 Affections of the seventh pair, 790 Blepharospasm, 790 Affections of, from diseases of the sexual organs, 755 Affections of the sixth pair, 789 Symptoms, 789 Affections of the third pair, 780 Associated movements of the head and eyes, 782 Double third-pair paralysis, 780 Nystagmus, 783 Autopsies in, 784 Definition, 783 Frequency, 783 Pathology, 784 Symptoms, 783 Ophthalmoplegia interna, 781 Description of, 781 Paralysis of, 781 Ptosis, 781 Affections of the twelfth pair, 790 Bulbar paralysis, 790 Labio-glosso-laryngeal paralysis, 790 Mental affections, 791 Dementia, 792 General paralysis, 792 Mania, 792 Melancholia, 792 Spinal cord, 792 Injuries to, 792 Tabes dorsalis, 793 Unclassified nervous affections, 796 Basedow's disease, effects of, 799 Diabetes mellitus, effects of, 796 Epilepsy, idiopathic, effects of, 797 Exophthalmic goitre, effects of, 799 Graves' disease, effects of, 799 Toxic amblyopia, 803 Alcohol, 803 Lead-poisoning, 803 Quinine, 804 Salicylate of sodium, 804 Santonin, 804 Tobacco, 803 Blindness after pneumonia, 748 Congestion and inflammation of ovaries, 758 Displacement of uterus, 757 Lactation, 760 Masturbation, 758 Menstruation, 755 Pathology, 660 Pelvic cellulitis, 757 Pregnancy, 759 Puerperal phlebitic ophthalmitis, 759 In relation to diseases of the skin and kidneys, 752 Diseases of, febrile and post-febrile ophthalmitis, 761 Erysipelas, 769 Intermittent fever, 768 Relapsing typhus, 765 Rubeola, 763 Scarlatina, 764 Typhoid fever, 767 Variola, 761 Yellow fever, 767 Effects of diseases of kidneys and skin on, 752

Eye-ground, changes in, due to diseases of circulatory apparatus, 738 Effects of hemorrhage on, 745 Leukæmic retinitis, 744 Pathology, 746 Pernicious anæmia, 745 Retinal aneurism, 743

F.

Factitia, 604

Fallopian dropsy, 295

Febrile and post-febrile ophthalmitis, 761

Feigned deafness, methods of detecting, 840

Ferrocyanide of potash as a test for albumen in albuminuria, 37

Fever as a symptom of progressive muscular atrophy, 552 relapsing, in pregnancy, 427 scarlet, in pregnancy, 426 typhoid, in pregnancy, 426 typhus, in pregnancy, 427

Fibroid tumors of ovary, 297

Fibroma of skin, 686

Fibrous tumors of uterus, 245 of vagina, 381

Fifth pair of cranial nerves, affections of, 785

Filaria as a cause of elephantiasis, 674 medinensis, 732

Flexions of uterus, 166, 174, 176, 177

Floating kidney, 21

Forceps for arresting hemorrhage in ovariotomy, 322

Foreign bodies in external ear, 815

Frequency of abortion, 468 of acne, 642 of floating kidney in sex, 22 of herpes iris, 609 of lichen scrofulosis, 625 of nystagmus, 783 of pelvic hæmatocele, 240 of sarcoma of the skin, 710 of tinea circinata, 718 favosa, 715 sycosis, 724 tonsurans, 720

Functional disorders of bladder in women, 349 in connection with menopause, 432

Functions of uterus, disordered, 182

Furuncle of external auditory canal, 813

Furuncles of labia, 392

Furunculus, 604

G.

Gallic acid in treatment of hemorrhage from bladder, 135

Galvanism in the treatment of chronic perimetritis, 237

General paralysis of the insane in relation to diseases of the eye, 792 treatment of chronic metritis, 459

Geographical distribution of chyluria, 115

Giddiness in acute catarrh of middle ear, 821

Glycerin tampons in treatment of chronic metritis, 458

Goitre, exophthalmic, in medical ophthalmology, 799

Gout, effects of, in medical ophthalmology, 800

Graves' disease, in medical ophthalmology, 799

Great thirst as a symptom of polyuria, 29

Growths in the vagina, 381

Gymnastics in treatment of progressive muscular atrophy, 555 of seminal incontinence, 143

Gynæcological treatment of vomiting of pregnancy, 412

H.

Hæmatoma, 401

Hæmaturia, 104

Hæmoglobinuria, 104 in albuminuria, 35

Hæmophilia as a disorder of pregnancy, 407

Hæmostatics in treatment of hemorrhage from bladder in women, 340

Hair in tinea tonsurans, 720

Headache as a symptom of polyuria, 30

Heart disease in pregnancy, 430

Hemeralopia, 751

Hemianopia, 775

Hemianopsia, 775

Hemiopia, 775

Hemorrhage, arresting of, in ovariotomy, 322 as a local cause of abortion, 490 during menopause, 438 from bladder, 134 in women, 340 its effects on the eye, 745

Heredity of lupus vulgaris, 693

Hernia of ovary, 289 pudendal, 398

Herpes facialis, 785 as an affection of fifth pair of cranial nerves, 785 iris, 609 simplex, 607 zoster, 610 ophthalmicus, 785 as an affection of fifth pair of cranial nerves, 785

High temperature, effects on foetus in acute infectious diseases of pregnancy, 424

Histology of progressive muscular atrophy, 543

History, natural, of change of life, 434 of abortion, 470 of Menière's disease, 839 of myalgia, 529 of ovariotomy, 313 of progressive muscular atrophy, 540 of pseudo-hypertrophic paralysis, 557 of retroversion of uterus, 166

Horseshoe kidney, 20

Hot-water douche in treatment of chronic metritis, 457 in treatment of parametritis, 220

Hyaline casts in pyelitis, 54

Hydræmia as a disorder of pregnancy, 405

Hydrocele in women, 397

Hydro-nephrosis, 56 Causes of, 56 Diagnosis, 58 Effects of, 58 Treatment of, 59

Hygienic treatment of diseases of kidneys in pregnancy, 419 of vomiting of pregnancy, 410

Hyoscyamus in acute cystitis, 127

Hyperæmia as a cause of chronic metritis, 451 of bladder in women, 339

Hyperidrosis as a disorder of secretion in diseases of skin, 583

Hypertrichosis, 669

Hypertrophies of skin, 658

Hypertrophy of bladder in women, 348 of vulva, 398

Hysterical diathesis as a cause of polyuria, 31

Hysteria during menopause, 443

Hystero-epilepsy in relation to diseases of eye, 799

I.

Ice in treatment of hemorrhage from bladder, 135

Ichthyosis, 666

Icterus in pregnancy, 414 malignant, in pregnancy, 415

Impacted cerumen in the external auditory canal, 811

Imperforate hymen, 374

Impetigo, 651 contagiosa, 652

Importance of abortion, 468

Incision in treatment of furuncle in external auditory canal, 815 stricture of the urethra in women, 364 line of, in ovariotomy, 322

Indications for ovariotomy, 316

Infectious diseases in pregnancy, acute, 424

Inflammation of bladder, 123 of middle ear, causes of, 818 of ovaries as a cause of disturbed vision, 758 of ovary, 283

INFLAMMATION OF THE PELVIC CELLULAR TISSUE AND PELVIC PERITONEUM--General considerations, 208 Parametritis, 209 Anatomy, course, 210 Cases of, 217 Complications, 210 Course, 210 Definitions and symptoms, 209 Differential diagnosis, 215 Etiology 209 Parturition as a cause, 210 Pathology and termination, 210 Physical signs, 214 Prognosis, 219 Symptomatology, 213 Treatment, 219 Aconite in, 221 Aspiration in, 225 Blistering in, 222 Hot water in, 220 Iodine in, 221 Medicinal, 227 Morphia in, 220 Operation, 223 Perimetritis, 227 Course, 229 Definition of, 227 Diagnosis, 231 Etiology of, 228 Pathology, 229 Physical signs, 231 Prognosis, 232 Symptoms, 230 Synonyms for, 227 Termination, 229 Treatment, 232 Blisters in, 236 Galvanism, 237 Local, 234 Of chronic perimetritis, 233 Packing in, 236

Inflammation of the urethral glands in women, 354

Inflammations, 593

Injections in the treatment of vaginitis, acute, 372

Injuries of the fifth pair of cranial nerves, 788 to the spinal cord in relation to diseases of the eye, 792 to the spine in relation to diseases of the eye, 792

Insanity during the menopause, 445

Insects in the external ear, 815

Instruments for the examination of the external auditory canal, 809 for the operation of ovariotomy, 319 in treatment of abortion, 512

Intermittent fever as a cause of ophthalmitis, 768

Internal ear, 835 treatment of alopecia areata, 681 of psoriasis, 617 of urticaria, 599

Inversion of urethral mucous membrane in women, 362

Iodide of potash in the treatment of fibrous tumors of the uterus, 259 of syphiloderma bullosum, 707

Iodides as a cause of dermatitis medicamentosa, 603

Iodine in the treatment of parametritis, 221

Iron in the treatment of acute parenchymatous nephritis, 80 of hemorrhage from bladder, 135 of pernicious anæmia of pregnancy, 406

Irrigation in the treatment of vaginitis, acute, 372

Ixodes, 733

J.

Jaborandi in the treatment of nephritis, 83

K.

Keloid, 685

Keratosis pilaris, 660

Kidney, absence of one, 21 Anomalies of, 19 Horse-shoe, 20 Description of, 19

Kidneys, alterations in functions of, during the menopause, 437

KIDNEYS, DISEASES OF THE--Albuminuria, 34 Albuminoids in, 35 Causes of, 39 Definition of, 34 Estimation of albumen in, 38 Hæmoglobinuria in, 35 In pregnancy, 416 Nephrozymase in, 35 Of nervous affections, 40 Of pregnancy, 40 Tests for albumen in, 35 Ferrocyanide of potash, 37 Nitric acid, 36 Salt solution with hydrocyanic acid, 36 Treatment of, 42 Astringents in, 42 Bright's disease, 72 Albuminuria in, 75 Blood in, 77 Casts in urine in, 76 Cerebral symptoms in, 77 Dyspnoea in, 76 Retinitis, 77 Calculous pyelitis, 47 Diagnosis of, 49 Examination of urine in, 49 Pus as an aid to, 49 Thompson's method in, 49 Symptoms of, 51 Albuminuria in, 47 Casts in, 51 Dropsy in, 51 Treatment of, 51 Diuretics, 51 Operative, 51 Nephrectomy, 51 Nephro-lithotomy, 51 Palliative, 51 Rest, 51 Varieties of, 47 Chyluria, 114 Constituents of urine in, 115 Definition of, 114 Distribution, geographical, 115 Etiology, 116 Morbid anatomy of, 119 Pathology of, 115 Symptoms of, 119 Treatment of, 120 Congestion, chronic, 69 Course of, 71 Cardiac disease in, 71 Dyspnoea in, 71 Duration of, 72 Etiology of, 69 Lesions of, 69 Atrophied tubercles, 69 Unnatural hardness as a, 69 Symptoms of, 70 Albuminuria as a, 70 Casts as a, 70 Coma as a, 70 Dropsy as a, 70 Dyspnoea, 70 Loss of flesh, 70 Synonyms, 69 Treatment of, 72 Caffeine in, 72 Convallaria in, 72 Digitalis in, 72 Ether in, 72 Opium in, 72 Cysts, 63 Symptoms of, 63 Varieties of, 63 Malignant growths, 60 Symptoms of, 61 Treatment, 62 Nephritis, 82 Acute diffuse, 82 Etiology of, 82 Morbid anatomy of, 82 Prognosis of, 83 Symptoms of, 82 Albumen in urine, 82 Bloody urine, 82 Cerebral, 82 Dropsy, 82 Micturition, painful, 82 Pericarditis, 83 Peritonitis, 83 Pleurisy, 83 Pneumonia, 83 Treatment of, 83 Dry cups, 83 Jaborandi in, 83 Purgatives in, 83 Acute diffuse, of scarlatina, 84 Prognosis, 84 Symptoms of, 84 Dropsy, 84 Time of occurrence, 84 Acute parenchymatous, 78 Duration of, 79 Etiology of, 79 Pathological anatomy of, 78 Prognosis of, 80 Symptoms of, 79 Treatment of, 80 Iron, 80 Milk diet, 80 Oxygen, 80 Pilocarpine, 80 Sweating, 80 Chronic diffuse, 84 Albuminuria in, 96 Casts in urine in, 96 Complications of, 94 Definition of, 85 Etiology of, 87 Lesions of, 86 Morbid anatomy of, 85 Large white kidney, 90 with waxy infiltration, 92 Symptoms of, 88 Treatment of, 95 Chronic parenchymatous, 80 Definition, 80 Duration of, 81 Etiology of, 81 Lesions of, 81 Prognosis of 81 Symptoms of, 81 Albumen in urine, 81 Change in specific gravity of urine, 81 quantity of urine, 81 Dropsy, 81 Dyspnoea, 81 Pyelo-, 99 Causes of, 99 Cystitis in, 100 Etiology of, 100 Prognosis, 101 Treatment of, 101 Symptoms of, 99 Treatment of, 99, 101 Varieties of, 99 Parasites, 65 Treatment of, 66 Varieties of, 65 Perinephritis, 102 Etiology, 102 Lesions, 102 Symptoms of, 102 Rupture of abscess into peritoneal cavity, 102 Treatment of, 103 Polyuria, 27 Course of, 30 Diagnosis, 32 Large quantities of water consumed during, 30 Origin of, 31 After acute diseases, 30 After meningitis, 31 Hysterical diathesis in the, 31 Sudden fright in the, 31 Pathology, 31 Nerve lesions, 31 Symptoms, 27 Dryness of skin, 29 Great thirst, 29 Headache, 30 Phosphates in urine, 30 Termination, 30 Treatment, 33 Atropia in, 34 Ergot in, 34 Nitric acid in, 33 Opium in, 33 Pilocarpine in, 34 Sufficient food in, 33 liquids in, 33 Pyelitis, secondary, 53 Causes of, 53 Diagnosis of, 54 Hyaline casts in, 54 Muco-pus in, 54 Pain in, 54 Treatment of, 55 Boric acid in the, 55 Carbolic acid, 55 Operative, 55 Washing-out of bladder as a, 55 Tuberculosis of, 64 Diagnosis, 65 Origin, 64 Prognosis, 65 Floating, 21 Diagnosis, 24 Difficulties in, 25 Frequency in sexes, 22 Symptomatology, 23 Treatment, 25 Palpation of, 20 Position of, 20 Supernumerary, 21

L.

Labio-glosso-laryngeal paralysis, 790 in medical ophthalmology, 790

Lacerated cervix uteri as a cause of chronic metritis, 451

Lactation as a cause of disturbed vision, 760

Laparo-hysterectomy in treatment of fibrous tumors of the uterus, 269

Laparotomy in treatment of fibrous tumors of the uterus, 269

Large quantities of water consumed in polyuria, 30

Large white kidney, 90 with waxy infiltration, 92

Lateral flexion of uterus, 174 locations of uterus, 153 versions of uterus, 174

Laxatives in constitutional treatment of eczema, 632

Lead-poisoning as a cause of toxic amblyopia, 803 effects of, on the eye, 803

Left hand in uterine examinations, 152

Lentigo, 658

Leptus, 731

Lesions of chronic diffuse metritis, 86 parenchymatous nephritis, 81 of congestion of kidney, 69 of perinephritis, 102

Leucorrhoea, 447, 455 during the menopause, 439

Leukæmic retinitis, 744

Lichen ruber, 623 scrofulosus, 624

Ligatures, silk, in the treatment of pedicle after ovariotomy, 326

Line of incision in ovariotomy, 322

Liver, diseases of, in pregnancy, 414 disorders of, during the menopause, 441

Local causes of abortion, 488 treatment of acne, 644 of chronic endometritis, 465 of metritis, 457 of perimetritis, 234 of psoriasis, 619 of syphiloderma bullosum, 707

Location of nævus pigmentosus, 666

Locomotion in pseudo-hypertrophic paralysis, 563

Loss of flesh as a symptom of chronic congestion of kidney, 70

Lotions in external treatment of eczema, 635 in treatment of lupus erythematosus, 691 of vulvitis, 390

Lumbago as a symptom of myalgia, 533

Lungs, diseases of, in pregnancy, 430

Lupus erythematosus, 689 vulgaris, 693

Lymphangioma of skin, 689

Lymph-space theory, 773

M.

Malarial fever in pregnancy, 427

Malformations of ovaries and oviducts, 282

Malignant growths of kidney, 60 icterus in pregnancy, 415 tumors of ovary, 298

Mammary glands, changes in, during menopause, 437

Mania in relation to diseases of eye, 792

Marriage, in treatment of inflammation of bladder, 125 of seminal incontinence, 146

Massage in treatment of progressive muscular atrophy, 555

Mastoid disease, following chronic inflammation of middle ear, 833

Masturbation as a cause of disturbed vision, 758

Measles as a cause of inflammation of middle ear, 819 in pregnancy, 426

Medical ophthalmology, see Ophthalmology.

Medical otology, see Otology. treatment of diseases of kidneys in pregnancy, 419 of vomiting of pregnancy, 411

Medicated cotton pledgets in treatment of anteversion of uterus, 176

Medication in treatment of abortion, 512

Medicinal treatment of pelvic abscess, 227

Medullary cancer of uterus, 274

Melancholia in relation to diseases of eye, 792

Menière's disease, see Otology.

Meningitis, purulent, as a sequel of chronic inflammation of middle ear, 831

MENOPAUSE, FUNCTIONAL DISORDERS IN CONNECTION WITH, 432 Alterations in functions of skin, 435 in nutrition, 437 in secretion by kidneys, 437 Hemorrhages, 438 Neuroses, 442 Cerebral hyperæmia, 443 Epilepsy, 445 Hysteria, 443 Insanity, 445 Monomania, 445 Pseudocyesis, 444 Of alimentary canal, 440 Constipation, 440 Diarrhoea, 440 Of liver, 441 Serous and mucous discharges, 438 Diarrhoea, 439 Leucorrhoea, 439 Date of cessation of menstruation, 432 Definition of, 432 Duration of, 432 Mammary glands, changes in, 437 Natural history of, 434 Respiratory changes, 435 Termination, 432

Menorrhagia, 200

Menstruation, 182 age of, 185 as a cause of disturbed vision, 755

Mental affections in relation to diseases of the eye, 791

Mercury as a cause of dermatitis medicamentosa, 603 in treatment of syphiloderma bullosum, 706

Methods for detecting feigned deafness, 840 of examination of Eustachian tube, 809

Metritis, acute, 447 chronic, 450

Middle ear, acute catarrh of, 821 anatomy of, 817 diseases of, 817

Miliaria, 654

Milium, 592

Milk diet in treatment of acute parenchymatous nephritis, 80

Morbid anatomy of abortion, 494 of acute diffuse nephritis, 82 of chronic diffuse nephritis, 85 of chyluria, 119 of elephantiasis, 675 of lupus vulgaris, 694 of myalgia, 534

Molluscum epitheliale, 661

Monomania during menopause, 445

Morphia as a cause of dermatitis medicamentosa, 603 in treatment of parametritis, 220 of pelvic hæmatocele, 244 suppositories in treatment of cystitis in women, 346

Morphoea, 672

Movements of uterus, normal, 149

Muco-pus in pyelitis, 84

Multiple fibroma of skin, 686

Mumps, deafness after, 839

Muscles affected in pseudo-hypertrophic paralysis, 560

Muscular atrophy, progressive, 540 fibres in pathological anatomy of pseudo-hypertrophic paralysis, 570

Mutism, 840

MYALGIA, 529 Complications, 534 Course, 533 Definition, 529 Diagnosis, 537 Duration, 533 Etiology, 530 Exciting causes, 530 Predisposing causes, 530 History, 529 Morbid anatomy, 534 Pathology, 534 Prognosis, 538 Sequels, 534 Symptomatology, 531 Cephalodynia, 532 Dorsodynia, 532 Lumbago, 533 Omodynia, 532 Pleurodynia, 532 Scapulodynia, 532 Torticollis, 532 Synonyms, 529 Termination, 533 Treatment, 538

Myoma of skin, 687

N.

Nævus pigmentosus, 666

Natural history of change of life, 434

Nephrectomy in treatment of calculous pyelitis, 51

Nephro-lithotomy in treatment of calculous pyelitis, 51

Nephrozymase in albuminuria, 35

Nerve-centres in pathological anatomy of pseudo-hypertrophic paralysis, 572

Nerve-lesions in polyuria, 31

Nerves, fifth pair, affections of, in relation to diseases of eye, 785 seventh pair, affections of, in relation to diseases of eye, 790 sixth pair, affections of, in relation to diseases of eye, 789 third pair, in relation to diseases of the eye, 780 twelfth pair, affections of, in relation to diseases of eye, 790

Nervi optici, neuritis of, 771

Nervous diseases, unclassified, in relation to diseases of eye, 796 system, diseases of, affecting eye, 771

Neuritis of nervi optici, 771

Neuroma of skin, 686

Neuro-paralytic ophthalmia, 787

Neuroses during menopause, 442 of bladder, 132 of pregnancy, 421 of skin, 711

New growths of bladder, 136 of skin, 685

Nitrate of silver in treatment of acute urethritis in women, 353 of chronic purulent inflammation of middle ear, 829 of cystitis in women, 347 of furuncles of labia, 392 of hemorrhage from bladder, 135 of lupus vulgaris, 696 of seminal incontinence, 145

Nitric acid as a test for albumen in albuminuria, 36 in polyuria, 33

Nocturnal pollutions in seminal incontinence, 137

Nomenclature of displacement of uterus, 150

Normal location of uterus, 147 movements of uterus, 149 supports of uterus, 150

Nutrition, alterations in, during the menopause, 437

Nystagmus, 783

O.

Objective symptoms of acute catarrh of middle ear, 822 of purulent inflammation of middle ear, 828

Obstetrical treatment of vomiting of pregnancy, 412

Oestrus, 732

Ointments in external treatment of eczema, 635 in treatment of angioma of skin, 688 of inflammation of bladder, 125 of lupus vulgaris, 697 of pruritus, 713 of seborrhoea, 589 of tinea tonsurans, 722

Omodynia as a symptom of myalgia, 532

Onychauxis, 669

Oöphorectomy, 290 dressings in, 292 effects of, 293 indications for, 290 varieties of, 291

Operative treatment of calculous pyelitis, 51 of chronic metritis, 459 of lupus vulgaris, 697 of pelvic abscess, 223 of pelvic hæmatocele, 244 of pyelitis, 55

Opium as a cause of dermatitis medicamentosa, 603 in acute cystitis, 127 in polyuria, 33 in treatment of chronic congestion of kidney, 72 in treatment of hemorrhage from bladder, 135

Ophthalmitis, puerperal phlebitic, 759

OPHTHALMOLOGY, MEDICAL, 737 Affections of the eye from diseases of the digestive organs, 749 of intestines, 750 of liver, 750 of spleen, 751 of stomach, 750 of teeth, 749 Hemeralopia, 751 Affections of the fifth pair, 785 Herpes facialis, 785 zoster ophthalmicus, 785 Prognosis, 786 Symptoms, 785 Injuries of, 788 Neuro-paralytic ophthalmia, 787 Affections of the general system, 800 Cholera, 800 Gout, 800 Rheumatism, 800 Syphilis, 800 Tuberculosis, 802 Affections of the second pair, 771 Choked disc, 772 Lymph-space theory, 773 Neuritis, 771 Affections of the seventh pair, 790 Blepharospasm, 790 Affections of the sixth pair, 789 Symptoms, 789 Affections of the third pair, 780 Associated movements of the head and eyes, 782 Causes of, 782 Nystagmus, 783 Autopsies in, 784 Definition, 783 Frequency, 783 Pathology, 784 Symptoms, 783 Ophthalmoplegia interna, 781 Description of, 781 Paralysis of, 780 Ptosis, 781 Affections of the twelfth pair, 790 Bulbar paralysis, 790 Labio-glossal-laryngeal paralysis, 790 Blindness after pneumonia, 748 Changes in eye-ground and its appendages due to diseases of the circulatory apparatus--heart, blood-vessels, and blood, 738 Hemorrhage, 745 Leukæmic retinitis, 744 Pathology, 746 Pernicious anæmia, 745 Prognosis, 746 Retinal aneurism, 743 Diseases of kidneys and skin affecting the eyes, 752 of the nervous system affecting the eyes, 771 of the organs of respiration, 748 Disturbances of vision caused by disease of the sexual organs, 755 Menstruation, 755 Congestion and inflammation of ovaries, 758 Displacements of the uterus, 757 Lactation, 760 Masturbation, 758 Pathology, 760 Pelvic cellulitis, 757 Pregnancy, 759 Puerperal phlebitic ophthalmitis, 759 Febrile and post-febrile ophthalmitis, 761 Erysipelas, 769 Intermittent fever, 768 Relapsing typhus, 765 Rubeola, 763 Scarlatina, 764 Typhoid fever, 767 Variola, 761 Yellow fever, 767 Hemianopia, 775 Cases of, 776 Symptoms, 778 Mental affections, 791 Dementia, 792 General paralysis, 792 Mania, 792 Melancholia, 792 Nervous system, unclassified diseases of, affecting the eye, 799 Basedow's disease, 799 Diabetes, 796 Epilepsy, idiopathic, 796 Exophthalmic goitre, 799 Graves' disease, 799 Toxic amblyopia, 803 Alcohol, 803 Lead-poisoning, 803 Quinine, 804 Salicylate of sodium, 804 Santonin, 804 Tobacco, 803 Spinal cord, 792 Injuries to, 792 Tabes dorsalis, 793 Ophthalmoplegia interna, 781 as an affection of third pair of cranial nerves, 781

Origin of polyuria, 31 of tuberculosis of kidney, 64

OTOLOGY, MEDICAL, 805 Diseases of external auditory canal, 811 Impacted cerumen, 811 Causes, 812 Diagnosis, 813 Prognosis, 813 Symptoms, 812 Treatment, 813 Eczema of the auricle, 810 Course, 811 Diagnosis, 811 Treatment, 811 Examination of Eustachian tube, 809 methods of, 809 of external canal and tympanic membrane, 808 by ear speculum, 808 instruments in, 809 of patients by the tuning-fork, 807 by the voice, 807 by the watch, 807 Foreign bodies in the ear, 815 Insects, 815 Varieties of, 816 Diagnosis, 816 Symptoms, 816 Treatment, 816 Vegetable parasites, 815 Prognosis, 815 Symptoms, 815 Treatment, 815 Furuncle, 813 Diagnosis, 814 Etiology and pathology, 813 Prognosis, 814 Symptoms, 814 Treatment, 814 Internal ear, anatomy of, 835 Diseases of, 835 Deaf-mutism, 840 Treatment, 840 Deafness after cerebro-spinal meningitis and mumps, 839 Menière's disease, 839 Treatment, 840 Tinnitus aurium, 836 Prognosis, 838 Treatment, 838 Varieties, 836 Methods for detecting feigned deafness, 840 Middle ear, anatomy of, 817 Diseases of, 817 Acute catarrh, 821 Diagnosis, 822 Symptoms of 821 Deafness, 821 Giddiness, 821 Objective, 822 Pain, 821 Tinnitus aurium, 821 Treatment, 822 Acute purulent inflammation, 825 Course, 825 Diagnosis, 826 Prognosis, 826 Symptoms, 826 Treatment, 826 Chronic catarrh, 823 Classification, 823 Causes, 824 Description, 824 Prognosis, 825 Treatment, 825 Chronic purulent inflammation, 827 Causes, 828 Diagnosis, 828 Morbid anatomy, 828 Sequelæ, 830 Abscess of brain from, 831 Location of, 831 Symptoms, 832 Brain involvement, 830 Mastoid disease, 833 Symptoms, 834 Treatment, 834 Phlebitis with thrombosis, 832 Symptoms, 833 Prognosis, 833 Purulent meningitis, 831 Symptoms, 831 Symptoms, 828 Treatment, 829 Boric acid, 829 Nitrate of silver, 829 Inflammation, causes of, 818 Bright's disease, 820 Diphtheria, 820 Measles, 819 Retro-nasal catarrh, 819 Scrofulosis, 819 Smallpox, 819 Syphilis, 820 Tuberculosis, 819 Typhoid fever, 820 Whooping cough, 820

Ovarian cysts, treatment of, aspiration in the, 308 Electrolysis in the, 313 Radical surgical, 312 Tapping in the, 308 Use of trocar in the, 308

Ovarian tumors, 297 Cystic, 301 Causation of, 302 Description, 301 Diagnosis, 304 Ascites in the, 305 Obesity in the, 308 Phantom tumors in the, 308 Pregnancy in the, 306 Renal cysts in the, 307 Spina bifida in the, 307 Uterine fibroids in the, 306 History, 303 Symptoms, 303 Treatment of surgical, 308 Palliative, surgical, 308 Aspiration in the, 308 Tapping through the abdominal wall, 310 methods of, 310 Tapping through the vagina, 311 Use of the trocar in the, 308 Radical, 312 Electrolysis in the, 313 Dermoid cystic, 299 Description of, 299 Symptoms of, 294 Treatment of, 300 Fibroid, 297 Diagnosis, 297 Prognosis, 297 Recoveries in, 297 Malignant, 298 Description, 298 Diagnosis, 298 Treatment, 299

OVARIES AND OVIDUCTS, DISEASES OF, 282 Cysts of the oviducts, 295 Contents of, 295 Diagnosis of, 295 Treatment of, 295 Cysts of the parovarium, 293 Description, 293 Differential diagnosis, 294 Treatment, 295 Cysts of terminal vesicle of the oviduct, 296 Hernia, 289 Treatment, 290 Inflammation, 283 Ovaritis, acute, 283 Chronic, 284 Causation of, 284 Prognosis, 285 Symptoms, 285 Treatment, 285 Bromide of potash in, 286 Fowler's solution in, 286 Rest-cure in, 286 Suppositories in, 285 Oöphorectomy in, 287 Prolapse, causation of, 287 Description, 287 Diagnosis, 288 Symptoms, 287 Treatment, 288 Knee-chest position in, 289 Oöphorectomy in, 289 Tumors of the round ligament, 296 Description of, 282 Malpositions of, 282 Diagnosis, 283 Treatment, 283 Ovariotomy, 313 Accidents and complications of, 336 After-treatment of cases of, 333 Arrangement of tables for, 320 Articles needed for the operation of, 318 Assistants in, 320 Position of, 321 Carbolic-acid spray in, 320 for instruments, 321 Causes of death after, 314 Contraindications for, 316 Counting the sponges after, 330 Definition of, 313 Drainage-tubes after, 332 Dressing the wound after, 331 History of, 313 Indications for, 316 Instruments, 319 Cautery-irons, 319 Forceps, 319 Gauze, 319 Needles, 319 Sponges, 319 Line of incision in, 322 Performance of the operation of, 322 Preparation of the patient for, 317, 321 Diet in the, 317 Drugs in the, 317 Pressure-forceps for arresting hemorrhage in, 322 Statistics of, 314 Surgical after-treatment of cases of, 335 Time for the performance of, 318 Treatment of pedicle after, 325 By actual cautery, 326 By clamp, 325 Silk ligatures in, 326

Ovum, development of, 477 as a local cause of abortion, 489

Oxygen in the treatment of acute parenchymatous nephritis, 80

P.

Pain in acute catarrh of the middle ear, 821 in chronic cystitis, 129 in pyelitis, 54

Painful micturition as a symptom of nephritis, 82

Palliative treatment of calculous pyelitis, 51

Palpation of kidney, 20

Paralysis, double, of third pair of nerves, 780 of bladder, 133 in women, 350 of third pair of cranial nerves, 780 pseudo-hypertrophic, 557

Parametritis, 209

Parasites in pathology of comedo, 590 of kidney, 65 of skin, 715 vegetable, in the external ear, 815

Parasiticides in treatment of scabies, 728 in treatment of tinea favosa, 716

Parenchyma of the uterus, diseases of, 447

Parenchymatous nephritis, acute, 78 chronic, 80

Parturition in the etiology of parametritis, 210

Pathogeny of progressive muscular atrophy, 546 of pseudo-hypertrophic paralysis, 576 of seminal incontinence, 140

Pathological anatomy of acute endometritis, 461 of acute metritis, 448 of acute parenchymatous nephritis, 78 of chronic endometritis, 462 of chronic metritis, 452 of progressive muscular atrophy, 543 of prolapse of uterus, 157 of pseudo-hypertrophic paralysis, 569 anteflexion of uterus, 176 anteversion of uterus, 174

Pathology and etiology of the vomiting of pregnancy, 409 of abortion, 494 of chronic cystitis, 130 of chyluria, 115 of comedo, 590 of cystitis in women, 341 of diseases of kidneys in pregnancy, 418 of disturbed vision, 760 of eczema, 629 of elephantiasis of the vulva, 399 of impetigo, 651 of inflammation of bladder, 124 of keloid, 685 of lupus erythematosus, 690 of malignant icterus in pregnancy, 415 of milium, 592 of molluscum epitheliale, 662 of myalgia, 534 of nystagmus, 784 of parametritis, 210 of pelvic hæmatocele, 240 of perimetritis, 229 of pernicious progressive anæmia of pregnancy, 406 of polyuria, 31 of prolapsus vaginæ, 377 of prurigo, 640 of retroflexion of uterus, 166 of stricture of the urethra in women, 363 of urethral caruncle, 403 of urticaria, 598 of vaginismus, 385

Pedicle, treatment of, after ovariotomy, 325

Pediculosis, 728 capitis, 729 corporis, 730

Pedunculus, 227

Pelvic abscess, treatment of, 222 Cellular tissue, inflammation of, 208 Cellulitis as a cause of disturbed vision, 757 Causes, 241 Complications, 243 Course of, 243 Definition and synonyms of, 240 Differentiation, 243 Duration, 243 Frequency, 240 Hæmatocele, 239 History of, 239 Pathology, 240 Physical signs of, 242 Prognosis, 243 Symptoms, 242 Termination, 243 Treatment of, 243 Morphia in the, 244 Operative, 244 Varieties, 241

Pemphigus, 656

Performance of anterior elytrorrhaphy for prolapse of uterus, 161

Pericarditis as a symptom of nephritis, 83

Perineorrhaphy for prolapse of uterus, 163

Perinephritis, 102

Peritoneum, pelvic, inflammation of, 208 inflammation of, 208

Peritonitis as a symptom of nephritis, 83 in prolapse of uterus, 158 pelvic, in prolapse of uterus, 158

Permanganate of potash in treatment of amenorrhoea, 191

Pernicious anæmia, effects on the eye, 745

Pernicious progressive anæmia of pregnancy, 406

Pessaries in pathological anteversion of uterus, 176 in prolapse of uterus, 160 in retroflexion of uterus, 171 in treatment of prolapse of uterus, 160

Phantom tumors in the diagnosis of cystic tumors of ovary, 308

Phlebitis with thrombosis following chronic inflammation of middle ear, 832

Phlegmonous inflammation of the labia majora, 391

Phosphates in polyuria, 30

Phosphoric acid as a cause of dermatitis medicamentosa, 603

Phosphoridrosis as a disorder of secretion in diseases of skin, 585

Physical signs of chronic metritis, 454 of parametritis, 214 of pelvic hæmatocele, 242 of perimetritis, 231

Physiology of early pregnancy, 474

Pilocarpine in polyuria, 34 in treatment of acute parenchymatous nephritis, 80 of diseases of kidneys in pregnancy, 419

Pityriasis rosea, 621 rubra, 622

Placenta, the, as a local cause of abortion, 490

Plethora as a disorder of pregnancy, 407

Pleurisy as a symptom of nephritis, 83

Pleuritis, acute, in pregnancy, 431

Pleurodynia as a symptom of myalgia, 532

Pneumonia, blindness after, 748 acute lobar, in pregnancy, 439

Polyuria, 27 after acute diseases, 30 after meningitis, 31

Pompholyx, 655

Position of assistants in ovariotomy, 322 of kidney, 20

Poultices in treatment of carbunculus, 607

Predisposing causes of abortion, 480 of myalgia, 530

Pregnancy as a cause of disturbed vision, 759

PREGNANCY, DISORDERS OF, 405 Acute infectious diseases, 424 Cholera, 428 Effects of high temperature on the foetus, 424 Malarial fever, 427 Measles, 426 Other causes of death of foetus in, 425 Relapsing fever, 427 Scarlet fever, 426 Smallpox, 425 Syphilis, 428 Treatment, 429 Typhoid fever, 426 Typhus fever, 427 Alterations in the condition of the blood, 405 Chlorosis and hydræmia, 405 Etiology, 406 Treatment, 406 Hæmophilia, 407 Treatment, 407 Plethora, 407 Treatment, 407 Progressive pernicious anæmia, 406 Pathology, 406 Prognosis, 406 Treatment, 406 Iron in, 406 Cardiac diseases, 429 Acute endocarditis, 430 Chronic heart disease, 430 Circulatory disturbances, 407 Treatment, 408 Diabetes mellitus, 416 General consideration of, 416 Prognosis, 416 Treatment, 416 Diseases of the kidneys, 416 Etiology and pathology, 417 Prognosis, 418 Symptoms, 418 Convulsions, 418 Vertigo, 418 Treatment, 418 Hygienic, 419 Medical, 419 Cathartics, 419 Diuretics, 419 Pilocarpine, 419 Diseases of the liver, 414 Icterus, 414 Etiology, 414 Simple, 414 Symptoms, 415 Malignant, 415 Diagnosis, 415 Etiology, 415 Pathology, 415 Prognosis, 415 Symptoms, 415 Diseases of the lungs, 430 Acute lobar pneumonia, 430 Prognosis, 431 Treatment, 431 Acute pleuritis, 431 Pulmonary tuberculosis, 431 Diseases of the skin, 420 Disorders of alimentary canal, 408 Constipation, 413 Diarrhoea, 414 Ptyalism, 413 Toothache, 413 Vomiting, 408 Course, 409 Diagnosis, 410 Pathology and etiology, 409 Prognosis, 410 Serious effects, 408 Treatment, 410 Gynæcological, 412 Hygienic, 410 diet in, 410 Medical, 411 Obstetrical, 412 Disorders of special sense, 423 Neuroses, 421 Chorea, 422 Course and symptoms, 422 Etiology, 422 Prognosis, 422 Treatment, 423 Epilepsy, 423 Diagnosis, 423 Tetanus, 421

Pregnancy, early physiology of, 474 in the diagnosis of cystic tumors of the ovary, 306

Preparation of patient for ovariotomy, 317

Preparations for treatment of abortion, 509

Preventive treatment of abortion, 515

Prognosis of abortion, 508 of acute cystitis, 127 diffuse nephritis, 83 endometritis, 461 lobar pneumonia in pregnancy, 431 metritis, 449 parenchymatous nephritis, 80 purulent inflammation of middle ear, 826 of anteversion of uterus (pathological), 175 of carcinoma of uterus, 277 of chorea in pregnancy, 422 of chronic catarrh of middle ear, 825 cystitis, 130 endometritis, 464 metritis, 456 ovaritis, 285 parenchymatous nephritis, 81 of diabetes mellitus in pregnancy, 416 of dilatation of urethra in women, 359 of diseases of kidneys in pregnancy, 418 of dislocations of urethra in women, 361 of dysmenorrhoea, 197 of eczema, 631 of epithelioma of uterus, 280 of fibroid tumors of ovary, 297 of fibrous tumors of uterus, 254 of furuncle of external auditory canal, 814 of herpes zoster ophthalmicus, 786 of ichthyosis, 668 of impacted cerumen in external auditory canal, 813 of imperforate hymen, 375 of inversion of urethral mucous membrane in women, 362 of malignant icterus in pregnancy, 415 of myalgia, 538 of neurosis of bladder, 133 of paralysis of bladder in women, 351 of parametritis, 219 of pelvic hæmatocele, 243 of perimetritis, 232 of pernicious progressive anæmia of pregnancy, 406 of progressive muscular atrophy, 554 of pyelo-nephritis, 101 of renal colic, 45 of retroversion of uterus, 165 of sarcomatous tumors of uterus, 272 of scarlatina in nephritis, 84 of seminal incontinence, 142 of stricture of urethra in women, 368 of tinea tonsurans, 721 of tinnitus aurium in diseases of internal ear, 838 of tuberculosis of kidney, 65 of vaginismus, 385 of vaginitis, 371 of vegetable parasites in external ear, 815 of vomiting of pregnancy, 410

PROGRESSIVE MUSCULAR ATROPHY, 540 Age, 542 Complications, 552 Definition, 540 Diagnosis, 552 Etiology, 541 Histology, 543 History, 540 Pathogeny, 546 Pathological anatomy, 543 Prognosis, 554 Sex, 542 Symptoms, 547 Fever as a, 552 Synonyms, 540 Treatment, 554 Electricity, 554 Gymnastics, 555 Massage, 555

Progressive pernicious anæmia as a disorder of pregnancy, 406

Prolapse of ovary, 287 of uterus, 154

Prolapsus vaginæ, 376

Prophylactic treatment of chronic endometritis, 464

Prophylaxis of prolapse of uterus, 159

Prurigo, 639

Pruritus, 711 hiemalis, 714 vulvæ, 392

Pseudo-cyesis during the menopause, 444

PSEUDO-HYPERTROPHIC PARALYSIS, 557 Autopsies, 558 Course and prognosis, 568 Definition, 557 Diagnosis, 578 History, 557 Pathogeny, 576 Pathological anatomy, 569 Central nervous organs, 572 Connective tissue, 571 Muscular fibres, 570 Symptoms, 558 Electrical reaction as a, 560 In upper part of body, 565 Locomotion, 563 Muscles affected, 559 Reflex excitability in, 561 Synonyms, 557 Treatment, 579 Electricity in, 579

Psoriasis, 614

Psychical influences as a cause of amenorrhoea, 187

Ptosis, 781 of third pair of cranial nerves, 781

Ptyalism in pregnancy, 413

Pudendal hernia, 398

Puerperal phlebitic ophthalmitis, 759

Pulex irritans, 733 penetrans, 732

Pulmonary symptoms of abortion, 499 tuberculosis as a cause of amenorrhoea, 186 in pregnancy, 431

Purgatives in treatment of nephritis, 83

Purulent inflammation of middle ear, acute, 825 chronic, 827 meningitis as a sequel of chronic inflammation of middle ear, 831

Pus as an aid to diagnosis in calculous pyelitis, 49

Pyelitis, calculous, 47

Pyelo-nephritis, 99

Q.

Quinine as a cause of dermatitis medicamentosa, 603 of toxic amblyopia, 804 effects of, on the eye, 804

R.

Race in scrofuloderma, 699

Radical surgical treatment of ovarian cysts, 312

Recto-vaginal hernia, 378

Reflex excitability in pseudo-hypertrophic paralysis, 561

Relapsing fever as a cause of ophthalmitis, 765 in pregnancy, 427 typhus as a cause of ophthalmitis, 765

Removal of causes in treatment of seminal incontinence, 143

Renal colic, 42 cysts in the diagnosis of cystic tumors of ovary, 307

Reposition in retroflexion of uterus, 170

Respiratory changes in connection with the menopause, 435

Rest-cure in treatment of chronic ovaritis, 286

Rest in treatment of calculous pyelitis, 51

Retinal aneurism, 743

Retinitis, 77 leukæmic, 744

Retrocele in prolapse of uterus, 158 vaginalis, 378

Retroflexion of uterus, 166

Retro-locations of uterus, 153

Rheumatism and gout in relation to diseases of the eye, 800

Rhinochoprion penetrans, 732

Round ligament, tumors of, 296

Rubeola as a cause of ophthalmitis, 763

Rue in treatment of amenorrhoea, 190

Rupture of abscesses into peritoneal cavity as a symptom of perinephritis, 102

S.

Saffron in treatment of amenorrhoea, 190

Salicylate of sodium as cause of toxic amblyopia, 804 effects of, on the eye, 804

Salicylic acid as a cause of dermatitis medicamentosa, 603

Salt solution with hydrochloric acid as a test for albumen in albuminuria, 36

Santonin as a cause of dermatitis medicamentosa, 604 of toxic amblyopia, 804 effects of, on the eye, 804

Sarcoma of the skin, 710

Sarcomatous tumors of the vagina, 381

Savin in treatment of amenorrhoea, 190

Scabies, 726

Scapulodynia as a symptom of myalgia, 532

Scarlatina, acute diffuse nephritis of, 84 as a cause of ophthalmitis, 764

Scarlet fever as a cause of inflammation of middle ear, 818 deafness after, 839 in pregnancy, 426

School-life as a cause of amenorrhoea, 188

Sclerema neonatorum, 671

Scleroderma, 671

Sclerosis as a cause of inflammation of middle ear, 819

Scrofuloderma, 698

Seat of eczema vesiculosum, 627

Seats of cornu cutaneum, 664 of eczema erythematosum, 626 of epithelioma, 708 of keloid, 685 of lupus erythematosus, 690 vulgaris, 693 of tinea versicolor, 725

Seborrhoea as a disorder of secretion in diseases of skin, 586

Secondary pyelitis, 53

Second pair of nerves, cranial, affections of, 771

SEMINAL INCONTINENCE, 137 Anatomical characteristics of, 141 Classification, 137 Diurnal pollutions, 138 Nocturnal pollutions, 137 Spermorrhagia, 138 Clinical history, 138 Definition, 137 Diagnosis, 141 Etiology, 140 Pathogeny, 140 Prognosis in, 142 Treatment of, 143 Atropia, 146 Bougies, 144 Bromide of potash, 145 Cantharidal collodion, 145 Gymnastics, 143 Marriage, 146 Nitrate of silver, 145 Removal of causes, 143 Sitz-baths, 145

Sequelæ of chronic purulent inflammation of middle ear, 830

Sequels of myalgia, 534

Serious effects of vomiting of pregnancy, 408

Serous and mucous discharges during menopause, 438

Seventh pair of cranial nerves, affections of, 790

Sex in epithelioma, 709 in progressive muscular atrophy, 542

Signs of parametritis, 214

Silk ligatures in treatment of pedicle of ovariotomy, 326

Simple icterus in pregnancy, 414

Sitz-baths in acute cystitis, 127 in treatment of seminal incontinence, 145

Skin, alteration of functions of, during menopause, 435

SKIN, DISEASES OF (classified), 583 Atrophies, 676 Albinismus, 676 Definition, 676 Alopecia, 678 areata, 680 Causes, 681 Description, 680 Diagnosis, 681 Symptoms, 680 Treatment, 681 External, 681 Internal, 681 Atrophia cutis, 683 Definition, 683 pilorum propria, 682 Definition, 682 Diagnosis, 683 unguis, 683 Diagnosis, 683 Canities, 678 Vitiligo, 677 Definition, 677 Synonyms, 677 Treatment, 677 Hypertrophies, 658 Callositas, 662 Definition, 662 Symptoms, 662 Synonyms, 662 Treatment, 662 Chloasma, 659 Causes, 659 Definition, 659 Clavus, 663 Definition, 663 Treatment, 663 Cornu cutaneum, 663 Definition, 663 Seats of, 664 Treatment, 664 Dermatolysis, 675 Definition, 675 Elephantiasis, 674 Cause, 674 Filaria as a, 674 Definition, 674 Morbid anatomy, 675 Synonyms, 674 Treatment, 675 Hypertrichosis, 669 Causes, 670 Definition, 669 Synonyms, 669 Treatment, 670 Caustics, 670 Electrolysis, 670 Ichthyosis, 666 Prognosis, 668 Symptoms, 667 Synonyms, 666 Treatment, 668 Varieties of, 666 Keratosis pilaris, 660 Causes, 661 Definition, 660 Treatment, 661 Lentigo, 658 Definition, 658 Molluscum epitheliale, 661 Cause, 661 Diagnosis, 662 Pathology, 662 Synonyms, 661 Morphoea, 672 Definition, 672 Diagnosis, 673 Treatment, 674 Nævus pigmentosus, 666 Definition, 666 Locations, 666 Treatment, 666 Onychauxis, 669 Definition, 669 Symptoms, 669 Synonyms, 669 Treatment, 669 Sclerema neonatorum, 671 Definition, 671 Scleroderma, 671 Causes, 672 Definition, 671 Synonyms, 671 Treatment, 672 Verruca, 664 Definition, 664 Diagnosis, 665 Etiology, 665 Treatment, 665 Caustics in, 665 Inflammations, 593 Acne, 641 Definition, 641 Diagnosis, 642 Frequency, 642 Treatment, 642 Local, 644 Varieties, 641 rosacea, 647 Definition, 647 Diagnosis, 647 Treatment, 648 External, 648 Internal, 648 Carbunculus, 606 Causes, 607 Definition, 606 Synonyms, 606 Treatment, 607 Dressings in, 607 Poultices in, 607 Dermatitis, 600 calorica, 601 Treatment, 601 exfoliativa, 623 factitia, 604 gangrænosa, 604 herpetiformis, 611 Changes in, 613 Definition, 611 Diagnosis, 612 Symptoms, 612 Treatment, 613 Varieties, 612 medicamentosa, 601 Causes, 602 Arsenic, 602 Atropia, 602 Belladonna, 602 Bromides, 602 Cannabis indica, 602 Chloral, 602 Copaiba, 602 Cubebs, 603 Digitalis, 604 Iodides, 603 Mercury, 603 Opium, 603 Morphia, 603 Phosphoric acid, 603 Quinine, 603 Salicylic acid, 603 Santonine, 604 Stramonium, 604 Strychnia, 604 Turpentine, 604 traumatica, 600 venenata, 600 Treatment, 601 Ecthyma, 653 Causes, 653 Definition, 653 Diagnosis, 653 Treatment, 654 Eczema, 625 Symptoms, 625 erythematosum, 626 Course, 626 Seats of, 626 Symptoms, 626 papulosum, 627 pustulosum, 627 Symptoms, 627 squamosum, 628 vesiculosum, 627 Definition, 627 Symptoms, 627 Eczemas in general, 629 Diagnosis, 629 Etiology, 629 Pathology, 629 Prognosis, 631 Treatment, 632 Constitutional, 632 Arsenic, 632 Laxatives, 632 External, 634 Lotions, 635 Ointments, 635 Erythema intertrigo, 594 Treatment, 594 multiforme, 595 Description, 595 Treatment, 596 nodosum, 596 Causes, 596 Definition, 596 Treatment, 597 simplex, 593 Treatment, 594 Furunculus, 604 Aleppo bouton, 606 Biskra bouton, 606 Boil or evil, 606 Definition, 604 Delhi boil, 606 Diagnosis, 605 Symptoms, 605 Synonyms, 604 Treatment, 606 Herpes iris, 609 Definition, 609 Diagnosis, 609 Frequency, 609 Treatment, 609 simplex, 607 Definition, 607 Varieties, 608 Treatment, 608 zoster, 610 Causes, 610 Definition, 610 Diagnosis, 611 Symptoms, 610 Treatment, 611 Impetigo, 651 Definition, 651 Pathology, 651 contagiosa, 652 Causes, 652 Definition, 652 Diagnosis, 652 Symptoms, 652 Treatment, 653 Lichen ruber, 623 Definition, 623 Diagnosis, 624 Etiology, 624 Treatment, 624 Arsenic, 624 Baths, 624 Tonics, 624 Varieties, 623 scrofulosus, 624 Diagnosis, 625 Miliaria, 654 Definition, 654 Diagnosis, 655 Treatment, 655 Pemphigus, 656 Definition, 656 Diagnosis, 657 Treatment, 657 Pityriasis rosea, 621 Course, 621 Definition, 621 Diagnosis, 621 Treatment, 621 rubra, 622 Course, 622 Definition, 622 Etiology, 622 Symptoms, 622 Treatment, 622 Pompholyx, 655 Definition, 655 Treatment, 656 Prurigo, 639 Definition, 639 Diagnosis, 640 Pathology, 640 Symptoms, 640 Treatment, 641 Psoriasis, 614 Definition, 614 Diagnosis, 616 Duration, 614 Symptoms, 614 Treatment, 617 Internal, 617 External, 617 Local, 619 Varieties, 615 Urticaria, 597 Definition, 597 Pathology, 598 Treatment, 599 External, 599 Internal, 599 Varieties, 598 pigmentosa, 599 Neuroses, 711 Dermatalgia, 711 Pruritus, 711 Causes, 712 Definition, 711 Diagnosis, 712 Treatment, 712 Drugs in, 712 Ointments in, 713 Washes in, 713 hiemalis, 714 Definition, 714 Treatment, 714 New Growths, 685 Angioma, 688 Course, 688 Definition, 688 Treatment, 688 Caustics, 688 Cauterization, 688 Electrolysis, 689 Ointments, 688 Epithelioma, 707 Age in, 709 Seats of, 708 Sex in, 709 Treatment, 709 Caustics in, 709 Curette in, 710 Varieties, 707 Fibroma, 686 Absence of pain, 686 Definition of, 686 Multiple, 686 Keloid, 685 Definition, 685 Pathology, 685 Seats of, 685 Treatment, 685 Lupus erythematosus, 689 Causes, 690 Definition, 689 Diagnosis, 691 Pathology, 690 Seats of, 690 Symptoms, 689 Treatment, 691 Curette, use of, in, 692 Lotions in, 692 vulgaris, 693 Definition, 693 Diagnosis, 694 Heredity, 693 Morbid anatomy of, 694 Seats of, 693 Symptoms, 693 Treatment, 695 Caustic potash, 696 Corrosive sublimate, 696 Nitrate of silver, 696 Ointments in, 697 Operative, 697 Lymphangioma, 689 Myoma, 687 Neuroma, 686 Sarcoma, 710 Definition of, 710 Diagnosis, 710 Frequency of, 710 Symptoms, 710 Scrofuloderma, 698 Definition, 698 Race in, 699 Symptoms, 698 Treatment, 699 Varieties, 698 Syphilis cutanea, 699 Definition of, 699 Syphiloderma bullosum, 705 Anatomy, 705 Treatment, 705 Mercury, 706 Iodide of potash, 707 Local, 707 erythematosum, 700 Symptoms of, 700 Diagnosis, 700 gummatosum, 705 papulosum, 701 Varieties, 701 pigmentosum, 701 pustulosum, 703 Varieties, 703 tuberculosum, 704 vesiculosum, 702 Synonyms for, 702 Xanthoma, 687 Parasites, 715 Acanthia lectularia, 733 Cimex lectularius, 733 Culex, 733 Cysticercus cellulosæ, 732 Demodex folliculosum, 732 Filaria medinensis, 732 Ixodes, 733 Leptus, 731 Varieties, 731 Oestrus, 732 Pediculosis, 728 Synonyms, 728 Varieties, 728 capitis, 729 Symptoms, 729 Treatment, 729 corporis, 730 Cause, 730 Description, 730 Symptoms, 730 pubis, 731 Definition, 731 Treatment, 731 Pulex irritans, 733 penetrans, 732 Rhinochoprion penetrans, 732 Scabies, 726 Cause, 726 Definition, 726 Diagnosis, 727 Symptoms, 726 Treatment, 728 Parasiticides, 728 Tinea circinata, 717 Course, 717 Definition, 717 Diagnosis, 718 Frequency, 718 Treatment, 719 favosa, 715 Definition, 715 Diagnosis, 716 Frequency, 715 Symptoms, 715 Treatment, 716 Parasiticides in, 716 sycosis, 723 Definition, 723 Frequency, 724 Treatment, 724 tonsurans, 720 Baldness, 720 Definition, 720 Diagnosis, 721 Frequency, 720 Hair in, 720 Prognosis, 721 Treatment, 722 Ointments in, 722 trichophytina, 717 Definition, 717 versicolor, 724 Cause, 725 Definition, 724 Diagnosis, 725 Seats of, 725 Treatment, 726 Secretion, Disorders of, 583 Anidrosis, 584 Bromidrosis, 584 Treatment, 585 Chromidrosis, 585 Comedo, 589 Pathology, 590 Parasites in, 590 Treatment, 591 Hyperidrosis, 583 Treatment, 583 Milium, 592 Description of, 592 Pathology of, 592 Treatment of, 592 Phosphoridrosis, 585 Seborrhoea, 586 Definition of, 586 Treatment, 588 Applications in, 589 Ointment in, 589 Varieties of, 587 Steatoma, 592 Treatment, 593 Sudamen, 586 Course of, 586 Treatment of, 586 Sycosis, 649 Definition, 649 Diagnosis, 650 Synonyms, 649 Treatment, 650 Uridrosis, 585

Skin, diseases of (unclassified). Acanthia lectularia, 733 Acarus, 732 Acne, 641 rosacea, 647 vulgaris, 641 Albinismus, 676 Aleppo boil, 606 Alopecia, 678 areata, 680 Angioma, 688 Anidrosis, 584 Anthrax, 606 Atrophia pilorum propria, 682 cutis, 683 unguis, 683 Bedbug, 733 Biskra bouton, 606 Boil, 604 Bromidrosis, 584 Callositas, 662 Canities, 678 Carbunculus, 606 Chigoe, chigger, or jigger, 732 Chloasma, 659 Chromidrosis, 585 Cimex lectularius, 733 Clavus, 663 Comedo, 589 Corn, 663 Cornu cutaneum, 663 Culex, 733 Cysticercus cellulosæ, 732 Delhi boil, 606 Demodex folliculorum, 732 Dermatalgia, 711 Dermatitis, 600 calorica, 601 exfoliativa, 623 gangrænosa, 604 herpetiformis, 611 medicamentosa, 601 traumatica, 600 venenata, 600 Dermatolysis, 675 Dermato-syphilis, 699 Dracunculus, 732 Ecthyma, 653 Eczema, 625 erythematosum, 626 papulosum, 627 pustulosum, 627 vesiculosum, 627 Elephantiasis, 674 Epithelioma, 707 Erythema, 593 intertrigo, 594 multiforme, 595 nodosum, 596 simplex, 593 Exanthematous syphilide, 700 Favus, 715 Fibroma, 686 Filaria medinensis, 732 Flea, 733 Furunculus, 604 Gad-fly, 732 Gnat, 733 Guinea-worm, 732 Herpes, 607 facialis, 608 iris, 609 simplex, 607 zoster, 610 Hyperidrosis, 583 Hypertrichosis, 669 Ichthyosis, 666 Impetigo, 651 contagiosa, 652 Itch, 726 Ixodes, 733 Jigger, 732 Keloid, 685 Keratosis pilaris, 660 Lentigo, 658 Leptus, 731 Lichen ruber, 623 scrofulosus, 624 Lousiness, 728 Lupus erythematosus, 689 vulgaris, 693 Lymphangioma, 689 Macular syphiloderm, 700 Miliaria, 654 Milium, 592 Mole, 666 Molluscum epitheliale, 661 fibrosum, 686 Morphoea, 672 Mosquito, 733 Myoma, 687 Nævus pigmentosus, 666 Neuroma, 686 Oestrus, 732 Onychauxis, 669 Pediculosis, 728 capitis, 729 corporis, 730 pubis, 731 Pemphigus, 656 Phosphoridrosis, 585 Phtheiriasis, 728 Pityriasis rosea, 621 rubra, 622 Pompholyx, 655 Prurigo, 639 Pruritus, 711 hiemalis, 714 Psoriasis, 614 Pulex penetrans, 732 irritans, 733 Rhinocoprion penetrans, 732 Roseola syphilitica, 700 Sarcoma, 710 Scabies, 726 Sclerema neonatorum, 671 Scrofuloderma, 671 Seborrhoea, 586 congestiva, 689 Senile atrophy, 684 Steatoma, 592 Sudamen, 586 Sycosis, 649 Syphilis cutanea, 699 Syphiloderma bullosum, 705 erythematosum, 700 gummatosum, 705 papulosum, 701 pigmentosum, 701 pustulosum, 703 tuberculosum, 704 Ticks, 733 Tinea circinata, 717 favosa, 715 sycosis, 723 tonsurans, 720 tricophytina, 717 versicolor, 724 Uridrosis, 585 Urticaria, 597 pigmentosa, 599 Verruca, 664 Vitiligo, 677 Vitiligoidea, 687 Wart, 664 Wood-ticks, 733 Xanthelasma, 687 Xanthoma, 687

Smallpox as a cause of inflammation of middle ear, 819 in pregnancy, 425

Soft cancer of the uterus, 274

Sound, use of, in uterine explorations, 152

Sounds in treatment of inflammation of bladder, 125

Special sense, disorders of, in pregnancy, 423

Specula, use of, in uterine explorations, 153

Spermorrhagia in seminal incontinence, 138

Spina bifida in the diagnosis of cystic tumors of ovary, 307

Spinal cord, relation of, to diseases of the eye, 792

Stages of chronic metritis, 452

Statistics of ovariotomy, 314

Steatoma as a disease of the skin, 592

Sterility as a symptom of acquired anteflexion of uterus, 178

Stramonium as a cause of dermatitis medicamentosa, 604

Stricture at junction of urethra and bladder in women, 365 of urethra in women, 363

Strychnia as a cause of dermatitis medicamentosa, 604 in treatment of atony of bladder, 134 of paralysis of the bladder in women, 351

Subacute urethritis in women, 355

Subinvolution as a cause of chronic metritis, 450

Sudamen, as a disorder of secretion in diseases of skin, 586

Sufficient food in polyuria, 33 liquid in polyuria, 33

Sulphate of zinc in the treatment of acute urethritis in women, 353

Supernumerary kidney, 21

Supports of uterus, normal, 150

Surgical treatment of fibrous tumors of the uterus, 266

Sweating in the treatment of acute parenchymatous nephritis, 80

Sycosis, 644

Symptomatology and course of prolapsus vaginæ, 377 of dilatation of the urethra in women, 358 of dislocations of the urethra in women, 361 of floating kidney, 23 of myalgia, 531 of parametritis, 213 of phlegmonous inflammation of the labia, 391 of stricture of the urethra in women, 363 of vaginismus, 384 of vulvitis, 389

Symptoms of abortion, 500 preliminary, 499 of acute catarrh of middle ear, 821 cystitis, 126 diffuse nephritis, 82 metritis, 448 parenchymatous nephritis, 79 purulent inflammation of middle ear, 826 of alopecia areata, 680 of amenorrhoea, 187 of anteflexion of uterus (acquired), 178 of anteversion of uterus (pathological), 174 of atrophy of the bladder in women, 348 of brain abscess following chronic inflammation of middle ear, 832 of calculous pyelitis, 51 of callositas, 662 of carcinoma of uterus, 276 of chorea in pregnancy, 422 of chronic cystitis, 129 diffuse nephritis, 88 metritis, 453 ovaritis, 285 parenchymatous nephritis, 81 purulent inflammation of middle ear, 828 of chyluria, 119 of congestion of kidney, 70 of cystic tumors of the ovary, 303 of cystitis in women, 343 of cysto-vaginal hernia, 377 of cysts of kidney, 63 of dermatitis herpetiformis, 612 of dermoid cysts of the ovary, 300 of diseases of kidneys in pregnancy, 418 of displacements of uterus, 151 of eczema, 625 erythematosum, 626 pustulosum, 627 vesiculosum, 627 of foreign bodies in the external ear, 816 of furuncle of the external auditory canal, 814 of furunculus, 605 of hæmatoma, 401 of hemianopia, 778 of hemorrhage from the bladder in women, 340 of herpes zoster, 610 ophthalmicus, 785 of hyperæmia of bladder in women, 339 of hypertrophy of bladder in women, 348 of ichthyosis, 667 of impacted cerumen in external auditory canal, 812 of imperforate hymen, 374 of impetigo contagiosa, 652 of inflammation of bladder, 124 of lupus erythematosus, 689 vulgaris, 693 of malignant growths of kidney, 61 of mastoid disease, 834 of nephritis in scarlatina, 84 of neuro-paralytic ophthalmia, 787 of nystagmus, 783 of onychauxis, 669 of pediculosis capitis, 729 of pelvic hæmatocele, 242 of perimetritis, 230 of perinephritis, 102 of phlebitis with thrombosis following chronic inflammation of middle ear, 833 of pityriasis rubra, 622 of polyuria, 27 of progressive muscular atrophy, 547 of prolapse of ovary, 287 uterus, 158 of prurigo, 640 of pruritus vulvæ, 393 of pseudo-hypertrophic paralysis, 558 in the trunk, 565 of psoriasis, 614 of pudendal hernia, 398 of purulent meningitis as a sequel of chronic inflammation of middle ear, 831 of pyelo-nephritis, 99 of renal colic, 43 of retroflexion of uterus, 167 of retroversion of uterus, 165 of sarcoma of skin, 710 of scabies, 726 of scrofuloderma, 698 of simple icterus in pregnancy, 415 of syphiloderma erythematosum, 700 of tinea favosa, 715 of urethral caruncle, 403 of vegetable parasites in the external ear, 815

Synonyms and classification of prolapsus vaginæ, 376 of abortion, 467 of callositas, 667 of carbunculus, 606 of chronic congestion of kidney, 69 metritis, 450 of elephantiasis, 674 of furunculus, 604 of hypertrichosis, 669 of ichthyosis, 666 of molluscum epitheliale, 661 of myalgia, 529 of onychauxis, 669 of parametritis, 209 of pediculosis, 728 of perimetritis, 227 of progressive muscular atrophy, 540 of pseudo-hypertrophic paralysis, 557 of scleroderma, 671 of sycosis, 649 of syphiloderma vesiculosum, 702 of vaginitis, 368 of vitiligo, 677

Syphilis as a cause of inflammation of middle ear, 819 cutanea, 699 in abortion, 491 in pregnancy, 428 in relation to diseases of the eye, 800

Syphiloderma bullosum, 705 erythematosum, 700 gummatosum, 705 papulosum, 701 pigmentosum, 701 pustulosum, 703 tuberculosum, 704 vesiculosum, 702

Systemic diseases in relation to diseases of the eye, 800 treatment of vaginismus, 386

T.

Tabes dorsalis in relation to diseases of the eye, 793

Tampons in treatment of carcinoma of the uterus, 278 of fibrous tumors of the uterus, 258

Tannic acid in treatment of dilatation of urethra in women, 359 of hemorrhage from bladder, 135

Tapping in treatment of ovarian cysts, 308

Termination of abortion, 504 of functional disorders in connection with the menopause, 432 of myalgia, 533 of pelvic hæmatocele, 243 of perimetritis, 229 of polyuria, 30 of vaginismus, 384

Terminations of chronic metritis, 456

Tests for albuminuria, 35

Tetanus in pregnancy, 421

Third pair of cranial nerves, affections of, 780

Thompson's method in diagnosis of calculous pyelitis, 49

Tinea circinata, 717 favosa, 715 sycosis, 723 tonsurans, 720 tricophytina, 717 versicolor, 724

Tinnitus aurium as a symptom of acute catarrh of middle ear, 821 in diseases of internal ear, 836

Tobacco as a cause of toxic amblyopia, 803

Tonics in treatment of lichen ruber, 624

Toothache in pregnancy, 413

Torticollis as a symptom of myalgia, 332

Toxic amblyopia, 803 in medical ophthalmology, 803

Treatment of abortion, 509 of acne, 642 rosacea, 648 of acute catarrh of middle ear, 822 cystitis, 127 endometritis, 461 lobar pneumonia in pregnancy, 431 metritis, 449 parenchymatous nephritis, 80 purulent inflammation oi' middle ear, 826 urethritis in women, 353 of albuminuria, 42 of alopecia areata, 681 of amenorrhoea, 189 of angioma of the skin, 688 of anteversion of uterus (acquired), 179 (pathological), 175 of atony of bladder, 134 of atrophy of bladder in women, 349 of bromidrosis as a disease of the skin, 585 of calculous pyelitis, 51 of callositas, 662 of cancer of the vagina, 383 of carbunculus, 607 of carcinoma of the uterus, 277 of chlorosis and hydræmia as a disorder of pregnancy, 406 of chorea in pregnancy, 423 of chronic catarrh of middle ear, 825 congestion of kidney, 72 cystitis, 131 diffuse nephritis, 95 endometritis, 464 metritis, 457 ovaritis, 285 perimetritis, 233 purulent inflammation of middle ear, 829 of chyluria, 120 of circulatory disturbances in pregnancy, 408 of clavus, 663 of comedo, 591 of cornu cutaneum, 664 of cystitis in wound, 345 of cysts of canal of Nuck, 397 of cysts of parovarium, 295 of deaf-mutism, 840 of dermatitis calorica, 601 herpetiformis, 613 venenata, 601 of dermoid cysts of the ovary, 300 of diabetes mellitus in pregnancy, 416 of dilatation of urethra in women, 359 of diseases of kidneys in pregnancy, 418 of dislocations of the urethra in women, 362 of dysmenorrhoea, 198 of ecthyma, 654 of eczema, 632 of the auricle, 811 of elephantiasis, 675 of the vulva, 460 of entero-vaginal hernia, 379 of epithelioma, 709 of the uterus, 280 of erythema intertrigo, 594 multiforme, 596 nodosum, 597 simplex, 594 of fibrous tumors of the uterus, 257 of floating kidney, 25 of foreign bodies in the external ear, 816 of furuncle of the external auditory canal, 814 of furuncles of labia, 392 of hæmatoma, 401 of hæmophilia as a disorder of pregnancy, 407 of hemorrhage from bladder, 135 in women, 340 of hernia of the ovary, 290 of herpes iris, 609 simplex, 609 zoster, 611 of hyperæmia of bladder in women, 339 of hyperidrosis as a disease of the skin, 583 of hypertrichosis, 670 of hypertrophy of the bladder in women, 348 of the vulva, 399 of ichthyosis, 668 of impacted cerumen in the external auditory canal, 813 of imperforate hymen, 375 of impetigo contagiosa, 653 of inflammation of bladder, 125 of inversion of urethral mucous membrane in women, 362 of keloid, 685 of keratosis pilaris, 661 of lichen ruber, 624 of lupus erythematosus, 691 vulgaris, 695 of malformations of ovaries and oviducts, 283 of malignant growths of kidney, 62 tumors of the ovary, 299 of mastoid disease, 834 of Menière's disease, 840 of menorrhagia, 203 of miliaria, 655 of milium, 592 of morphoea, 674 of myalgia, 538 of nævus pigmentosus, 666 of nephritis, 83 of neurosis of bladder, 133 of onychauxis, 669 of ovarian cysts, 308 of paralysis of the bladder in women, 351 of parametritis, 219 of parasites of kidney, 66 of pedicle after ovariotomy, 375 of pediculosis capitis, 729 of pelvic abscess, 222 hæmatocele, 243 of pemphigus, 657 of perimetritis, 232 of perinephritis, 108 of pernicious progressive anæmia of pregnancy, 406 of phlegmonous inflammation of the labia majora, 391 of pityriasis rubra, 622 of plethora as a disorder of pregnancy, 407 of polyuria, 33 of progressive muscular atrophy, 554 of prolapse of ovary, 288 of uterus, 159 of pruritus, 712 hiemalis, 714 vulvæ, 393 of pseudo-hypertrophic paralysis, 579 of psoriasis, 617 of pudendal hernia, 398 of pyelitis, 55 of pyelo-nephritis, 101 of renal colic, 45 of retroflexion of uterus, 168 of retroversion of uterus, 166, 168 of sarcomatous tumors of the uterus, 273 vagina, 382 of scabies, 728 of scleroderma, 672 of scrofuloderma, 699 of seborrhoea, 588 of seminal incontinence, 143 of stricture of the urethra in women, 364 of sudamen, 586 of sycosis, 650 of syphilis in pregnancy, 429 of syphiloderma bullosum, 705 of tinea circinata, 719 favosa, 716 sycosis, 724 tonsurans, 722 versicolor, 726 of urethral caruncle, 403 of urticaria, 599 of vaginismus, 385 of vaginitis, 371 of vegetable parasites in the external ear, 815 of verruca, 665 of vitiligo, 677 of the vomiting of pregnancy, 410 of vulvitis, 390

Tuberculosis as a cause of inflammation of middle ear, 819 in pregnancy, 431 in relation to diseases of the eye, 802 of kidney, 64

Tumors, uterine, 245 Carcinomatous, 274 Medullary, or soft, 274 Clinical history of, 275 Diagnosis, 276 Etiology of, 274 General symptoms, 276 Prognosis, 277 Treatment, 277 Operative, 278 Tampons in, 278 Epitheliomatous, 278 Clinical history, 279 Diagnosis, 279 Prognosis, 280 Treatment, 280 Operative, 280 Fibroid, 245 Clinical history, 250 Development, mode of, 246 Diagnosis, 252 Effects of, 248 Etiology of, 250 Locations of, 248 Prognosis, 254 Relations and structure, 245 Treatment of, curative, 259 Ammonium chloride, 259 Ergot, 259 Iodide of potash, 259 Palliative, 257 Tampons, 258 Tents, 258 Surgical, 266 Laparotomy, 269 Laparo-hysterectomy, 269 Sarcomatous, 271 Clinical history of, 271 Diagnosis, 272 Prognosis, 272 Treatment, 273

Tuning-fork in examination of the ear, 807

Turpentine as a cause of dermatitis medicamentosa, 604

Typhoid fever as a cause of inflammation of middle ear, 820 of ophthalmitis, 767 in pregnancy, 426

Typhus fever in pregnancy, 427

U.

Umbilical cord, the, as a local cause of abortion, 491

Unnatural hardness in congestion of kidney, 69

Ureters, diseases of, 67

Urethral caruncle, 403

Urethritis, acute, in women, 353

Uridrosis, 585

URINARY ORGANS, DISEASES OF THE-- Bladder, diseases of, 123 Acute cystitis, 126 Atony and paralysis, 133 Catarrh, 128 Chronic cystitis, 128 Hemorrhage from, 134 Inflammation, 123 Neuroses of, 132 New growths, 136 Paralysis and atony, 133 Chyluria, 114 Hæmaturia and hæmoglobinuria, 103 Malarial, 107 Malignant, 112 Kidneys, 19 Albuminuria, 34 Bright's disease, 72 Calculous pyelitis, 47 Chyluria, 114 Congestion, chronic, 69 Cysts, 63 Floating, 21 Malignant growths, 60 Nephritis, 82 Acute diffuse, 82 of scarlatina, 84 parenchymatous, 78 Chronic diffuse, 84 parenchymatous, 80 Parasites, 65 Perinephritis, 102 Polyuria, 27 Pyelitis, 53 Pyelo-nephritis, 99 Tuberculosis, 64

URINARY ORGANS IN WOMEN, DISEASES OF, 339 Functional Diseases, 349 Acute urethritis, 353 Diagnosis, 353 Treatment, 353 Nitrate of silver in, 353 Sulphate of zinc in, 353 Varieties of, 353 Circumscribed urethritis, 355 Dilatation of the urethra, 355 Description, 355 Diagnosis, 358 Etiology of, 357 Prognosis, 359 Symptomatology, 358 Treatment, 359 Alum in, 359 Excision in, 359 Tannic acid, 359 Dislocations of the urethra, 360 Description of, 360 Diagnosis of, 361 Etiology of, 361 Prognosis of, 361 Symptomatology, 361 Treatment of, 362 Inflammation of the urethral glands, 354 Description of, 354 Inversion of urethral mucous membrane, 362 Causes, 362 Prognosis, 362 Treatment, 362 Paralysis, 350 Invasion of, 351 Prognosis of, 351 Treatment of, 351 Electricity, 351 Strychnia, 351 Prolapsus of urethral mucous membrane, 362 Stricture at junction of urethra and bladder, 365 Description, 365 Morbid anatomy of, 365 Symptoms, 365 Treatment, 365 Stricture of the urethra, 363 Diagnosis, 364 Pathology, 363 Prognosis, 364 Symptomatology, 363 Treatment, 364 Incision in, 364 Use of dilators, 364 of urethrotome, 364 Subacute urethritis, 355 Organic Diseases, 339 Atrophy, 348 Symptoms and diagnosis, 348 Treatment of, 349 Cystitis, 341 Diagnosis, 344 Etiology, 341 Pathology, 341 Symptoms of, 343 Albuminuria in urine, 343 Nervous, 344 Pain, 343 Specific gravity of urine in, 343 Tenesmus, 343 Toxic, 344 Treatment, 345 Antiseptics in, 347 Borax and water in, 346 Diet, 345 Dover's powder in, 346 Milk diet in, 345 Morphia suppositories in, 346 Nitrate of silver in, 347 Hemorrhage, 340 Causes of, 340 Symptoms of, 340 Treatment of, 340 Hæmostatics in, 340 Hyperæmia, 339 Diagnosis of, 339 Etiology of, 339 Morbid anatomy of, 339 Symptoms of, 339 Treatment of, 339 Hypertrophy, 348 Diagnosis, 348 Etiology, 348 Symptoms, 348 Treatment, 348

Urticaria, 597 pigmentosa, 599

Use of trocar in treatment of ovarian cysts, 308 voice in examination of the ear, 807 watch in examinations of the ear, 807

Uterine axis, 148

Uterine fibroids in the diagnosis of cystic tumors of ovary, 306 mucosa as a local cause of abortion, 488 in early pregnancy, 476

Uterus, anteflexion of, 176 Definition of, 176 Diagnosis of, 178 Etiology of, 177 Pathology of, 177 Symptoms of, 178 Dysmenorrhoea as a, 178 Sterility as a, 178 Vesical, 178 Treatment of, 179 By rapid dilatation of cervix, 179 Sims's method of, 179 Ante-locations of, 153 Anteversion of, 174 Diagnosis of, 175 Etiology of, 174 Prognosis in, 175 Symptoms of, 175 Dragging sensation in, 175 Treatment of, 175 Medicated cotton pledgets in, 176 Pessaries in, 176 Ascent of, 153 Axis of, 148 Carcinoma of, 274 Descent of, 154

Uterus, diseases of--endometritis, acute, 460 Diagnosis, 461 Etiology of, 460 Pathological anatomy, 461 Prognosis, 461 Treatment, 461 Endometritis, chronic, 462 Chronic catarrh, 462 Diagnosis, 464 Dysmenorrhoea membranacea, 463 Etiology, 462 Pathological anatomy, 462 Prognosis, 464 Treatment, 464 Curative, 465 Local, 465 Prophylactic, 464 Metritis, acute, 447 Diagnosis, 449 Etiology, 447 Pathological anatomy, 448 Prognosis, 449 Symptoms, 448 Treatment, 449 Metritis, chronic, 450 Definition of, 450 Diagnosis, 456 Etiology, 450 Hyperæmia, 451 Lacerated cervix in the, 451 Subinvolution in the, 450 Pathological anatomy of, 452 Stages in the, 452 Physical signs, 454 Prognosis, 456 Symptoms, 453 Synonyms for, 450 Treatment, 457 General, 459 Ergot in the, 460 Local, 457 Alterations, 459 Castration, 459 Depletion, local, 458 Glycerin tampons, 458 Hot-water douche, 457 Operative, 459 Terminations, 456 Disorders of functions of, 182 Amenorrhoea, 183 Cause of, 184 Atrophy as a, 186 Chlorosis as a, 185 Exposure as a, 187 Psychical, 187 Pulmonary tuberculosis, 186 Diagnosis of, 186 Pathological conditions in, 185 Symptoms of, 187 Constipation as a, 189 Treatment of, 189 By apiol, 190 By electricity, 191 By permanganate of potash, 191 By rue and saffron, 190 By savin, 190 Dysmenorrhoea, 192 Diagnosis of, 194, 195 Prognosis, 197 Treatment of, 198 Menorrhagia, 200 Causes of, 201 Treatment of, 203 Displacement of, as a cause of disturbed vision, 757 Definition of, 150 Diagnosis of, 151 Nomenclature of, 150 Symptoms of, 151 Epithelioma of, 278 Examinations of, 151 Digital, 152 Left hand in, 152 Explorations of, 152 Specula in, 153 Use of sound in, 152 Fibrous tumors of, 245 Lateral flexions of, 174 Locations of, 153 Versions of, 174 Normal location of, 147 Movements of, 149 Supports of, 150 Prolapse, 154 Course of, 158 Degrees of, 154 Diagnosis of, 159 Etiology of, 154 Pathological anatomy of, 157 Prophylaxis of, 159 Symptoms of, 158 Acute vaginitis, 158 Bearing-down feeling, 158 Catarrh of bladder, 157 Cystocele, 158 Enlargement of cervix, 157 Erosion of cervix, 157 Pelvic peritonitis, 158 Rectocele, 158 Vesical irritation, 156 Treatment of, 161 Anterior elytrorrhaphy, 161 After-treatment in, 163 Performance of, 162 Methods of, 159 Perineorrhaphy, 163 Performance of, 164 Pessaries in, 160 Functions of, 160 Retroflexion, 166 Diagnosis of, 168 Etiology of, 166 Pathology, 166 Symptoms of, 167 Treatment of, 168 Bimanual replacement in, 170 Digital touch in, 168 Dry cupping in, 168 Pessaries in, 171 Danger in use of, 173 Reposition in, 171 Vaginal touch in, 168 Retro-locations, 153 Retroversion, 165 Course of, 166 Diagnosis of, 166 Etiology of, 166 History of, 166 Prognosis of, 166 Symptoms of, 167 Bearing-down feeling in, 166 Constipation in, 166 Treatment of, 166, 168 Bimanual replacement, 170 Sarcomatous tumors of, 271 Tumors of, see Tumors.

V.

Vagina, anatomy of, 367 Atresia of, 373, 376 Definition, 373 Hymenalis, 374 Cancer of, 382 Diagnosis of, 383 Treatment of, 383 Cicatrices, 380 Cystic tumors of, 381 Cystocele vaginalis, 377 Cysto-vaginal hernia, 377 Symptoms, 377 Diseases of, 367 Double, 380 Enterocele vaginalis, 378 Entero-vaginal hernia, 378 Treatment, 379 Fibrous tumors of, 381 Growths in, 381 Imperforate hymen, 374 Diagnosis, 374 Prognosis, 375 Symptoms, 374 Treatment, 375 Prolapsus of, 376 Definition, 376 Etiology, 377 Pathology, 377 Symptomatology and course, 377 Synonyms and classification, 376 Recto-vaginal hernia, 378 Retrocele vaginalis, 378 Sarcomatous tumors of, 381 Diagnosis, 382 Treatment of, 382

Vaginal douche in retroflexion of uterus, 168

Vaginismus, 383 Complications, 384 Course, 384 Diagnosis, 385 Duration, 384 Etiology, 384 Pathology, 385 Prognosis, 385 Symptomatology, 384 Termination, 384 Treatment of, 385 dilators in the, 386 systemic, 386

Vaginitis, 366 Acute, in prolapse of uterus, 158 Complications, 369 Course, 369 Decubitus in, 371 Definition of, 368 Diagnosis, 371 Duration, 369 Etiology of, 368 Pathology, 369 Prognosis, 371 Symptomatology, 369 Synonyms of, 368 Terminations, 369 Treatment, 371 Chloral in the, 372 Infections in the, 372 Irrigation in the, 372 Varieties of, 368

Varieties of acne, 641 of acute urethritis in women, 353 of atrophia cutis, 684 of calculous pyelitis, 47 of cysts of kidney, 63 of dermatitis herpetiformis, 612 of epithelioma, 707 of foreign bodies in the external ear, 816 of herpes simplex, 608 of ichthyosis, 666 of inflammation of bladder, 123 of leptus, 731 of lichen ruber, 623 of pessaries, 160 of psoriasis, 615 of pyelo-nephritis, 99 of oöphorectomy, 291 of parasites of kidney, 65 of pediculosis, 728 of pelvic hæmatocele, 241 of sarcomatous tumors of the uterus, 272 of scrofuloderma, 699 of seborrhoea, 587 of syphiloderma papulosum, 701 pustulosum, 703 vesiculosum, 702 of urticaria, 598 of vaginitis, 368 of verruca, 665 of vulvitis, 391

Variola as a cause of ophthalmitis, 761

Vegetable parasites in the external ear, 815

Verruca, 665

Versions of uterus, 165, 174

Vertigo as a symptom of diseases of kidneys in pregnancy, 418

Vesical irritation caused by prolapse of uterus, 156 symptoms of acquired anteflexion of uterus, 178

Vision, disturbed, caused by disease of the sexual organs, 755

Vitiligo, 677

Vomiting in pregnancy, 408

Vulva, anatomy of, 388 Diseases of, 388 Atresia of, 373 Cancer of, 402 Treatment, 402 Cysts of the canal of Nuck, 397 Definition, 397 Treatment, 398 Elephantiasis, 399 Definition, 399 Etiology, 399 Pathology, 399 Treatment, 400 Furuncles of the labia, 392 Definition, 392 Treatment of, 392 Nitrate of silver in, 392 Hæmatoma, 401 Definition of, 401 Diagnosis, 401 Etiology, 401 Symptoms, 401 Treatment, 401 Hydrocele in women, 397 Hypertrophy, 398 Treatment, 399 Phlegmonous inflammation of the labia majora, 391 Definition, 391 Diagnosis, 391 Symptomatology, 391 Treatment, 391 Pruritus vulvæ, 392 Course, 393 Definition, 392 Etiology, 392 Symptoms, 393 Treatment, 393 Pudendal hernia, 398 Definition, 398 Etiology, 398 Symptoms, 398 Treatment, 398 Urethral caruncle, 403 Definition of, 403 Diagnosis, 403 Etiology, 403 Pathology, 403 Symptoms, 403 Treatment, 403 Vulvitis, 389 Course, 389 Definition, 389 Duration, 389 Etiology, 389 Symptomatology, 389 Treatment of, 390 Lotions in the, 390 Varieties of, 391

W.

Washes in the treatment of pruritus, 713

Washing out of bladder in the treatment of pyelitis, 55

Water, hot, in the treatment of parametritis, 220

Whooping cough as a cause of inflammation of middle ear, 820

X.

Xanthoma, 681

Y.

Yellow fever as a cause of ophthalmitis, 767

END OF VOLUME IV.

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