Publications of Dr.H.O.Gunewardene, M.B.,B.S. Lond. D.M.R.E. Cant. Consultant Cardiologist, Radiologist. Dr. Gunewardene was the father of Ian Gardner who was born Basil Ian Gunewardene in Sri Lanka, then Ceylon. This file was compiled for the benefit of posterity.
1 DR. H. O. GUNEWARDENE M.B.,B.S. Lond., D.M.R.E. Cant. . December 1942 Hubert Oliver Gunewardene was born in Sri Lanka, then Ceylon, on June 6 th . 1890. He was educated at the Colombo Academy, which later became Royal College, studied medicine at the Medical College, Colombo, and did his post graduate work in London, England, where he later had rooms in Harley Street as a Consultant Cardiologist. He later returned to Ceylon to practice. In about 1933, at the behest of the Government, he returned to England to study radiology to set up and head, in Colombo, Ceylon’s first Department of Radiology and X-ray facility. 1
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DR. H. O. GUNEWARDENEM.B.,B.S. Lond., D.M.R.E. Cant.
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December 1942
Hubert Oliver Gunewardene was born in Sri Lanka, then Ceylon, on June 6th. 1890. He was educated at the Colombo Academy, which later became Royal College, studied medicine at the Medical College, Colombo, and did his post graduate work in London, England, where he later had rooms in Harley Street as a Consultant Cardiologist. He later returned to Ceylon to practice. In about 1933, at the behest of the Government, he returned to England to study radiology to set up and head, in Colombo, Ceylon’s first Department of Radiology and X-ray facility.
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Dr. Gunewardene, second from right, with friends and his son Ian*, on his right, in 1952.*On leaving Sri Lanka in 1969 Ian changed his surname to Gardner.
Mrs. H.O.Gunewardene, fifth from left, her daughter, second from left, her then daughter-in-law, seventh from left, with relatives in England in 1957.
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POSTED HERE ARE SOME OF
DR. GUNEWARDENE’S PUBLICATIONS
ON
HEART DISEASEET AL
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DR. H. O. GUNEWARDENEM.B.,B.S. Lond., D.M.R.E. Cant.
1890 - 1954
Thirty-five Years Study Of Clinical Heart Disease*Being
The unfinished manuscript of a paper written by the late Dr. H.O.Gunewardene, Consultant Cardiologist, Colombo.
*Read by Dr.Stanley de Silva at the 67th.Anniversary Meeting of the Ceylon Medical Association (Section on Medicine) on 15th. November 1954.
This document was posted from May & Baker Ltd., Dagenham, England on 28 June 1966 to Dr Guy de Silva, nephew of Dr. Gunewardene, who handed it over to Dr. Gunewardene's widow who added the notation "Unfinished Manuscript".
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JAN. 4; 1936 ~~~~~~~~~~~~CORl?ESPOND)EN' E tEIMABITURN't 87JAN.~~-496-C.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~EIA ..tNA" The Local Origin of Cancer. The application of these
observations, Dr. Gye continues, lies in the fact that almostall the ' cancer cures ' which are produced from time to timeare based on the idea that the tumours arise from some con-stitutional defect in the body of the patient. . . Thetheories upon which these practices are based are in obviousconflict with the conception of the nature of cancer indicatedabove. "As the heading indicates, the section is devoted to stress-ing the view that the constitutional and local origintheories are opposed and mutually exclusive: " Constitu-tion Avenue Closed." In the next section we read,inter alia:
" Professor Kennaway and his collaborators have been ableto synthesize chemically pure substances with definite carcino-genic Properties. Some of these stubstances are relatedchemically to the sterols, which are normal constituents ofthe body." (Italics mine.)
Really, Sir, but for the prominent notice we saw Ishould have said we were in Constitution Avenue after all." Normal constituents of the body," " related chemi-cally," " carcinogenic properties ": did I hear someonesay " It is Constitution Avenue "? How came we here,then? That side entrance you cannot have noticed,marked " Private, for Laboratory Workers Only ; for KeyApply in Person to Director." Shelley, long ago, wrote:
"Nature has gifted Man with all-subduing will;Matter, with all its transitory shapes,Lies subjected and plastic at his feet."
Cancer has not quite yielded yet to that all-subduingweapon. There are many whose lot does not permit ofwhole-time devotion to that end. There are intelligentpeople among the laity as sincerely interested in thecampaign- as the whole-timers. To these classes annualreports are the most authentic sources of information.While no one would claim for them infallibility, yetcoming with the imprimatur they do, they are takenas of ex cathedra status, so it is of some importance thatthey shall be at once intelligible and trustworthy guidesto the existing situation. Incompatibles, besides beingunpalatable, are unaesthetic.Only when the goal has been reached will it be seen
what body of opinion and method of attack has been mostnearly on the direct course. Wait and see. Meantime,could the director, be directed to rewrite this report-omitting the sobstuff and the special pleadings but care-fully correlating the data-it would be time well spent.Also we may remind ourselves that progress is not neces-sarily rectilinear as in Euclidean postulate. It may besinusoidally serpentine, corkscrew, or (even as appearsin this case) a kind of zigzag.-I am, etc.,London, W.6. Dec. 19th, 1935. W. M. HEWETSON.
Heart Disease in the TropicsSIR,-Will you permit me to make a reference to one or
two points in the review of my book Heart Disease in theTropics which appeared in a recent issue of your Journal?The " perhaps unnecessary detail" appeared necessary tome as author because I felt that no detail should be leftout in support of an observation that diastolic murmurswhich were diagnosed by most competent observers-oneof them a gold medallist in medicine in the London M.D.-as aortic regurgitation or mitral stenosis disappeared in thecourse of treatment, a fact in favour of which no moderntextbook gives any support. The reference to diabeteswas made owing to the very common prevalence of highgrades of glycosuria in men and women in Ceylon, and inkeeping with my concurrence with the author in his viewcontained in the best book on the heart I have read inrecent years: " Toxic blood states such as occur indiabetes and nephritis must act deleteriously on themyocardium and vessels " (Vital Cdrdiology, by Bruce
Williamson, 1934). High blood pressure was given specialspace because it should have a place similar to rheumaticcarditis in the textbooks now in use in the Tropics, whichdo not give it the consideration it deserves. I consideredit needed a special place in view of the fact that a fewyears ago there were not, in a country with severalhundred practitioners, any more than half a dozen bloodpressure instruments, and consequently that hypertensionwas not recognized as a common cause of cardiacdisability.-I am, etc.,December 16th, 1935. H. 0. GUNEWARDENE.
Medico-Legal
DEATH FROM AMIDOPYRINE POISONINGA death from amidopyrine poisoning, the second in thecourse of a few weeks, was the subject of an inquestheld by Dr. Bentley Purchase, H.M. Coroner for St.Pancras, on December 13th and 20th. Sir BernardSpilsbury, who performed the necropsy, said that thedeceased was a stout woman of 60 with signs of chronicosteo-arthritis and rheumatism. The heart was enlargedand its cavities all dilated ; the surface showed somepetechial haemorrhage. There was also fatty disease ofthe -heart muscle and brown atrophy. The cause of deathas certified was acute bronchopneumonia, the lungs beingcongested, especially in the lower lobes. The thyroid wasrather small, the liver fatty, and there were small haemor-rhages in the spleen; the kidneys were enlarged and con-gested, and the suprarenal glands somewhat enlarged.There was acute inflammation of the tonsils which hadspread over the wall of the pharynx, with some mem-brane on the surface; the entrance to the larynx wasoedematous. There was a certain amount of chronicgastritis. The marrow in the femoral shafts was a deepred. The white cell count on admission had been 4,400cells per c.mm., dropping to 1,000 and rising to 2,000,the figure obtained on the last count before death (fourdays after admission). No polynuclear cells were seen.There was a history that to relieve her rheumatism thepatient had- been in the habit of taking some anti-rheumatic pills.The coroner adjourned the first hearing in order to
allow the chemists who had made the pills to appear ifthey wished. Accordingly, at the adjourned hearing arepresentative of the firm gave evidence that the bottlefrom which the deceased had been taking pills had con-tained when full forty tablets, the analysis of which wasaspirin 21 grains, amidopyrine 1/8 grain, and caffeine1/8 grain. Not only was the prescription stated on thebottle, but the word " Poison " also appeared, as this wouldbe required under the new Poisons Act next May. Thetablets Fjvere packed by a large firm of manufacturingchemists, and were the same as others sold by manyretailers. They had sold large quantities for several yearsand had never before heard of any untoward result.There was no evidence to show the period over whichthe deceased had taken the pills. Sir Bernard Spilsbury,in explaining the aetiology of agranulocytosis, said thatthe sensitivity to amidopyrine could hardly be caused inless than six weeks, and usually took over a year to beestablished. The dosage given on the bottle was twotablets three times a day. Analysis of the organs-wouldprobably have shown no amidopyrine, as the drug wasnot retained in the body.The coroner said that after the last case he had
investigated he had communicated with the Poisons Boardand the Home Office. They had shown great interest,and- he understood that provision was being made toput amidopyrine into the same group as the barbiturates,which were controlled without being labelled as poisonousor dangerous. He considered that the chief requirementwas not to brand the drug as dangerous, but to checkits promiscuous use. On the evidence, he assumed thatthe deceased was one -of the few persons who were sus-ceptible to the action of amidopyrine. He entirelyaccepted the evidence of the chemist's representative that
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OCT. 13, 1934] CORRESPONDENCE THE BRITTSH 699L[MEDICAL JOURNA
CORRESPONDENCE
PublicitySIR,-From time to time you publish in your corre-
spondence columns and elsewhere indignant protests frompractitioners whose articles have been quoted by the laypress, and who wish to repudiate any responsibility fortheir appearance. I wonder if there is any advantage insuch disclaimers., Those who are familiar with the profes-sional status of their colleagues require no such assurance.Others acquainted with the methods of journalism areperfectly well aware that no precautions can preventthese occurrences. And a tiny minority who might bewilling to accuse your correspondents of seeking publicityor notoriety may even interpret the disclaimer as cor-roboration of the original intention! In any case nothingcan prevent the lay journals from quoting from yourcolumns, extracting the relatively dramatic, and un-happily, on occasion, misquoting and misrepresenting.For the author of the original article to protest isobviously useless. Is it too much to say that not oniyis it useless but it is quite unnecessary?
There is another aspect of this subject to which refer-ence may not be inappropriate. The interests of medicalmen are not by any means restricted to their professionallife, and there are certain, outside activities upon whichthey are, rightly or wrongly, 'regarded as authorities, andupon which their opinion is considered to be correspond-ingly desirable. From their familiar-association with theuse of the telephone doctors are particularly fair gamefor attack through this convenient but highly dangerousmedium. And once your ear is at the instrument andyour arrival admitted, and you are inveigled into sayingsomething, no matter what, the mischief is done. If,good-naturedly, you believe you may be doing a serviceto the public-and that really is the motive on mostoccasions-publicity is inevritable. The most ferventrequest to withhold your name is unlikely to be respected,since any news value attaching to the opinion of onewho is being represented to be an authority depenidsentirely upon his name being mentioned. Alternatively,a curt refusal' may rebound upon you'to your subsequentdiscomfiture, and those who have once suffered in thisway have learnt that it pays to be courteous.At midnight a few weeks ago the news editor of one of
the daily papers felt unable to rest until he had telephonedto take my opinion upon a " story " just to hand fromSouth Africa: an indignant protest against holdingOlympic Games for women because there was abundantevidence that some men had actually competed. It sayssomething for my forbearance that my only observation,even at this hour, was that I knew absolutely nothingabout it. Yet this became ingeniously interpreted as anauthoritative denial of the rumour. A week later-againat the (apparently critical) hour of midnight-I wasapproached by another journal in reference to an inquestthat had been held that afternoon, at which the coronerhad expressed his opinion that the suicide of someunhappy young man was due to his " having lived toostrenuously.-" " Did I think the coroner was right?'and " What did I suppose the coroner meant? "
It may be that some of us might succeed in fencingourselves round by a complete secretarial inaccessibility(more appropriaxte, perhaps, to a Pope than to a medicalman), and thus receive adequate protection from tele-phonic assault. But by the time we had acquired aneminence commensurate with such a state we should be" in the news " anyway.-I am, etc.,
London, WV., Oct. 8th. ADOLPHE ABRAHAMS.
Is High Blood Pressure a Risk?SIR,-In your issue of August 25th " M.S., F.R.C.S."
appears to call for a review of the vast amount of workwritten on high blood pressure. The cases to which hemakes reference appear to cast a cynical doubt on thenow recognized fact that, as a rule, high blood pressurecertainly carries with it a risk which, to our shame itmust be admitted, has been seriously overlooked sinceClifford Allbutt drew attention to this disorder. Thecondition, according to Fahr, claims 10,000,000 afflictedin America, and 200,000 deaths a year-an incidence ascommon as cancer and tuberculosis together accordingto Parkinson it is a " very common disease, which isresponsible for so much suffering and mortality in latemiddle life and early old age." I can endorse Parkinson'sobservations even more strongly from my experience inthis country, where the ravages of rheumatic fever arenot so prevalent as in the West, and therefore show uphypertensive failures more readily.One is tempted to ask: Has " M.S., F.R.C.S." met no
other cases of high blood pressure? If he has not he isan extremely lucky medical man. If he has met manycases with such high diastolic pressures, surely there musthave been many with serious complications. I have hadseveral friends and many patients with diastolic pressuresof 170; very few indeed are alive. I have seen fourcases which had systolic pressures of over 300. Thesecould not be recorded, as the manometer only read up tothis figure. The diastolic pressures in them were over 160.All these patients were over 60 years of age, and untila short time prior to a fatal issue had nothing more thanthe mildest general symptoms. One patient of mine, 68years old, apparently in good health, had a systolicpressure of 210 and a diastolic of 95; another, a lady,a systolic of 300 and a diastolic of 90. These strikingexceptions, and many more like them, have not made meceaseu to believe that high blood pressure, particularlywhen it occurs under 50 years of age and once anysymptoms are manifested, is a danger to life of whichsome kind of notice should be taken.An account of the numerous strokes which appear in
these cases is given in my Sir Charles Hastings prize essayon "The Stroke in High Blood Pressure," published inthe British Medical Journal of January 30th, 1932.I am, etc.,General Hospital, Colombo, H. 0. GUNEWARDENE.
Ceylon, Sept. 22nd.
Preliminary Ligature in Toxic GoitreSIR,-The correspondence concerning preliminary liga-
ture in toxic goitre has probably contLnued long enoughfor adequate ventilation of the different opinions thatare held. An excellent summary of the position wassupplied in your issue of September 29th by Sir W. I.de Courcy Wheeler. I cannot, however, remain silent inview of the repetition by Mr. G. Bankoff in your lastissue of the astonishing and dangerous fallacy that thedegree of the reaction depends, not on the amount ofthyroid tissue that is removed, but on how much is leftbeh:nd. If this were true, the only logical inference wouldbe that the lowest mortality rate would be obtained byperforming a total thyroidectomy in all the worst cases.This is contrary to clinical experience, and the principlewould be most dangerous if generally applied. I fullyagree with Mr. Hawe and Mr. Bankoff that " for thegood success of the operation it is imperative to removeat least three-quarters of the gland," and in fact I fre-quently remove more than this. In the great majorityof patients it can be done in one operation, but in a
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THE STROKE IN HIGH ARTERIAL -PRESSURE r THEBRITISH 181L MEDICAL JOURNAL
lesions have developed, the patient has already ceased orforgotten to look upon the earlier symptoms as part cfthe same disease in its undeveloped state.High blood pressure, whatever its etiology, is common
enough in general practice. No one is in a better positionto study those aspects of it which throw light on itscausation, and on some of the features which forecast thefinal doom, than the family practitioner. Methods ofinvestigation are no doubt limited, but the mass of clinicalmaterial is heavy. No apology is made for not resortingto those special tests which can be carried out only ina fully equipped laboratory with a full staff, for thepurpose of this essay is to record the clinical observationsmade on the so-called " stroke " as it occurs in higharterial pressure.
DEFINITION OF "STROKEA stroke is defined in Dorland's Medical Dictionary asa sudden severe attack, as of apoplexy or paralysis."
Saville considers " stroke " to be synonymous withapoplexy, for he defines each word as " a term whichmay be conveniently retained to indicate a sudden un-consciousness due to a vascular lesion within the skull."I propose to resort to a certain degree of licence in theuse of the word, interpreting it as a " sudden severeattack," not necessarily apoplectic, and thus implyingthat these attacks are not confined only to the motor side.There appears to be somb justification for such adeparture, for one finds Batty Shaw saying (under theheading " Persistent or temporary hyperpiesic paralysis "):" Sometimes the paralysis affects the sensory instead ofmotor areas, so that the patient becomes blinded withoutany changes being discovered in the retina or the brain."A little elasticity in my definition seems justified, not onlybecause it helps to explain more fully the various formsthese attacks take, particularly in the earlier stages ofhigh blood pressure, but also because it helps to give amental picture of the much-neglected sensory forms.
FREQUENCY OF STROKEStroke occurs so commonly in high pressure, at
least in Ceylon, that the scant references to it instandard textbooks is surprising. Theodore Thomson inPrice's Textbook of Medicine says, " sometimes transientparalysis occurs," without any mention of the sensoryattacks. Batty Shaw makes the statement quoted abovein a superficial but none too impressive way. East andBain, in Recent Advances in Cardiology, make no referenceto the sensory stroke. In what they call the second stage,they say, " symptoms will rarely be experienced whichrefer to the pressure," also stating that the clinical features" are strikingly few "-this is in contrast to my findingth'at the strokes, all except the apoplectic, are mostcommon at this stage. Vaquez, on the other hand, statesclearly: " Transient aphasia and fleeting paresis, speciallybrachial monoplegia, are frequent incidents in vascularhypertension. They appear and disappear suddenly,leaving no traces, and may occur several months later."He lays some stress on the mental symptoms (uncommonin my series), which, he maintains, assume the mostvaried forms-for example, amnesia, mental confusion,and suicidal tendency.
MOTOR AND SENSORY STROKESDefining " the stroke" as a sudden severe attack
drawing the attention of the subject of hypertension toa change in his normal motor or sensory phenomena, onecan classify " motor strokes " under the main heads ofthe paralytic and the paretic. These can be describedaccording to distribution as: (1) hemiplegic; (2) mono- j
plegic; (3) localized-for example, tongue; and (4) diffuse.The last variety usually occurs as a terminal event, beingdue to a severe haemorrhage which causes sudden death,or to one which produces paralysis, first of one side ofthe body and then of the other. According to theirduration, we may say that they are: (1) permanent,(2) present for a few days or weeks, and (3) transient.The annexed diagram gives a clear picture of what mayoccur on the motor side.
StRO/E
PQtMOR f R SW SoR
, ^tJ PER,IANiNF1W/N O>R s ffwD4Ys OR wEiea
* Dysarthria or aphasia.
On the sensory side we get similar changes: completeloss of sensation, as in coma, and changes in sensation-named " incomplete " for the purpose of the diagram-these being analogous to the paralytic and the pareticforms on the motor side. The distribution and durationare similar to those occurring in the motor phenomena.The diffuse form, including cases in which tingling ornumbness, or " a peculiar feeling all over the head andbody," has been reported, is rare. Changes in sensationhave been variously described by the patients themselves,and may occur associated. with, in the absence of, orfollowing motor phenomena. Tingling and numbness are
common. One patient of mine described the sensation as" a cotton-woolly feeling-the face feels heavy o-fi thatside." A doctor, in whom a monoplegia had disappeared,described as irritating " the peculiar dry feeling of thelimb, as though it had been immersed in formalin andtaken out "; again, " When warm water is taken I feelit hotter on one side of the tongue; and, further, onshaving I do not feel the razor well on the recentlyaffected side." In another case a patient complained ofnurnbness of the ear, left upper limb, and distal part ofthe left leg after motor power had returned His descrip-tion was: " as though I have placed my hand on a lumpof ice and removed it." Of the ear he said: " When Iscratch my ear it feels plain.'
JAN. 30, 1 9321
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182 JAN. 30, 1932] THE STROKE IN HIGH ARTERIAL PRESSURE
DIASTOLIC PRESSURE IN STROKEIt is interesting to study very clearly at what stages
in high arterial pressure the stroke supervenes. In my
series of cases the stroke, sensory or motor, has notappeared in a single instance in which the diastolic bloodpressure was under 115. In 20 per cent. of the cases thestroke-in most transient, in a few permanent, in one
fatal-occurred with a diastolic blood pressure between115 and 120. In ten out of the 150 cases death resultedfrom what appeared clinically to be definite cerebralhaemorrhage; in nine of these, the patients were activelyor restrictedly pursuing their usual occupations. Again, innine of these ten the diastolic blood pressure was over 135,the systolic being 200 and over. In 10 per cent. of theseries the transient and permanent strokes occurred incases with a diastolic blood pressure of over 125.
It seems, therefore, that sudden changes in the normalsensory and motor phenomena appear most commonlywith a diastolic blood pressure between 115 and 125,and are altogether absent in cases with diastolic bloodpressures under 115. Cerebral haemorrhage seems to beuncommon in patients under observation, and they are
warned against any but a very quiet life. Fatal haemor-rhage seems to ensue mostly in patients who carry on
ordinary occupations without making allowances for theirabnormal pressure. Indeed, it seems that the catastropheof fatal haemorrhage is the one phase of high arterialpressure in which the practitioner or specialist can give
little relief. There is therefore all the more urgent needto study the earlier signs and symptoms very fully, forthen therapeutic measures can be resorted to in time,and where these are likely to be of no avail, relativesand dependants may be warned of the possibilities ahead,and adjustments relating to business, finance, or familymatters may be made.
HEART FAILURE AND STROKF,The relation of the stroke to heart failure consequent
on high arterial pressure is worth studying. My observa-tions seem to suggest that fatal cerebral haemorrhage,or even transient strokes, are very uncommon once
failure has set in or the heart has begun to show consider-able enlargement, with dyspnoea and other symptomsof a tiring cardiac musculature-even though at thisstage it is observed that the blood pressure, systolic anddiastolic, remains high. In three cases of mine, however,there was very marked enlargement of the heart withthe apex in the sixth- space- and anterior axillary line,with thickened vessels and a locomotor pulse (brachial),but with practically no symptoms referable to the heart.These three patients are reported to have died of cerebralhaemorrhage. The impression is gained, in a review ofmy cases, that patients with hyperpiesis, showing few or
no symptoms referable to the heart, with or withoutcardiac enlargement, are particularly prone to die ofcerebral haemorrhage.
DIAGNOSIS AND PROGNOSISIn this country (Ceylon) there is a popular belief
that the native doctor, so called because he practisesAyurvedic medicine, excels the practitioner of Westernmedicine in the diagnosis and treatment of paralysis.This is no doubt due, in my opinion, to our mistakes inthe matter of prognosis in these cases, and to our failureto appreciate the transient nature of the attacks.A common procedure is as follows. A man gets hemi-
plegia. The nearest practitioner is sent for; he diagnosescerebral haemorrhage and gives a gloomy prognosis,hinting at the possibility or probability of death withintwenty-four hours. The blood pressure is not taken.
In despair the relatives run to the native doctor, to whomno circumstances are hopeless, and who not only promises
relief, but paints the picture of a permanent cure. Thecase falls into the hands of the latter, and time, withrestricted diet on the one hand and rest on the other,works the miracle. In one case the patient gives thisversion: " Dr. X saw me, and said it was a ' spasmodic '
stroke. We took native treatment, as Dr. X said recoverywould take three months, and it was due to highpressure." If the possibility of recovery in a few hoursor days had been mentioned with confidence thepractitioner would have retained his patient as wellas his fees.
In sensory cases the phenomena are generally classedunder neurasthenia, neuritis, and hysteria, and the possi-bility of pressure as a causative factor is missed. Thusin this country, and elsewhere too, misdiagnosis must be
common.These observations have been made with one object in
view-namely, to invite the study of this commondisease, and so to correct or amplify the present findings.From the point of view of the practitioner there is every-
thing to gain and nothing to lose by agreeing withCabot that " the measurement of blood pressure is themost important of all the recourses that have been addedto our armamentarium in the last fifteen years." Whenthe frequent occurrence of sudden motor and sensorychanges as a result of high arterial pressure is more
widely recognized, the diagnosis and prognosis will beplaced on more reliable data.
CONCLUSIONS AND SUMMARYIn a final review of these observations on the stroke
in high arterial pressure, one appears entitled to infer:1. That transient or permanent paralyses of varied
distribution occur fairly frequently.2. That the hitherto neglected sensory phenomena have
a distribution similar to the motor phenomena; that theyalso occur frequently, and are probably caused througban affection of the sensory areas, the pathogenesis beingsimilar to that in the motor cases.
3. That strokes often attributed to other factors, suchas shock, exertion, and emotion, are the result of an
already existing pressure exacerbated by the influenceof these factors.
4. That cerebral haemorrhage does not seem to occur
with diastolic blood pressures of under 115 (whatevermay be the systolic), and that prognosis may be basedon this observation.
5. That cerebral haemorrhage occurs most commonly inpeople working in defiance of an already existing pressure,and without taking any account of this abnormality.
6. That any kind of paresis or paralysis is very rare incases in which the diastolic blood pressure is under 115.If they do occur, the minimum diastolic pressure is over
115 at the time of the stroke. Strokes at this pressure are
rarely fatal or permanent. The former occurs in patientswith thickened vessels or other disease ; the latter in an
unfortunate few, or in those in whom the causative factoris other than hypertension.
7. That cerebral haemorrhage seems to occur more
frequently in those cases of hypertension which showneither marked cardiac enlargement nor symptoms, andrarely in those cases in which there are signs both ofconsiderable cardiac enlargement and symptoms of heartfailure.
I am grateful to my medical colleagues at the GeneralHospital, Colombo, for givinlg me opportunities for verifyingmy observations with cases inl their wards.
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I 14 DEC.~~~~~~~~~~~~~~~~~~~~~~ A E ~~~~~~~~~THrE BRITISH111 DEC. 16, 1933] ACASE OF ADDISON'S DISEASE MEDICAL JOURNAL11 14 D' rm~~~~~~~~~~~~~~shadows which suggested old calcified tuberculous gland atthe root of the lung, but there was no evidence of any changesin the suprarenal glands. A Mantoux test gave a markedpositive reaction with vesiculation, followed by induration,which persisted for several weeks in dilution 1 in 10,000;with dilutions 1 in 100,000 and 1 in 1,000,000 the resultswere negative. There was a marked general reaction, thetemperature rose to 103.80 F. and the pulse to 112 perminute, with headache, recovery being only completed on thefifth day. There were no symptomns pointing to a focalreaction. Laboratory investigations showed: red cells perc.mm., 6,010,000; haemoglobin, 94 per cent.; colour index,0.78 ; white cells per c.mm., 6,800. Differential count gave:polymorphonuclears, 43.2 per cent. ; lymphocytes, 51.2 percent. ; and eosinophils, 5.6 per cent. Meinicke reactionnegative. Blood urea 40 mg. per cent. Urine normal. Bloodsugar fasting, and twenty-four hours after an injection ofeucortone, 72 mg. per cent. ; after 50 grams dextrose half-hourly readings gave the figures 109, 83, 72, and 80. Onanother occasion, ninety-six hours after the last injectionof eucortone, the blood sugar was 80 mg. per cent. ; the boyfelt weak and fainted. The blood pressure was 78/50.After the administration of eucortone, 5 c.cm. intravenously,and 50 grams of dextrose by mouth half-hourly estima-tions of blood sugar yielded the following results, 117, 113,94, 68, and 78. Blood pressure readings taken at ten-minuteintervals after an injection of eucortone showed no rise ofblood pressure.
Progress of CaseFrom February 6th till March 15th, inclusive, the patient
received 5 c.cm. eucortone intravenously each day, with theexception of the ninety-six hours above-mentioned. Underthis treatment he remained free of most of his symptoms,e;uch as vomiting, insomnia, anorexia; but there was onlya gain of 2 lb. in weight. There was but slight lesseningof pigmentation, and the blood pressure varied between 70/50and 78/50. On March 1st three horizontal lineae atrophicaehad appeared on either side of the spine opposite the eighthand ninth dorsal spinous processes. Lines of lighter colour,like those already mentioned above, had appeared, two oneach' side, symmetrically placed along the pectoral margin ofthe axilla, and one running from the sternal notch towardsthe umbilicus.On March 16th whole-gland suprarenal (Armour) was sub-
stituted for the eucortone ; three tablets, each of 2 grainsdried gland (= 10 grains fresh gland), were given by mouththrice daily. Within two days the patient expressed himselfas feeling much better and stronger than he had done formany weeks. In the following ten days he gained 3 lb. inweight and the blood pressure rose to 90/55.On March 31st whole-gland suprarenal was replaced by a
special extract of cortex prepared by Allen and Hanburys fororal administration. It was given in doses as suggested, butthe gland equivalent was unknown to me at the time. Withintwenty-four hours the lad said he did not feel so well, hisappetite began to fail, there was immediate loss of weight,and the blood pressure fell to 78/48. It was then found thatthis liquid extract, which was being given in doses of half ail.ounce thrice daily by mouth, only contained 1 gram of cortexper 3 c.cm. It also contained 0.05 per cent. adrenaline. Areturn to whole gland by mouth was made on April 5th, withimmediate benefit; all previous symptoms disappeared, theblood pressure rose to 88/58 in forty-eight hours, weightincreased, and appetite was excellent. During the ensuingtwo weeks improvement was rapid; he was able to walkseveral miles, muscular power was good to exercises directedto correct the kyphosis he responded well. The pigmentationwas diminishing very considerably, and the blood pressureremained higher than previously. The pulse sounds notedduring sphygmomanometrical readings appeared almost normal.About the middle of April it was noticed that the breastswere enlarged, resembling those of a girl a year beforepuberty, but without changes in the nipples. During forty-eight hours, April 18th to 20th, treatment was discontinued,with no obvious ill effect.On April 21st cortin organon, 5 c.cm. by mouth, was given.
By the evening of that day symptoms of suprarenal insuffi-ciency developed. These had not been noticed during theprevious two days, when treatment had been withheld. After
three days on 5 c.cm. by mouth, 5 c.cm. were given twicedaily intramuscularly, with some improvement. Cortin isa preparation of suprarenal cortex made at Oss in Hollandby N. V. Organon, who very kindly sent me a supply fora trial at the instance of Dr. Alison Macbeth: 1 c.cm. repre-sents 50 grams of fresh gland. The dose advised-namely,5 c.cm., intravenously-for maintenance is doubtless aboutcorrect, and corresponds fairly closely, to that of eucortone.A second return was made to dried whole gland, and the
patient took his discharge from hospital on May 4th, 1933,with a supply of tablets. He came up once two weeks laterfor more tablets, and then disappeared; all efforts to tracehim failed. On July 1st, 1933, he returned in a conditionof collapse, with all his previous symptoms returned. Weight,119 lb.; temperature, 980 to 990 F.; pulse 72/84; bloodpressure, 60/36. There were present extreme asthenia,negativism, nausea, vomiting, and abdominal pain. Duringthe first week, 10 c.cm. eucortone was given daily; later anoral preparation of eucortone, made by Allen and Hanburys,was tried, and the addition of adrenaline subcutaneously wasmade. The patient continued to lose weight, and it was
impossible to get him to take nourishment. A return wasmade to intravenous eucortone, kindly provided by Allenand Hanburys: 10 c.cm. were given twice on the first day(July 22nd) and the second day, then 10 and 5 c.cm., andthereafter 5 and 5 c.cm. each day. There was some responsein that a little nourishment was taken and the extreme senseof weakness was less marked; the blood pressure remainedat 60/36. Eucortone was then discontinued, as the supplyhad come to an end. Twenty-four hours later the patientcollapsed, became comatose, and died. Necropsy was refused.
LATE CLINICAL ASSISTANT, NATIONAL HOSPITAL FOR DISEASESOF THE HEART, LONDON
In 1917 Cyriaxl reported good results in cases of moder-ately high blood pressure obtained by what he describedas " mobilization of the spinal column," by which hemeant active and passive movements of the vertebraljoints, and passive manipulations, vibrations, petrissage,etc., of the erector spinae muscles. His explanation ofraised, pressure was, apparently, that congestion of theseparts led to irritative states of the erector spinae, settingup a series of sensory stimuli to the posterior spinal nerves,which in turn gave rise to a series of pressor effects.Whatever the -explanation, his figures seemed to show adefinite diminution of the blood pressure in his pat:ents.
Although unwilling to accept the theory on which thetreatment was based, I ventured to modify his method bysubstituting electrical stimulation of the skeletal muscles,and submitting patients with high grades of pressure totreatment on these lines. As a preliminary the patientswere tested to see what effect the resulting muscular con-tractions had on the pulse rate, particularly as some ofthem were on the verge of cardiac failure, a few actuallyexhibiting oedema of the ankles and a more than moderateenlargement of the heart. In every case the pulse ratedropped, sometimes by eight beats to the minute; in a
few it ramained stationary in none did it rise. It was on interrogation, breathlessness and pain over the lower partargued, therefore, that the method of treatment, instead of the sternum following exertion (of two years' durationl).of throwing a burden on the heart, actually relieved it, Family history: father died of enlarged liver at the age ofand the treatment was carried out with greater zest. 48; mother died suddenly of " debility "; of six brothers,
one had kidney disease, two were dead-one dying of typhoid.CLINICAL MATERIAL Previous history: none of any significance. Habits: a little
alcohol occasionally, but no tobacco; exercise, a little walking;Case 1.-A woman, aged 58, and unmarried, complained food, three good meals a day.,;that her left leg had suddenly become stiff, and that her Condition before treatment: Tightness under the sternum,speech had become bad two years previously. Family
histry:faterad ded f "strke at he ge f 6 ; alpiltationl, dyspnoea on exertion, slight giddiness ; badhistory: father had died of "stroke" at the age of 62; teeth ; bowels constipated. Pulse 90, regular, and of highhe was paralysed for two months; mother had died of tension. Heart: apex beat in the sixth space, anteriorbronchitis at the age of 40w ; one brother had died of axillary line. VesseIs,: palpable. Blood pressure 260/160.nephritis, while twvo were well - one sister had high blood Urn no alui. Lnsni.p Urine: no albumin. Lungs: nil.pressure, one had -died of stroke, six were well. Prevlous On May 25th the blood pressure had fallen to 218/142,history: none of any significance; patient 'was fat two years and the patient said he felt better. The following were theago. Habits: no alcohol, no smoking; exercise, housework. blood pressure readings:
Condition before- treatment:. the patient was thin, hadleft-sided hemiparesis, with dysarthria ; she could not getinto her car, and walked very slowly. Heart: left border Blood Pressureone inch outside- mid-clavicular line,- first sound +, aortic Date Renwrkssecond sound + +. Lungs: nil. Blood pressure 240/140. Systolic DiastolicUrine: specific gravity 1014 no albumin or sugar. Aftertreatment the blood pressure readings were as follows: May 18th, 1932 260 160
May 25th, ,, 218 142Date Systolic Diastolic May 28th, ,, 210 120 No pain under the sternum; heart
16th, ,, ... 200 136 June 3rd, ,, 190 122 Left border of heart finger-breadth outside nipp)le line,,21st, ,, ... ... 133 , June 6th, ,, - - Left border of heart just outside21st, 184 13) ~~~~~~~~~~~~~~~~~~~~nippleline,,27th, ,, ... ... 180 122 June 17th, ,, - - Left border of heart in nipple line
230 122 June 22nd, ,, 182 118,,30th, , ... - 200120 Aug. 16th, ,, 180 115 Left border of heart in nipple
line; no pain under sterntumOctober Eth, ,, ... ... 175 120 Aug. 19th, ,, - - Patient ceased attendance
The patient states that she can now get into the car alone, Case 4.-A carpenter, aged 60, married, with nine children,"feels lighter," and walks better. -The left border of the was admitted to hospital on June 17th, 1932,' complaining ofheart is just outside the mid-clavicular line, with a heaving loss of power of the right limb; he had had a similar attackapex beat and an accentuated aortic second sound. three years before.' Family history: father died, aged 60
Case 2.-A woman, aged 56, unmarried,' complained of a (? boil in chetk) ;. mother died, aged 83, 'of old age. Previousswaying feeling in the head " of s-ix months' duration. history: malaria, nothing else of significance. Habits: a little
Family history: as for Case 1. Previous history: none of alcohol occasionally, but no tobacco; exercise, his work;any significance. Habits: no -exercise ; no tobacco or alcohol. food, formerly two good meals a day.Heart: left border just outside mid-clavicular line ; aortic Condition before treatment: Slight paresis of left side ofsecond sound +. Lungs: nil. Urine: specific gravity face, speech slurring. Pulse 90 ; rhythm regular, high tension.1012 ; no albumin or sugar. Blood pressure readings were Vessels: thick. Heart: left border half an inch outside theas follows: nipple line ; aortic second sound accentuated. Blood pressure
-______________________ ___________ - 210/110. Urine: a trace of albumin, no casts. Lungs: nil.Date Systolic Diastolic Wassermann reaction negative. Nervous system: knee-jerks
_______________________-_________ and biceps response normal on the left side.September 12th, 1932 ... ... 210 128 July 4th, 1932: Babinski's reflex positive on right side
no sensory phenomena. After daily treatment blood pressure,,16th, ,, ... ... 170 110 'is 132/92. The patient's speech is normal, and power of the21st, ,, ... ... 158 105 lower limbs has returned ; the left border of the heart is
I 160 105 internal to the nipple line.. 23rd, 178 108 Case 5.-Hotel manager, aged 56, married, with tenchildren, was admitted on April 3rd, 1932. He complained of
27th, ... ... 148 98 breathlessness and palpitation, and occasional swelling of' the(Exercise started) legs. Family history: father died of old age at 72; mother
September'30th, 1932 ... ... 170 112 died of heart trouble at 68 ; five brothers, all well; fourOctober Eth, 1932 ... ... ... 155 106 sisters-one dead, the remainder well. Previous history: was
in the police force, 1895-1918 ; admitted to hospital fourtimes, once with diabetes; had had malaria in 1892. Habits:
On October 8th, 1932, the' left border of the heart was a fair quantity of alcohol, but no tobacco; nO exercise now.in- the mid-clavicular line; the patient stated that she felt Condition before treatment: Fat and short-necked typequite well, and had no swaying feeling in the head. had palpitation and shortness of breath, while teeth were
In neither of these cases was rest enjoined or medicine slightly infected ; legs were swollen. Pulse 40, regular.given, and there was no restriction of dliet. In both there Heart: three-quarters of an inch outside the nipple line,was marked diminution of the size of the heart, disappear- aortic second sound accentuated. Blood pressure 180 / 120.ance of symptoms, a considerable fall in the pressure, and Lungs: nil. Urine: a trace of albumin, but no0 casts.obvious general improvement. But one of the patients, the On July 29th the blood pressure was still 180 / 120, butyoungern, seemed to have improved more than the elder, .who there was no swelling of the legs; the heart was as before;appeared, wchen she first came to me, to have reconciled pulse 84 * no oedema. Patient complained of headache aboutherself to a condition of inactivity engenldered by a fear of 1L30 a.m. Renal involvrement was feared, and a urea con-fatal apoplexy. centration test was done on August 2n-l (blooXd urea 27 mg.
Case 3.-A clerk, aged 49, married, with seven children, per 100 c.cm.). Concentration before test 1.3 per cent. ; afterwhen seen on May 18th, 1932, complained of weakness, and, 'one hour 2.5 per cent. ; after two hours 2.0 per cent. ; after
27
28
moo, r ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~THE ERrTTSWIii o16 DEC. 16, 1933] ESSENTIAL HYPERTENSION I MEDICAL JOURNAL
three hours 2.0 per cent. The treatment was continued, andthe following were the subsequent blood pressure readings:
Date Systolic Diastolic Remarks
August 8th ... 162 100 Patient felt much better; no head-ache; no swelling of the feet
August 13th ... 170 106 Left border of heart in the nippleline. Patient felt much better
August 18th ... _ Left border of heart in the nippleline
In this case the failure to respond to treatment in the earlystages suggested renal involvement and impaired renal func-tion, but the blood urea and the urea concentration test gavefigures which indicated efficient functioning. Therefore thetreatment was continued until the diastolic pressure fell to100, and the patient felt very much better.
Case 6.-Hotel manager, aged 41, married, with twochildren. He complained of occasional throbbing in the head.Family history: father died at the age of 54 years, and motherat the age of 66; two brothers and five sisters, all well.Previous history: patient consulted a doctor about four yearspreviously for " feeling dizzy suddenly," and one year pre-viously had complained of headache; no history of any otherillnesses. Habits: alcohol formerly, but little now ; exercise,only walking associated with work ; tobacco, fifteen cigarettesa day; food, had eaten well previously.
Condition before treatment: Headache occasionally,dyspnoea slight; nothing else of significance. Pulse: 85,regular, good volume and tone. Heart: left border in nippleline, second aortic sound accentuated. Urine: specific gravity1011, a trace of albumin. Blood pressure 220/150. -Three weeks of treatment made no reduction in his blood
pressure. Renal involvement was suspected, and the ureaconcentration test was done ; the concentration in the secondhour specimen was 1.7 per cent. Treatment was discon-tinued, but the patient " felt very much better."The patients whose records are given above received
no special medicine, nor was absolute rest ordered for anyof them. Cases 4 and 5 happened to be in hospital; theothers came for treatment from home. The diet wasrestricted in all of them.
DIscusSIONPrior to adopting this method of treatment I had tried
diathermy in a large number of cases of hypertension.I was never able to convince myself that pressure wasreduced to an extent which could not be explained by thesimultaneously ordered rest, in spite of Clifford Allbutt's2statement nine years ago that " d'arsonvalizatiou bythe auto-condensation method is the most valuable im-mediate aid we possess for hyperpiesia." But it wasalways strikingly evident that this treatment made thepatients feel better, particularly when the kidneysappeared to be involved. They nearly always stated theywere much better. With the diathermy I often combinedradiant heat, particularly in renal cases. The striking re-duction of pressure obtained in non-renal cases in theabove series would therefore appear to be due to themobilization of the muscles in the manner described.The results recorded above indicate:1. IThat in some cases of hyperpiesia the blood pressure
drops to low limits, even to normal figures, without rest ormedicinal aid ; there is also relief from distressing symptoms.
2. That in other cases the patients are relieved of theirsymptoms and proclaim that they feel better, but thatpressures will not fall. These cases show impaired renal func-tion as gauged by the urea concentration test.
3. That the heart enlarged as a result of the strain of hyper-tension gets astonishingly smaller with the fall of pressure.
It is difficult to give an explanation of the mechanismby which the reduction of pressure is brought about. Iwas encouraged to try it by my belief that sedentaryoccupations or lack of sufficient exercise play an im-portant part in the aetiology of essential hypertension,and, if I may be allowed to put it figuratively, that therusty arterioles and capillaries of sluggish muscles were acause of elevated pressure. It was found in the series thatwhen an appreciable degree of diminution of pressure wasnot obtained the urea concentration test showed im-paired renal efficienlcy.
All the patients were treated in hospital. The machineused was the ordinary pantostat-the faradic current-with a Lewis Jones interrupter in-circui topreventirregular contractions and uneven, unpleasant shocks.Ordinary batteries have not so far been used, but thereis no reason why any method of stimulation should notanswer, so long as sudden shocks and irregular contractionsare avoided. The Smart-Bristowe coil ought to proveuseful. In the absence of electricity, massage would, Iimagine, answer; but I am not in a position to vouch forgood results. When pressures drop low as a result oftreatment-namely, below a diastolic pressure of 110-thepatients are taught exercises with which the muscles maybe kept in action-particularly the trunk muscles-oradvice is given that mild exercises may be resorted to.The patient should be carefully watched, particularly whencardiac enlargement and symptoms are present, or thedoctor may one day be called upon to face a charge of" electrocution " when death due to heart failure is attri-buted to electrical shock. I have deliberately refrainedfrom using subsidiary measures in order to establish theefficacy of this method of treatment, but I am of thebelief that therapeutic doses of the drugs ordinarily used(not patent medicines) would prove very useful in main-taining the good results obtained, particularly in thosecases in which the blood pressures have not fallen too nearnormal limits. To establish that the combined measureswill give more satisfactory results than those alreadyobtained must remain part of the programme of the future.So widely is it accepted that arterial hypertension, when
it throws its strain on the myocardium, takes the patientgradually to hypertrophy, dilatation, and failure, that wefind East and Bain in Recent Advances in Cardiologydescribing " the third stage " of high blood pressure, asmuch as to imply that the changes are irrevocable. Theyprobably are, but only when the vessel changes havetaken place. If such changes have not taken place itwould appear from these observations that' extreme gradesof enlargement can be reduced to moderate grades, andmoderate grades to slight ones.
It is now sixteen years since Cyriax published his paper,but the methods of treatment which might have beenceveloped from his findings are still not in vogue. Thismethod of treatment was referred to briefly by me at thediscussion on essential hypertension at the Annual Meetingof the British Medical Association in Dublin.
I have to acknowledge here my gratefulness to Miss Bevan,sister-in-charge of the electrotherapeutic department, GeneralHospital, Colombo, for the pains she has taken in connexionwvith these cases, and mny indebtedness to my colleagues of thatinstitution for helping me to carry out this treatment on theirpatients.
REFERENCES1 Cyriax, E. F.: Practitionier, 1917, xcix, 468.2Allbutt, Sir Clifford: Arteriosclerosis, 1925, p. 91.
This case is of interest because symptoms were due tospinal cord compression, and the nature of the primarygrowth remained unsuspected till necropsy was performed.A labourer, aged 50, on May 10th, 1933, noticed pains in
both shoulders and in his back, which came on suddenly andforced him to leave his work; he said he was not subjectto backache or rheumatism: 1)uring the next few days thepains were less troublesome, but on May 13th he becameconstipated, and medicine afforded him little relief. At thesame time he noticed that his urine was cloudy. On May30th he complained of weakness and numbness of his lowerlimbs, the right leg becoming slightly weaker than the left.The next day he was unable to pass water, and was admittedto the medical ward of this hospital.On examination he was found to be a well-developed man,
of good colour, with no signs of muscular wasting. No
END
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Ocr. 3, 1942 RENAL IMPAIRMENT DUE TO CRUSHING LIMBS MEDICALJOURNAL 393
creatinine from the concentrated urine in the tubules back intothe blood. The renal damage described above is probably notdue mainly to reduction in glomerular filtration rate, becauseoliguria from this cause is associated with very high creatinineand low chloride concentration in the urine, whereas in theseexperiments the creatinine concentrations are low and thechlorides may be increased. Microscopically the damagedorgan appears fairly vascular.
Blockage of the tubules, suggested as a possible factor bythe appearance of the deposit in them, should produce a tensekidney, in contrast with the striking flaccidity observed in thesedamaged kidneys. The deposit does not appear compact enough,nor does it occur in a sufficiently high proportion of tubules,to lead one to expect that it could reduce the creatinine outputto one-quarter. A more likely hypothesis would involve releaseof a poison from the damaged limbs that affects the tubule cellsby increasing their permeability to creatinine, urea, and othersubstances which are concentrated by the kidney. Thesesubstances would diffuse from the concentrated solution inthe distal parts of the tubules across the tubule wallsto the blood in the venules. Hastening the flow of liquiddown the tubules with diuretics should reduce the loss byleakage of creatinine and so increase the creatinine clearance,an expectation which accords with observation. The mainobjection to regarding this as a self-sufficient hypothesis isthat poisons such as cyanide or mercury salts produce anincreased urine flow, due to inhibition of water reabsorption,before they produce the anuria due to increased permeability.Correspondingly, organs poisoned in this way are usually tense.This is, however, not an insuperable objection to the view thatthe poison here in question affects the permeability mainly.
Such a poison might reach the tubule cells either from theblood"stream or, if diffusible, from the lumen of the tubule. Inthe latter event the poison itself might well be a substancewhich is concentrated in the tubules, and act the more potentlyin virtue of its concentration. This possibility has, however,been excluded in the following way. Partial obsftction of onekidney by an increase of ureter pressure resulted in a fourfoldconcentration of urine (as evidenced by creatinine-U/P ratio)compared with the unobstructed side. If the toxic agentreleased from the limbs had been similarly more concentratedon the obstructed side the severity of the damage should havebeen greater on that side. In fact, the obstructed side, afterremoval of the obstruction, was, if- anything, a little less severelydamaged than the unobstructed side.So far as available evidence goes, the injury to the kidneys
in our series of dogs appears to be of the same kind as that inman after comparable prolonged crush injury to the limbs.The essential nature of the renal damage has not yet beendetermined, but the evidence suggests that the main factor maybe concerned with increase in permeability of the renal tubulesdue to a toxic agent released from the damaged limbs, whilethere may be an additional factor involving reduction in therate of glomerular filtration probably due to lowering ofglomerular capillary pressure.
VARIATIONS IN THE RESPIRATORYRHYTHM OF PROGNOSTIC SIGNIFICANCE
IN MALIGNANT HYPERTENSIONBY
H. 0. GUNEWARDENE, M.B., B.S., D.M.R.E.Radiologist, General Hospital, Colombo
Recently I drew attention to varlations in the respiratoryrhythm in a case of malignant hypertension in its terminalstages (Gunewardene, 1938). A similar type of respira-tion has been noticed in cases of meningitis (Hutchisonand Hunter, 1929). The characteristic feature is that therespirations are grouped; in each group the initial excur-sion in the tracing is the largest, the subsequent ones get-ting smaller, until the movements cease for a moment.This means that the depth of the respiration graduallydeclines as in the waning phase of Cheyne-Stokes respira-tion. In that case, however, there was no period of apnoea.
This type of respiration is seen in the terminal stage otmalignant *hypertension when pronounced albuminuria, per-sistent hypertension, and extensive eye changes (haemorrhages,exudates, cotton-wool patches, oedema of the disks, etc.) arepresent. The patient is generally quiet and lies flat on theback without a suggestion of the breathlessness of the cardiactype which previously had been well marked. A little restless-ness, not continuous, is often observed; he opens his mouthfrequently and breathes as though he is yawning half-heartedly.Occasionally he is irrational. Sometimes there is maniacalexcitement ; at.other times a little drowsiness suggestive of auraemic state. Uraemic twitching or convulsions were notobserved.
These variations in the respiratory rhythm in associationwith malignant hypertension have not been described before,so far as I can gather from the literature available in Ceylon.Their cause has yet to be explained. Are they due to cerebraloedema, or to the effects of toxins on the respiratory centre?Is the alteration in the chemistry of the blood responsible forthem? Eyster has shown that Cheyne-Stokes breathing canbe produced in dogs by a rise and fall of the blood pressurein the presence of raised intracranial pressure.
In the following case, grouping of respiratory movementssimilar to those in the case referred to above was noticed, buteach group was followed by a period of apnoea. The tracingis unlike Biot's type, but resembles that of Cheyne-Stokesrespiration with the waxing phase absent. The rhythm isirregular and the depth of the respirations varies.
Case ReportThe patient, a male sedentary clerical' worker aged 42, was
admitted on March 7, 1939, complaining of occasional occipitalheadache, giddiness on and off, and blurring of vision. He waslying quiet, but a few days previously he had been verydyspnoeic. Examination revealed the following characteristics.Heart: heaving apex beat-in fifth space, midclavicular line;second aortic + + ; no murmurs. The lungs were clear. Bloodpressure: systolic 300, diastolic 180. The brachial and radial
*.t5."'.arteries did not feel much thickened, nor did palpation suggestsuch high pressure. Pulse 78, regular. Urine: scanty; S.G.1010; albumin 0.7%; no sugar. Fundi showed oedema of thedisks; flame-shaped haemorrhages, exudates, thickened arteries,very congested veins. Blood urea, 224 mg. per 100 c.cm. ; ureaclearance, mean 7.26% normal.
Treatment consisted of venesection; administration of sodiumnitrite, theominal, etc.
During his stay in hospital the blood pressure varied between210/140 and 260/170 (not eliminating effects of drugs). Hebecame somewhat irrational, yawned half-heartedly, and laterbecame a little drowsy and quiet. Just, before his death (underayurvedic treatment) on April 7, 1939, he complained that he" couldn't breathe." The accompanying illustration shows therespiratory tracing (thoracic) of this case.
According to Harrison (1939), the carbon dioxide tension inmalignant hypertension is abnormally low and patients withperiodic breathing have arterial blood which is under-ventilatedas regards oxygen and over-ventilated as regards carbondioxide. It has also been shown that the administration ofcarbon dioxide abolishes periodic breathing. The fairly suddentransition of a dyspnoeic. sometimes orthopnoeic, patient intoa condition of -tranquillity would suggest that changes in thechemical constituents of the blood gases and the tissue fluidsplay a significant part in the production of periodic breathingand the cessation of dyspnoea.
SummaryA form of variation in the respiratory rhythm associated
with malignant hypertension is described.There are changes in the periodicity as well as the depth of
the respiratory movements.These changes are of grave prognostic significance even when
the patient does not look seriously ill, the duration of life inthe cases described being not more than 6 weeks after theironset.
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394 OCT. 3, 1942 VACCINATION IN GLASGOW DOCKS MEBRITISH
I gratefully acknowledge the co-operation of Dr. J. R. Blaze andDr. Cyril F. Fernando, under whose care the patient Was; also thekind services of the Physiological Department, Ceylon MedicalCollege. REFERENCESGunewardene, H. 0. (1938). J. Ceylon Br. Brit. med. Ass., 35, 391.Harrison, T. R. (1939). Failure of the Circulation, p. 206, Bailliere, London.Hutchison, R., and Hunter, D. (1929). Clinical Methods, p. 279, London.
VACCINATION IN GLASGOW DOCKSBY
GEORGE BUCHANAN, L.R.C.P., L.R.C.S.D.P.H., D.P.A.
Medical Officer, Clyde Navigation TrustAND
STUART LAIDLAW, M.D., B.Sc., D.P.H., D.P.A.Senior Assistant Medical Officer of Health, Glasgow
The following is an account of an investigation into thepotency of vaccine lymph and the effect of vaccination onthe sickness and industrial accident rates among Glasgowdock workers.As a result of small-pox of a severe type occurring in
Glasgow, the medical officer of health, on June 29, 1942, issuedan appeal for mass vaccination of the city's population. Sincethe disease had presumably entered through the Port it wasfelt that every endeavour should be made to have dock workersVaccinated at once. At all times close co-operation is main-tained between the city's health services and the Port Authority(Clyde Navigation Trust), so that the drawing-up and comple-tion of the scheme here outlined naturally fell to be dealtwith by us. The scheme was approved by the medical officerof health, the Clyde Navigation Trust, and the port regionaldirector.
Outline of SchemeThe first essential was to carry out vaccination promptly
and with the minimum interference with the normal workingof the harbour; secondly came the necessity of informing thedock workers of the need for vaccination; and, thirdly, con-veniently situated vaccination centres had to be establishedin the Docks.
It was decided to utilize the existing gas-cleansing stationsin each dock as vaccination centres and, on the day beforethe opening of the centres, to make use of a broadcasting vanto explain the need for vaccination and to announce the timeand place for workers to attend. This scheme answeredextremely well, and over 60% of the workers in the Port ofGlasgow availed themselves of the opportunity. The medicaland nursing staff employed were directed to pay particularattention to the technique of vaccination as outlined bySir Alexander Macgregor in his communication.
Result of VaccinationOf the lymph used 95% was supplied by the Government
Lymph Establishment, the remaining 5% being from othermanufacturers. Our impression was that the Governmentlymph was somewhat more potent, although all the othervarieties gave satisfactory reactions. The follow-up of mnanyof the workers was far from easy owing to the constant changesof working shifts and the movement of gangs of dockers fromone dock to another as ships arrived and departed, and we, ofnecessity, had to satisfy ourselves with records of 1,000 out
of the total vaccinated. The accompanying table shows underfour headings the results we obtained. (A) Severe reactionevidenced by constitutional upset, enlarged axillary glands,fairly extensive localized reaction, with inflammation extending
from the pock sometimes up to the shoulder and down to theforearm. (B) A normal vaccination pock with little or no con-stitutional upset. (C) An immune reaction sometimes describedas the papule of immunity of Pirquet. (D) No reaction.From the table it is evident that the lymph used was particu-
larly potent, 84% of the cases showing severe or normalvaccinations and a further 10% an immune reaction due inpractically every instance to a previous successful vaccination.The 58 cases which showed no reaction were all revaccinated,when only two showed an immune reaction.
Effects on IndustryWe feared that mass vaccination would interfere with the
normal work in the harbour and thus slow down the nationaleffort, but this has not been so. In fact, less than 3% of allclasses of workers were off work on account of vaccination.The maximum period of incapacity was one week, the greatmajority being back at work within 48 hours. Scrutiny ofthe sickness rate among dockers, office staff, and Clyde Trustemployees for the 28 days subsequent to vaccination showedno increase over the normal rate prevailing at this time of year.The industrial accident rate has also shown no increase
above the normal, despite .the fact that many crane drivers,capstanmen, and winchmen were vaccinated successfully, andwere plucky enough to continue at work despite very sore arms.
CommentsA good previous vaccination scar was no guarantee of im-
munity. For example, one female who had five large foveatedscars resulting from vaccination in infancy, and subsequently in1921, had a very severe reaction.
Stout persons generally had much more severe local reactionsthan thin persons.
Elderly persons often showed severe reactions even althoughpreviously vaccinated.Many suffered from a coryza, sometimes associated with
sore throat, of about three days' duration from the 8th tothe 11 th day after vaccination. In no case was the coryzasevere enough to cause incapacity for work.Women reacted more severely than men in the same age
groups.We found that vaccination of the lower limbs caused much
more discomfort than vaccination of the upper limbs.Nine cases in our series showed a post-vaccinial rash; four
of these were urticarial in type and associated with previousacne or scabies, three morbilliform, and two scarlatiniform.They all occurred between the 9th and the 10th day followingvaccination and disappeared within 48 hours. We noted nocase of papular urticaria, nor did any of the dock workersdevelop pustular rashes resembling small-pox. Neither didwe see any case of post-vaccinial encephalitis nor any personwho developed nervous symptoms following vaccination.Several cases showed a somewhat delayed local reaction tovaccination.
This investigation' was made possible only by the willing co-operation of all classes of dock workers, and we wish to thank themedical officer of health, the general manager of the Clyde Naviga-tion Trust, and the port regional director for permission to printthis short review.
The Chadwick Trustees have arranged for the following publiclectures to be given on Tuesdays at 2.30 p.m.: Oct. 6, at Roya!Society of Tropical Medicine, 26, Portland Place, W., Sir LeonardHill, F.R.S., " The Interrelation of Clothing and Shortage of Fuelin Matters of Health "; Oct. 27, at Royal Sanitary Institute, 90,Buckingham Palace Road, S.W., Mr. W. T. Creswell, K.C., "TheForensic Aspects of Wartime Public Health Legislation "; Nov. 10,at London School of Hygiene and Tropical Medicine, Keppel Street,W.C., Bossom Lecture by Miss Jocelyn Adburgham, " Land Settle-ment-Its Sanitary and Architectural Aspects and After-war Possi-bilities "; Nov. 24, at Westminster Hospital Medical School,Horseferry Road, S.W., Malcolm Morris Memorial Lecture by SirArthur MacNalty, "' The Prevention of Tuberculosis in Peace andWar "; Dec. 8, at Royal Society of Tropical Medicine, Dr. W.Norwood East, " The Differentiation, Prevention, and Treatment ofAnti-social Behaviour Disorders." Admission to the lectures is free,and further particulars can be had from the secretary, ChadwickTrust, 204, Abbey House, Westminster, S.W.I.
END top left.
30
31
180 JAN. 30, 1932] THE SIGNIFICANCE OF HAEMATURIA LMEDICA JouRNIL
-Tubular Adenocarcinomna.-The tumour of the secretingelement is the tubular adenocarcinoma. It is much moremalignant, rapidly infiltrating the parenchyma in whichit ariseg. It involves the perinephric tissue early, andproduced metastases in the adjacent lymphatic glands.It thus comes about that the kidney, although increasedin size, may have a normal contour and the drainagesystem be only slightly damaged, so that pyelographyreveals little deformity, the cavity appearing probablydilated and at one part slightly deformed. When exam-ined by excretion urography, however, it is demonstratedto be a functionless organ by the absence of any shadow.A rare tumour of the renal parenchyma is a haemangio-blastoma.Papillary Adenocarcintoina.-The commonest malignant
tumour arising from the collecting element is the papillaryadenocarcinoma. Many of these were formerly mistakenfor hypernephromata, and, like the latter, they formeda tumour mass, usually palpable and demonstrable. Thecharacteristic local destruction of the drainage system,with the neighbouring calyces elongated and flattened,is observed on pyelographic examination. Functionalactivity as estimated by excretion urography, however,is poor. From the pelvis or calyces an epidermoidcarcinoma may arise.
Villous Papillorna.-The innocent tumour of the kidneythat is met with clinically is a villous papilloma. Itis similar to that which occurs in the bladder. Itspresence can be recognized by pyelography. At firstsight, when the film is inspected, the pelvis and calycesappear normal, but on more careful examination thedensity of the media within the cavity is seen at onepart to be diminished-namely, where the villous growthis occupying the cavity. In some cases a definite fillingdefect is observed, and when this is combined with aninterference with the entrance of the pyelographic mediato one of the calyces it may be suspected that the villousgrowth has overstepped the borderline and become amalignant papilloma. Functional activity as estimatedby excretion urography in these cases is good.
Tuberculous disease of the kidney produces variousappearances on pyelographic examination, which arecharacteristic and diagnostic.Renal Calculus.-If the shadow of a stone is seen in
the renal region at the preliminary x-ray examination,its accurate localization can be simply achieved by takinganother photograph with the patient lying on his side.If the concretion -be situated within the renal pelvis, thislateral view will show it lying opposite the anterior thirdof the body of the corresponding lumbar vertebra. If theshadow be intra-abdominal, it will be seen in front of thebodies of the lumbar vertebrae. The exact situation ofthe stone within the pelvis or calyces can be demon-strated by pyelographic examination.
IDIOPATHIC HAEMATURIAEssential or idiopathic haematuria is the one renal
disease producing haematuria whose diagnosis is arrivedat by a process of exclusion. The source of the bleedinghaving been localized to one kidney, no further abnor-mality of this organ can be revealed by any of the variousmethods that are employed; the urine collected is foundto be sterile and free from pus cells, such as would bemet with if the bleeding was from an inflamed pelvisthe pyelographic contour is normal. In some cases ofessential haematuria the bleeding may be most persistent.Eight years ago I operated on a man who had sufferedfrom haematuria from this cause for twenty out oftwenty-one years since it originally appeared. Nephrec-tomy was performed, and he has had no recurrence ofthe bleeding since then. Anatomically, after the kidney
was removed it appeared normal, and on histologicalexamination all that was revealed was a certain increaseof the intrarenal pelvic fat, and a varicosity of the venuleswithin it.
CONCLUSIONWhen a case of haematuria comes under our observation
it is our duty to demand that the cause of the bleedingbe forthwith determined. This may necessitate a some-what tedious examination, buit the ultimate result iscertain. Fortunately, in most cases, when the cause ofthe bleeding has been determined, a speedy and certaincure can be obtained. In others, especially where malig-nant disease is present, the outlook is graver. In allof them, however, the earlier the diagnosis is arrived atthe better will be the result of treatment, and in all ofthem, whether they are innocent or malignant, the pro-gress of the case afterwards should be followed up byre-examination at regular intervals of three months, sixmonths, and a year. It is difficult to persuade patientswho have been pronounced cured after operative treatmentof the necessity of this, and the temptation sometimes is todismiss them with a reassurance that all is well for alltime. Fortunately, in many this will prove to be correct,but in others, slight recurrence may take place, and, ifso, by an accurate follow-up system such recurrence canbe observed at its earliest stage and dealt with simply andpromptly.
THE STROKE IN HIGH ARTERIALPRESSURE *
A STUDY OF 159 CASESBY
H. 0. GUNEWARDENE, M.B.., B.S.LOND.D.,M.R.E.CANTAB.
FORIMERLY CLINICAL ASSISTANT, NATIONAL HOSPITAL FOR DISEASESOF THE HEART, LONDON
The prominence given to the study of high arterialblood pressure seems to be ever increasing, both in therecognized textbooks and in the medical journals. SinceClifford Allbutt's lucid exposition of the conditicn calledby him " hyperpiesis," Batty Shaw, Geoffrey Evans,Lord Dawson, and others have contributed to the elucida-tion of some of the clinical and pathological aspects ofthis type of high arterial pressure and of that associatedwith renal disease. But much remains still hazy, un-known, and unexplained. Etiology is but vaguely under-stood; some of the clinical manifestations have receivedno uniform explanation, physiologically or pathologically;and the lines of treatment indicated touch no specificmethods which can be relied on to help the practitioner,who is left to turn for relief to general measures adoptedin the treatment of other diseases-for example, rest,restricted diet, hydrotherapy, and the removal of septicfoci.On the whole, one feels that there is some justification
for striking a note of disappointment, and that, in spiteof the valuable contributions hitherto made, very littlesubstantial advance has taken place in our knowledge bywhich the disease can be arrested or relief be given tothose in danger of being afflicted with its unpleasantsequels. One reason for this slow progress seems to heclear-namely, that the malady has not been thoroughlyinvestigated or its early stages closely followed. Cerebralhaemorrhage and heart failure as terminal events in highblood pressure may be encountered commonly enough inhospital practice, but the earlier phases and the lessserious and striking manifestations are very seldom seei.Indeed, it is true to say that, by the time the grosser
* Awarded Sir Charles Hastings Clinical Prize, 1930.
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32
THE STROKE IN HIGH ARTERIAL -PRESSURE r THEBRITISH 181L MEDICAL JOURNAL
lesions have developed, the patient has already ceased orforgotten to look upon the earlier symptoms as part cfthe same disease in its undeveloped state.High blood pressure, whatever its etiology, is common
enough in general practice. No one is in a better positionto study those aspects of it which throw light on itscausation, and on some of the features which forecast thefinal doom, than the family practitioner. Methods ofinvestigation are no doubt limited, but the mass of clinicalmaterial is heavy. No apology is made for not resortingto those special tests which can be carried out only ina fully equipped laboratory with a full staff, for thepurpose of this essay is to record the clinical observationsmade on the so-called " stroke " as it occurs in higharterial pressure.
DEFINITION OF "STROKEA stroke is defined in Dorland's Medical Dictionary asa sudden severe attack, as of apoplexy or paralysis."
Saville considers " stroke " to be synonymous withapoplexy, for he defines each word as " a term whichmay be conveniently retained to indicate a sudden un-consciousness due to a vascular lesion within the skull."I propose to resort to a certain degree of licence in theuse of the word, interpreting it as a " sudden severeattack," not necessarily apoplectic, and thus implyingthat these attacks are not confined only to the motor side.There appears to be somb justification for such adeparture, for one finds Batty Shaw saying (under theheading " Persistent or temporary hyperpiesic paralysis "):" Sometimes the paralysis affects the sensory instead ofmotor areas, so that the patient becomes blinded withoutany changes being discovered in the retina or the brain."A little elasticity in my definition seems justified, not onlybecause it helps to explain more fully the various formsthese attacks take, particularly in the earlier stages ofhigh blood pressure, but also because it helps to give amental picture of the much-neglected sensory forms.
FREQUENCY OF STROKEStroke occurs so commonly in high pressure, at
least in Ceylon, that the scant references to it instandard textbooks is surprising. Theodore Thomson inPrice's Textbook of Medicine says, " sometimes transientparalysis occurs," without any mention of the sensoryattacks. Batty Shaw makes the statement quoted abovein a superficial but none too impressive way. East andBain, in Recent Advances in Cardiology, make no referenceto the sensory stroke. In what they call the second stage,they say, " symptoms will rarely be experienced whichrefer to the pressure," also stating that the clinical features" are strikingly few "-this is in contrast to my findingth'at the strokes, all except the apoplectic, are mostcommon at this stage. Vaquez, on the other hand, statesclearly: " Transient aphasia and fleeting paresis, speciallybrachial monoplegia, are frequent incidents in vascularhypertension. They appear and disappear suddenly,leaving no traces, and may occur several months later."He lays some stress on the mental symptoms (uncommonin my series), which, he maintains, assume the mostvaried forms-for example, amnesia, mental confusion,and suicidal tendency.
MOTOR AND SENSORY STROKESDefining " the stroke" as a sudden severe attack
drawing the attention of the subject of hypertension toa change in his normal motor or sensory phenomena, onecan classify " motor strokes " under the main heads ofthe paralytic and the paretic. These can be describedaccording to distribution as: (1) hemiplegic; (2) mono- j
plegic; (3) localized-for example, tongue; and (4) diffuse.The last variety usually occurs as a terminal event, beingdue to a severe haemorrhage which causes sudden death,or to one which produces paralysis, first of one side ofthe body and then of the other. According to theirduration, we may say that they are: (1) permanent,(2) present for a few days or weeks, and (3) transient.The annexed diagram gives a clear picture of what mayoccur on the motor side.
StRO/E
PQtMOR f R SW SoR
, ^tJ PER,IANiNF1W/N O>R s ffwD4Ys OR wEiea
* Dysarthria or aphasia.
On the sensory side we get similar changes: completeloss of sensation, as in coma, and changes in sensation-named " incomplete " for the purpose of the diagram-these being analogous to the paralytic and the pareticforms on the motor side. The distribution and durationare similar to those occurring in the motor phenomena.The diffuse form, including cases in which tingling ornumbness, or " a peculiar feeling all over the head andbody," has been reported, is rare. Changes in sensationhave been variously described by the patients themselves,and may occur associated. with, in the absence of, orfollowing motor phenomena. Tingling and numbness are
common. One patient of mine described the sensation as" a cotton-woolly feeling-the face feels heavy o-fi thatside." A doctor, in whom a monoplegia had disappeared,described as irritating " the peculiar dry feeling of thelimb, as though it had been immersed in formalin andtaken out "; again, " When warm water is taken I feelit hotter on one side of the tongue; and, further, onshaving I do not feel the razor well on the recentlyaffected side." In another case a patient complained ofnurnbness of the ear, left upper limb, and distal part ofthe left leg after motor power had returned His descrip-tion was: " as though I have placed my hand on a lumpof ice and removed it." Of the ear he said: " When Iscratch my ear it feels plain.'
JAN. 30, 1 9321
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182 JAN. 30, 1932] THE STROKE IN HIGH ARTERIAL PRESSURE
DIASTOLIC PRESSURE IN STROKEIt is interesting to study very clearly at what stages
in high arterial pressure the stroke supervenes. In my
series of cases the stroke, sensory or motor, has notappeared in a single instance in which the diastolic bloodpressure was under 115. In 20 per cent. of the cases thestroke-in most transient, in a few permanent, in one
fatal-occurred with a diastolic blood pressure between115 and 120. In ten out of the 150 cases death resultedfrom what appeared clinically to be definite cerebralhaemorrhage; in nine of these, the patients were activelyor restrictedly pursuing their usual occupations. Again, innine of these ten the diastolic blood pressure was over 135,the systolic being 200 and over. In 10 per cent. of theseries the transient and permanent strokes occurred incases with a diastolic blood pressure of over 125.
It seems, therefore, that sudden changes in the normalsensory and motor phenomena appear most commonlywith a diastolic blood pressure between 115 and 125,and are altogether absent in cases with diastolic bloodpressures under 115. Cerebral haemorrhage seems to beuncommon in patients under observation, and they are
warned against any but a very quiet life. Fatal haemor-rhage seems to ensue mostly in patients who carry on
ordinary occupations without making allowances for theirabnormal pressure. Indeed, it seems that the catastropheof fatal haemorrhage is the one phase of high arterialpressure in which the practitioner or specialist can give
little relief. There is therefore all the more urgent needto study the earlier signs and symptoms very fully, forthen therapeutic measures can be resorted to in time,and where these are likely to be of no avail, relativesand dependants may be warned of the possibilities ahead,and adjustments relating to business, finance, or familymatters may be made.
HEART FAILURE AND STROKF,The relation of the stroke to heart failure consequent
on high arterial pressure is worth studying. My observa-tions seem to suggest that fatal cerebral haemorrhage,or even transient strokes, are very uncommon once
failure has set in or the heart has begun to show consider-able enlargement, with dyspnoea and other symptomsof a tiring cardiac musculature-even though at thisstage it is observed that the blood pressure, systolic anddiastolic, remains high. In three cases of mine, however,there was very marked enlargement of the heart withthe apex in the sixth- space- and anterior axillary line,with thickened vessels and a locomotor pulse (brachial),but with practically no symptoms referable to the heart.These three patients are reported to have died of cerebralhaemorrhage. The impression is gained, in a review ofmy cases, that patients with hyperpiesis, showing few or
no symptoms referable to the heart, with or withoutcardiac enlargement, are particularly prone to die ofcerebral haemorrhage.
DIAGNOSIS AND PROGNOSISIn this country (Ceylon) there is a popular belief
that the native doctor, so called because he practisesAyurvedic medicine, excels the practitioner of Westernmedicine in the diagnosis and treatment of paralysis.This is no doubt due, in my opinion, to our mistakes inthe matter of prognosis in these cases, and to our failureto appreciate the transient nature of the attacks.A common procedure is as follows. A man gets hemi-
plegia. The nearest practitioner is sent for; he diagnosescerebral haemorrhage and gives a gloomy prognosis,hinting at the possibility or probability of death withintwenty-four hours. The blood pressure is not taken.
In despair the relatives run to the native doctor, to whomno circumstances are hopeless, and who not only promises
relief, but paints the picture of a permanent cure. Thecase falls into the hands of the latter, and time, withrestricted diet on the one hand and rest on the other,works the miracle. In one case the patient gives thisversion: " Dr. X saw me, and said it was a ' spasmodic '
stroke. We took native treatment, as Dr. X said recoverywould take three months, and it was due to highpressure." If the possibility of recovery in a few hoursor days had been mentioned with confidence thepractitioner would have retained his patient as wellas his fees.
In sensory cases the phenomena are generally classedunder neurasthenia, neuritis, and hysteria, and the possi-bility of pressure as a causative factor is missed. Thusin this country, and elsewhere too, misdiagnosis must be
common.These observations have been made with one object in
view-namely, to invite the study of this commondisease, and so to correct or amplify the present findings.From the point of view of the practitioner there is every-
thing to gain and nothing to lose by agreeing withCabot that " the measurement of blood pressure is themost important of all the recourses that have been addedto our armamentarium in the last fifteen years." Whenthe frequent occurrence of sudden motor and sensorychanges as a result of high arterial pressure is more
widely recognized, the diagnosis and prognosis will beplaced on more reliable data.
CONCLUSIONS AND SUMMARYIn a final review of these observations on the stroke
in high arterial pressure, one appears entitled to infer:1. That transient or permanent paralyses of varied
distribution occur fairly frequently.2. That the hitherto neglected sensory phenomena have
a distribution similar to the motor phenomena; that theyalso occur frequently, and are probably caused througban affection of the sensory areas, the pathogenesis beingsimilar to that in the motor cases.
3. That strokes often attributed to other factors, suchas shock, exertion, and emotion, are the result of an
already existing pressure exacerbated by the influenceof these factors.
4. That cerebral haemorrhage does not seem to occur
with diastolic blood pressures of under 115 (whatevermay be the systolic), and that prognosis may be basedon this observation.
5. That cerebral haemorrhage occurs most commonly inpeople working in defiance of an already existing pressure,and without taking any account of this abnormality.
6. That any kind of paresis or paralysis is very rare incases in which the diastolic blood pressure is under 115.If they do occur, the minimum diastolic pressure is over
115 at the time of the stroke. Strokes at this pressure are
rarely fatal or permanent. The former occurs in patientswith thickened vessels or other disease ; the latter in an
unfortunate few, or in those in whom the causative factoris other than hypertension.
7. That cerebral haemorrhage seems to occur more
frequently in those cases of hypertension which showneither marked cardiac enlargement nor symptoms, andrarely in those cases in which there are signs both ofconsiderable cardiac enlargement and symptoms of heartfailure.
I am grateful to my medical colleagues at the GeneralHospital, Colombo, for givinlg me opportunities for verifyingmy observations with cases inl their wards.
