numerous reports of heliotherapy being carried out in low altitudes. I have no statistics as to how

keys, and secured a diplococcus culturally identical with that of Laveran & Catrin, and states that

but from the small series of cases that I have treated with heliotherapy I feel encouraged to the extent that I would not dare to deny heliotherapy to a case of surgical tuberculosis if it could be accorded to it.

SOME AURAL COMPLICATIONS OF ACUTE EPIDEMIC PAROTITIS*

GEORGE C. ALBRIGHT, M.S., M.D., Iowa City Acute epidemic parotitis is one of the most common diseases of childhood and one which has long been regarded with little concern. Occurring in adults, however, its presence excites a little more apprehension because of the complications, which sometimes arise-chiefly orchitis or oophoritis. Aural complications of this disease are not common, yet occur in a sufficient percentage of cases to warrant our consideration. The aural complications which have been most frequently observed are (1) acute suppurative otitis media; (2) auditory neuritis, occurring either (a) through the meninges or (b) through the middle ear; (3) labyrinthitis. It will be my purpose to consider briefly the last two of these complications, particularly the last.

Before presenting this study may I note a few points regarding the disease itself, which will put us all on a common ground.

Etiology-Mumps is an acutely infectious and contagious disease whose etiological factor is still in dispute. Much work has been done to isolate a causative organism. Ollivier (1), in 1885, published the results of his researches which confirmed the work of Capitan & Charrin by which he concluded cocci, single and diplococci, were constantly present and probably the causative factor of mumps. Laveran & Catrin (2), in 1893, secured a diplococcus in sixty-seven out of ninety-two patients, by examining the parotid, and the spinal, pericardial and peritoneal fluid. Michaelis (3), in 1897, secured bacteria from Steno's duct, from the parotid, and in the blood. Cocci were also found. He believes the bacteria to be the etiological agent. Osler (4), in 1912, states "the virus is unknown" but in 1913 seems to accept the work of Laveran & Catrin as worthy of endorsement. Herb (5), in 1905, carried out extensive work in the Memorial Institute for Infectious Diseases, Chicago, using dogs and mon

*Presented at the Sixty-Ninth Annual Session, Iowa State Medical Society, Section Ophthalmology, Otology and RhinoLaryngology, Des Moines, May 12, 13, 14, 1920.

cause of mumps. Wollstein (6), in 1915, working at the Rockefeller Institute used cats, and by work apparently as painstaking as that of Herb arrived at the conclusion that the causative factor of mumps is a filterable blood borne virus, bacterially sterile by present cultural methods and ultra microscopic.

Period of Incubation-This is long, usually two to three weeks, sometimes as long as six (Osler & McCrae (7). It is important that this be kept in mind because some of the complications, the ones we are to consider, may arise before the appearance of the parotitis. The infection probably enters the parotid by way of Steno's duct, though there is evidence that it enters by way of the respiratory system, digestive system, and through the blood or lymph, to the parotids.

Nature of the Disease--Concerning the disease itself there is not much to be emphasized here. It is a diffuse infiltration of the parotid gland, with very little tendency to suppuration. Suppuration may occur, however, possibly due to a secondary invader.

Two views of the nature of the disease prevail -the distinction being more or less an academic one. First, that mumps is a general infection of which the parotitis and the so-called complications are merely separate and distinct manifestations. The predominance of certain localizations, i. e., parotid, testis, ovary, etc., is due to unusual susceptibility. This view is held by Combeau (8), Brunner (9), Leichenstern (10), Hubbard (11), Alt (12), Colin (13), and others. The second view is that the parotid is the original site of infection, and the affection of the other parts, or the complications, are metastatic in nature. So far as I have been able to learn the majority of internists today incline to this latter concept. With the establishment of the fact that the virus is blood borne (Ollivier, Laveran & Catrin, Michaelis, Herb, Wollstein), there is not really much difference between the two views.

That conditions strongly resembling clinical mumps in the human, with pathological changes in parotid gland and testis identical with those of mumps, can be produced by the injection of bacterially sterile blood serum of patient's ill with mumps into the parotid and testis of healthy laboratory animals has been definitely shown (Woelstein (6).

Complications-The important fact about the disease, which concerns us as otologists, is the

marked tendency to complications. The most common are, of course, orchitis and oophoritis. Mammitis, meningitis, neuritis, and labyrinthitis occur less frequently. Of these meningitis, auditory neuritis and labyrinthitis should interest us. At this time may I again mention the other aural complications-otitis media, serosa and suppurative, and note that these occur usually only when there is a suppurative process in the parotid. Meningitis, auditory neuritis and labyrinthitis occur when there is no suppuration present.

The clinical picture which we shall consider at some length, is relatively rare, i. e., sudden profound deafness, either unilateral or bilateral, appearing usually with a fairly definite chain of symptoms.

Frequency-Early literature on mumps and on ear diseases contain no reference to mumps deafness. Thus the work of von Rochard (14), 1750, von Dogny (15), 1828, von Leitzen (16), 1837, all dealing with epidemics of mumps in army garrisons with thousands of cases, do not mention deafness as one of the complications (Seligsohn (17). Kramer's (18) Text on Ear Diseases in 1863 contains no reference to mumps deafness. Vogel (19), writing on aural diseases in Ziemssen's cyclopedia, a year or two later, does not mention the condition. When Toynbee (20), in 1860, reported a case and gave us the first postmortem findings, and stated that the "poison of mumps is very often the source of complete deafness" he gave impetus to several similar observations. Hinton (21), 1874, placed mumps next to scarlet fever as a cause of deafness. Roosa (22), in 1881, in discussing two cases reported by Buck to the American Otological Congress, stated he had seen so many cases, that mumps "caused him great concern." Brunner's (23), rather caustic comment published in 1882 after Roosa's statement, asked that the profession be shown the "great frequency" alluded to by Roosa. Later, in 1883, Roosa (24), retracted his statement and reported only ten cases out of 5,000 ear cases studied. Dalby (25), in 1883 (Roosa), said that mumps deafness occurs in a very large number of cases. Buck (25), in reporting two cases regarded the condition as very rare. Seligsohn (27), also, in 1883, insisted that the condition is rare and questioned the broad statements made by the above men. Pierce (28), in 1885, collected forty cases seen by him in thirteen years of practice, but reports only four of these. Texier (29), in 1902, collected a series of thirty-four cases. Mygind (30), gives mumps as the cause of deaf-mutism in 0.3 per cent of cases in Saxony, and 0.5 per cent in America (Boot). Buerk

ner (31), in the Goettengen Clinic (Weinstein) gives mumps as the cause of labyrinthine deafness in 2 per cent of the cases. Lake (32), 1905, and Barr (33), ibid, state it is "frequent" but cite no statistics. Hubbard (34) 1910, estimates 3 to 5 per cent of all deaf mutes in United States as due to mumps. Radin (35), 1918, in 5,000 cases of mumps at Camp Wheeler reports twenty cases of ear troubles, all otitis media suppurativa, and none of labyrinthitis.

Since 1881 a number of cases have been reported and a few fairly comprehensive reviews of the subject published. Chief among these we would mention the articles by Buck, Roosa, Seligsohn, Pierce, Connor (36), Minor (37), Texier, Boot (38), Hubbard, and Weinstein (39).

The type of cases to which we wish to limit our discussion is well described by Boot. "Cases in which the labyrinth is involved in the course of mumps, not by a suppurative process, nor by the extension of a middle ear process to the labyrinth, nor by an extension of an inflammatory process in the vicinity of the ear, but apparently by metastases or by a primary localization of the disease. in the labyrinth."

Ths history of these cases is substantially as follows: At some time during an attack of mumps, the patient who may have had no previous ear trouble suddenly discovers that hearing in one or both ears is impaired, or may be suddenly gone, e. g., overnight. This may be the only symptom. In certain cases there is tinnitus, vertigo, nausea, and vomiting indicating involvement of the static labyrinth. After a varying period of time the accompanying symptoms subside, but as a rule the deafness persists. If bilateral deafness occurs in early childhood it usually results in deaf-mutism.

4

Cases of this type have been reported by the following authors: Roosa (24), six cases; Minor (37), Heilskov (40), Hubbard (11), Pierce (28), four cases each; Knapp (41), Moos (42), Alt (12), three cases each; Hodgson (43), Buck (26), Noyes (44), Tsakyroglous (45), Kipp (46), Lake (32), Crockett (47), Burnett (48), Dreyfuss (49), Willcutt (79), two cases each; Connor (36), Lemoine & Lannois (50), Seitz (51), Brunner (9), Field (52), Dalby (53), Pomeroy (54), Buerkner (31), Harlan (55), Foster (56), Kayser (57), Dempsey (58), Haug (59), Brieger (60), Urbantschitsch (61), Hail (62), Boot (38), Shambaugh (63), Cheatham (64), Gruening (65), Duel (66), Mauther (67), Haike (68), Jollye (69), Calmette (70), Moure (71), Seligsohn (17), Sewel (72), Weinstein (39), Wilson (73), Albright (74), one case each.

In all to date, so far as I am able to find, eightyone cases have been reported. The case I wish to report to you at this time makes eighty-two cases. The majority of these cases I have been able to find as originally reported. A few I have accepted as reported by writers in reviewing the subject. Grandinigo (34) (Hubbard), Yearsley (39 Weinstein), Barr (33), Alt (12), Baruich (75), and Bliss (76), each report cases of deafness due to mumps, but give no data on the findings.

Case Report-E. D., female, nineteen, teacher. Seen first May 31, 1918. Her family and previous medical history are excellent. In January, 1918, had bilateral mumps. Five days before appearance of parotitis her right ear suddenly felt as if "something had passed over it" and she noticed that the ear was deaf. There was tinnitus but no dizziness at the time. There was slight pain in the right ear three days later, only slight and for short time. On the fifth day of the deafness the parotitis appeared, at which time she was dizzy and nauseated but did not vomit. Dizziness worse when lying down. Tinnitus persisted. She felt always as though falling to right, did so in the night on attempting to walk in the dark. The dizziness lasted for ten to twelve days. When seen in May, 1918, examination showed: Hearing right 0. Drum slightly retracted, ossicles freely movable. Rinne negative (probably heard in the other ear). No air conduction. With Barany's apparatus in sound ear no tuning fork could be heard. A careful examination by Mr. C. C. Bunch, Research Associate in Psycho-physics of Otology in the University of Iowa, of the complete hearing range from sixteen double vibrations to 49,000 double vibrations showed total deafness, right, except for a tone island between 10,922 to 20,480 double vibrations.

The caloric test showed the right labyrinthine function impaired-water at 64 degrees for 90 seconds produced slight rotatory nystagmus and tendency to fall and past point to right. Prolonged ir

eyes made the dizziness so much worse that it was impossible to observe nystagmus, though nystagmoid movements could be seen beneath the lids. Upon forcing the lids open, the eyes were seen drawn clear over to the left, that is, toward the sound side. In about three hours the acute symptoms had subsided and the patient was able to go about as usual. Ex

amination the next day showed the deafness still

present, static labyrinth still active, but much less so than when the caloric was first done. No spontaneous nystagmus. Tinnitus still persisted.

April 16, 1920, she reported that there had been no dizziness since October, but that the deafness and tinnitus remained unchanged.

May 7, 1920, she had another very similar attack with similar findings, the attack lasted about three hours. This attack was followed on May 10, by a slight attack lasting two hours. No vomiting. A caloric on the right ear shows the reactions about the same as in October. A caloric left shows the labyrinth functioning. An examination on May 11. by Mr. Bunch, shows the tone island of May, 1918, changed. Now hearing the Galton whistle from 7,000 to 8,000 dv. and the Koenig cylinders from 12,000 to 36,000 dv.

An analysis of all the cases reported brings ou a few points of interest. Of the eighty-two cases forty-three are female, thirty-two male, and seven the sex not stated. Of the eighty-two cases. fifty-two are unilateral; right and left sides about equally divided; bilateral, thirteen; while in seventeen it is not stated whether unilateral or bilateral. The preponderance of unilateral cases is one source of gratification.

Thirty-four of the cases are in the decade between eleven and twenty years; thirteen below the age of ten. In a number the age is not stated.

The deafness appears at varying periods, from the first day of the mumps until the sixteenth day, usually about the fifth to eighth day. In only four cases, one reported by Heilskov (40), one

. nausea. A caloric on the left, or sound side, produced normal reactions in sixty seconds, including marked dizziness and nausea.

This case has remained under observation for nearly two years. In that time she has had several attacks of vertigo, more or less severe.

In some

there has been nausea and vomiting. In all except the last she has noted a tendency to fall to the right; if walking keeps bumping into people or objects at her right, and in two or three attacks has required support to keep from falling. In the last attack, October, 1919, she did not note the direction, but said it was not so definite as formerly. I saw her during this attack. She complained of great pain in her head, arms and legs. She was not comfortable in any position, but seemed best sitting with the head inclined forward about sixty degrees. Opening the

(37), and my own, did the deafness appear before the parotitis. In all but two, where stated, the onset was sudden, although in some cases this point was overlooked because being unilateral the deafness might not have been discovered if only the cochlear portion of the labyrinth was involved. Vertigo was noted in forty-nine cases, tinnitus in forty-six. Their presence is much more constant in the cases observed in later years, where the records are more complete. Earlier cases at times report a "staggering gait," but say nothing of dizziness or tinnitus.

Pathology-The site of the lesion and the nature of the pathology have been, in the absence of careful post-mortems, necessarily matters of dis

pute. So far Toynbee (20) has the only recorded case where the pathology was definitely determined post-mortem. He found hemorrhage into the labyrinth. With the refinement of labyrinthine tests that has come about the past few years more definite data will undoubtedly be collected. Auditory neuritis or acute exudative labyrinthitis, either serous or hemorrhagic, or both neuritis and labyrinthitis seem to be the most probable pathology. A few observers have considered the lesion wholly of the middle ear, but an analysis of the cases they present shows that the cases are not of the type under consideration-usually they are suppurative. Among those who regard auditory neuritis as the pathology we find Connor (36), Roosa (24), Buck (26), Politzer (77), Heilskov (40), Stein (78), and others. Some of these regard the neuritis as descending, i. e., from the meninges toward the labyrinth, while others consider the neuritis ascending, from the labyrinth toward the brain center. The great majority of later observers regard the labyrinth as the seat of the lesion. Buck (26), Vogel (19), Hinton (21), Foster (56), Hubbard (34), Harlan (55), H. Knapp (41), Moos (42), Brunner (9), Seitz (51), Toynbee (20), Alt (12), Minor (37), Willcutt (79), and Boot (38), are among those that favor the labyrinthine lesion. In my own case I am certain the lesion was undoubtedly labyrinthine.

The cases are divided into three classes from the standpoint of pathology:

(a.) Those in which the cochlear fibres only are affected. These cases note only sudden, complete loss of hearing. If unilateral, it may be some time after deafness really occurs before it is discovered. Tinnitus aurium is quite common. There is no pain. In my own case, an unusually intelligent young woman, at first the only symptom noted was as though some one had simply "passed something over the ear so she could not hear." Later the process extended to the static labyrinth producing the dizziness, staggering gait, nausea and vomiting, as reported above.

(b) Those in which the static labyrinth only is affected. These cases get all the symptoms of labyrinthitis, vertigo, staggering gait, tendency to fall toward the affected ear, tinnitus, nausea and vomiting. Recent cases may show nystagmus. The distressing symptoms usually subside in a variable period-from a few days to several weeks. Caloric. tests made after subsidence of acute symptoms show the static labyrinth to be dead or its function greatly ablated.

(c) Those in which both are affected. There

cases usually note first the symptoms of labyrinthitis, occasionally also the impairment of hearing, but more frequently this latter is not discovered until the acute labyrinthine symptoms subside. In the case just reported this order was reversed--the loss of hearing was noted first with only slight static labyrinthine symptoms, but later, after hearing was totally lost, static labyrinthine symptoms developed over a long period of time. The only possible explanation for the number of brief attacks of vertigo, nausea and vomiting from which the patient suffered, would be that the labyrinthitis, after the destruction of the cochlea, was temporarily circumscribed in the semi-circular canals. Each fresh extension of the process was marked by an exacerbation of symptoms, which subsided as soon as the extension was stopped and compensation established.

What is the nature of this labyrinthitis? In most cases evidently something acute, rapidly fulminating, reaching its peak in a short time. Coming as a complication of mumps-which is a rapidly swelling parotitis with little tendency to suppurate comparing it to the orchitis-again a rapid swelling with little tendency to suppurate, and followed by tendency to atrophy-the most obvious explanation is that here is a rapid serous exudative labyrinthitis, in some cases probably hemorrhagic, as in the case reported by Toynbee (20). If we consider the anatomy of the labyrinth-a delicate nervous structure within a membranous capsule, and this again enclosed in a dense bony capsule with only four points that can relieve the pressure-the two fenestræ, the saccus endolymphaticus and the internal auditory meatus, we can readily see how a small amount of exudate could cause serious trouble. A few cases recover, in these the amount of exudate is small-and it is probably serous. Reasoning by analogy from the known pathology in the testis following the acute inflammation, we may safely. assume that atrophy of the delicate nerve fibres in both cochlea and static labyrinth occurs.

Mode of Infection--So long as the exact etiological agent of mumps remains unknown or at least not agreed upon, there will be difference of opinion regarding the transmission of the virus from the parotid to the other organs affected. A brief review of these theories will be given. One theory was that of direct transplantation. This was evolved first to explain the occurrence of orchitis. The virus would travel from parotid to saliva, lips to hand, then to penis, up urethra and into the testis. In the ear this would occur by the virulent saliva working its way up the eustachian

tube to the middle ear, through the fenestra ovale into the vestibule and into the inner ear. Minor (37), Seligsohn (27), Cruveilhier (80) and Mosler (81) have championed this view.

Another theory is that of direct extension from the parotid, to the middle ear, thence to the internal ear by direct continuity of structure. Most of the cases considered as a basis for this theory were suppurative. Roosa (24), Seligsohn (27). Vogel (19), Connor (36), Juergens (82), and Ballenger (83) have endorsed this theory.

A third theory is that the infection travels from the parotid to the internal ear by way of the vessels or nerve sheaths, or through the fissure of Santorini a retrograde infection, depending upon direct anatomical connection. Some of

those who regard the nerve as the path of the infection consider that it travels along the sheath of the facial until it reaches the sheath of the eighth, and then in the eighth either sets up a neuritis of the trunk, or, descending, involves the terminal filaments in the labyrinth. Vogel (19), Politzer (77), Virchow (84), Eloy (85), Alt (12), and Buck (26), are among the proponents of this theory.

Still another theory is that in cases of labyrinthitis there may be a preceding meningitis of the base near the exit of the eighth, and the meningitis becomes a neuritis by direct extension. Cases of meningitis due to mumps have been reported, particularly by Kaunitz (86). Heilskov (1917) (40), proposes this latter theory.

The most widely accepted theory of the mode of involvement of the labyrinth, and the one that is accepted by the majority of those studying labyrinthine deafness, and the one that seems most logical in view of the nature of the disease itself, and the other complications, is that it is a purely metastatic lesion, blood borne. Moos (42), Brunner (9), Barr (33), Weinstein (39). Barnhill & Wales (87), Boot (38), Hubbard (11), Kaunitz (86), and Braun & Friesner (89), are among those who believe this to be the proper theory in most of the cases. Why the internal ear should be selected as one of the infrequent sites for the localization of a metastasis is no more settled than is the reason for the orchitis being so frequently right sided. Certain it is that the eighth nerve is the most vulnerable of the cranial

nerves.

Whether we accept the explanation of Moos (42) that metastasis occur in organs with "complicated, richly anastomosing circulation" or Hubbard's (11) theory that the virus is present in all the circulation, and that it produces symptoms only in those organs which are contained in a

more or less "unyielding capsule" is a matter of personal reasoning.

Prognosis-This is usually bad as regards recovery of hearing. The vertigo and nausea usually subside in a few days, but deafness usually is permanent. The limited number of cases seen by otologists early after the appearance of the ear symptoms with the consequent lack of opportunity to study the cases or to try treatment has contributed to the gloomy outlook. Cases are usually first seen by the family physician, and unfortunately the aural symptoms are too often overlooked or regarded in the wrong light, e. g., the nausea and vomiting have been ascribed by very recent observers as due to a testicular reflex, resulting from an orchitis.

Cases of deafness which have recovered are probably cases of slight serous labyrinthitis. In some of them the character of the treatment and the improvement resulting makes one doubt the diagnosis.

Treatment-First preventitive:

Since the

mumps, as a rule, precedes the ear complications such measures should be taken as are taken to light nutritious diet, free elimination. After the prevent metastasis from occurring bed rest, labyrinth is invaded treatment seems unavailing. In the earlier cases, the old reliable K. I. was given in full doses-and some cases noted as improved, but none cured. In these cases lues was not excluded. Pilocarpin, hypodermically, pushed by many-chiefly Dundas Grant (88), Sauther to the physiological limit has been recommended (90), Jollye (69), and Yearsley (39). The latter two report a case each as completely cured. More recent cases, in which more accurate localization of the lesion has been possible, have had pilocarpin tried, without any improvement.