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THE MITIGATION OF STREET NOISES

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1542 Again, Dr. West refers to Hyde Salter’s case in which asthma and epilepsy alternated. The same alternation occurs in migraine and epilepsy,7 in epilepsy and angina pectoris, 0 in asthma and migraine,9 and in asthma and angina,10 not to mention many other pairs of neurosal affections, less well known and less understood. And many such alternating neuroses may be led up to by similar or even identical auras. None of these observations can be correlated and explained except on the view that all such clinically diverse neuroses are manifestations of disordered vaso-motor action ; on this view they present no difficulty whatever. Now the vaso-motor theories of migraine, asthma, angina pectoris. and epilepsy, major and minor, are all already accepted by physicians whose scientific position none can question. But unfortunately for the sake of correct generali- sation, all are not accepted by the same physicians. And for this there can be no doubt that extreme specialisation, necessary as it is, is almost solely to blame. I will refer to a few names. Sir William Osler regards asthma as "a neurotic affection characterised by hypersemia and turgescence of the mucosa of the smaller bronchial tubes." 11 Sir Lauder Brunton demonstrated that peripheral vaso-constriction is essential to the paroxysm of angina pectoris. Sir William Gowers, long an opponent of vaso-motor theories as regards both migraine and epilepsy, has recently seen reason to modify his views, at least, as regards migraine,12 while the vaso- motor theory of epilepsy has gained a most valuable sup- porter in Dr. A. E. Russell.13 Considered separately the arguments in favour of a vaso-motor mechanism in each of the four neuroses seem sufficiently cogent ; considered collectively they gain, at any rate, a hundredfold in power. Let the above four physicians be imagined to form a commission to sit on this question, having before them all the clinical evidence. This is already in existence, and needs but collecting and arranging. I feel confident they could arrive at but one conclusion as regards the mechanism of the four paroxysmal neuroses. This I will attempt to outline. Primarilv there is a more or less widespread peripheral vaso-constriction common to all. This affects most frequently, or at any rate most obviously, the cutaneous area. As a result there is a tendency to a rise in the general or aortic blood pressure. This tendency is met, and more or less compensated-i.e., inhibited-in different ways, varying with the neurosis. In migraine there is a compulsory vaso- dilation localised in the head-scalp, pericranium, or mem- branes of the brain-any or all of these. Such localised vaso-dilation of necessity gives rise in the circumstances (the blood stream being largely shut off from other wide areas) to an intense vascular distension (arterial hypersemia), which is the cause of the intense throbbing headache. In asthma the compensating vaso-dilation affects the bronchial arteries. The resulting vascular distension causes turgescence of the bronchiolar mucosa with obstruction to respiration in the smaller tubes. In epilepsy there are two varieties of mechanism. In one the peripheral vaso-constriction extends to the cerebral arterioles and so causes sufficient cerebral anaemia, local or general, to induce convulsions, local or general. In the other, the peripheral vaso-constriction, being widespread and rapid, causes so sudden a rise in general blood pressure that vagus inhibition of the heart-beat, partial or complete, occurs, and is responsible for the sudden cerebral ansemia, unconsciousness, and general convulsions. In angina pectoris there is a failure of compensation ; the peripheral vaso-constriction is uncompensated, or at least inadequately compensated. Hence a sudden and actual rise in the aortic blood pressure. Distension of the aorta will explain the anginal pain in the breast, which will, of course, be greatly intensified if aortitis be present. But distension of the aorta involves distension of the coronaries and of the tissues, including the aortic and coronary plexuses, which they supply. The communications of these plexuses with the brachial, &:.c., would explain the referred pains in the arm and elsewhere. 7 Gowers: Prodromas of Migraine, Brit. Med. Jour., June 12th, 1909, p. 1400, et seq. 8 Rowe: Journal of Mental Sciences, January, 1905. 9 Liveing: Migraine and Sick-headache, 1873, p. 212. 10 Ibid., p. 200. 11 Principles and Practice of Medicine, 1894, p. 499. 12 Prodromas of Migraine, Brit. Med. Jour., June 12th, 1909, p. 1400, et seq. 13 Pathology of Epilepsy. Transactions of the Royal Society of Medicine, Medical Section, Nov. 26th, 1907; also Gulstonian Lectures. I believe I am correct in saying that there is no single clinical observation on any of the four neuroses which can be shown to be inconsistent with the vaso-motor theory above stated. I am, Sir, yours faithfully, Beckenham, Nov. 16th, 1912. FRANCIS HARE To the Editor of THE LANCET. SIR,-I was greatly interested in reading Dr. William Russell’s lecture on Cerebral Angiospasm in THE LANCET of Nov. 16th (p. 1349), and also Dr. Samuel West’s article on Respiratory Neurosis at page 1352 of the same issue. There was one symptom which was not mentioned in either paper to which I may draw attention-viz., yawning. In the Edinbmrgh Mediecal Journal, May, 1893, I published some cases of Raynaud’s disease, and perhaps a brief note on one of them may be of interest after having been buried so long. A woman, aged 60, complained of giddiness, faintness, some paresis of left leg, and slight aphasia. Not been well for a few days. History: Twelve years ago, when 48, she first became subject to symmetrical dead fingers, which were very painful. Ten years ago epistaxis occurred, and a slight injury to a toe caused profuse bleeding. Attacks of epistaxis frequent, but she was somewhat alcoholic. Never had chil- blains. The condition of hands and toes not varied much lately, but often unable to do domestic duties on account of pain in hands after washing. On examination, Feb. 24th, 1891, three hours after the aforesaid symptoms, she was strange and dazed. No facial or other marked paralysis, but paresis of left arm. Feet colder, hands warmer than rest of body. Pulse regular, 80. No marked increase of tension. Still some aphasia, left- sided headache ; breathing quiet and regular. Pupils equal ; react normally. Superficial plantar and patellar tendon reflexes exaggerated, specially the former. When taken ill to-day the hands were said to have been almost black, face pale, sight dim. Nails are overgrown, being so tender to cut, and so on. Feb. 25th: Speech almost right; no giddiness, though still left-sided headache. LTrine 10 oz., 1025 ; no blood, no sugar. Albumin doubtful. March 1st: Fingers better, nails able to be pared. Spasmodic cough, 3 to 5 A.M. No headache. March 3rd : Been yawning all day, though cannot sleep. Periodic cough continues. March 6th: Cough ceased, but replaced by watery diarrhoea at same hour. Yawning passed off, having lasted two and a half days. It was remarked that these varying symptoms can only be accounted for by corresponding attacks of cerebral ansemia or congestion affecting different areas of the brain, as they are compatible with no single lesion." I once attended a stout lady who had repeated severe attacks of "air hunger," associated with extensive angio-neurotic oedema of the arms. I have under my care at present an old man, 78, who has recovered from a patch of gangrene of the lung with empyema which I opened freely. Two weeks ago he had a series of eight convulsive seizures in the course of a few hours. Conjugate deviation to the right, marked paresis of the right arm and leg, both of which, however, were at times convulsed. I gave him hypodermic injections of heroin and hyoscine, and next morning he was apparently all right, in his previous condition, which was one of more or less aphasia, &c., the result of a lesion during his previous illness, but he is able to be up and walk about. Two similar cases in old people have been patients of mine-one an elderly lady who had five or six illnesses, each with a series of convulsive attacks. Such convulsions are evidently due to cerebral anaemia from one cause or another. The New Sydenham Society published in 1859 a monograph by Kussmaul and Jenner on this subject, and on page 104 one of the causes is given thus : " Spasms of the iiiiiseles of the blood-vessel, with four sub-divisions. I am, Sir, yours faithfully, J. CHRISTIAN SIMPSON, M.D. Edin. Cambridge, Nov. 19th, 1912. THE MITIGATION OF STREET NOISES. To the Editor of THE LANCET. SIR,—You were good enough last September to grant me space in your columns to invite the support of the profession in approaching the authorities with a view to mitigating street noises. I have now to thank you very much for that favour and to express my gratitude to those medical men
Transcript
Page 1: THE MITIGATION OF STREET NOISES

1542

Again, Dr. West refers to Hyde Salter’s case in whichasthma and epilepsy alternated. The same alternation occursin migraine and epilepsy,7 in epilepsy and angina pectoris, 0in asthma and migraine,9 and in asthma and angina,10 notto mention many other pairs of neurosal affections, less wellknown and less understood. And many such alternatingneuroses may be led up to by similar or even identical auras.None of these observations can be correlated and explainedexcept on the view that all such clinically diverse neurosesare manifestations of disordered vaso-motor action ; on thisview they present no difficulty whatever.Now the vaso-motor theories of migraine, asthma, angina

pectoris. and epilepsy, major and minor, are all alreadyaccepted by physicians whose scientific position none canquestion. But unfortunately for the sake of correct generali-sation, all are not accepted by the same physicians. Andfor this there can be no doubt that extreme specialisation,necessary as it is, is almost solely to blame. I will refer toa few names.

Sir William Osler regards asthma as "a neurotic affectioncharacterised by hypersemia and turgescence of the mucosaof the smaller bronchial tubes." 11 Sir Lauder Bruntondemonstrated that peripheral vaso-constriction is essential tothe paroxysm of angina pectoris. Sir William Gowers,long an opponent of vaso-motor theories as regards bothmigraine and epilepsy, has recently seen reason to modifyhis views, at least, as regards migraine,12 while the vaso-motor theory of epilepsy has gained a most valuable sup-porter in Dr. A. E. Russell.13 Considered separately thearguments in favour of a vaso-motor mechanism in each ofthe four neuroses seem sufficiently cogent ; considered

collectively they gain, at any rate, a hundredfold in power.Let the above four physicians be imagined to form a

commission to sit on this question, having before them allthe clinical evidence. This is already in existence, andneeds but collecting and arranging. I feel confident theycould arrive at but one conclusion as regards the mechanismof the four paroxysmal neuroses. This I will attempt tooutline.

Primarilv there is a more or less widespread peripheralvaso-constriction common to all. This affects most frequently,or at any rate most obviously, the cutaneous area. As aresult there is a tendency to a rise in the general or aorticblood pressure. This tendency is met, and more or lesscompensated-i.e., inhibited-in different ways, varyingwith the neurosis. In migraine there is a compulsory vaso-dilation localised in the head-scalp, pericranium, or mem-branes of the brain-any or all of these. Such localisedvaso-dilation of necessity gives rise in the circumstances (theblood stream being largely shut off from other wide areas)to an intense vascular distension (arterial hypersemia), whichis the cause of the intense throbbing headache. In asthmathe compensating vaso-dilation affects the bronchial arteries.The resulting vascular distension causes turgescence of thebronchiolar mucosa with obstruction to respiration in thesmaller tubes. In epilepsy there are two varieties ofmechanism. In one the peripheral vaso-constriction extendsto the cerebral arterioles and so causes sufficient cerebralanaemia, local or general, to induce convulsions, local or

general. In the other, the peripheral vaso-constriction, beingwidespread and rapid, causes so sudden a rise in general bloodpressure that vagus inhibition of the heart-beat, partial orcomplete, occurs, and is responsible for the sudden cerebralansemia, unconsciousness, and general convulsions. In

angina pectoris there is a failure of compensation ; the

peripheral vaso-constriction is uncompensated, or at least

inadequately compensated. Hence a sudden and actualrise in the aortic blood pressure. Distension of the aortawill explain the anginal pain in the breast, which will, ofcourse, be greatly intensified if aortitis be present. Butdistension of the aorta involves distension of the coronariesand of the tissues, including the aortic and coronary plexuses,which they supply. The communications of these plexuseswith the brachial, &:.c., would explain the referred pains inthe arm and elsewhere.

7 Gowers: Prodromas of Migraine, Brit. Med. Jour., June 12th, 1909,p. 1400, et seq.

8 Rowe: Journal of Mental Sciences, January, 1905.9 Liveing: Migraine and Sick-headache, 1873, p. 212.

10 Ibid., p. 200.11 Principles and Practice of Medicine, 1894, p. 499.

12 Prodromas of Migraine, Brit. Med. Jour., June 12th, 1909, p. 1400,et seq.

13 Pathology of Epilepsy. Transactions of the Royal Society ofMedicine, Medical Section, Nov. 26th, 1907; also Gulstonian Lectures.

I believe I am correct in saying that there is no singleclinical observation on any of the four neuroses which canbe shown to be inconsistent with the vaso-motor theory abovestated. I am, Sir, yours faithfully,Beckenham, Nov. 16th, 1912. FRANCIS HARE

To the Editor of THE LANCET.SIR,-I was greatly interested in reading Dr. William

Russell’s lecture on Cerebral Angiospasm in THE LANCET ofNov. 16th (p. 1349), and also Dr. Samuel West’s articleon Respiratory Neurosis at page 1352 of the same issue.There was one symptom which was not mentioned in eitherpaper to which I may draw attention-viz., yawning. Inthe Edinbmrgh Mediecal Journal, May, 1893, I publishedsome cases of Raynaud’s disease, and perhaps a brief note onone of them may be of interest after having been buried solong.A woman, aged 60, complained of giddiness, faintness,

some paresis of left leg, and slight aphasia. Not been wellfor a few days. History: Twelve years ago, when 48, shefirst became subject to symmetrical dead fingers, which werevery painful. Ten years ago epistaxis occurred, and a slightinjury to a toe caused profuse bleeding. Attacks of epistaxisfrequent, but she was somewhat alcoholic. Never had chil-blains. The condition of hands and toes not varied much

lately, but often unable to do domestic duties on account ofpain in hands after washing.On examination, Feb. 24th, 1891, three hours after the

aforesaid symptoms, she was strange and dazed. No facialor other marked paralysis, but paresis of left arm. Feetcolder, hands warmer than rest of body. Pulse regular, 80.No marked increase of tension. Still some aphasia, left-sided headache ; breathing quiet and regular. Pupils equal ;react normally. Superficial plantar and patellar tendonreflexes exaggerated, specially the former. When taken ill

to-day the hands were said to have been almost black, facepale, sight dim. Nails are overgrown, being so tender to cut,and so on. Feb. 25th: Speech almost right; no giddiness,though still left-sided headache. LTrine 10 oz., 1025 ; noblood, no sugar. Albumin doubtful. March 1st: Fingersbetter, nails able to be pared. Spasmodic cough, 3 to 5 A.M.No headache. March 3rd : Been yawning all day, thoughcannot sleep. Periodic cough continues. March 6th: Coughceased, but replaced by watery diarrhoea at same hour.Yawning passed off, having lasted two and a half days.

It was remarked that these varying symptoms can onlybe accounted for by corresponding attacks of cerebralansemia or congestion affecting different areas of thebrain, as they are compatible with no single lesion." I onceattended a stout lady who had repeated severe attacks of"air hunger," associated with extensive angio-neuroticoedema of the arms.

I have under my care at present an old man, 78, who hasrecovered from a patch of gangrene of the lung with empyemawhich I opened freely. Two weeks ago he had a series of eightconvulsive seizures in the course of a few hours. Conjugatedeviation to the right, marked paresis of the right arm andleg, both of which, however, were at times convulsed. I

gave him hypodermic injections of heroin and hyoscine, andnext morning he was apparently all right, in his previouscondition, which was one of more or less aphasia, &c., theresult of a lesion during his previous illness, but he is able tobe up and walk about.Two similar cases in old people have been patients of

mine-one an elderly lady who had five or six illnesses,each with a series of convulsive attacks. Such convulsionsare evidently due to cerebral anaemia from one cause or

another. The New Sydenham Society published in 1859 amonograph by Kussmaul and Jenner on this subject, andon page 104 one of the causes is given thus : " Spasms of theiiiiiseles of the blood-vessel, with four sub-divisions.

I am, Sir, yours faithfully,J. CHRISTIAN SIMPSON, M.D. Edin.

Cambridge, Nov. 19th, 1912.

THE MITIGATION OF STREET NOISES.To the Editor of THE LANCET.

SIR,—You were good enough last September to grant mespace in your columns to invite the support of the professionin approaching the authorities with a view to mitigatingstreet noises. I have now to thank you very much for that

favour and to express my gratitude to those medical men

Page 2: THE MITIGATION OF STREET NOISES

1543

who were kind enough to communicate with me. You and

they will, no doubt, be pleased to learn that, following myrepresentation, the authorities have issued an order pre-scribing the use of silencers for motor cycles after March 31stnext, and have informed me that borough and countycouncils are empowered under Section 23 MunicipalCorporation Act, 1882, Section 16 Local Government Act,1888, and Section 5 London Government Act, 1899, to makeby-laws dealing with the other noises complained of.

I am, Sir, yours faithfully,CHAS. MONK,

Lieutenant-Colonel, I.M.S. (retired).Burlton Lodge, Station-road, Barnes, S.W., Nov. 25th, 1912.

CATTLE AND HORSES AS TYPHOIDCARRIERS.

To the Editor of THE LANCET.

SIR,—Practising as I have been for the last 24 years inSouth Africa, I have been often struck with the way entericfever spreads, apparently without any regard for time-honoured principles. I have had experience of several

epidemics, and I think it may be useful to put certain ideasof mine on paper, which are the result of observation, andwhich may explain the apparently erratic behaviour of thisdisease. Even if the explanation should turn out to beincorrect or inaccurate, it might at any rate lead to furtherobservation on a line which, as far as I am aware, has notbeen suggested-namely, that cattle, horses, and perhapsother animals may be typhoid carriers.When I first started practice in Clanwilliam in the early

part of 1888 the country was flooded by the heaviest rainsthat had occurred in the memory of the proverbial oldestinhabitant. Typhoid fever had made a start before the

rain, however, had begun, continued more or less duringthe rainy season, but assumed its greatest severity as thedry weather set in. I was then quite unable to accountfor its spread and severity, the farms being isolated

dwellings often at a considerable distance from one another.Its greatest intensity was along the course of the OliphantsRiver, but as the river water was not used for drinking orhousehold purposes, and was a large rapidly flowing stream,I did not think the river could be to blame. Drinking waterwas obtained from mountain springs that ran down andcollected into furrows from which all water for householduse and irrigation was drawn. The doctrine of typhoidcarriers was unknown or known to but few, and the idea of" carrying" by means of cattle had never occurred to me.The next severe outbreak that I had to deal with was

during the concluding stages of the war-that is to say,from January, 1901, until September or October, 1902, whenthe country was still being largely policed. Then I noticedhow typhoid fever occurred constantly in the neighbourhoodof remount camps or in places where large numbers ofhorses had congregated and where manure in largequantities was lying about the ground, and I came to theconclusion that horse-dung probably made an excellentculture medium for the typhoid bacillus, and was carried byflies from place to place.Within the last few days I was sent by the Divisional

Council to investigate an outbreak that had occurred ontwo farms about 50 miles from Clanwilliam ; the farms wereabout four miles from each other. On the first farm I foundtwo European children suffering from the disease. Theowners of the farm were cleanly, intelligent Dutch people,and they used every precaution to prevent the spread of thedisease. The second farm, however, was quite different.Not only were the inhabitants uncleanly and careless,but the houses were built on a marsh with water

flowing all about them, and it was upon this farmthat the disease originated. Here I found in all eightcases in different stages. The water-supply in bothcases, as stated before, was from a mountain spring wherecattle were in the habit of drinking, and the water, afterbeing contaminated with their fasces, was freely used forhousehold purposes. At the time of the present outbreakthere was no enteric fever in the neighbourhood, and theidea struck me that possibly some of the cattle might becarriers, who deposit the bacillus in a suitable medium forits growth, and are thus able to start an outbreak of entericfever in the neighbourhood.

I remember that during the war the spread of enteric fevercould not always be accounted for, and from time to time Ihave thought that possibly horses, cattle, and other animals,who do not suffer themselves from the disease, might be ableto carry it and deposit its bacilli in various places. If thisview be correct, it would readily explain the apparentlyerratic behaviour which characterises so many of the SouthAfrican epidemics.

I should be glad if you would give publicity to this, if youthink it would create discussion, as it is a question of con-siderable importance to South Africa, where typhoidfever epidemics often assume a very serious character.

T am Rir vniirq faithfully

ALFRED A. HAYES,Clanwilliam, Cape Province, South Africa. District Surgeon.

THE ADVISORY COMMITTEE UNDER THENATIONAL INSURANCE ACT.

To the Editor of THE LANCET.

SIR,-The numerous letters I have received from membersof the medical profession and the announcement of Sir JohnCollie’s resignation make it necessary for me to explain myattitude towards the Advisory Committee of the NationalHealth Insurance Act. I did not respond to the request ofthe British Medical Association that I should resign for tworeasons. The Association had accepted sanatorium benefit,and I was placed on the committee chiefly for the purpose ofadvising with regard to the regulations of that benefit.Further, I thought it my duty to remain on the committee solong as there appeared to be any hope of the Chancellor ofthe Exchequer coming to some arrangement which wouldsatisfy the legitimate and reasonable demands of the

profession.In view of the terms of the British Medical Association’s

resolution of Nov. 20th, which is now before the Chancellorand which does not preclude the possibility of a settlement,I feel it to be my duty to continue to serve on the committeeuntil the Association finds that it is unable to obtain satis-faction for what it authoritatively defines as the reasonabledemands of the profession.

T :1.m. Sir voiirq faithfully

Portland-place, W., Nov. 21st, 1912. ARTHUR LATHAM.

FIRE PROTECTION IN LONDON AND THELONDON COUNTY COUNCIL.

To the Editor of THE LANCET.

SIR,-The coroner in summing-up at the Kensington fireinquest on Nov. 21st, is reported to have spoken as

follows :-

The calamity made one wonder how many other buildings inLondon were in the same condition as they were told Messrs. Barkers’premises were; how the many negotiations were going on, and howmany buildings were waiting before the necessary alterations were tobe made.

I wish to take the earliest opportunity of publicly replying _

to these questions. There are upwards of 50,000 buildingsin the metropolis at the present moment to which the LondonBuilding Act Amendment Act of 1905 has not yet beenapplied. Although this Amendment Act has been in forcenow for upwards of seven years, the superintending architectof the London County Council, giving evidence before theHouse of Commons Committee on the London CountyCouncil General Powers Bill (1912) in June last, stated thatonly 2330 buildings had been scheduled for action at thatdate, and that the Building Act Committee of the LondonCounty Council had only considered 1203 of those cases. Ofthese 1203 cases only 527 had at that date been satisfactorilyequipped by the provision of suitable means of escape, andthe balance were in what might be termed a state of

negotiation.That so few buildings (527) should have been put in order

out of approximately 50,000 cases in the long period ofseven years is a matter of the gravest import, but the blameshould not in any way be attributed to the superintendingarchitect nor his officer,,, but specifically to the London

County Council in its corporate capacity, which does notgive its Building Act department the necessary means,the necessary staff, or the necessary encouragement to carry


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