TUBERCULAR MENINGITIS;WITH REPORT OF A

PECULIAR CASE.

BY

H. X. POTTER, M.l).

Reprint from September number, Vol. X,

Annals of Gynecology and Pediatry

Boston, 1897.

TUBERCULAR MENINGITIS; WITH REPORT OF APECULIAR CASE.

H. N. POTTER, M.D.

Among the diseases that are gen-erally regarded as affections of earlylife, there is not one that is really solittle understood and so unsuccessful-ly treated as tubercular meningitis.While this disease is not an uncom-mon affection, it is very often the casethat a post-mortem reveals the factthat a wrong diagnosis had been madewhich is only proven when it is toolate. This, then, brings up the ques-tion regarding a primary and second-ary form of this disease and it maywell be asked—“Why does tubercu-losis first make its appearance in theform of meningitis, and why does itnot show symptoms of a general tu-berculosis before becoming localizedin the meninges?”

If the authorities of most of ourwriters can be recognized whereinthey assert that this disease is almostalways secondary to the affection insome other part of the body, why dowe find tubercular meningitis in chil-dren who have been apparently

healthy prior to the attack of the dis-ease?

Many eminent writers assert that inprimary cases, which are especiallyfrequent in children and young peo-ple, it seems to arise in persons pre-viously quite healthy, or at most aftera weeks’ malaise; but even inthese instances, after death, it is near-ly always the case that some other le-sion is present , such as caseatingbronchial glands, or miliary tubercu-losis of the lungs and other viscera, ora caseous nodule in the brain itself.

Generally speaking, tuberculosisinvades the body or it becomes sus-ceptible through three and possiblyfour channels: hereditary taint,partaking of milk from a cowinfected with tuberculosis, nurs-ing by a tubercular woman, andpossibly by the bacilli finding an en-trance through a wound. It is onlyin rare cases, however, that it invadesthe body through the last-mentionedchannel As regards a hereditary

2 H. E T. POTTER.

predisposition there is no doubt; asmay be said, also, of the infectionthrough cow’s milk and the breastmilk of the mother or wet nurse, in-fected with tuberculosis.

I have referred to this disease as be-ing little understood and unsuccess-fully treated, by which I wish to con-vey the idea that while we know ofthe bacilli of tuberculosis, know theresults of its invasion of the body andthe very unsuccessful treatment ofthe conditions that arise, we are verymuch in the dark regarding a diagno-sis and causes that localize this dis-ease without first showing symptomsof a general or miliary form whichreasonably should occur.

It is not difficult to find a cause fortubercular meningitis when the pa-tient is already affected with phthisis,hip-joint disease, caries of the spineor other tubercular or strumous com-plaints, which make the disease sec-ondary; but the reason for a primaryform of this disease is very much inthe dark, and our knowledge of thelocal invasion, especially in the formof meningitis, is very little.

Etiology. —This disease occurs atall ages, but is generally regarded asmore frequent in children thanadults, and it is very certain it affectsmales more than females. It isclaimed by medical writers in generalthat so far as its causation is con-cerned, it is constantly associated with

tubercle elsewhere in the body, and isreally secondary. Primary caseswhich are found in children andyoung people, seem to arise in personspreviously quite healthy or after afew weeks of ill health; still it isclaimed that even in such cases thecondition is due to tuberculosis insome other region of the body. Theremay be a discharge from the ear, butif it has any relation to the disease, itis either that it indicates general ill-health, or that it opens a passage forthe entrance of the tubercle bacilli.Sometimes the glands of the neck en-large, break down and suppurate priorto this disease being manifested.

We know that the cause of tuber-culosis, no matter what part of thebody is affected, is due to a bacillus,which may invade the body throughinfected cow’s milk or the breast milkof a tubercular woman and possiblythrough a wound. Experiment hasclearly shown that the introduction oftubercle bacilli into the tissues willproduce tubercles; and this must beby some special irritant properties ofthe bacillus. In relation to the occur-rence of tuberculous disease in man,we have before us the question, how isit usually introduced into the system,so as to produce the numerous tuber-cular lesions of the bones, joints,lungs, peritoneum and other organs?If this cannot in every case be an-swered, it is in many instances suf-

TUBERCULAR MENINGITIS,

ficiently obvious. Tlie bacillus mayenter from without through the mu-cous passages, of which the respira-tory gives the preponderating numberof instances; thus, tuberculosis of thelungs follows the lodgment of thebacillus in the bronchioles or lung tis-sue. With comparative rarity, thebacillus may enter through a wound.In most cases we must suppose a spe-cial predisposition on the part of theindividual (hereditary), or of the tis-sue first affected (depressed vitalityfrom inflammation), which allows thetubercle to establish itself and thrive.Allowing this to be true, it still doesnot account for a primary meningitisbeing manifested when it is so reason-able to suppose that other organs ofthe body, more exposed, should be af-fected first and show unmistakablesymptoms of the disease.

Moi'bid Anatomy.—The character-istic appearances are seen in the piamater and consist of the effusion oflymph, and the presence of tubercles.The lymph is gelatinous and translu-cent, or more opaque, and gray or agrayish-yellow, rarely or never puru-lent and is contained in the meshes ofthe pia mater, especially at the base ofthe brain, over the cliiasma, thespace behind it and the adjacent cruraand pons. It commonly extends intothe Sylvian fissure on each side, alongthe course of the middle cerebral ar-tery. The surface of the hemis-

pheres is free from lymph, but itis found at the top of the cerebellum,at the anterior part. With thelymph are mixed tubercles, of dif-ferent sizes, gray and opaque, occa-sionally commencing to caseate. Un-der the microscope the smaller tu-bercles present lymphoid corpusclesin the perivascular sheath; the largertubercles may present giant cells andbacilli. There may be abundantlymph in the characteristic situations,with few, if any, tubercles, or theremay be a number of tubercles withlittle lymph. Occasionally there maybe symptoms indistinguishable fromthose of tubercular meningitis, inwhich tubercles are found on the sur-face with no meningitis. The ven-tricles of the brain are commonly dis-tended with fluid, the convolutionsare flattened against the skull, the for-nix and septum lucidum are generallysoft, and the ependyma of theventricles presents a granular orsanded appearance. The cranial duramater is not usually affected, but thespinal dura mater sometimes showsminute tubercles, and lymph may ex-tend from the pia mater to the cervi-cal region of the spinal cord. A gen-eral tuberculosis is not uncommon.Tubercles may be found in the lungs,liver, spleen and kidneys. In bothsecondary and primary cases the mod-ern view.is that the meninges are in-fected from a preceding tubercular

H. N. POTTER.4

deposit in the lung, kidneys, bron-chial gland, brain or elsewhere; orpossibly from outside.

Symptomatology.—The symptomswill be first described as they com-monly occur in children, and the dif-ferences in secondary cases afterwardsmentioned.

There is often a stage of ill health.The child is restless, loses appetite,may be occasionally sick and has con-stipation. The illness beginsdefinitely by headache, vomiting or aconvulsion. The headache is severeand continuous, and there is moaningor occasionally a sudden cry. Thereis a moderate degree of fever, quickpulse, sensibility to light and sound.The child shuts its eyes and resentsbeing disturbed. The vomiting doesnot generally last long, and the con-vulsions that occur at the beginningare seldom repeated.

After a few days there may beslight delirium and the patient be-comes drowsy. The head is some-times retracted and neck stiff. Theabdomen becomes hollowed out or re-tracted, the margins of the ribs andiliac crests being prominent. Thepulse may be slow, and often irregu-lar; the respirations slow, sighing andirregular; the temperature is general-ly high, oscillates between 101° and103°. There is a tendency to vaso-motor paralysis as seen in the flushingof the face. If the finger is drawn

across the skin of the forehead or ab-domen, a broad red line quickly ap-pears which may last as long as fiveminutes. This condition, which isnot peculiar to, but only more markedin meningitis, is called the cerebralstreak. Changes often occur veryearly in the optic disk, which at firstbecomes vascular and then shows defi-nite optic neuritis. Food is takenbadly and the bowels are constipated.

From this point the case may go toa fatal termination without othersymptoms. The drowsiness increasesto coma, optic neuritis is moremarked, the abdomen becomes morehollowed, pulse more irregular,feebler and generally quicker, therespiration may take on the characterof Clieyne-Stokes breathing, the tem-perature may fall more or less rapid-ly, or before death rise quickly to106° or 107°. Mucous accumulatesin the bronchial tubes and with fail-ing pulse death takes place. It is veryoften the case that the last few daysare marked by local symptoms. Anarm or leg, or the arm and leg on oneside become rigid or paralyzed. Theremay be facial paralysis or ptosis. Thepupils are very often unequal andmay be insensitive to light. In thisstage convulsions may occur. Withthese symptoms coma becomes moreprofound and death takes place asabove shown or the patient is asphyxi-ated in a convulsion.

TUBERCULAR MENINGITIS.

The duration of the illness variesbetween ten days and three weeksfrom the beginning of the pro-nounced symptoms, but it may be fiveor six weeks. The above course ofthe disease has been divided intothree stages—irritation, compressionand paralysis, but it is not alwayseasy to distinguish between them, andin some cases the more typical symp-toms may be little marked, comaalone being prominent.

In secondary tubercular meningitisthe symptoms are often more rapidlydeveloped. The patient may, withlittle warning, become delirious orhave paralysis of a limb or face, orhave a convulsion, quickly becomingcomatose, and dying in a few days.

Diagnosis. —This is sometimeseasy, but at other times difficult andimpossible until late in the illness. Wemust expect meningitis when thereare decided head symptoms accom-panied by fever, but headache alonewould not be a diagnostic symptom.In young children otitis may causeheadache, moaning, vomiting, photo-phobia and the desire to be undis-turbed. A careful examination of theear and mastoid process may revealthis localized condition. Enteric fe-ver may for some days resemble men-ingitis, but in that fever, headacherarely persists after the tenth day, andgenerally by that time the bowelmovements or the rose spots on a full

abdomen, will decide the diagnosis,which will be confirmed later bythe absence of convulsions, rigidityor paralysis. The mistake is oftenmade in cases of meningitis, withoutprominent headache, but with flushedface, delirium and pyrexia, they be-ing diagnosed as enteric fever. Themost useful symptoms are irregularpulse, sighing or irregular respiration,rigidity of muscle or paralysis, con-vulsions and optic neuritis. However,optic neuritis may occur in enteric fe-ver. Tubercle of the choroid only oc-curs in a small percentage of casesand is not to be depended upon alonefor a diagnosis. In young children,decided cerebral symptoms accom-pany other acute sickness, as in pneu-monia and broncho-pneumonia; theremay occur drowsiness with a retractedhead, and convulsions may occur to-wards the end, These symptomswould be explained by the detectionof localized dnllness with bronchialbreathing, but rales over the wholechest might indicate a general tuber-culosis. The exhaustion followingmal-nutrition, bad feeding or severediarrhoea in young infants may simu-ulate this disease. The child is drow-sy or comatose, with pale face, sunkeneyes, dilated, irregular pupils, andirregular, sighing respiration. Itwas formerly called hydrocephaloiddisease. It is distinguished frommeningitis by the history, absence of

6 II. K POTTER.

fever and local paralysis, the de-pressed fontanelle and its speedy im-provement under supporting treat-ment. The distinction of the tuber-cular from other forms of meningitisrests largely upon the absence of lo-cal cause for a suppurative menin-gitis, as cranial injury or otitis; theprevious existence of strumous or tu-bercular lesions, the paralysis of cra-nial nerves, indicating that the men-ingitis is situated at the base ratherthan over the vertex; the duration,which is generally much shorter insuppurative meningitis. So far as theclinical history goes, and the absenceof any local exciting cause, the samediagnostic points cover those cases ofmeningitis which mostly affect in-fants or very young children, inwhich no tubercles can be found, butonly a grayish lymph at the base. Inevery respect but the absence of tu-bercles they resemble tubercular men-ingitis, from which they cannot bedistinguished during life. With men-ingeal symptoms and tubercidosis ofthe choroid a diagnosis may be madeof tubercular meningitis. With men-ingitis a lumbar puncture may give adiagnosis also.

Prognosis. —The prognosis in thisdisease is very grave, and it is a ques-tion whether there is ever a recovery.In the cases reported as recovering,there is a just suspicion that a wrongdiagnosis had been made. We rarely

find traces of a past tubercular menin-gitis in those who die of other diseases,and it is very difficult to prove duringlife that the case is tubercular, even ifmeningitis is present. Still a certainnumber of patients with apparent tu-bercular meningitis do get well. Therecovery is slow, the speech, vision,etc., remaining imperfect for weeksor months. The prognosis, then, isunfavorable, especially in the second-ary form where phthisis, hip diseaseor other well-marked tubercular le-sions are present. Yet primary casesneed not be considered absolutelyhopeless.

Treatment.—With the prognosisunfavorable, the treatment is reducedto a small limit. Cold should be ap-plied to the head by means of an icebag, the bowels kept open and milkgiven in small quantities, frequently.Blisters are sometimes applied to theback of the neck, but are of doubtfulvalue iu the tubercular form of men-ingitis. Irritant applications havebeen used upon the close-shaven scalp,but here, too,they seem to be general-ly of little benefit. In some cases iodo-form ointment may show some bene-ficial results. Of the internal reme-dies, iodide of potassium has been ex-tensively used iu the hope of influenc-ing the morbid process. The bro-mide is given to allay the pain in thehead. A combination of the five bro-mides has also been used.

TUBERCULAR MENINGITIS. 7

A Somewhat Peculiar Case.—Knowing that cases of this disease arealways interesting to the profession,and especially so when they varyfrom the usual course, I will give ahistory of one that I recently discov-ered which assumed a somewhat dif-ferent formfrom the typical ones. Thehistory of the case with its develop-ments made the diagnosis reasonablysure, although no post-mortem wasperformed. The peculiarity of thecase is in its changeable nature, for al-though the child was paralyzed fromtime to time, this would pass away,then occur again. The child had sev-eral spells of apparent collapse butwould recover. As early as the fourthday the arm and limb on the rightside were paralyzed, which passedaway after a few days. Then the leftarm and limb were affected, whichalso passed away, and finally, whenthe child died on the seventeenth(17th) day, there were no signsof paralysis. Another somewhat un-common condition was the fact of thetemperature gradually rising severaldays before death, instead of the sud-den rise that occurs so often. Thecase is as follows:

A few weeks ago I was called to seea little girl one year of age who hadbeen slightly ill for about a week pre-vious. There had been no markedsymptoms until the day I saw herwhen she was taken with vomiting

and convulsions. I liad treated thechild a short time before for enlarge-ment of the glands of the neck and adischarge from the ear, from whichshe fully recovered. The mother in-formed me that for the past few weeksthe child had shown symptoms of hermilk disagreeing with her, and hadnursed but very little. Plenty ofcow’s milk had been given and ithad received sufficient nourishment.While treating the child for its for-mer trouble I got a history of tuber-culosis, the mother’s two sisters andher mother having died from it in apulmonary form. I advised the moth-er to wean the child at once on ac-count of the possible danger of its con-tracting the disease, the mother beingpredisposed, although no signs oftuberculosis were manifested as yet.The mother, however, did not heedmy warning and continued to nursethe child and also gave it cow’s milk.

At my first call I found the child inconvulsions, pulse 110, temperature100° (axilla), respiration about nor-mal. There had been several convul-sions and vomiting and the childnursed badly. On the second day thepulse reached 120, temperature (axil-la) 101°, respiration irregular andquickened, with no convulsions orvomiting, which never occurredagain. The pupils were dilated andunequal, which continued throughoutthe course of the disease. The tem-

8 14. N. POTTER.

perature then indicated tuberculosisinasmuch as it had the evening riseand the morning fall. On the thirdday the pulse reached 136, tempera-ture 101° (axilla) and Cheyne-Stokesbreathing. Fourth day symptomsabout the same with paralysis of rightarm and limb lasting about forty-eight hours; coma. From the fourthto eighth day symptoms about thesame, temperature varying from 101°to 103°(axilla). On the eighth day thearm and limb on left side became par-alyzed. From the eighth to eleventhday, symptoms the same with a grad-ual elevation of temperature. Elev-enth day, pulse irregular and hard tocount,temperature 104° (axilla), othersymptoms the same. Twelfth daymore normal pulse and respiration,temperature remaining at 104° (ax-illa). Thirteenth day, temperature

(axilla), collection of mucus inbronchial tubes, other symptoms thesame. Fourteenth day showed pulse140, respiration oppressed, tempera-ture 104-J0 (axilla), with increased col-lection in throat. Fifteenth day nochange. There were no symptoms ofparalysis. Sixteenth day, throat par-alyzed. Up to this time nourishmenthad been given by the mouth, al-though coma was present. Uourish-

ment was now given by the rectum.The collection of mucus increased,respiration oppressed, heart weak,temperature 104° (axilla), child in astate of collapse. Seventeenth day,child died from failure of heart.There were no symptoms of generalparalysis. Unequal dilated pupilspresent. The other symptoms in thiscase did not differ from a typical caseof the disease. The bowels were con-stipated, abdomen sunken, cerebralstreak, delirium, dilated unequal pu-pils, etc. I examined the child bothat morning and night for several daysand noted the evening rise and themorning fall of the temperature. Acareful examination of the caseshowed no symptoms of any other dis-order, not even a general or miliarytuberculosis, and a cause for the con-dition in this case might be due to ahereditary taint as the child was stru-mous, from being fed on cow’s milkinfected with the germ or possibly bythe entrance of the infection throughthe discharging ear. The mother’smilk was not analyzed as she showedno signs of tuberculosis, althoughthere is no doubt a hereditary predis-position.

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