Chapter L: Part II: , Showing Predominance of Malarial Element . . . . 617 (49)

The physical causes that give rise to the pains which have just been described likewise occasion the spasmodic and tetanoid phenomena that are so peculiar to this disease. In general terms, they are most marked in cases attended with inflammatory exudation, and least so when, instead of this lesion, there is only vascular congestion of the meninges of the spinal cord. But the rule is, of course, not absolute, for individuals are so differently constituted that one will remain impassive under an irritation that will throw another into convulsions. There is no doubt that spinal rigidity may be produced by mere congestion of the cord, and, on the other hand, that it may be absent even when plastic exudation is abundant. This symptom is, however, more than any other one, characteristic of the disease. It existed in the original epidemic at Geneva, attracted the attention of the earliest American observers of the disease, and elsewhere has marked a greater or a smaller proportion of the cases in every epidemic. It was described by such terms as these: "a drawing-back of the head;" "a corpse-like rigidity of the limbs;" "the form of tetanus called opisthotonos;" "spastic rigidity of the muscles of the lower jaw and the posterior muscles of the neck;" "rigidity of the posterior cervical muscles, retracting the head considerably backward." The historians of the disease in Europe are, if possible, still more emphatic in their elaborate descriptions of this phenomenon, and, on the Continent at least, it seems to have been more uniformly present than it was in Ireland or in this country. Tourdes, in describing the epidemic of 1842 at Strasburg, said: "The decubitus of the sick was distinguished by a backward flexion of the head and spine; most frequently the neck alone was affected, but sometimes the whole trunk was arched." And again: "The contraction often involved all of the extensor muscles of the spine, and the trunk formed an arch opening backward and resting upon the occiput and sacrum." In Ireland, Gordon says of a patient, "Her spine presented a most wonderful uniform curve concave backward; her head was also curved backward on the spine of the neck." During an epidemic at Birmingham in 1875 in one case "the retraction was so marked that a slough formed from the occiput pressing between the scapulæ."[23] In some cases rigid flexion of the body forward or laterally has been noticed. The rigidity persists, as a rule, until death, but sometimes ceases a short time before that event. If recovery takes place, this symptom gradually subsides, and disappears within a few days; but, on the other hand, more or less stiffness of the spine may last for several weeks. In one case it continued for more than two months, and in another until death on the forty-ninth day.

[Footnote 23: Hart, _St. Bart's Rep._, iv. 141.]

The same physical cause that occasions rigidity, when acting less intensely or when a special susceptibility of the nervous system exists, also excites clonic convulsions. They are oftenest observed in patients of the {810} age especially liable to spasmodic affections--in children before the completion of the first dentition. They vary in degree from twitching or subsultus affecting particular muscles, as of the eyes, the face, a limb, etc., to general epileptiform convulsions with loss of consciousness. They may be associated with paralysis, as where the two halves of the body are, the one convulsed and the other paralyzed. A case occurred in Dublin which "presented the very striking phenomenon of continued and violent convulsions during the whole of the brief course of the illness."[24] These convulsions, like others occurring at the commencement of acute diseases, are by no means always fatal, even when they are general. In the case of a robust adult convulsions occurred repeatedly during the first two days, and less frequently during the two following days, but the patient ultimately recovered.[25]

[Footnote 24: _Dublin Quart. Jour._, xlvi. 187.]

[Footnote 25: _Boston Med. and Surg. Jour._, Feb., 1884, p. 121.]

Paralysis, it may be inferred from the statements already made, is an incident of this disease, for an excess of the action causing tonic or clonic spasm must induce paralysis. Paralysis of an arm or leg or of the muscles of deglutition was long ago noticed among even the initial symptoms of the attack. In Dublin (1865) it was said of a patient, "All his members seemed to be paralyzed; he could move neither arms nor legs." Wunderlich describes the case of a man who "on the second day of the disease lost both sensibility and motility in the lower limbs and over the greater part of the trunk, while his left arm also was partially paralyzed." In another case complete paralysis of the right side occurred on the third day, the left side being rigid.[26] Baxa relates the case of a soldier in whom paralysis of the left side persisted after recovery from the disease,[27] and that of a woman in whom paralysis of the left lower limb continued along with right ciliary paralysis. Ptosis, strabismus, paralysis of the bladder and rectum, of the muscles of deglutition, and even general paralysis, have been observed. Aphasia also has been recorded by Hirsch and by Hayden.[28]

[Footnote 26: _Dublin Quart. Jour._, 1867, p. 431.]

[Footnote 27: _Wiener med. Presse_, No. 29, p. 715.]

[Footnote 28: _Dublin Quart. Jour._, xlvi. 187.]

The condition of the eyes and of vision in this disease is directly due to pressure of the exudation at the base of the brain upon the nerves and blood-vessels that supply these organs. One of the most striking peculiarities of the countenance of a patient at the beginning of an attack is the diffused and uniform redness of the conjunctivæ. In children it has a light tint, but a darker one in adults, and in some cases the eye becomes suffused with an extravasation of blood. The conditions of the pupil are also very peculiar. Very long ago it was observed to undergo sudden changes from contraction to dilatation, or the reverse. Dilatation is, however, its ordinary condition, especially in the fully-formed attack. Very often the pupils of the two eyes are in opposite states. In cases of long duration, with great exhaustion, they are almost invariably dilated. Photophobia is not uncommon, and oscillation of the pupils and spasmodic movements of the eyeball have frequently been observed. Strabismus is a symptom of very ordinary occurrence, particularly when other paralytic or spasmodic phenomena exist. It may be convergent or divergent, but most commonly is the former, and may be either a transient or a {811} permanent symptom. Like other individual symptoms, it may be present rarely or frequently in a particular epidemic.

Blindness has been repeatedly observed. At first it seemed to be noticed as a transient symptom only. Fish (1809) states that it was sometimes the first deviation from health, and then was followed by paralytic spinal symptoms. He also observed that sight was sometimes restored in a few hours, and in no case did he know it to be permanently lost. American as well as European physicians, however, have met with many cases in which the sight was seriously and permanently impaired or altogether destroyed. In 1873 the changes affecting the eye were more fully and accurately described, especially those which tend to the structural injury of the organ. The abnormal appearances included cloudiness of the media, discoloration of the iris, irregularity of the pupils, and their obstruction with exudate. In exceptional cases the cornea ulcerated, and the globe collapsed after losing its contents. Ordinarily, however, says Lewis, "no ulceration occurs, and as the patient convalesces the oedema of the lids, the hyperæmia of the conjunctiva, the cloudiness of the cornea and of the humors gradually abate, and the exudation in the pupils is absorbed. The iris bulges forward, and the deep tissues of the eye, viewed through the vitreous humor, which had a dusky color from hyperæmia, now present a dull white color. The lens itself, at first transparent, after a while becomes cataractous, and sight is lost totally and for ever."

Impairment or loss of hearing has been occasionally observed during the successive epidemics of this disease, even from the beginning of its history, and it was early noticed that the symptom was often quite independent of any cognizable lesion of the ear itself. It was also observed that the sense of smell sometimes became impaired or was lost at the same time with that of hearing. More recently, Collins reported a case in which the patient lost the sight of one eye and became permanently deaf in both ears. Knapp states that in all of thirty-one cases examined by him the deafness was bilateral, and, with two exceptions of faint perception of sound, complete. Among twenty-nine cases of total deafness only one seemed to give some evidence of hearing afterward.[29] This surgeon holds that the deafness results from a purulent inflammation of the labyrinth, and his judgment has been confirmed by Keller and Lucas. When the impairment of hearing occurs simultaneously, or nearly so, in both ears, it is probable that the chief cause of the deafness is the pressure of the plastic exudation in which the auditory nerve is imbedded. Such deafness is rarely permanent. When the loss of hearing, whether complete or partial, does not improve, there is reason to believe that the internal ear has suffered great and incurable changes of structure. Sometimes this follows a distinct attack of suppurative inflammation of the middle ear; but as complete and permanent deafness sometimes occurs without being preceded by any such affection, it must be inferred that atrophic changes have taken place in some portion of the nervous apparatus of hearing. It is stated by Moos that of sixty-four cases of recovery from cerebro-spinal meningitis, which showed disturbance of hearing as a sequel, one-half manifested in addition a more less disordered equilibrium. Of these twenty-nine were totally deaf on both sides, two totally deaf on one and hard of hearing on the other side, and one case had merely {812} impaired hearing in both ears. The disturbance of locomotion had existed for periods varying from three weeks to five years from the inception of the disease, and was chiefly characterized by a staggering or waddling gait.[30] In the deaf-mute institutions at Bamberg and Nürnberg it is said that out of 91 pupils, 80 owed their infirmity to this disease (Ziemssen). Salamo states that some awake out of sleep totally deaf, and remain so for a long time, or, it may be, permanently (Moos).

[Footnote 29: Smith, _loc. cit._]

[Footnote 30: _Mening. Cerebro-spinal epid._, p. 11.]

The expression of countenance in this disease is peculiar. When the pain in the head is severe and paroxysmal the features are apt to be violently distorted; when it is more persistent the face assumes a fixed or rigid expression, or is at the same time dull, particularly after a long continuance of the pain. In the apoplectic form the expression may be set and stupid, but the features have neither the dark, dull, swollen, and duskily-flushed aspect of typhus, nor the languid, sleepy expression, and circumscribed flush on the cheek which are so characteristic of typhoid fever. Except during absolute insensibility in rapidly fatal cases there is a look of greater intelligence than belongs to either of the diseases mentioned. Indeed, in the beginning of the attack in regular cases the distinctive facies presents pale and sunken features, with paleness of the skin over the whole body.

Delirium in this disease exhibits a great many degrees and varieties. It may occur among the earliest symptoms in certain rapid cases not of the congestive type, but is more apt to arise on the second or third day in those more typically developed. It may be mild, reasoning, hysterical, or maniacal, or it may change from one to another of these forms during the same attack. Fish states that it is apt to be violent if it comes on at the commencement of the illness, but that when it begins at a later period it is milder, and sometimes playful, the patient being sociable and humorous. All good observers have furnished similar descriptions of this symptom; some have added that the mental condition is often desponding and apprehensive, and others that certain patients remain sombre and silent; and it sometimes happens that the delirium comes on abruptly, as when a patient "woke suddenly in the middle of the night and began to hum tunes, to fancy that people were conversing with him," etc. (Gordon).

Coma is met with sooner or later in nearly all fatal cases, but rarely in a marked degree until the approach of death. If anything is surprising in epidemic meningitis, it is the absence of that deep and prolonged stupor that characterizes the typhoid state, notwithstanding the pressure of the exudation upon the brain in most cases, and in others such a profound alteration of the blood that it exudes through the tissues as water passes through a porous body. Another striking phenomenon of the disease is that the patient after recovery has generally a complete oblivion of all that happened to him between the beginning of the attack and convalescence. This is true even of cases in which the brain symptoms are far from being conspicuous.

Another symptom closely related to the local lesion and the blood-change in this disease is vertigo. As originally described by Miner in 1823, it occurred from the very commencement of the attack, and was even then regarded as denoting a deficient supply of the blood to the {813} brain, so that when the patient rose to an erect posture it was felt along with uneasiness in the stomach, acceleration of the pulse, dimness of sight, nausea, and fainting. Tourdes, speaking of it as it occurred in the Strasburg epidemic, says that it confused the mind and rendered walking impossible. In two cases patients were seized with a giddiness which compelled them to whirl around, when they fell and did not rise again. According to Moos (1881) unilateral affections of the labyrinth give rise to vertigo, and bilateral lesions to a staggering gait. Bilateral hemorrhage or acute suppuration of the ampullar terminations of the auditory nerve occasions paralysis and staggering. Children, and those who at the same time have the sight impaired, are apt to remain affected for a long time. Otherwise, prolonged and systematic muscular exercise may remove the tottering walk.

To the same causes must doubtless be attributed the debility which is so early and so conspicuous a symptom in this disease, and which gave it one of the names, typhus syncopalis, by which it was first known in this country. It was manifested by the vertigo already noticed, by a sense of sinking in the epigastrium, by a quick, frequent, feeble, and irregular pulse, and by a sudden and extreme loss of muscular power, so that the patient found himself unable to raise his hand before he was sensible of being ill. This state of asthenia is conspicuous throughout the whole of the disease, and is the immediate cause of the slow and irregular convalescence which is characteristic of it.

Of the symptoms peculiar to the digestive apparatus hardly any belong to it directly. They are nearly all the effect of reflex influences. The condition of the tongue is for the most part quite unlike that which belongs to the typhoid state. The fuliginous condition of the tongue, gums, cheeks, and lips which characterizes that state is seldom met with in epidemic meningitis. The older writers agreed that even when the tongue does grow dry and brown the condition is not of long continuance, and later observers have confirmed their statements. Thus, J. L. Smith (1872) says, "Occasionally, in cases attended with great prostration, the fur of the tongue is dry and brown, but only for a few days, when the moist whitish fur succeeds." We have generally found it moist, whitish in the centre and at the tip and edges.

Nausea and vomiting are very constant among the initial symptoms of the disease, and, as already pointed out, are due to irritation of the cerebro-spinal ganglia. Very often the vomiting is not preceded by nausea, and is brought on by the patient's raising himself, etc. The stomach itself undergoes no change. Both symptoms are usually accompanied by faintness or giddiness, and are more decided in the initial than in the later stages of the attack. The matters vomited, varying with the contents of the stomach and the urgency and duration of the symptom, consist of ingesta, mucus, serum, or bile, and in some grave cases of a dark grumous matter taken to be altered blood. In some epidemics, apparently, more than in others, this symptom is very distressing, as it was at Birmingham in 1875.[31] The inability of the stomach to retain food necessarily leads to a rapid wasting of the flesh, which is aggravated by the patient's suffering, restlessness, and want of sleep. Nevertheless, no sooner is the vomiting appeased than a desire for food is felt, and when {814} it is retained it generally undergoes digestion. Indeed, in no other disease is the return of a good appetite and digestion so prompt and complete. It is true that the recovery of flesh and strength is not always in proportion to the appetite. As might be expected in a disease in which fever plays so subordinate a part, there is seldom urgent thirst. But epidemics differ in this as in so many other respects. In that which we witnessed in the Philadelphia Hospital in 1866-67 the patients were clamorous for liquids. Constipation is the rule among patients with this disease, as, indeed, might naturally be expected, for no lesion affects the bowels and little or no food is retained by the stomach. Yet in a few cases diarrhoea accompanies persistent vomiting.

[Footnote 31: Hart, _St. Bart's Rep._, xii. 112.]

The fauces appear to have been more or less inflamed in some epidemics; swelling of the parotid glands is an occasional occurrence, and sometimes they undergo suppuration. Aphthæ have also been met with.

The secretion of urine is not affected in any uniform manner. Sometimes it is diminished and sometimes increased in quantity. The latter symptom has occasionally long survived the disease. It retains its normal acidity. In rare cases either albumen or sugar has been detected; the former may have been due to the action of blisters of cantharides used in the treatment of the disease.

One of the most curious and unintelligible phenomena occasionally met with in this disease is a peculiar affection of the joints, which first was observed in this country. Jackson (1810 and 1813) wrote: "In some cases swellings have occurred in the joints and limbs. They have been very sore to the touch, and their appearance has been compared to that of the gout. The parts so affected feel as if they had been bruised. These swellings arise on the smaller as well as on the larger joints, and are often of a purple color." So Collins[32] reports: "The joints sometimes become swollen, red, and tender; at other times red and painful without any swelling; while, again, intense pain and rapid enlargement from effusion have occurred unattended with redness. The joints most usually attacked are the knee, elbow, wrist, and the smaller articulations of the fingers and toes." In an epidemic which occurred in Greece in 1869 articular swellings similar to those of inflammatory rheumatism were observed.[33] These descriptions, which apply to some cases in most epidemics, are of more than casual interest, for they demonstrate conclusively, as we think, the truth which the whole history of the disease confirms--viz. that it is a systemic and not a local affection, and is dependent for its existence upon a specific poison which is absolutely unlike every other morbid poison known to pathology.

[Footnote 32: _Dublin Quart. Jour._, Aug., 1868, p. 170.]

[Footnote 33: _Archives générales de med._, Mai, 1883, p. 622.]

The act of respiration is variously modified in this disease, as might, indeed, be expected from the seat and nature of the cerebro-spinal lesions. It is sighing, labored, and interrupted. Burdon-Sanderson describes its differences from the so-called Cheyne-Stokes respiration; it is, he says, "marked by a slow, labored inspiration, followed by a quick expiration and a long pause." When opisthotonos is very great and persistent, it necessarily interferes with the dilatation of the lungs, and leads to oedema of those organs, and even to sanguineous effusions into them. {815} Pneumonia is not an unusual complication of the disease when it prevails in cold weather.

The distinguishing characters of the pulse are diminished force and volume, and a tone so much impaired that slight causes produce extreme variations in its rate and rhythm. If the disease be a fever, as is by some maintained, then it is the only fever in which the pulse-rate is often far below the normal, and at the same time neither full nor tense, unless transiently and in altogether exceptional cases. In no other disease attended with inflammation do the rate and quality of the pulse vary so greatly within short intervals. It may be said, in general terms, to be variable in rate and strength even in the most sthenic cases of the disease, and in those which tend to a fatal issue to be small, thready, weak, intermittent, or imperceptible for a longer or shorter time before death. It is no uncommon thing for the pulse-rate at the beginning of an attack to fall as low as 40, or even 27, and afterward rise to 120 or even more, in a minute, without necessarily indicating a fatal issue. Muscular exertion, rising from a recumbent posture, etc., will sometimes double its frequency, besides producing irregularity. Read, describing the pulse as he observed it in Boston in 1873-74, speaks of cases in which "both the rhythm and the force of the beats are entirely destroyed; ... one moment, while beating very fast, it will suddenly drop to a much lower rate.... These conditions also may outlast apparent convalescence." Some fatal cases are attended by distressing palpitations of the heart.

Nothing is more remarkable in the early histories of this affection than their unanimous statement that it is not distinguished by a febrile temperature. It is true that the observers of those days had not the advantage of using clinical thermometers, but they were too nearly agreed in their judgments and harmonious in their descriptions to permit any serious doubt of the substantial accuracy of their conclusions, which were expressed in such terms as these: "A diminution of heat may be considered as among this most striking symptoms of this disease" (Strong); or, "the temperature never exceeded the standard of health in more than three or four cases, ... and a great majority of the patients had no fever at all" (Miner); or, again, "A high febrile movement took place only in a limited number" (Gilchrist); or, "The heat of the surface was less in all cases than is usually observed in acute diseases" (Jenks). It will be observed that these statements, and very many others which agree with them, were founded upon the perception of the patients' temperature by the hand, which was of course applied to the most accessible parts of the body--the face, neck, arms, and hands--but they have more real value and significance than the more recent measurements taken in the mouth, axilla, rectum, or vagina, for we know that, however valuable the temperatures of these parts may be for comparative studies, they do not really indicate the condition of the individual who presents them. It is a familiar fact that the difference of temperature in cholera when taken in the rectum and the axilla may be 4° F., or even more than this.

Since the thermometer has been used in the study of epidemic meningitis greater accuracy of results has been attained, and yet the general statements of the earlier observers have been confirmed. Thus, Githens has shown that the temperature of the body in this disease is lower than that recorded of any other fever or inflammatory affection; the average, {816} indeed, of his cases was lower by four or five degrees than that of typhus or typhoid fever, pneumonia, etc. In 2 cases only did the thermometer in the axilla reach 105°. The highest temperature in 15 cases was between 104° and 105°; in 12, between 103° and 104°; in 7, between 102° and 103°; in 6, between 101° and 102°; and in 2 it was below 100°.[34] Tourdes, Niemeyer, and others have noted the slight rise of temperature during the first and second days of the attack, and Wunderlich found fever of very unequal degrees and with very variable maxima, but the highest temperatures were observed by him as well as others in fatal cases and immediately before death. In one instance it reached 107.5° F. Burdon-Sanderson and others have found that an increased temperature always attended exacerbations of pain. Von Ziemssen gives the average temperature as varying from 100.4° to 103° F., but with variations between higher and lower points, and particularly notes the persistence of a normal temperature while the other symptoms are undergoing a variety of changes, as well as the fact that, unlike other febrile affections, this disease has no representative temperature curve. In his clinical observations Hart found for several successive days as much as six degrees of difference between the morning and evening temperatures. A morning rise for several days was noticed in four cases, and usually there was no relation between the pulse and the temperature, nor any uniformly between the temperature and the gravity of the attack.[35] But not rarely it has been noticed that the daily exacerbations, if any, did not occur in the afternoon, but with great irregularity, so that the maxima and minima might occur on successive days and at the same hour of the day. Dr. J. L. Smith, whose thermometric observations in this disease seem to have been carefully made, used the thermometer in the rectum, and thus obtained temperatures higher that the average of other observations, such as 105.4/6° to 107.2/6° in several cases. Yet he found the fluctuations of rectal temperature remarkable, though less so than the surface temperature, of which he states that sometimes it rose above or fell below the normal standard several times in the course of the same day.

[Footnote 34: _Amer. Jour. of Med. Sci._, July, 1867, p. 38.]

[Footnote 35: _St. Bart's Reports_, xii. 112.]

Nothing can be more irregular, uncertain, or various than the eruptions and other cutaneous symptoms that have been met with in this disease. When it first appeared in New England a large proportion of the cases, and especially of the grave cases, exhibited petechial eruptions and ecchymotic spots, whence the disease presently received the name of spotted fever. Yet even then, North and the other historians of its epidemics were careful to state that spots on the skin were by no means characteristic of the disease, and very often were not present at all, especially in cases that terminated favorably. Woodward, for example, wrote (1808): "An eruption on the skin so seldom appeared that it could no longer be considered a characteristic symptom of the disease." In various American local epidemics an eruption of some kind seems to have existed in about one-half of the cases. In one that we observed in the Philadelphia Hospital no eruption whatever was observed in thirty-seven out of ninety-eight cases. In the epidemic at Chicago in 1872, N. S. Davis says:[36] "About one-third of the cases presented some red erythematous spots" between the third and the seventh day. In mild cases they were few and {817} bright red; in grave cases, darker and larger, with some swelling of the skin; and in the worst cases, purple spots one or two or more inches in diameter. In that of Louisville,[37] Larrabie states that the eruption "was generally herpetic in its character, and accompanied by sudamina; but in several instances an urticarious eruption suddenly appeared and disappeared." Nothing is said of petechiæ or ecchymoses. In the New York epidemic of 1873[38] the skin in grave cases presented dusky mottlings, especially when the animal temperature was reduced; also a punctated red eruption, bluish spots a few lines in diameter, and large patches of the same color. Herpes also was common. It is chiefly in cases of a malignant type and rapid and fatal course that ecchymoses have been observed. Of this statement illustrations will be given in the paragraph relating to the duration of the disease.

[Footnote 36: _Louisville Med. Jour._, June, 1872, p. 705.]

[Footnote 37: _Louisville Med. Jour._, Dec., 1872, p. 782.]

[Footnote 38: _Amer. Jour. of Med. Sci._, Oct., 1873, p. 329.]

In continental European epidemics of meningitis the proportion of cases in which a general eruption existed seems to have been smaller than it was in this country. In the Geneva epidemic of 1805 a considerable number of cases at the point of death presented purplish spots, some earlier than this, and some after death only. In the Neapolitan epidemic of 1833, and in that which occurred in Dublin in 1867-68, ecchymoses were often present, and in a very marked degree. Stokes and Banks mention that in some rare instances the spots ran together and coalesced over some portions of the body, so as to cover a large extent of the skin and render it completely black, as though it were wrapped in some dark shroud. The entire right arm and half of the right side of the chest in one case, and in the other the whole of the lower portion of one leg and foot, were thus affected.[39] In Strasburg, on the other hand, only three cases of petechiæ were observed by Tourdes; at Rochefort and Versailles, in 1839, they were rarely noticed; at Gibraltar, in 1844, they do not seem to have been observed; in 1848-49, at the Val de Grâce Hospital (Paris), they appear not to have attracted attention; and at Petit Bourg they were not noticed, although the state of the skin was fully described. In Prussia, in 1865, neither Burdon-Sanderson nor Wunderlich mentions petechiæ or vibices as occurring during life; and Hirsch, after noting their occasional presence, is obliged to draw upon American authors for an account of them.

[Footnote 39: _Dublin Quart. Jour._, xlvi. 199.]

Of the eruptions other than petechiæ and ecchymoses, several of which have already been mentioned, it is necessary to take some notice here. They are, chiefly, and in general terms, exanthems, including erythema, roseola, and urticaria, and in addition herpes, particularly of the lips. The last has no special relation to this affection, as it is met with in almost every febrile disease, but it has sometimes extended to the whole face in this one. The former may be connected pathologically either with the altered condition of the blood or with the irritation produced by the exudation in the spinal nervous centres. They have frequently been compared to measles and to scarlatina, but sometimes they have assumed the form of bullæ. Thus, in the case of a child four years old, described by Grimshaw,[40] an eruption of pemphigus occurred over the whole body. Jackson long before had mentioned, as one of the eruptions belonging to this disease, "large bullæ, as if produced by cantharides." Jenks {818} described "large elevated spots of a very dark color, presenting outside of the dark color a blistered appearance." In some cases gangrene of the skin has been observed when the spots have been exceptionally dark, and occasionally has been produced by pressure.

[Footnote 40: _Jour. of Cutaneous Med._, ii. 37.]

The cause of death in many of the more rapid cases is coma, which is often preceded by convulsions, especially in children; but in many others, even when attended with all the marks of dissolution of the blood, consciousness may be but slightly impaired until the actual imminence of death. In many other cases, which are fatal in the midst of an attack with spinal symptoms, death is due to asphyxia, partly owing to pressure on the medulla oblongata, and partly to the interference with the respiratory act due to this pressure, and occasioning excessive bronchial secretion. Again, death may occur through a gradual exhaustion of the powers of life, without marked spasm, blood-change, or complication. In these cases also the intelligence remains unimpaired almost until the moment of dissolution. Death is not very rarely due to pneumonia, and when the disease is greatly prolonged or the convalescence from it is imperfect a fatal termination by dropsy of the brain is still among its dangers.

Hirsch once declared that the duration of epidemic meningitis "is between a few hours and several months," and, however hyperbolical the phrase may seem, it is quite accurate. Such inequalities are more characteristic of acute blood diseases than of inflammations, and in this case the coexistence of elements of both kinds doubtless accounts for the extreme irregularity of the symptoms and duration of the attack. The early American writers insisted strongly on this as a characteristic feature of the disease. They record an unusually large proportion of cases that were fatal within the first day, and even after an illness of five hours, although they agree that the most usual date of death was between the fourth and seventh days--a result that has been confirmed by subsequent observation. Dr. N. S. Davis gives the duration of the disease, as seen by him, as between twenty hours and twenty-eight days. Out of 469 fatal cases in the city of New York in 1872, 334 are said to have terminated within eleven days, and of this number 270 were fatal in the first six days of the attack, including 52 who died on the first day, and 51 in from one to two days. It is perhaps worthy of note that while from the eleventh to the fourteenth day only 11 deaths occurred, 20 took place on the fourteenth and fifteenth; and while from the fifteenth to the twenty-first day only 16 died, yet from the twenty-first to the twenty-second 12 deaths were reported. This would seem to indicate a peculiar danger on the days represented by multiples of seven. Of cases that recover, the duration is even more indefinite than that of fatal cases, owing to complications that occur in many, and especially such as involve the cerebro-spinal centres. When death takes place within a few hours it usually, if not always, is attended with symptoms that denote a disorganization of the blood. In 1864 we attended a young man previously in perfect health, but who died in twenty-one hours after the first seizure. His mind was unclouded throughout his brief but fatal illness. Within seven hours of death a purpurous discoloration of the skin began, and about an hour before that event the surface everywhere assumed a dusky hue. The forearms and hands were almost uniformly purple and the face turgid; many ecchymotic spots on the trunk and lower limbs were nearly black and measured {819} one or two inches in diameter.[41] In the case of a child of five years death in convulsions took place after an illness of ten hours, the skin presenting purpurous spots, some of them very large and of a deep bluish livid hue. On post-mortem examination there was not the slightest appearance of any meningeal lesion, except a few dark spots like sanguineous effusion under the arachnoid. The heart was full of dark blood in a semi-coagulated state, and the white corpuscles were three times as numerous as the red.[42] A case is reported by Gordon[43] in which the entire duration of the illness until death was five hours. This is probably the shortest case on record. A lady aged twenty-two years died in sixteen hours, the skin covered with livid ecchymoses, some of them measuring an inch or an inch and a half in diameter.[44]

[Footnote 41: _Amer. Jour. of Med. Sci._, July, 1864, p. 133.]

[Footnote 42: _Dublin Quart. Jour._, 1867, ii. 441.]

[Footnote 43: _Loc. cit._]

[Footnote 44: _Med. Press and Circular_, May, 1866. For other cases see _ibid._, pp. 296, 298-300.]

The character of the convalescence from epidemic meningitis must evidently be affected by the causes that determine its duration, the grade of the disease, the development and extent of the lesions, etc.; but it is certain that, except in those imperfect and, as it were, shadowy cases which denote a very slight action of the morbid cause, its subjects do not recover rapidly. The essential lesion of the fully-formed disease requires time for its removal, just as in typhoid fever the intestinal ulcers are often slow of healing, and hence become a cause of tardy recovery and even of unlooked-for death. The convalescence, then, from the disease we are now studying is slow and irregular, is attended often with debility and emaciation, and sometimes with persistent headache, neuralgia, convulsions, stiffness of the neck and pain in moving it, hyperæsthesia of portions of the skin, palpitation of the heart, dyspepsia, etc. Relapses are very far from being uncommon.

Among the causes of tardy convalescence in this disease are those lesions and disorders which may be embraced by the term sequelæ. Impaired vision, due to various affections of the eyes, has already been considered among the symptoms proper of the disease, but they are not infrequently developed after the acute attack has subsided. Thus, in a case reported by Larrabie:[45] "Just as convalescence seemed beginning the left eye became affected in all its parts, with entire loss of vision and also complete deafness. After a short remission hydrencephaloid symptoms appeared, followed by the same changes in the hitherto sound eye, complete blindness and deafness, general cachexia and marasmus, rigid flexion of the right limbs, and death by exhaustion at the end of sixteen weeks." The impairment of hearing, which also was described as a symptom of the acute attack, is apt to become more marked after the acute stage has passed by, and, as before stated, is very often permanent. Occurring in young children, it then involves deaf-mutism. It is in many cases associated with defective vision, weakness or loss of memory, mania, impairment of intelligence, persistent pains in the head or chronic hydrocephalus. Sometimes to one or more of these symptoms is added more or less general paresis or complete paralysis. Southhall[46] mentions the case of a child two years old whose attack was followed by incomplete paralysis, and death at the end of eight months with softening {820} of the brain. Gordon thus describes the conclusion of a case: "The man has gradually passed into a state of almost organic life; he eats, drinks, and sleeps well; he passes solid feces and urine without giving any notice, yet, evidently, not unconsciously; ... he seems to understand, but cannot answer; ... he can draw up his legs and arms, but he cannot use his hands at all." Hirsch has remarked that disorders of speech are met with, due apparently to an inability to articulate certain sounds. Von Ziemssen regards chronic hydrocephalus as not a rare consequence of epidemic meningitis, and as one not absolutely or immediately fatal. Its symptoms include severe paroxysmal pain in the head or neck or extremities, with vomiting, loss of consciousness, convulsions, and involuntary evacuation of excrements. Between the paroxysms, which sometimes occur periodically, the patient generally suffers from neuralgic pains, hyperæsthesia, and various motor and even mental disorders; but in other cases the intervals are free, or nearly so, from all morbid manifestations. Davis (1872) and many others speak of severe neuralgic pains following this disease; according to Dr. D., they are most frequent at the heads of the gastrocnemii muscles, in the abdomen, and the head; a very fretful disposition, variable appetite, and disturbed sleep are often observed. Relapses have been noticed in almost all the epidemics, and it seems probable that they are often due to the influence of accidental exciting causes, mental or physical, in renewing the inflammation around the cerebro-spinal lesions. Miner (1825) remarked that they were most apt to occur within the first week, but that when the disease had once run its course there were very few relapses during convalescence. But, he adds, there were several repeated attacks after the most perfect recovery, and several of the patients had had the disease the preceding year.

[Footnote 45: _Richmond Journal of Med._, Dec., 1872, p. 779.]

[Footnote 46: _Ibid._, Aug., 1872, p. 141.]

Like other epidemic diseases, meningitis presents itself with every possible degree of gravity between that of a slight indisposition and that of a malignant and deadly malady. The mortality in a number of epidemics compared by Hirsch varied between 20 per cent. and 75 per cent. It changes with the locality. Thus, nearly at the same time that the death-rate from this disease in Massachusetts was 61 per cent., it was but 33 per cent. in the Philadelphia Hospital. In 1872 the whole number of deaths caused by it in Philadelphia was 133, while at St. John's College, Little Rock, Ark., 21 cases out of 29 were fatal (Southhall). It differs, also, at different periods; for while ten epidemics in various places, occurring between 1838 and 1848, presented an average mortality of 70 per cent., a similar number, occurring between 1855 and 1865, gave an average mortality of only 30 per cent. It must, however, be confessed that such statistics cannot be relied upon as accurate, for in private practice many cases occur that are never reported unless they end fatally.

MORBID ANATOMY.--The lesions found after death from epidemic meningitis consist essentially of congestion or inflammation of the cerebro-spinal meninges, but they also include in many cases hemorrhage, serous effusion, plastic exudation, and tissue-changes in the brain and spinal marrow, and in many other cases an impaired constitution of the blood. As the signs of the latter, and not the former, alterations are met with in the more malignant cases, it is evident that, looking at the disease as a {821} whole, it must involve a toxic element of whose operation the various post-mortem lesions are only effects. These lesions, on the whole, vary with the type of the disease, and also with its duration, but some are chiefly met with in cases of a malignant and others in cases of an inflammatory type.

The exterior of the body after death in the early stages of this disease almost always presents the marks of transudation of the contents of the blood-vessels. The dependent parts of the body exhibit large livid patches or a uniform discoloration of the same hue. In acute cases the muscles are more deeply colored than natural, and when the attack is prolonged they are said to have their cohesion impaired by fatty degeneration. Congestion of the brain is an unfailing accompaniment of the first stage of the disease; its blood-vessels are all distended with dark blood; the sinuses of the dura mater are usually filled with coagula of the same hue, though sometimes very dense. Serum abounds in the arachnoid cavity and in the ventricles of the brain; it may be clear or milky, and sometimes it is quite purulent. It is alleged by one reporter that no less than three pints of turbid serum escaped in a case in which, however, death did not occur until the thirty-fifth day. Craig found eight and twelve ounces of a limpid fluid in two cases; and Tourdes found pus in more than one-half of his cases, either unmixed or forming a milky liquid. J. L. Smith refers to the case of an infant who had the disease at the age of five months, and two months subsequently great prominence of the anterior fontanelle, and other symptoms which indicated the presence of a considerable amount of effusion within the cranium. In a case in Dublin,[47] there was no meningeal lesion except in a "few dark spots like sanguineous effusion under the arachnoid." White[48] mentions the case of an adult that terminated fatally in thirty-six hours, in which the vessels of the pia mater were very much congested, and sanguineous effusions existed above and below the cerebellum, and a clot of blood three inches long and external to the theca extended downward from the lowest portion of the medulla oblongata. In all of these instances, then, congestion, the first stage of inflammation, existed. That such was its real nature is proved by what follows.

[Footnote 47: _Dublin Jour._, July, 1867, p. 441.]

[Footnote 48: _Med. Record_, iii. 198.]

The most characteristic lesion is a fibrinous or purulent exudation in the meshes of the pia mater. American physicians described it as early as 1806 in such terms as these: "The dura mater and pia mater in several places adhered together and to the substance of the brain; ... between the dura mater and the pia mater was a fluid resembling pus" (Danielson and Mann). In 1810, Bartlett and Wilson found "an extravasation of lymph on the surface of the brain;" and in the same year Jackson and his colleagues, after describing the congestion and serous effusion found within the cranium "in those who perished within twelve hours of the first invasion," state that the arachnoid and pia mater present an effusion between them of "coagulated lymph or semi-purulent lymph" both on the convexity and at the base of the brain. These descriptions correspond in all respects with those of Mathey relating to the epidemic at Geneva in 1805, for he says: "The meningeal blood-vessels were strongly injected. A jelly-like exudation tinged with blood covered the surface of the brain; ... on its lower surface and in the ventricles a {822} yellowish puriform matter was found." Such lesions have been described by a long line of observers--by Wilson in 1813, Gamage in 1818, Ames and Sargent in 1848; by Squire, Upham, and a host of others since 1860 in the United States, and by Tourdes, Gilchrist, Ferrus, Wilks, Gordon, Banks, Gaskoin, Niemeyer, Burdon-Sanderson, and many more in Europe.

It is evident, therefore, that in a certain number of fatal cases only sanguineous congestion of the membranes of the brain and spinal cord are found, and in certain others--constituting, it may be added, nine-tenths of the whole number--evidences exist of cerebro-spinal meningitis. Hence the natural conclusion is that the congestive lesions represent the first stage of a process which if prolonged and perfected occasions the lesions peculiar to inflammation. For the development of the latter two factors would seem to be essential--not only a fibrinous condition of the blood, but also sufficient time for exudation to occur. But when we come to study the actual results of examinations post-mortem, it is found that the duration of the attack does not determine absolutely the nature of the lesions. On the one hand, in a case which terminated fatally after a week's illness there was found reddish serum between the arachnoid and the pia mater and in the lateral ventricles, with intense injection of the pia mater of the base, medulla oblongata, and upper part of the spinal cord, but no exudation of lymph.[49] And, on the other hand, numerous cases have been published in which, although death occurred within twenty-four hours from the onset of the attack, coagulated lymph and also pus were found upon the brain and spinal marrow. For example, during the winter of 1861-62, in the army, that then lay near Washington, D.C., a soldier was attacked with a chill, severe fever, and headache, followed by opisthotonos and repeated convulsions before his death, which occurred in about twenty-four hours. No eruption or discoloration of the skin is mentioned in the history. On examination there was found beneath the arachnoid a thin layer of lymph and abundant exudation over the posterior lobes of the cerebrum, and also at the base of the brain and on the medulla oblongata.[50] In a case reported by Gordon[51] the entire duration of the illness was under five hours, and after death the cerebral arachnoid was more or less opaque, and in some spots had a layer of very thin purulent matter beneath it. And, again, not only may the symptoms belonging to blood-dissolution be consistent with a certain prolongation of life, but also with decidedly inflammatory tissue-changes. Thus, in another case of Gordon's the duration of the illness was at least six days, and the patient presented all the characteristic symptoms of the disease, including "a most wonderful and uniform curve of the spine and head backward," "spots black as ink," "bullæ which rapidly became opaque and dusky," "herpetic eruption, etc." After death the body had a very frightful appearance. It was still prominently arched forward. It was of a dusky blue color, with a copious eruption of black spots of various sizes, and one or two of them were gangrenous.... When the theca vertebralis was opened purulent matter flowed out, and a purulent effusion was found in patches on the brain. {823} The cerebral arachnoid was all opaque, the lateral ventricles were filled with serum, and the blood in all the cavities was very fluid and dark colored. From all that precedes, therefore, it must be inferred that the nature of the lesions in this disease depends not on the type alone, nor on the duration merely, of the attack--that a very brief course is compatible with marked inflammatory lesions, and a prolonged one with profound alterations in the condition of the blood. In other words, it seems that there must be something besides the appreciable lesions that influences, if it does not determine, the issue of an attack of this affection. While bringing forward prominently this proposition, and the facts on which it rests, we have no intention of under-estimating the relative significance of the two most conspicuous types of the disease, the purely inflammatory and the adynamic, or calling in question the fact that the evolution of the former is most usually comparatively slow and regular, and of the latter rapid and irregular. In the one, when death takes place early, congestive changes are found, and when later these have merged into exudative lesions; in the other or adynamic cases congestion and liquid transudation prevail, and the results of complete inflammation are seldom seen. When the disease has been very much prolonged the exudation becomes tough, adherent, and shrivelled.

[Footnote 49: Davis, _Richmond Med. Jour._, June, 1872, p. 709.]

[Footnote 50: Frothingham, _Amer. Med. Times_, Apr., 1864, p. 207.]

[Footnote 51: _Dublin Quart. Jour._, May, 1867, p. 409.]

The brain-tissue has generally been found softer than natural, and, although in some cases this diminished consistence might be attributed to post-mortem changes, yet on the whole it must be associated with the inflammatory lesions of the meninges. As a rule, it is greater the longer the attack has lasted, and is by no means equally diffused, but is more marked where the meningeal alterations are greatest. Ames found softening in nine out of eleven cases, and chiefly in the cortical substance, but also in the fornix and septum lucidum; and Chauffard states that in protracted cases "the interior surface of the ventricles, the fornix, and septum lucidum, were reduced to a pultaceous and creamy consistence." But it is by no means true that softening is met with in all cases of long duration.

The lesions of the spinal marrow and its membranes correspond with those of the brain. The dura mater is often very dark, its blood-vessels engorged, its arachnoid cavity distended with serum more or less bloody, turbid, or purulent. Two ounces of pus have been removed from it through a puncture. Fibrinous and purulent exudation fills the meshes of the pia mater, and is usually most abundant in the cervical and dorsal portions, and generally upon the posterior rather than upon the anterior surface of the organ; but sometimes large accumulations of lymph and pus are found at the lower end of the cord. Gordon[52] relates of a case that "when an opening was made into the lower part of the theca vertebralis purulent matter flowed out, and the entire surface of the pia mater was covered with a coating of thin purulent matter, which, like a thin layer of butter, remained adherent to it." Occasionally the cavity of the spinal arachnoid contains blood. Softening of the spinal cord has been often noticed. Chauffard states that in some cases of particularly long duration it was reduced to a mere pulp, and he adds, "in the place of portions of the spinal marrow, completely destroyed, was found only a yellowish liquid, or the empty membranes fell into contact where it was {824} wanting." Similar disorganization has been described by Ames, Klebs, and others. Fronmüller reports the case of a girl aged fourteen years in whom the central canal of the spinal cord was distended with pure pus.

[Footnote 52: _Dublin Quart. Jour._, xliii. 414.]

The lesions of the internal auditory apparatus consist of softening in the fourth ventricle and of the root of the auditory nerve, yet such lesions are said to have been found even when no defect of hearing had existed. In other cases in which deafness did occur the lesions consisted of inflammatory changes in the cavity of the tympanum and suppuration of the labyrinth. They probably arose from an extension of inflammation from the pia mater along the trunk of the auditory nerve (Von Ziemssen). In like manner, the inflammatory and destructive changes in the eye which have been elsewhere described arise from an analogous cause affecting the optic nerves.