ABSTRACT OF THE Gulstonian Lectures ON SOME CEREBRAL LESIONS
2
739 ABSTRACT OF THE Gulstonian Lectures ON SOME CEREBRAL LESIONS. Delivered at the Royal College of Physicians, BY G. NEWTON PITT, M.A., M.D., F.R.C.P. LECTURE I. FATAL CASES OF EAR DISEASE. IN making a study of cerebral lesions some are found to occur so infrequently that no one can have a very large personal experience of them, and in order to obtain any thorough knowledge of the various complications and the frequency with which they take place it is usually necessary for authors to collect the many cases scattered through current literature. These reports vary much in value, and they all labour under the great defect that they have been published because they illustrated some special point or on account of their rarity. Deductions drawn from such sources are therefore defective, owing to the omission of less striking cases. The alternative is to collect the experience of a large institution, such as a London hospital; the series will then be free from gaps, and it will be possible to form a much truer estimate of the disease as a whole; the dis- advantage, of course, is that the number of cases is much more limited. I have therefore confined myself to the unpublished records of Guy’s Hospital, and among these have taken only those which proved fatal during their stay. I desire to express my appreciation of the kindness of my colleagues in placing their cases at my disposal, and I am more particularly indebted to Dr. Goodhart, who made a large number of the post-mortem examinations. I intend first to deal with the cases of ear disease which have proved fatal from the secondary complications they have set up in the cranial cavity. Two of the commonest complications to which they may give rise are cerebral abscesses and thrombosis of the sinuses. In my second lecture I propose to discuss the other causes of these affections, and to analyse the sym- ptoms which were recorded. In my last lecture I shall examine the fatal cases of cerebral emboli and of cerebral aneurysms, which are for the most part included among them, as there are but few which are not due to this cause. I have examined the post-mortem records from 1869 to 1888, a period of twenty years, and have found fifty-seven inspections in which ear trouble had set up disease in the cranial cavity, which ultimately proved fatal. During this period there were nearly nine thousand inspec- tions. No case of simple otitis media, with or without disease of the mastoid cells, was fatal during the whole of this period, and only twice was the fatal complication out- ;side the cranial cavity, it being in one a retro-pharyngeal abscess and in the other haemorrhage from ulceration into the internal carotid artery. The difficulties of diagnosis in -ear disease are much increased by the fact that not only may a patient die without any otorrheea being noticed, but in two instances the membrana tympani was found intact at the inspection. Of the 57 cases, 34 were males and 23 females; the left ear was rather more frequently affected than the right. Seventeen of the patients were under ten, 17 were between ten and twenty. 14 between twenty and thirty, and only ’9 over thirty. The acute symptoms in ear disease appear sometimes to come on spontaneously ; at others, they have followed exposure to cold, a blow on the ear, mastoid suppuration, the introduction of foreign bodies into the external meatus, or the removal of a polypus. Any of these causes may start acute inflammation, which will be indicated by an increase in the otorrhoea if there be a sufficient outlet, but by a cessation of the discharge if the swollen mucous membrane blocks up the exit. If the pus is pent-up under tension, earache and headache will develop ; but only those cases, in this series, proved fatal in which the inflammation had spread outside the petrous bone. The majority of the- cases, if freely drained by opening up the mastoid cells, recover, and many of them ultimately discharge their pus externally without surgical aid. Toynbee thought that affections of the external meatus and mastoid cells produced disease in the lateral sinus and cerebellum, that affections in the tympanic cavity produced disease in the cerebrum, and that affections of the vestibule and cochlea pro- duced disease in the medulla oblongata. As I shall show later on, thrombosis of the lateral sinus often has originated from caries of the posterior wall of the tympanic cavity, and mastoid disease sometimes spreads to the middle fossa of the skull; still, the usual sequence is that indicated by Toynbee. Disease of the internal ear appears usually to set up meningitis in the posterior fossa of the skull. Anatomical and post-mortem evidence have led me to the conclusion that the condition of the mastoid cells, and of the roof of the tympanum, and the situation of the lateral sinus, play the most important part in determining the direction in which the disease shall spread, and that therefore too great stress should not be laid on the presence or absence of disease of the mastoid, although it may be somewhat of a guide to the seat of the mischief. The condition of the wall of the middle ear teaches nothing which can be of assistance in diagnosis. The most convenient arrangement of the complications to be discussed will be according to their site: (1) dura mater, (2) cerebral tissue, (3) sinuses (4) pia-arachnoid. Owing to the thinness of the tympanic roof, the dura mater over the anterior surface of the petrous bone is rather more often inflamed than that over the posterior wall of the middle ear, but less often if we include the part bounding the mastoid cells as well. The otorrhoea in these cases is of old standing; generally the bone beneath is inflamed, discoloured, carious, or necrosed, and in some of the cases the bone presented carious apertures, through which the infection had spread directly. Inflammation or sloughing of the dura mater occurred in ten out of twelve cases of temporo-sphenoidal abscess, and probably seven of these could not have recovered unless the dura mater as well as the abscess could have been allowed to drain. In extra- dural abscesses, which may produce optic neuritis, the in- flammation has probably spread along the lymphatics around the veins. In three cases of mastoid disease which recovered after trephining, and one without trephining, there was optic neuritis. Of eighteen cases of cerebral abscess, nine occurred on each side of the brain, and the preponderance which Gull and Sutton found in their twenty-four cases in favour of the right side was probably accidental. In the cases I am considering all of the patients were men, and thirteen of the cases occurred between the ages of ten and twenty-nine, the only case over forty being one of pontic abscess. They agreed with the general experience that otorrhoea does not set up cerebral abscess until it has lasted months or years, for in only two was its duration under a year. Three of the abscesses were in the cerebellum, one in the pons, two in the centrum ovale, and the remaining twelve in the temporo-sphenoidal lobes within a very short distance of the tympanic roof. The dura mater in this latter group was healthy in only two, in eight it was sloughing, in two inflamed, and in one there was a localised extra-dural abscess. When there is healthy brain tissue between the temporo- sphenoidal abscess and the bone it is probable that the infection has been spread by the veins which empty into the superior petrosal sinus from the temporo-sphenoidal lobe on the one hand, and the tympanum on the other, by means of a septic phlebitis, or, more pro- bably, by means of the perivascular lymphatics ; for if it had been due to a phlebitis, thrombosis of the superior petrosal sinus would have been occasionally noticed. Frequently the brain adheres to the anterior surface of the petrous bone over which the dura is inflamed, and thence infection spreads by contact to the cerebral tissue. The two abscesses in the centrum ovale originated, the one from thrombosis of a vein from the Sylvian fissure to the dura. mater, and the other from pyaemic infection due to an old septic thrombus in the lateral sinus on the opposite side. An extra-dural abscess behind the petrous bone started one of the cerebellar abscesses, and another had originated near the torcular Herophili from an old thrombus in the lateral sinus. Only five of the abscesses were less than an inch in diameter, while ten exceeded two inches. Death was preceded by coma in the majority of instances.
Transcript of ABSTRACT OF THE Gulstonian Lectures ON SOME CEREBRAL LESIONS
739
ABSTRACT OF THE
Gulstonian LecturesON
SOME CEREBRAL LESIONS.Delivered at the Royal College of Physicians,
BY G. NEWTON PITT, M.A., M.D., F.R.C.P.
LECTURE I.FATAL CASES OF EAR DISEASE.
IN making a study of cerebral lesions some are found tooccur so infrequently that no one can have a very largepersonal experience of them, and in order to obtain anythorough knowledge of the various complications and thefrequency with which they take place it is usually necessaryfor authors to collect the many cases scattered throughcurrent literature. These reports vary much in value, andthey all labour under the great defect that they have beenpublished because they illustrated some special point or
on account of their rarity. Deductions drawn from suchsources are therefore defective, owing to the omission of lessstriking cases. The alternative is to collect the experienceof a large institution, such as a London hospital; the serieswill then be free from gaps, and it will be possible to form amuch truer estimate of the disease as a whole; the dis-advantage, of course, is that the number of cases is muchmore limited.
I have therefore confined myself to the unpublished recordsof Guy’s Hospital, and among these have taken only thosewhich proved fatal during their stay. I desire to expressmy appreciation of the kindness of my colleagues in placingtheir cases at my disposal, and I am more particularlyindebted to Dr. Goodhart, who made a large number of thepost-mortem examinations. I intend first to deal withthe cases of ear disease which have proved fatal fromthe secondary complications they have set up in the cranialcavity. Two of the commonest complications to which theymay give rise are cerebral abscesses and thrombosis of thesinuses. In my second lecture I propose to discuss theother causes of these affections, and to analyse the sym-ptoms which were recorded. In my last lecture I shallexamine the fatal cases of cerebral emboli and of cerebralaneurysms, which are for the most part included amongthem, as there are but few which are not due to thiscause. I have examined the post-mortem records from1869 to 1888, a period of twenty years, and have foundfifty-seven inspections in which ear trouble had set updisease in the cranial cavity, which ultimately proved fatal.During this period there were nearly nine thousand inspec-tions. No case of simple otitis media, with or withoutdisease of the mastoid cells, was fatal during the whole ofthis period, and only twice was the fatal complication out-;side the cranial cavity, it being in one a retro-pharyngealabscess and in the other haemorrhage from ulceration intothe internal carotid artery. The difficulties of diagnosis in-ear disease are much increased by the fact that not only maya patient die without any otorrheea being noticed, but intwo instances the membrana tympani was found intact atthe inspection.Of the 57 cases, 34 were males and 23 females; the left
ear was rather more frequently affected than the right.Seventeen of the patients were under ten, 17 were betweenten and twenty. 14 between twenty and thirty, and only’9 over thirty. The acute symptoms in ear disease appearsometimes to come on spontaneously ; at others, theyhave followed exposure to cold, a blow on the ear,mastoid suppuration, the introduction of foreign bodiesinto the external meatus, or the removal of a polypus.Any of these causes may start acute inflammation, whichwill be indicated by an increase in the otorrhoea if therebe a sufficient outlet, but by a cessation of the dischargeif the swollen mucous membrane blocks up the exit. Ifthe pus is pent-up under tension, earache and headachewill develop ; but only those cases, in this series, provedfatal in which the inflammation had spread outside thepetrous bone. The majority of the- cases, if freely
drained by opening up the mastoid cells, recover, andmany of them ultimately discharge their pus externallywithout surgical aid. Toynbee thought that affectionsof the external meatus and mastoid cells produced diseasein the lateral sinus and cerebellum, that affections inthe tympanic cavity produced disease in the cerebrum,and that affections of the vestibule and cochlea pro-duced disease in the medulla oblongata. As I shallshow later on, thrombosis of the lateral sinus oftenhas originated from caries of the posterior wall of thetympanic cavity, and mastoid disease sometimes spreads tothe middle fossa of the skull; still, the usual sequenceis that indicated by Toynbee. Disease of the internalear appears usually to set up meningitis in the posteriorfossa of the skull. Anatomical and post-mortem evidencehave led me to the conclusion that the condition of themastoid cells, and of the roof of the tympanum, and thesituation of the lateral sinus, play the most importantpart in determining the direction in which the disease shallspread, and that therefore too great stress should not belaid on the presence or absence of disease of the mastoid,although it may be somewhat of a guide to the seat of themischief. The condition of the wall of the middle earteaches nothing which can be of assistance in diagnosis. Themost convenient arrangement of the complications to bediscussed will be according to their site: (1) dura mater,(2) cerebral tissue, (3) sinuses (4) pia-arachnoid.Owing to the thinness of the tympanic roof, the dura mater
over the anterior surface of the petrous bone is rather moreoften inflamed than that over the posterior wall of themiddle ear, but less often if we include the part boundingthe mastoid cells as well. The otorrhoea in these cases isof old standing; generally the bone beneath is inflamed,discoloured, carious, or necrosed, and in some of the casesthe bone presented carious apertures, through which theinfection had spread directly. Inflammation or sloughingof the dura mater occurred in ten out of twelve cases oftemporo-sphenoidal abscess, and probably seven of thesecould not have recovered unless the dura mater as well asthe abscess could have been allowed to drain. In extra-dural abscesses, which may produce optic neuritis, the in-flammation has probably spread along the lymphaticsaround the veins. In three cases of mastoid disease whichrecovered after trephining, and one without trephining,there was optic neuritis.Of eighteen cases of cerebral abscess, nine occurred
on each side of the brain, and the preponderance whichGull and Sutton found in their twenty-four cases in favourof the right side was probably accidental. In the cases I am
considering all of the patients were men, and thirteen of thecases occurred between the ages of ten and twenty-nine,the only case over forty being one of pontic abscess. Theyagreed with the general experience that otorrhoea does notset up cerebral abscess until it has lasted months or years,for in only two was its duration under a year. Three ofthe abscesses were in the cerebellum, one in the pons, twoin the centrum ovale, and the remaining twelve in thetemporo-sphenoidal lobes within a very short distance ofthe tympanic roof. The dura mater in this latter groupwas healthy in only two, in eight it was sloughing, in twoinflamed, and in one there was a localised extra-duralabscess.When there is healthy brain tissue between the temporo-
sphenoidal abscess and the bone it is probable that theinfection has been spread by the veins which empty intothe superior petrosal sinus from the temporo-sphenoidallobe on the one hand, and the tympanum on theother, by means of a septic phlebitis, or, more pro-bably, by means of the perivascular lymphatics ; for ifit had been due to a phlebitis, thrombosis of the superiorpetrosal sinus would have been occasionally noticed.Frequently the brain adheres to the anterior surface ofthe petrous bone over which the dura is inflamed, andthence infection spreads by contact to the cerebral tissue.The two abscesses in the centrum ovale originated, theone from thrombosis of a vein from the Sylvian fissureto the dura. mater, and the other from pyaemic infection dueto an old septic thrombus in the lateral sinus on the oppositeside. An extra-dural abscess behind the petrous bonestarted one of the cerebellar abscesses, and another hadoriginated near the torcular Herophili from an old thrombusin the lateral sinus. Only five of the abscesses were lessthan an inch in diameter, while ten exceeded two inches.Death was preceded by coma in the majority of instances.
740
The following conclusions may be drawn from the presentseries of cases. Abscesses in the temporo-sphenoidal lobe,which is the most common situation, are often associatedwith an inflamed or sloughing dura mater over theanterior surface of the petrous bone, or with a collectionof pus beneath it. Other complications are infrequentexcept meningitis, which is generally due to the exten-sion or to the rupture of the abscess, which is almostalways situated very close to the roof of the tympanum. Afoul discharge is often a source of danger, and frequently,if not invariably, the spread of the mischief is due toimperfect drainage of the middle ear. Mastoid suppurationoften infects the posterior surface of the petrous bone, butit may be associated with disease limited to the middlefossa of the skull. Cerebral abscesses only occur when theotorrhcea has lasted for months or years. The symptomsusually come on insidiously, being vague for a considerabletime, which may be called the latent period; during thistime headache, vomiting, and a slow dull mental conditionare usually present. After a variable period the acute stageis entered upon, which may last less than a week; agonisingheadache is the most marked symptom, but it may not benoticed if the patient be very lethargic. The temperatureis rarely high with uncomplicated cerebral abscess; it wasnot above the normal in six cases; in eight it was high,but three of these had meningitis, two thrombosis of thelateral sinus, and two marked lesion of the dura mater.The pulse is often increased in rate, but when the abscessis large it may become slow and irregular. Tenderness ofthe scalp was not especially noticed. Rigors and pyrexiaare not frequent in uncomplicated cases, but they bothoccur occasionally. A headache of intense severity and adull, sluggish mental state are the two most characteristicsymptoms. Optic neuritis is but infrequently noticed, andis often in such cases due to a complication.The three cases of cerebellar abscess presented no very
marked signs. They appear to be less common, and willbe probably found associated with disease of the dura materbehind the petrous bone or with thrombus of the sinus.There is no evidence, pathological or other, that cases
of cerebral abscess ever recover without the aid of asurgeon, and although a few successful cases have beendrained, even now almost every one is fatal. The objectsto be aimed at in treatment are—() In every case toimprove the drainage of the ear by gouging away ortrephining the mastoid sufficiently to open up the hori-zontal cells or antrum, where pus is often found, andto break a hole through the deeper part of the posteriorwall of the external meatus, so as to allow no secretion tobe retained. The cavity should be rendered aseptic as soonas possible, and in a case of otitis media this should becarried out as soon as there is evidence of a fresh accession ofsevere mischief; should further exploration be necessary lateron, one great source of danger, the septic otorrhcea, will bemuch reduced. The external ear should be dressed apartfrom other openings, if any are made. (b) To expose theanterior surface of the petrous bone so as to allowfree drainage for any pus or debris which may haveformed in connexion with the dura mater, which isoften inflamed or gangrenous. This is best reached ata point half an inch above the external meatus. Shouldthere be any pus retained, some will often be found in thediploe of the bone removed, in which case the bone shouldbe broken away to a quarter of an inch above and just infront of the meatus, so as to expose the most dependentpart of the anterior surface (c) to drain the abscess frombelow when possible. In the case of a temporo-sphenoidalabscess, the area beneath which it will almost universallybe found may be said to be bounded anteriorly andposteriorly by curved lines drawn through the temporo-maxillary joint and the middle of the mastoid, running atright angles to the sagittal suture and lying between halfan inch to two inches above the meatus. The lower partof this area should therefore be explored with trocar andcannula after breaking the bone away, or trephining afresh hole, unless special symptoms indicate that theabscess is higher. If the attempt to find pus is un-successful, the lateral sinus should be exposed half aninch behind the meatus and examined ; if there isno extra-dural abscess and the sinus is healthy, thebone may be further broken away, and the outer and underpart of the cerebellum explored for abscess. By this methodall the likely seats for pus to accumulate can be systemati-cally examined, and we give the patient the best chance.It is necessary to examine all these seats in doubtful cases,
because, although in some uncomplicated instances we maybe able to determine the lesion fairly definitely, yet wheretwo or more lesions are combined the uncertainty in thediagnosis is so great that the best method is to explore allpossible spots where pus may be collected.Thrombosis of the lateral sinus occurred twenty-two times.
The condition both of the wall of the vein and of its con-tents varied. In some there was well-marked phlebitis; inconsiderably more than half the thrombus was suppurating,and in others, where not breaking down, it had set up a pul-monary pyaemia, thus demonstrating its septic nature. Thedisease more often spreads from the posterior wall of the middleear than from the mastoid cells; this is important, for anytreatment to be successful must deal with the condition ofthe bone and dura mater as well as with the sinus. When-ever the mastoid vein, which perforates an inch and aquarter behind the meatus and on a level with it, is foundthrombosed, the sinus should be explored. The clot maybe a small one or it may occupy the whole of the sinus andspread into the internal jugular or general venous system ofthe skull. Thrombosis is a fatal lesion, but there is someevidence that patients with the typical symptoms appear torecover, at any rate for a time. The otorrhoea is generally,but not always, of long standing; in only five it lastedless than seven weeks. The onset is usually sudden, thechief symptoms being pyrexia, rigors, pain in the occipitalregion and in the neck, associated with a septicsemiccondition. Earache, as distinct from headache, is more com-mon than with meningitis and abscess; vomiting and comawere also met with. In no other complication are erraticpyrexia and rigors so constantly present, and it will bealways justifiable to assume that they probably indicatethrombosis in any patient in whom freely opening thedeeper mastoid cells and draining the ear have not beenfollowed by their subsidence. Well-marked optic neuritis.may be present, and is more suggestive of sinus thrombosisthan of other lesions. The appearance of acute localpulmonary mischief or of distant suppuration is almostconclusive of thrombosis ; and, as death in three-quarters ofthe cases ensues from pulmonary pyaemia after a courseof but three weeks, treatment, to be of any value, mustbe directed to the prevention of the pysemia. Whensuch a danger has to be combated we must be willingto run great risks in order to save some of the patients.The internal jugular vein should be ligatured in theneck, the lateral sinus should be opened, and, if the clotbe very foul and septic, it may be scraped out, renderedaseptic as soon as possible, and, if desirable, irrigated. Insome instances it may be better to ligature the jugular veinlow down in the neck, seal the wound, then ligature anddivide the vein higher up, the upper end being brought outso as to allow any septic material that may pass down toescape externally. This line of treatment, which mayseem too heroic, has been recommended by surgeons, andcarried out successfully, and only some such method canavert the pulmonary infection which carries off thesepatients. This same treatment deals with the dura materover the posterior surface of the petrous bone, which,,if neglected, is a source of danger to nearly half itsvictims. If the lateral sinus, after it has been punc-tured, whether purposely or accidentally, be found to behealthy, thrombosis need not necessarily ensue. I haveseen this happen three times, and no evil results followed,the patients dying from other causes.
SUBACUTE INDURATIVE PNEUMONIA.1BY PERCY KIDD, M.D., F.R.C.P.,
ASSISTANT PHYSICIAN AND PATHOLOGIST TO THE BROMPTON HOSPITALFOR CONSUMPTION AND DISEASES OF THE CHEST.
IT is not intended on the present occasion to discuss thesubject of pulmonary induration in its general bearings,the object of this paper being to consider the group of casesin which fibrous changes in the lung are the direct sequel ofa more or less acute pneumonia. Contradictory opinionshave been expressed concerning the termination of acutelobar croupous pneumonia in induration. Some authorities,among whom are Rokitansky, Buhl, Wilks, and Wagner,deny that the acute classical pneumonia ever passes into a
1 Paper read at the Medical Society of London, March 24th.
