SPORADIC CEREBRO-SPINAL MENINGITIS.

MALONE DUGGAN, M. D.,

EAGLE PASS, TEXAS.

Epidemic cerebro-spinal meningitis and sporadic cerebro-spinal meningitis are essentially the same in pathology and symptomatology, they differing only in their etiological factors. The specific cause of the epidemic form has been found to be the diplococcus intracellularis meningitidis of Weichselbaum, while the sporadic cases are caused by different infectious agencies, viz.: streptococcus pyogenes, pneumococcus, bacillus typhosus, the micro-organism of influenza and others. Meningitis may occur independently of any of these diseases, or in the course of them or as a sequela of them. Very frequently some advance has been made in diagnosis by the examination of the cerebro-spinal fluid. In this way, some infectious organism can usually be found. Also, what appears to be a distinction of considerable importance, is the presence in all cases of multinuclear cells, and a slightly lower freezing point of the fluid.

Meningitis is very irregular in its distribution, and has many typical forms. However, the differential diagnosis from other acute infectious diseases should not be very difficult. It differs from them greatly in the severity of the nervous symptoms, which, together with continued stupor or coma, opisthotonos, slow pulse, and irregular respiration, point very clearly to the nature of the trouble. In addition to these symptoms, in most cases, there will be present high fever, rigidity of the lower extremities, contracted abdomen, and the Kernig sign.

To give a more general description of the various types, it would unnecessarily lengthen this paper; besides, I wish especially to call attention to the symptoms observed by me in four cases which

came under my observation during the past year. In each instance there was no connection or suggestion of infection. Each case occurred in widely separated localities, after several months interval between them, and under different social conditions. Of these cases, one was under a year old, two under two years, and one was five years old. The infant was bottle-fed and poorly nourished, though its surroundings were healthful. It had had previously several attacks of entero-colitis, but for a month or so prior to this its health had been very good. The attack was preceded by a mild diarrhea and slight fever lasting for three days, when suddenly the fever rose to 104° F., and a convulsion followed. After the convulsion, there was opisthotonos, and vomiting at intervals. The fever soon subsided. The child was extremely restless, and the entire body seemed to be hyperæsthetic. After twenty-four hours, the restlessness gave place to coma, and towards the last there was Cheyne-Stokes respiration. Death occurred on the fourth day.

The second and third cases were in children very strong and robust. Each had had a cold and some fever for three or four days, which resisted the usual treatment administered in such cases. The first of these, after the fourth day, had diarrhea and frequent vomiting spells. The fever became high and ran a very irregular course. On the sixth day there developed a very severe laryngitis, without the appearance of any membrane. This persisted for two days, with very great embarrassment to the respiration. During this time the child was extremely restless and peevish. The vomiting ceased, and the croup became much better, but the respiration continued to be irregular and coma soon came on. There was also contraction of the abdomen and opisthotonos. This condition lasted for seven days, when death occurred.

The second child had no diarrhea or vomiting, but after the fifth day of the coryza he had some elevation of temperature, and a slight convulsion. The fever, however, never rose above 103° F., and it usually remained about 100° to 102° F. There was also great hyperæsthesia and nervousness, constipation and retention of urine. Coma occurred on the third day after the spasm. In this case the

thermo-cautery was applied along the spine, which caused some slight amelioration in the coma. This improvement continued for twelve hours. Toward the last, the temperature fell to below normal, and the body heat had to be maintained by external applications. Opisthotonos and Cheyne-Stokes respiration were present at the last. Death occurred on the fifth day after the spasm. The fourth case was five years old. She had always been delicate, though her surroundings were good. She had had a slow fever of a very irregular type for some two or three weeks, though the temperature was never very high. While apparently improving and without warning, twitching movements of the hands appeared, which grew more severe and more frequent between intervals. In twelve hours there was marked opisthotonos, contraction of the abdomen and the Kernig sign. The temperature was very irregular and the pulse was weak. I did not see the patient after this, but I was informed that she soon lapsed into a semi-conscious condition, and that the contraction of the arms continued. CheyneStokes respiration came on at the last, and death occurred on the eighth day.

The treatment of these cases depends almost entirely upon the symptoms present, and they being so irregular, no definite course can be followed out. In a general way, opium or bromide and chloral, given by mouth or by injection, will very greatly relieve the pain and control the spasms. But in the case of infants, opium must be given very cautiously, as an overdose may itself cause coma. Undoubtedly the thermo-cautery, applied along the spine, caused a temporary relief. Nourishment, as peptonized milk and beef juice, can be given, but after coma occurs it must be given by rectal injection or by gavage. The temperature is not usually hard to control. Occasionally, stimulation in the way of whisky or strychnine will be required. Withdrawal of the cerebro-spinal fluid has been recommended, and in as much as it affords an additional means of diagnosis, it should be practiced wherever means are at hand for detecting bacteria.

In discussing this affection, I wish to call attention to the fol

lowing suggestions: 1. In young children with colds, where the fever persists after appropriate treatment, suspicion should be aroused as to the possibility of meningeal infection. It was suggested by one of my colleagues that such cases were influenza, and that the cause of the meningitis was the direct infection of the meninges of the influenza bacillus. 2. The desirability of bacterial diagnostic methods being more generally used by the general practitioner. In such cases as I have cited, for instance, if it were possible to know the real etiological factors, a more rational treatment might be prescribed. 3. The distinction must be made between the epidemic or contagious form and the sporadic or noncontagious form. This is important, for protection should be given the public from the former, and the non-contagiousness of the latter should be fully explained for the good of the patient, and to relieve the public anxiety. The public generally look upon this disease as being very contagious, and the burial regulations affecting it in many places are very rigid and fail to make this important distinction.

PNEUMONIA.

JAMES H. EVANS, M. D.,

PALESTINE, TEXAS.

Pneumonia was recognized by Hippocrates and Galen in the early days of medicine, but was confounded with pleurisy to such an extent that the rusty sputa characterizing the former disease was described as an attribute of the latter, and pleurisy was said to be capable of producing cavities in the lung.

We will define pneumonia as a disease whose essential anatomical feature consists in the inflammation of the vesicular structure of the lung, which is thereby rendered impervious to air through the accumulation of the interim of the alveoli of the products of such inflammation. Clinically, it is characterized by pyrexia, which, in the majority of cases, when the disease is primary, commencs with rigors, or chills; it is also attended commonly by pain in the side, by dysponea: cough; sanguinolent; sputa, and great physical prostration.

We approach this subject with a degree of caution, and must admit that all we know positively about the nature of pneumonia is that it is anatomically an inflammation of the air vesicles and bronchioles. When we go beyond this fact and attempt to determine its cause, we leave the confines of positive knowledge and enter the illimitable realms of conjecture, or the more or less obscure nebula which surrounds the body of exact science, and is yet unincorporated.

To be sure the revelations of recent years along the lines of bacterial pathology lend a new interest to this subject, and very promptly suggest a reconsideration of the origin of the inflammatory lesion in pneumonia. Klebs, in 1877, created a great amount of enthusiasm when he declared he had found the key which was to unlock this particular pathological mystery. Eberth, in 1881,