TETANUS.

LECTURE DELIVERED AT THECOLLEGE OF PHYSICIANS

AND SURGEONS,CHICAGO.

BY

N. SENN, M. I).,

Milwaukee, wis.,

Surgeon to Milwaukee Hospital, Professor ofPrinciples and Practice of Surgery and

Clinical Surgery.

1886.

TETANUS

LECTURE DELIVERED AT THECOLLEGE OF PHYSICIANS

AND SURGEONS,CHICAGO.

BY

N. SENTNL M. D.,Milwaukee, Wis.,

Surgeon to Milwaukee Hospital, Professor of

Principles and Practice of Surgery andClinical Surgery.

183a

TETANUS.Gentlemen: Having finished the sub-

ject of wound infective disease proper, I shallcall your attention this evening to a more in-frequent wound complication, in which thesymptoms point towards the cerebro-spinalcentres as the primary and principal seat ofthe disease. This disease constitutes one ofthe most terrible in the long list of surgicalaffections, and up to the present time iswrapped in a great deal of obscurity. Irefer to tetanus. Terrible, from the greatmortality attending it, and from the intensesuffering with which it is accompanied; ob-scure, because from the present standpoint ofpathology, we are still in ignorance as far asits essential nature is concerned. Tetanus, Iwill define as being a disease of the nervoussystem, due to infection of a specific charac-ter, combined in many instances with peri-pheral irritation of a sensitive nerve; it ischaracterized by spasm of definite musculargroups, and attended by a continued form offever. If I include the adjective “infective”

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in tetanus, it is more on account of reasoningby analogy than positive pathological orclinical demonstration; nevertheless analogyshould teach us that the well-marked periodof incubation between the supposed time ofinfection and the development of the activesymptoms resemble other forms of infectivediseases very closely. That the direct causeof tetanus is due to a specific microbe, isclaimed by a number of the most eminentwriters, and further study and research willundoubtedly substantiate its infectious char-acter. This disease is not a new one, inas-much as it was well known to and describedby Hippocrates, who recognized both an idio-pathic and traumatic form, the latter ofwhich he referred to wounds, abrasions, andto various pathological conditions indepen-dently of traumatism. Most all of the oldclassical works contain lengthy chapters onthis subject, which reflect the most diverseopinions concerning its nature and etiology,which have been promulgated by differentauthors at various times.

In considering its geographical distribu-tion, it has been observed that it is more fre-quently met with in the torrid zone, andmore especially in Indiaand South America,Statistics also show that in these countriesthe disease is noted for the gravity of its

symptoms and its greater mortality. Inspeaking of race influence, it can be statedthat the colored races, as a rule, are moresubject to it, and when suffering from thedisease, it is usually attended by a greatermortality. Age appears to exert a predis-posing influence, as after exclusion of tetanusneonatorum, at least 40 per cent, have oc-curred in patients 10 to 30 years ofage. Inorder to prepare you for a pathological de-scription of this affection, I shall call yourattention to a form of toxic tetanus producedby the introduction into the circulation ofcertain chemical poisons. There is, how-ever, this difference between this form oftetanus and traumatic tetanus ; that in theformer case the active symptoms of the dis-ease make their appearance immediatelyafter the poison has been brought in contactwith the cerebro-spinal centres by the circu-lating blood. There is no period of incuba-tion ; no premonitory stage. The tetanicsymptoms are well marked and fully devel-oped as soon as the toxic effects of the drughave manifested themselves. The agents inour materia medica which are known to pro-duce certain forms of tetanus, are strych-nine, brucin, ergotine, and thebain; theforms of tetanic convulsions, however, varyaccording to the drug which has been ad-

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ministered. Taking strychnine poisoning asa type of toxic tetanus, we find that thepathological conditions are always referableto vascular changes in the brain and spinalcord—changes marked by an increased af-flux of blood, by an active hvperaemia orcongestion, which later result in morpholog-ical changes indicative of the first symptomsof inflammation. Experiment has estab-lished the fact that the reflex action attend-ing toxic tetanus is the result of excessiveinnervation from the spinal cord. If thespinal cord in an animal is crushed at a cer-tain point, tetanic convulsions will only takeplace in the muscles supplied by the nervesfrom the intact portion of the cord. If,again, you should divide the posterior rootsof the spinal cord near their exit from thespinal canal, or the posterior columns of thecord, there will be no response to the toxicirritation in the muscles supplied by thenerves which have been divided, or belowthe section of the cord. Furthermore, ifprevious to the intoxication you should re-move the brain, the pons, or even the me-dulla oblongata, the toxic effect of the drugwill not be impaired, showing conclusivelythat 'the tetanic convulsions or spasms arethe direct result from the toxic effect of thedrug upon the spinal cord.

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In considering tetanus as it presents itseltto the physician and surgeon, we still recog-nize an idiopathic and traumatic form. Bythe term “ idiopathic,” I mean a tetanus un-attended or preceded by an appreciabletraumatism. Traumatic tetanus, on theother hand, as its name indicates, is thatwhich follows an injury. We place greatstress upon the fact that there must havebeen somewhere a loss of continuity of sur-face, an infection atrium, as we term it,through which the specific germs gained en-trance into the circulation. In many casesof so-called idiopathic tetanus, the traumaticlesion may have been so slight as to eludedetection at the time when the disease madeits appearance, and yet the traumatism mayhave been the direct and only cause of thedisease. Of the seven hundred cases col-lected by Thamhayn, the disease had a well-defined traumatic origin in six hundredcases, while in the remaining one hundredcases there was no apparent evidence of pre-vious injury found, and they were conse-quently classified as belonging to the spon-taneous variety. To impress upon you thenecessity of looking carefully for the sourceof infection in doubtful cases, I will brieflyrefer to a case that recently came under myobservation, where from the history of the

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case I thought I was dealing with a genuinecase of idiopathic tetanus. The patient wasa child five or six years of age, who hadbeen ill for several days when it came undermy care. The case presented all the symp-toms of a mild type of tetanus, and in theabsence of traumatism as a cause, I consid-ered it as a typical case of so-called idio-pathic tetanus. I had trismus, opisthotonos,and a mild form of continued fever withconsiderable disturbance in the function ofthe vascular system. After treating thecase for a week or so, I accidentally one dayfound an exceedingly tender point in thesole of the right foot, which corresponded toa small cicatrix. On questioning moreclosely, the patient finally admitted havingstepped upon a nail some time before, anaccident which had been entirely overlookedby the parents and forgotten by the patient.Unless by accident the primary cause hadbeen detected, this case would have beenconsidered as belonging to the idiopathicvariety, when in fact it was a well markedbut mild case of traumatic tetanus. I sim-ply make this allusion to put you on yourguard in cases of so-called idiopathic tetanus,to search diligently and unceasingly for atangible primary cause, as a slight injury orobscure cause of peripheral irritation might

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be easily overlooked, which would lead to anincorrect interpretation of the etiology ofthe disease. There may be such a thing asidiopathic tetanus, without any apparentbreach of surface, as specific germs may pos-sibly gain entrance into the circulationthrough an intact mucous membrane in thesame manner as in other instances of woundinfective diseases, the microbes finding inthe cerebro-spinal centres a favorable placeof localization and reproduction. Futureresearch, however, will have to verify orcontradict this supposition.

In considering the exciting causes of tet-anus, I will allude first to peripheral irrita-tion. Before the infective nature of tetanuswas recognized, it was generally consideredthat the disease was invariably the directresult of peripheral irritation. Clinical ex-perience has demonstrated the importantbearing of irritation of sensitive nerves, atleast as a determining cause, inasmuch asin 380 cases reported by Thamhayn, it wasfound that 75 per cent, of them were theresult of injury to the fingers, toes, hands,and feet—localities where we have an abun-dant supply of sensitive nerve filaments,so that it may be accepted as a wellknown and established fact that injuries ofthe hands and feet are more prone to be fol-

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lowed by tetanus than wounds in any otherlocality.

Another form of peripheral irritation,aside from the traumatic, are pathologicalconditions due to inflammation, which affectthe sensitive nerves the same as when theirritation is produced by an injury. Tetanusproduced in this manner has been observedas a complication in pleuritis, pneumonia,metritis; in fact, as a result of pathologicalconditions which involve in the same manneran extensive area of sensitive nerves as theeffects of traumatism. In the idiopathic formof tetanus, authors still recognize a centrallesion or point of irritation independently ofany peripheral or eccentric pathological irri-tation. By this I mean central irritation bypathological conditions involving directly thebrain or spinal cord, independent of trau-matism. Cases have been observed in thepost-mortem room where well marked patho-logical conditions existed in the brain andspinal cord, independent of either traumaticpathological peripheral irritation, where dur-ing life the characteristic symptoms werewell marked. These cases may serve to ex-plain the theory that the specific germs oftetanus once introduced into the system mayhave a special elective affinity for the nervecentres, and mav there manifest their toxic

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influence by producing pathological condi-tions which induce tetanic spasms. Specificinfection, then, must be recognized as themost important and essential factor in theetiology of tetanus. Recent literature onthis subject seems to have established thefact, that like wound infective diseases,tetanus is simply an expression of a specificform of intoxication, which implicates, prin-cipally, the cerebro-spinal centres, the resultof the introduction of specific microbes.This hypothesis does not lack analogy in dis-eases which are marked by a well-definedperiod of incubation, where a certain timeelapses between the introduction of the virusand the active development of the symptoms;in other words, diseases preceded by a periodof incubation, in contradistinction to diseaseswhich are caused by the introduction of aformed chemical poison, means simply thatthe germs introduced at the time when theinjury was inflicted keep on multiplyinguntil a sufficient number of them have beengenerated in the system, when the toxic ef-fects are announced by the active develop-ment of symptoms. If tetanus were the re-sult of the introduction into the system of apre-formed or chemical poison, the activestage of the disease would commence as soonas the poison had entered the circulation,

12

which evidently has never been the case. If,however, a certain period elapses from thetime of supposed infection until the activedevelopment of the disease, we recognize thefact by well demonstrated analogy that thesespecific germs have been introduced into thesystem, and have found a favorable soil fortheir growth and multiplication in the cen-tral nervous system until their direct toxiceffects are manifested by tetanic convulsions.The period of incubation in tetanus is not aswell marked and definite as in some otherinfectious diseases, but the same can be saidof other affections where there can be nodoubt concerning their microbic origin, hy-drophobia, for instance. The most charac-teristic symptom of tetanus consists in tonicspasm of certain w7ell-defined musculargroups, as a rule, the affection following in adescending direction. We will, for the sakeof convenience, assume that tetanus has fol-lowed a compound comminuted fracture ofthe leg, and will describe the symptoms intheir proper order. About the fifth or sixthday (the earliest period of incubation) ourpatient will probably complain of a certainill-feeling in the broken limb, marked byirregular jerking; if, at the same time, hecomplains of general malaise, loss of appe-tite, of symptoms indicative of infection, we

should realize that these premonitory symp-toms are but the precursors of the gravest ofall wound complications—tetanus. If theseearly symptoms are followed a little later bythe appearance of trismus, there can be nofurther doubt as to the nature of the disease.By trismus, I mean a contraction of the mus-cles of mastication, as evidenced bv difficultyin opening the mouth. Going still furtherdown, other muscular groups are implicated,and we have what is known as opisthotonos,a bending backwards of the body in contra-distinction to emprosthotonos, a bending ofthe body in the opposite direction. If themuscles on one side of the chest areaffected, we have pleurosthotonos; if stillfurther, all the muscles in the body (usuallythe extensors, however,) are affected, and theentire body becomes rigid, we have ortho-totonos. If the muscular spasms have be-come well developed, involving the area ofthe respiratory muscles, we expect an impair-ment of the function of respiration. Byspasmodic contraction of the muscles con-cerned in that function, respiration becomesimperfect on account of the constant rigidityof the muscles which are active in producingthe respiratory movements.

The temperature is increased in almostevery case, the rise depending upon the in-

tensity of the infection, the acuity of theattack, and especially the rapidity withwhich the disease progresses. A limited areaof muscular rigidity and a slight rise in tem-perature, are favorable prognostic indications.In some instances the temperature has beenfound unusually high. A temperature of108°, even 110°, as observed by Wunderlichand Billroth, denotes great danger, and isalmost without exception followed by a fataltermination. These authors have placedstress upon the importance of temperaturein tetanus, watching its rise in the axilla atdifferent times of the day, and observing thatan increase of temperature beyond 104° or105° is usually followed by death. Anothercurious fact has been noticed, and that is anincrease in temperature after death. Wun-derlich explains the high temperature in tet-anus by assuming a loss of function, or a lossof control of the heat moderators in thebrain, the heat centres being impaired by thedirect action of the poison upon this particu-lar portion of the cerebral mass. The post-mortalrise in temperature has been attributedby Fick and Huppert to evolution of heatduring the coagulation of the myosin. Thesensorium usually remains unimpaired to thelast, showing distinctly that thatportion of thebrain concerned in that function remains un-

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impaired, that the disease for some unknownreason expends itself upon the motor tracts,and especially upon that portion of the cere-bro-spinal system connecting the brain andspinal cord, the medulla oblongata. Whenthe spasms are severe and prolonged, therespiration becomes impaired, the pulse smalland rapid, and the surface of the body isbathed with a profuse perspiration. As thedisease progresses, evidences of capillarystasis become more and more apparent, theeyes are suffused, and the visible mucous mem-branes livid; the tongue is coated, appetitediminished, and the bowels are obstinatelyconstipated; all causes of peripheral irritation,as a draft of air, loud noises, etc., will pro-voke easily a repetition of spasmodic attacks,

The first attempt at an intelligent explan-ation of the morbid anatomy af tetanus wasoffered by Rokitansky, who found on exam-ining the nerves supplying the injured partevidences of inflammation in the nerve it-self, and hence described the disease as aform of neuritis, a neuritis ascendens. Asproof of this view of the disease he de-scribed the pathological conditions found inthe affected nerves as consisting in an exuda-tion between the nerve fibres, granular de-generation and hyaline changes in the nervefibres themselves, finally resulting in com

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plete disorganization and disintegration. Heregarded the disease essentially as a “ neuritisascendens,” the morbid process commencingin the nerve at the point of injury, and ex-tending by continuity to the cerebro-spinalcentres. All pathologists agree that thebrain and spinal cord are always found in astate of congestion, but some go still further•—Lockhart, Clarke, and Dickinson, for in-stance, asserted that the brain was not onlyhvpersemic, but that there was an actual in-flammation of the cortex of the brain itself,resulting in granular disintegration. Othershave found, on examining the spinal cord,pathological changes well marked in thatportion of the nervous system, consisting ofhypersemia, extravasation, softening, in-creased proliferation of connective tissue, de-generation of the anterior and posterior col-umns. Tyson, on the other hand, found intwo cases well marked degeneration of thecentral canal and disintegration of the pos-terior columns of the cord. Aufrecht foundcellular atrophy in the anterior and posteriorcornua of the cord and granular degenera-tion of the gray substance of the cord.From all that I have stated it appears evi-dent that so far no unanimity exists amongpathologists in localizing the central lesion,but from what we have learned it becomes

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apparent that the most constant pathologicalchanges are found in the upper portion ofthe spinal cord.

In considering the diagnosis, particularattention should be paid to the history ofthe case, fully eliciting the possibility of anyprevious traumatism or infection serving asa tangible cause. In cases of spasm ofdefinite groups of muscles, we should ascer-tain the existence or absence of fever by theuse of the thermometer.

Although no uniform pathological condi-tion appears to have been found character-istic of tetanus, the weight of evidence pointstowards the spinal cord as the central seat ofthe lesion, in this respect showing a resem-blance to hydrophobia, an affection which itsimulates in many respects.

Muscular spasm resulting from a neuroticsource and limited to a group of musclesunattended by general infection, is notmarked by rise in temperature. If, on theother hand, we have muscular spasm at-tended by an increase of temperature (par-ticularly if we have reason to believe that itis the result of previous traumatism or infec-tion), the case becomes suspicious, and meritsa scrutinizing examination. In tetanus, asa rule, the muscles on the extensor side areaffected, while in cases of inflammatory dis-

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ease in bones and joints, the contractions oc-cur on the flexor side.

In the differential diagnosis, consider thepossibility of toxic tetanus from poisoningwith strychnine or any of that class of rem-edies which are known to produce tetanicspasms. The mental condition of the pa-tient and the surrounding circumstances ofthe case will aid you greatly in eliminatinguch a cause. In strychnine poisoning,

orthotonos is produced as soon as the drughas been absorbed, and tetanic spasms ofmuscular groups pass in a descending direc-tion.

Hysteria may simulate tetanus, but youmust remember that your hysterical patientcannot, for any length of time, maintainmuscular spasm limited to definite musculargroups. The pupils of the eyes in tetanusare generally contracted, and the tempera-ture is increased, while in hysteria both ofthese symptoms are absent.

The next disease which may be mistakenfor tetanus is cerebro-spinal meningitis. Ifan epidemic of this disease prevails in yourlocality, carefully consider the differentialdiagnosis. In cerebro-spinal meningitis thesymptoms point equally to an affection of thebase of the brain, while brain symptomsproper do not belong to the clinical history

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of tetanus; hence, you will encounter symp-toms in the former which point towards anactive inflammation of the meninges of thebrain, as well as of the spinal cord. If thedisease has lasted for a sufficient length oftime, you will look for the symptoms aside ofmuscular spasm which characterize cerebro-spinal meningitis. Basilar meningitis is at-tended by symptoms indicating irritation atthe base of the brain; and as it is almost al-ways of a tubercular nature, you will care-fully inquire into the history of the case, andconcomitant tubercular lesions.

The last disease which it might be mistakenfor is hydrophobia. The muscular spasmsin hydrophobia are more of a clonic charac-ter, and remain limited to the muscles ofdeglutition and respiration. In the progno-sis you must be guided, in the first place, bythe extent of the central lesion, as evidencedby the number of muscular groups affected.If the central irritation is circumscribed,only a limited number of muscular groupsare affected, and when this is the case, weare usually dealing with a mild form, of thedisease. If, on the other hand, in the earlyhistory of the disease there is rigidity of anextensive muscular area, the disease is agrave one ; and more particularly if at thesame time, as will likely be the case, there isa high temperature. Time is one of your

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most important elements in rendering a prog-nosis. Hippocrates always considered theprognosis dubious the first four days. Severecases may terminate fatally from the secondto the sixth day, usually, so that time gainedafter the sixth day, with the symptoms re-maining stationary, the prognosis becomesmore favorable as time increases. In themild cases of tetanus, terminating in recov-ery, it may take weeks and sometimes monthsbefore all muscular rigidity has disappeared.I have observed several severe and acutecases where within forty-eight hours after thecommencement of the first symptoms, deathoccurred; but after the sixth day, with symp-toms remaining stationary, the surgeon’s hopeincreases as time elapses.

Another important point is the probablecause of the disease. If the injury has beenslight, infection limited, the disease assuminga mild type, your prognosis may be favor-able ; but should the symptoms develop them-selves incidental to injuries grave in them-selves, the prognosis becomes correspondinglyserious, so that in tetanus attending severelesions, followed by traumatic infection ofother types, attended, perhaps, by septicaemiaor pyaemia, our prognosis always must be un-favorable ; in other words, if there is no pos-sibility of removing the primary cause or

source ofinfection or irritation, the prognosisincreases in gravity.

Like in all other forms of wound infectivediseases, the prophylactic treatment is themost important. Practically, it is importantto recognize the microbic origin, and insthtute early and efficient treatment in accord-ance with this supposition. I therefore,again, emphasize the necessity of adoptingaseptic measures in the treatment of wounds,with a view not only of preventing suppur-ation, but also other forms of infection.There can be no question but that since theintroduction of antiseptic surgery tetanushas been uncommon. The clinical fact ispatent that it is prone to follow injurieswhere a foreign body has remained in thewound, and where subsequently from thiscause there is greater danger of infection onthe one hand, and peripheral irritation onthe other ; this is especially true of injuriesabout the hand. It is therefore of para-mount importance to treat slight injuries ofthe hand, and more especially 4th of Julyinjuries, which so frequently end in tetanus,with the greatest care. No matter howtrifling the injury may be, disregard in thisdirection has only too often been followed bythe most serious consequences. A smallwound of the hand when neglected may serve

22as aii avenue for the ingress of germs, whichaccording to their action may destroy life ina variety of ways. If necessary, enlargethe wound, search carefully for foreignbodies, if there is reason to believe that theyare present; take plenty of time to securean aseptic condition for the wound, and con-duct the subsequent treatment on strictlyantiseptic principles. If suppuration shouldtake place, be sure to secure efficient drain-age, and resort to frequent antiseptic irriga-tions. By following these directions youwill not only have the satisfaction of secur-ing the most favorable conditionfor the heal-ing of the wound, but you will have, at thesame time, carried out the most efficient pro-phylactic treatment against tetanus.

In the curative treatment, we considerfirst the importance of removing the sourceof infection and irritation. If a foreignbody remains in the wound, search diligentlyfor it, and if possible remove it. If the in-jury is attended by inflammation, burrowingof pus, destruction of tissue underneath theskin, secure ample and efficient drainage;in other words, convert the wound, as nearas you can, from a septic into an asepticcondition. If we are dealing with a painfulor tender cicatrix, which by producingperipheral irritation may determine tetanic

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spasms, it is proper to excise it. We canreadily conceive that the infection may havebeen so mild as to produce only slightchanges in the spinal cord, which but forsome peripheral irritation would not haveresulted in muscular spasms, and these arethe cases where the removal of the excitingcause of* the spasms is followed by a cure.I recollect a case of a mild form of tetanus,the result of a slight injury at the distal ex-tremity of the index finger, which left apainful, tender scar, where the trismus wasalways increased by pressure, and whichyielded promptly to removal of the excitingcause.

Another practical point in the treatmentis the consideration of the propriety of am-putation. If we are dealing with a com-pound comminuted fracture of the leg ora rm, attended by all the symptoms of woundinfection, and if present indications pointtowards the fact that the limb, independentlyof the existence of this complication, couldnot be saved, it is only rational to resort toamputation. It is, however, proper to statethat in the great majority of the cases thustreated the tetanus continued unabated afterthe operation, and only in exceptional caseshas life been saved by this procedure. Rec-ognizing the fact that according to Rokitan-

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sky’s theory, tetanus simply means “ an as-cending neuritis from the point of injury tothe spinal cord,” attempts have been made toarrest the progress of the disease by inter-rupting the nerve above the disease by nervesection, but results have shown that this op-eration had no effect in modifying the ter-mination of the disease. You will readilyunderstand why, if you assume its centrallocation and its infective character. If tet-anus were simply a “ neuritis ascendens,”we might reasonably expect to arrest theprogress of the disease bv division of thenerve trunk, by making the section throughhealthy tissue on the proximal side of theinflamed portion of the nerve. Grantedthat this operation would be efficient in pre-venting extension of the inflammatory pro-cess, it would not be applicable in all in-stances, from the inability of the surgeon tolocate the disease with sufficient accuracy.Imagine an injury involving the palm ofthehand, where we have filaments of differentnerves implicated; it would be difficult if notimpossible to ascertain in every case whichnerve trunk was the seat of irritation. Tak-ing it for granted that the neuritis is simplya local expression of the nerve injury, andthat the real cause of tetanus consists in aspecific infection, expending itself upon the

brain and spinal cord, all efforts at correct-ing or curing the disease by submittingnerve trunks to operative measures are indiscord with the true pathology of the dis-ease. A somewhat similar and more recentoperation for the same object as nerve section,we find in nerve stretching. For the lastfew years it has become the operation for allobscure nervous diseases, such as locomotorataxia and central irritation of variouskinds ; consequently it is not surprising thatit has been resorted to in the treatment oftetanus.

Benedict collected twenty-four cases oftraumatic tetanus treated by nerve-stretch-ing, of which number four recovered. I havestated that the disease in the milder formshows a tendency to cure itself; consequently,all operative measures which have been re-sorted to for the purpose of arresting its pro-gress must be accepted with a great deal ofcaution, inasmuch as statistics have shown,on the whole, that twenty-five per cent, haverecovered without operative interference bythe ordinary treatment; consequently, wehave no proof that these four cases wouldnot have recovered without nerve-stretching.All the possible good that can accrue fromoperations on nerve-trunks is simply to in-terrupt the nerve-current between the central

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disease and the peripheral irritation, and inmany instances it is impossible to decidewhich of the larger trunks connects the two.

The medical treatment consists in the ad-ministration of drugs which are known torelieve muscular spasm. In animals tetan-ized with strychnine the spasms are promptlyrelieved by injecting hydrate of chloral intothe veins. Woorara has been given with aview of relieving muscular spasm. On ac-count of the potency of this remedy, its ef-fects must be carefully watched and its usepromptly suspended as soon as its physio-logical action becomes apparent. It is bestadministered hypodermatically. Bromide ofpotassium in large doses is well known tocause cerebral anaemia, and on this accountit should be given to relieve the hypersemiawhich is always present in the cerebro-spinalcentres. A combination best adapted to ful-fil the two most urgent indications, to relievecerebral and spinal congestion and to over-come muscular spasm, are chloral and bro-mide of potassium. The remedies should begiven in large doses, frequently repeated, un-til the desired result has been obtained. Insevere cases, chloroform should be adminis-tered by inhalation with a view of relievingurgent symptoms; cold drafts of air, noise,and all forms of peripheral irritation, should

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be carefully excluded from the patient’sroom, for the purpose of securing rest, andwith a view of not aggravating reflex spasm.Alcoholic stimulants and external heat areindicated when the heart’s action has becomefeeble from general capillary stasis.