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JANUARY 17, 1925.

An AddressON

ACUTE DRUNKENNESS.ITS MEDICO-LEGAL ASPECTS, SYMPTOMS,

AND TESTS.

Delivered before the Society for the Study of Inebriety onJan, 13th, 1925,

BY SIR JAMES PURVES-STEWART, K.C.M.G.,C.B., M.D. EDIN., F.R.C.P. LOND.,

SENIOR PHYSICIAN TO WESTMINSTER HOSPITAL.

ACCORDING to the Oxford Dictionary, a drunk manis defined as one who is " overcome with liquor."We note that this is not quite synonymous withalcoholic intoxication or poisoning by alcohol, for aperson may have taken a mildly toxic dose of alcoholwhich may be insufficient to overcome him andmake him drunk. We naturally inquire at whatstage, then, of alcoholic intoxication a person is tobe regarded as drunk. This is not a mere dialecticquibble but a very practical question, for, undercertain conditions, a. drunken person is liable to variouslegal penalties.

DEFINITION.

Curiously enough, according to Byrne’s Law Dic-tionary, no statutory definition of -drunkenness exists,and " a man may be held drunk for the purpose ofone offence when he would not be held drunk for thepurpose of another offence. The degree of intoxicationwhich would make an engine-driver drunk if he weredriving an express train would not make him drunkif he were walking along a country lane." Mr.Serjeant Stephen, in his Commentaries on the Lawsof England, defines drunkenness as " that whichdeprives men of their reason and occasions in theman artificial madness or phrenzy while it la,sts." Wemedical men have to be even more precise. Therefore,with all deference to the learned legal authoritiesalready quoted, I would submit the followingdefinition for consideration :-

" A drunk person is one who has taken alcohol in sufficientquantity to poison his central nervous system, producing inhis ordinary processes of reaction to his surroundings atemporary disorder, which causes him to be a nuisance ordanger to himself or others."

In the foregoing definition two classes of transientdisability are referred to. One, the intoxicatedperson’s personal incapacity, is mainly a medicalquestion ; the other (comprising the final phrase ofmy definition) has to do with the relations of thedrunk man to his fellow-citizens and is a medico-legalaffair. In the eyes of the law (and here I amstrengthened by the opinion of an eminent solicitor,Mr. H. C. Haldane) a prisoner is liable to punishment Inot for being merely drunk, but for the combinedoffences of being drunk and disorderly, drunk andincapable, drunk and unfit to drive a motor-car,and so on. I am not aware that there is now anypenalty for being drunk, so long as the drunkennessdoes not inflict harm or risk on other people. In thereign of James I. the offence of drunkenness was anoffence against public morals and convenience andwas punished (4 Jac. 1., Chap. 5, and 21 Jac. I.,Chap. 7, Sect. 3) with the forfeiture of 5s. to be paidwithin one week after conviction to the church-wardens for the use of the poor. These statutes,however, appear to have been repealed by theLicensing Act of 1872 (35 and 36 Vie., Chap. 94,Sect. 12), which runs as follows (the italics are not inthe original) :-

" Every person found drunk in any highway or otherpublic place, whether a building or not, or on any licensedpremises, shall be liable to a penalty not exceeding tenshillings, and on a second conviction within a period oftwelve months shall be liable to a penalty not exceeding

twenty shillings, and on a third or subsequent occasionwithin such period of twelve months shall be liable to apenalty not exceeding forty shillings.I " Every person who in any highway or other public place,whether a building or not, is guilty while drunk of riotousor disorderly behaviour, or who is drunk while in chargeon any highway or other public place of any carriage,horse, cattle, or steam-engine, or who is drunk when inpossession of any loaded fire-arms, may be apprehended,and shall be liable to a penalty not exceeding forty shillings,or in the discretion of the Court to imprisonment with orwithout hard labour for any term not exceeding one month.

" Where the Court commits any person to prison for non-payment of any penalty under this section, the Court mayorder him to be imprisoned with hard labour."

CAUSATION.

Alcoholic intoxication occurs when the quantityof alcohol absorbed becomes enough to poison thecentral nervous system, according to the abovedefinition, and to disturb its normal reactions. Thetotal amount necessary to produce nervous symptomsvaries widely in different cases. Habituation or

acquired tolerance to the drug is one factor ; theseasoned toper may consume large and increasingquantities daily for many years and may nevershow any symptoms of drunkenness, whereas a

moderate drinker, or still more a habitual teetotaler,will become acutely drunk if he attempts to keep upwith him for an hour. The degree of concentrationof the alcohol is another factor so self-evident as torequire no further discussion. The majority of casesof alcoholic intoxication nowadays are due to spiritdrinking; only in a small proportion is it attributableto light wines or beer. Another factor is the relationbetween drinking alcohol and the taking of food.Alcohol swallowed before or between meals--i.e.,unmixed with food-is more rapidly absorbed thanwhen taken with or immediately after food. Inci-dentally another curious fact is that sometimes thevomiting of alcohol, or of a mixture of food andstrong alcohol, instead of preventing the person frombecoming drunk, may actually precipitate thesymptoms of acute intoxication. This is probablydue to removal, during the act of vomiting, of theprotective barrier of mucus from the gastric mucousmembrane, thereby rendering the residue of alcoholwhich remains in the stomach more readily absorbedthan before. Fatigue and excitement may also befactors in predisposing to rapid alcoholic intoxication.A sudden fall in atmospheric temperature may alsoprecipitate intoxication. Many a man from sadexperience hesitates to leave his host’s firesidewithout an escort, owing to vivid memories of previousopen-air tragedies. The most rapid method ofalcoholic intoxication which I know of is bv meansof intravascular injection. Needless to say, this isan accidental and very exceptional affair, never

self-induced by the patient.I can recall the case of a restless young man in whom

I was injecting absolute alcohol into the stylo-mastoidforamen, for the purpose of inducing temporary facialpalsy so as to relieve facial hemispasm. During thisinjection he suddenly moved his head ; consequently someof the alcohol, perhaps 20 or 30 minims, was accidentallydelivered into the adjacent structures, probably into theinternal carotid artery, conveying it directly to the brain.Within a few seconds symptoms of acute alcoholic intoxica-tion supervened, with mental confusion, singing, shouting,and fighting ; these phenomena subsided completely aftera few minutes.

SYMPTOMS AND SIGNS.

The symptoms of alcoholic intoxication are familiarto us all (of course, I only mean by the observationof other persons). May I be allowed to recall the mostimportant of the clinical phenomena.The early effects of alcohol, like those of similar

narcotic drugs, vary from one individual to another,affecting different parts of the central nervous systemwith varying intensity according to each person’sspecial vulnerability. In moderate doses, one of itsearly effects is to dull the critical and inhibitorycentres in the cerebral cortex.. Thus the cares and

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worries of everyday life are less keenly felt, so thatthe individual becomes temporarily happier and moresociable. The Old Book tells us how " wine makethglad the heart of man," and if this were the end-result of alcoholic celebration many people would benone the worse and possibly the better for it. Youmay know the story of an eminent London physician,now dead, with a huge and complicated practice,who was asked what he did if he came home at nighttired out and found an unsually heavy pile of letterswaiting for him. He replied :

" I drink a half-bottleof champagne at dinner and then I don’t care a damnabout letters or anything else." Everyone whoorganises a charity dinner in aid of some benevolentinstitution knows how alcohol tends to set free thelatent generous impulses of the diners. Therefore thesubscription list is never sent round until near theend of the banquet, by which time the pangs ofhunger are allayed, the happy guests are sippingvintage port and smoking choice cigars, and theirgenerous instincts are no longer subject to the samedegree of inhibition as during the less altruistic periodof the hors d’oeuvres or soup.Somewhat larger doses of alcohol cause pathological

inhibition of various other functions, producing amild degree of mental confusion or toxic delirium.At this stage some individuals become humorous andhilarious ; others become gloomy and quarrelsome.The old dictum, in villo veritas, reminds us of the well-established fact that under the influence of excess ofalcohol the individual’s temperamental and emotionalreactions, no longer controlled by the higher inhibitorycentres, now reveal themselves to a critical world.One man becomes garrulous and tells stories, funnyor otherwise. Another becomes boastful and aggressive,or even " fighting drunk." Another becomes senti-mental and lacrymose ; Englishmen call this con-

dition maudlin, Scotsmen call it " greetin’ fou." Inmany persons the sexual passions tend to becomeuncontrolled. This combination of excess in 7?acc/!oel Vencre is familiar, and unhappily accounts for alarge proportion of cases where venereal diseases areacquired by persons who in their sober senses wouldhave taken care to avoid such infections.

Besides the higher psychical functions, the lowernerve-centres for muscular coordination, reflex tonus,&c., may also become imperfectly controlled. Thus,for example, the cerebellum may bear the brunt ofthe poisoning. The familiar reeling gait of acutealcoholic poisoning with inability to walk accuratelyalong a straight and narrow path is typically cerebellarin type ; it is accompanied by muscular hypotoniaand by a sensation of giddiness, sometimes moderatein degree, in other cases so severe that the patientlies helpless on the ground, distressingly conscious ofhis condition but unable to raise his head or trunkwithout the most violent vertigo, causing him tocollapse helplessly on the floor. Cerebellar incoordina- ’,tion may be brought to light by a sudden change ’,in posture. Many a guest realises that he has dined ’not wisely but too well only when the moment comes ’for him to rise and leave the festal board. Cerebellarataxia may also appear in the upper limbs whenexecuting fine movements ; the returning roysterer’sdifficulty in inserting the key into the keyhole ofhis home is part of the stock-in-trade of the comicjournals. These ataxic phenomena are unaccom-

panied by nystagmus, and this would indicate thatthe cells of the cerebellar cortex rather than the intra-cerebellar nuclei are mainly disabled by the poison.

Other familiar toxic phenomena are due to disorderof the ponto-bulbar nuclei, notably those for theocular muscles beneath the floor of the iter and forthe articulatory muscles in the lower part of themedulla. The pupils are usually moderately dilatedbut at this stage still react to light. Double vision isnot uncommon. To illustrate alcoholic diplopia,Hughlings Jackson used to tell of a Scotsman whoremarked to his friend at the end of a joyous alcoholicevening,

" When ye gang oot o’ the door, Tam, ye’llsee twa cabs. Jist get intae the first yin, for thesecond yin’s no there."

I Dysarthria or indistinctness of articulation isanother familiar symptom in alcoholic intoxication,well known to the man in the street. The sufferer whotries to pronounce difficult test-phrases, such as

" British Constitution," " terminological inexactitude,"" sixty-sixth battery of artillery," and so on, some-times omits a syllable here and there, or slurs hisconsonants into one another. In other cases he is alertenough to be conscious of his own difficulty andbravely tries to conceal it, but betrays himself by theundue emphasis with which he pronounces his words.sometimes repeating a specially difficult one twiceover, to make sure that he can do it.

Alcoholic vomiting sometimes appears at thisstage and may tend temporarily to aggravate thenervous symptoms as already explained ; in othercases vomiting is postponed until six or seven hourslater, accompanied by bursting headache, as the toxicsymptoms are wearing off. The smell of the breath,and of the stomach contents if the patient is vomiting,has a characteristic indescribable aroma, probablydue to the admixture of alcohol with the pharyngealand gastric secretions. The smell of alcohol is con-clusive evidence that the patient has recently swallowedalcohol but of nothing more, for it may be producedby a single glass of alcoholic refreshment. Neverthe-less, uncharitable observers so often place an unkindinterpretation on its presence that even temperateCity men, so I am told, often chew a couple of clovesafter their mid-day glass of sherry as a sort of smoke-screen. Onions, various cheeses, and other aromaticsmay also serve the same kindly purpose.

Hiccup, myoclonic contraction of diaphragm, is apathological bulbar reflex due to abnormal excita-tion of the inspiratory centre. It occurs in cases ofpoisoning by alcohol, but also from other blood-bornepoisons as in uraemia and from various reflex causes.Alcoholic hiccup occurs at a,n early or only moderatelyadvanced stage of alcohol poisoning and is commonlyassociated with dysarthria.’ A deeper stage of alcoholic poisoning is that ofalcoholic stupor, in which the individual is unconscious,with flaccid limbs and trunk, dilated and sluggishpupils, and warm, moist skin ; his temperature issubnormal and his breath, as in the lighter stages ofpoisoning, smells of alcohol. But even here we mustbe cautious in our diagnosis. The presence of analcoholic aroma in a comatose patient, althoughsuggestive, is not conclusive evidence that the comais of alcoholic origin. Firstly, a patient with anattack of cerebral haemorrhage may have had alcoholgiven him just at the onset of his symptoms ; or

whilst drinking alcohol an intercurrent attack ofapoplexy may have supervened ; or again, he mayhave fallen and sustained a head injury, producingcerebral compression. Therefore, every patient whois seen in a condition of stupor or coma coexistingwith an alcoholic breath, or in surroundings suggestiveof alcoholic poisoning, should be carefully examinedfor other causes of coma. Unilateral signs such aslocalised paralysis of a limb, an extensor plantarreflex on one side, inequality of the pupils, and so on,would point to a unilateral intracranial lesion.Pin-point pupils suggest either poniine haemorrhage(often associated with a high temperature), or opiumpoisoning (with a subnormal temperature and a, cold,clammy skin). The urine should be examined toexclude diabetic and ursemic poisoning, whilst variousother poisons, especially opium, veronal, and alcoholitself, can be recognised by appropriate tets of thegastric contents, the urine, and even the cerebro-spinal fluid, preferably withdrawn by cistern-puncture,if the observer is skilful enough. Typical alcoholicstupor has a less profound degree of unconsciousnessthan in opium or veronal poisoning or than in cerebralhaemorrhage, for the alcoholic patient can usually beroused temporarily by energetic stimulation. As thealcoholic stupor passes off, it is followed by sleep,from which the patient wakes up with an acutebursting headache, dryness of the mouth (the so-calledparrot’s tongue), intense thirst, nausea, and sometimesvomiting, after which he begins to feel better. The

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cortical symptoms, cerebral and cerebellar, togetherwith the diplopia, the dysarthria, and other ponto-bulbar phenomena which characterised the onset ofthe process of intoxication, do not recur on the"morning after the night before."Amongst the rarer paralytic phenomena following

acute alcoholic poisoning must be mentioned thetragic one of acute optic atrophy. No case of thissort, so far as I am aware, has yet been" recorded inEngland, but it has been frequently observed in theUnited States especially since the days of prohibitionand extensive smuggling, or as the Americans callit, " boot-legging." It results from the drinking ofmethylated alcohol or wood-spirit. Such a patient,after recovery from his alcoholic stupor, becomesrapidly and permanently blind owing to acute retro-bulbar degeneration of the optic nerves.

TESTS FOR DRUNKENNESS.

We now come to the practical problem which has tobe solved daily-namely, whether a given individualis drunk or not. The diagnosis is often so easy thatit is arrived at by what trade-unionists would termunskilled labour—i.e.. by non-medical observers.As a matter of fact, in most cases the diagnosis ismade by a policeman, who has then to decide whetherto take the person into custody, for the safety of thedrunk man himself or for that of his fellow-citizens.At the police-station the police officer’s diagnosis isconfirmed or otherwise by the police surgeon, who ’,may be too open to suggestion. And here I wouldlike to make it perfectly clear that in nine cases outof ten the policeman’s diagnosis is correct.A good deal of loose thinking has been going on

upon the subject of so-called tests for drunkenness.With the possible exception of a positive reaction foralcohol in the cerebro-spinal fluid, to which I shallrefer later, there is no single clinical sign which ispathognomonic of alcoholic poisoning of the centralnervous system, because drunkenness is not a simpleclinical entitv like a broken bone or a consolidatedlung, but a way in which certain nervous tissues react,evidenced by a whole series of transient phenomenafollowing an initial poisoning. I

The first question we always have to ask ourselvesis. " Has the person recently taken alcohol ? " If hehas not, we need proceed no farther. If we smellalcohol in his breath, this is prima facie evidence ofthe possibility of alcohol poisoning, but only so faras it goes. And, by the way, it is important that theobserver who claims to recognise the smell of alcoholin others, whether he be a police-officer or medicalofficer, shall himself be free from recent alcoholicconsumption. Second, has he taken alcohol in suchquantity as to produce disorder of the central nervoussystem and to render his reactions to the outer worldtemporarily abnormal ? This is where the variousso-called tests for drunkenness come in. But it mustbe remembered that these are not tests for alcoholicpoisoning itself, but only for cerebral, cerebellar,ponto-bulbar, or other disorders. Such disorders maybe due to alcoholic intoxication, but they may also beproduced by various other causes. Take, for example,the common case where a policeman arrests a man forbeing drunk and incapable in a public place. Whenasked in the witness-box what was the the condition ofthe accused, the consta,ble usually replies confidentlyand dogmatically, "He was drunk." If pressed bythe court or by the defending counsel to say how heknew that the accused was drunk, he generally says," IIe smelt of drink ; he was disorderly in his conduct ;he spoke indistinctly; and he staggered in walking."Such facts as these are certainly strong, presumptiveevidence of drunkenness. But, being human, even apoliceman may be mistaken, for, apart from the smellof alcohol, everyone of the foregoing evidences ofdrunkenness may be found in certain persons whoare perfectly sober. As crude examples of what Imean, it is easy to understand how an individual withthe unsteady gait of locomotor ataxia or of cerebellaror labyrinthine disease, or a patient with dysarthria

from bulbar palsy, palatal deficiency, or even with astammer, or another who is nervous, angry, or

emotionally excited from perfectly legitimate cause,say after a street accident, may quite innocently becharged with being drunk. How are we to avoid sucherrors ? Sometimes by obtaining evidence as to thepresence of these disabilities before the onset of thealleged intoxication, and in any case by examining himafter the supposed drunkenness has had time to passaway when, if he is suffering from a gross organiclesion, he will still be found to display the same clinicaldisorders, with the exception that the alcoholic aromahas now faded from his breath " like the snows ofyester year."A little while ago a medical colleague, who suffers from a

large perforation of the palate, together with chronicEustachian catarrh and frequent labyrinthine vertigo, wasdriving his motor-car when he had to swerve to avoidsomeone at a street corner. His car ran on to the side path,bruising the legs of a bystander. As bad luck would have it,he had recently had a glass of gin and vermouth. Thepolice-constable, noticing his alcoholic breath and observinghis unsteady gait and indistinct articulation, promptly, andquite reasonably, arrested him. He was accused, and con-victed, of being drunk in charge of a motor-car. Only onappeal was he able to establish the facts of his chronicpalatal deficiency and recurrent labyrinthine vertigo andto secure acquittal on the charge of drunkenness.

In doubtful cases the court, in my opinion, shouldinsist on a second examination being carried out morefrequently than it does at present, which is almostnever.

Common Clinical Phenomena Used as Tests.

Let us now briefly consider some of the commonerclinical phenomena employed by medical men as testsin the recognition of drunkenness at a given moment.And once more let me emphasise the fact that theseare not in themselves tests for alcoholic poisoning,but merely for cerebral, cerebellar, or ponto-bulbardisorders, as the case may be.

Disorder of the higher cerebral eenfre8 may be evi-denced by the presence of mental confusion, inco-herence of thought and speech, emotional excitementon the one hand or apathy on the other. Sensationmay also be disordered so that the patient is relativelyinsensitive to stimuli, especially painful stimuli, andmay cut, bruise, or otherwise injure himself withoutnoticing it. Such cerebral phenomena when transient,of recent origin, and associated with a recent dose ofalcohol, are strong presumptive evidence of drunken-ness. But we have to bear in mind the possibility thatthe patient may be habitually emotional or excitable,that he may have recently sustained some acuteemotional or physical shock adequate to producethese phenomena in a perfectly sober person, or thatthe patient may be actually insane.

Cerebellar disorder is recognised by its characteristicincoordination of voluntary movement and by itsmuscular hypotonia. It is most readily detected inthe lower limbs. The reeling cerebellar gait, whetherfrom alcoholic poisoning or from other causes, isnoticeable by onlookers and sometimes by the patienthimself, who takes " more than his share of the pave-ment." Amongst the common manoeuvres for elicitingthe presence of cerebellar ataxia, a favourite one is toask the patient to walk along a straight and narrowpath, then to turn quickly and come back again,The more difficult feat of walking heel-and-toe alonga chalk line is an entirely artificial test which quitea number of sober persons may fail to accomplish.Failure to stand on one leg with the eyes shut, ofwhich I have recently read as a supposed test ofcerebellar disorder, is a mild acrobatic feat which themost sober of us might easily fail to execute duringthe emotional excitement following police arrest.The most exemplary abstainer may well feel appre-hensive if he falls into the hands of a medical officerwho exacts so high a standard of cerebellar efficiency.

Cerebellar ataxia of the upper limbs is convenientlytested by asking the patient to place one fingerquickly on our own finger-tip, or to raise a glass of

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fluid (water, of course) to his lips, or to carry out themore domestic ordeal of putting a key into its keyhole.In cerebellar disorder these movements are performedjerkily, partly owing to deficient muscular tonus andpartly from inability correctly to estimate the range,so that the patient cannot arrest the movement at thedesired target but either plunges past it, or mayunderestimate the range of movement and stops shortbefore reaching the mark, finally swooping down on itwith excessive force.

Tabetic afaxia of the lower limbs may be mistakenfor drunkenness, but only by a careless medicalobserver. Unlike cerebellar ataxia, tabetic ataxiais aggravated by closing the eyes. Absence of theankle-jerks and usually also of the knee-jerks,together with the condition of the pupils, &c., willusually prevent a mistaken diagnosis of this sort.Turning now to the phenomena of po/o’&Mo’’

disorder, dilatation of the pupils is a sign upon whichconsiderable emphasis has often been laid. In myopinion, its importance is often exaggerated ; thepupillary dilatation in alcoholic intoxication is usuallymoderate in degree, and in slighter degrees of intoxica-tion sometimes absent. In alcoholic stupor, on theother hand, dilatation of the pupils is the rule withsluggish response to light.A few days ago, when sitting at a table in a Pullman

carriage, during a short railway journey of an hour and ahalf, I found myself opposite a fellow-passenger who con-sumed, under my own eyes, five large whiskies-and-sodasin rapid succession, thereby incidentally providing me withan opportunity of studying with ease and comfort the onsetof toxic nervous phenomena. Towards the end of the ’,journey he became mentally confused, happy, noisy, andslightly dysarthric. As he leaned hospitably across thetable to offer me, although a complete stranger, the compli-ments of the season, I carefully observed his pupils; theywere not dilated and reacted normally to light.

Transient weakness of the external ocular musclesis frequently produced during the process of alcoholpoisoning. In its milder degrees it manifests itselfby deficient power of convergence, and when combinedwith mild cerebral symptoms which so frequentlycoexist, this helps to account for the drunk man’sdifficulty in visual fixation and for his characteristicfatuous look. A somewhat greater degree of weaknessof the ocular muscles produces double vision, a

symptom which usually impresses itself even on thesufferer’s fuddled consciousness. Disorder of lowerbulbar nuclei may produce temporary indistinctnessof articulation or dysarthria. NA’e must be carefulto exclude dysarthia from various organic causes,-whether in the brain-stem or bulbar nerves, or inthe palate, lips, or tongue. Moreover, ocular andbulbar symptoms, not unlike those of alcoholicpoisoning, varying in degree and sometimes oftransient duration, are also met with in myastheniagravis, admittedly a rare disease.Amongst the vascular and visceral phenomena

indicative of disorder of the vegetative nerve-cells,some of which are situated within the brain-stem,we may mention the flushed face, rapid pulse, andwarm, sweating skin, also the occurrence of salivationand vomiting, although this latter symptom may bepartly gastric in origin.The pupils, when they happen to be dilated, still

preserve their reaction to light, contrasted with theextremely dilated and insensitive pupils of poisoningby belladonna, hyoscine, and similar drugs.

Disorder of the reflexes, in my opinion, is of no

practical value in the recognition of alcoholic poisoning.Exaggeration of the knee-jerks and other deep reflexesis sometimes mentioned by medical officers as a signindicating acute alcoholic poisoning, but the degreeof briskness of these reflexes varies so widely in normalindividuals that we cannot regard their exaggerationas of any diagnostic significance. Ankle clonus neveroccurs from acute alcoholic poisoning; nor do we findextensor plantar responses, which may be present inursemic coma or that of poisoning by opium, sul-phonal, veronal, or coal-gas.

UNCONSCIOUS STAGE OF ALCOHOLICINTOXICATION.

In the deepest stage of alcoholic intoxication, whenthe whole brain is inactive with the exception of thevital medullary centres, there results a condition inwhich the patient is unconscious with fiaccid limbsand trunk. The depth of unconsciousness rangesfrom stupor to coma, according to whether the patientcan be roused from his unconsciousness or not byenergetic stimuli. In profound alcoholic poisoningstupor and not coma is what we find, even when thepatient is what is called " dead drunk." In recog-nising the cause of such unconsciousness the smell ofthe breath is of value, with certain limitations to whichI have already referred. Alcoholic stupor is usuallyassociated with a warm, moist skin, and accompaniedby the characteristic alcoholic odour, coexisting withfairly wide dilatation of the pupils, which still reactto a bright light. The odour of the breath may pointto poisons other than alcohol. The smell of opium ischaracteristic when laudanum has been taken by themouth, and in opium or morphine poisoning thepupils are closely contracted. The toxic coma ofureemia is often accompanied by a urinous odour inthe breath and that of diabetic coma by the sweethay-like smell of acetone.

.4naly-sis of the urine is h8lpfuJ in cases of deepunconsciousness. In alcoholic poisoning alcohol canbe detected by adding bichromate of potassiumsolution followed by a few drops of strong sulphuricacid ; if alcohol is present, a bright green colourappears, together with a smell of aldehyde. Anothersimple test is by adding an equal quantity of a strongsolution of iodine in iodide of potassium, followed bya few drops of caustic potash, drop by drop, untilthe iodine is decolorised. Iodoform crystals are

produced, accompanied by a characteristic odour.Other substances should also be looked for in theurine in cases of unconsciousness. Patients withdiabetic coma will show not only sugar but alsooxybutyric acid, aceto-acetic acid, and acetone. Thepresence of albumin, on the other hand, togetherwith casts and epithelial elements, is suggestive ofursemic coma, although in some cases of interstitialnephritis albumin and casts may be scanty or absent.

Tests can also be carried out on the cerebro-spinalfluid. To my mind the presence of alcohol in thecerebro-spinal fluid is really the only sign at our

disposal which can be regarded as pathognomonic.If positive, it is conclusive evidence of alcoholicpoisoning which has actually reached the centralnervous system. LTnfortunately, it is not alwaysfeasible to carry out lumbar or; still more, cisternpuncture. Through the kindness of my housephysician, Dr..T. G. ’Vilson, I have recently had thecerebro-spinal fluid analysed for alcohol in three recentcases of severe alcoholic poisoning, with a positiveresult in each case. Incidentally, in ursemic comaurea is present in excess in the cerebro-spinal fluidand an excess of sugar in diabetic coma.

SUbIVI9RY OF DIAGNOSTIC PROCEDURE.

Let me here offer a short summary of the proceduresuitable to be adopted when we are called to see acomatose patient :-

First we inquire into the history, as to the patient’s previoushealth, whether he has recently had a head injury, underwhat circumstances he was discovered to be unconscious,whether the unconsciousness was sudden or gradual in onsetand whether it was preceded by other symptoms such asconvulsions or headache. We then examine the patient,feel the head for signs of injury, smell the breath, examinethe pupils, noting their size, equality or inequality, andtheir reaction to light. We examine the heart and note thecharacter and frequency of the pulse and respirations. Wenote the radial systolic blood pressure and measure it bya manometer if possible. We observe whether the face issymmetrical or not, and whether there is conjugate deviationof the head and eyes in any direction. The optic discs andfundi should be examined in all cases of coma or stupor.We lift the limbs in turn and let them fall, observing whether

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there is any difference between the flaccidity of the two sides.We test the knee- and ankle-jerks and examine the plantarand abdominal reflexes on both sides. Then we pass acatheter, draw off the urine, note its specific gravity, andtest it for albumin, for sugar, and for acetone. Finally wenote the temperature in both axillae, and in all doubtfulcases we perform a lumbar or cistern puncture and examinethe cerebro-spinal fluid. In patients from malarious districtswe should also examine a blood-film for the malaria parasite.

Looking back on the successive stages of alcoholicpoisoning of the nervous system, it is evident thatthe average case of drunkenness presents little or

no difficulty in. diagnosis. The really difficult casesare at the two extremes of the series-namely, thosein which the impairment of cerebral function isvery slight and those in which it is so profound as tocause deep unconsciousness or stupor.Let us take the slighter cases first. In such cases

two distinct and successive facts must be proved tohave occurred in order to establish a diagnosis ofdrunkenness. First, it must be shown that theperson has recently taken alcohol. The immediateantecedent history of the case, the surroundingsunder which the person came under observation bythe police, the alcoholic odour of the person’s breath,are all suggestive, so far as they go, but not con-clusive. Whilst a drunken man’s breath will usuallysmell of alcohol, so may a perfectly sober man’s,otherwise it would be dangerous for an a,rchbishopto drink a glass of sherry with his lunch. Conversely,the absence of alcoholic odour in the breath, so faras it goes, is against the presence of alcoholic poisoning.Second, the reactions of the person’s central nervoussystem to his surroundings must be shown to betemporarily so disordered as to be injurious to himselfor others.

If a person already suffers from disease of thecentral nervous system, thereby presenting corre-

sponding cerebral, cerebellar, ponto-bulbar, or othersymptoms, and happens to come under observationafter taking alcohol in the most moderate amount,he may easily be the victim of an injustice. But insuch a patient the phenomena will not be temporary ;they will be present both before and after the allegedalcoholic poisoning. Apart from pre-existing diseasesof the nervous system, even anatomical abnormalities.such as deformities of the lower limbs, have beenknown to give rise to mistakes. I remember the caseof a taxi-driver with deformed feet who had themisfortune to be arrested on a cold winter’s nightoutside a bar after consuming a single glass of gingerwine. A police officer, quite reasonably, suspectedhim of being drunk, but subsequent investigationshowed that the man’s deformity was the adequatecause of his chronic insecurity of gait.Excluding people with pre-existing disabilities of

various sorts, and coming to temporary disorders offunction, we have a class of persons in whom transientexcitement-e.g., the fact of being arrested-maysimulate alcoholic poisoning of the central nervoussystem. This is really the most difficult case of all.Where the decision is doubtful, it is the duty of themedical officer, resisting the human tendency tocorroborate without careful consideration the snapshotdiagnosis of the police-constable, to give the patientthe benefit of the doubt. And I am sure that manymedical officers do pursue this course. If an excitedperson, examined in the humiliating environment ofa police-station, is nevertheless able to give a clearand coherent account of his recent doings, histransient excitement and indignation are not neces-sarily evidence of toxic cortical disorder. If hisbreath does not smell of alcohol, this is in favour ofsobriety ; on the other hand, if it does smell of alcohol,this, so far as it goes, is in favour of alcoholic poisoning.]3ut again I would insist that even the combinationof an alcoholic odour with emotional excitement is notsufficient evidence of cerebral disorder due to alcohol.

Matters are different, however, in cases where,superadded to the alcoholic breath and emotionalexcitement, we have, as is so commonly found,incoherence of thought and speech together with

signs of temporary cerebellar and ponto-bulbardisorder. Unsteadiness of the limbs, evidenced by astaggering gait and by difficulty in performingcoordinated movements such as pointing to or

picking up a small object, true dysarthria, known tobe different from the sufferer’s ordinary articulation,and diplopia, if it can be demonst.rated. are, all ofthem, definite evidence of disorder of central nervousmechanisms. Accessory phenomena, inconclusive bythemselves, such as hiccup, a warm, moist skin,flushing of the face, &c., are valuable corroborativesigns. To my mind the best physical evidence of allis a positive reaction for alcohol in the cerebro-spinalfluid. It must be admitted, however, that fewpersons are likely to submit voluntarily, and fewerstill are likely to volunteer, to have this valuablediagnostic procedure carried out.

tn the deeper stages of alcoholic poisoning wherestupor has supervened, the history and surroundingsof the case, together with the appearance of thepatient are usually characteristic, but we must alwaysbe careful to exclude the possibility of other varietiesof coma, not only from outside poisons (such asopium, veronal, ether, the late stages of belladonnaand hyoscine poisoning, and so on), but from auto-genous toxins as in diabetic and ursemic coma. Grossvascular lesions must also be borne in mind, suchas cerebral or pontine haemorrhage, and traumaticlesions, as in head injuries.

There is no short cut to accurate diagnosis. Ouronly safe guide is by means of careful and systematicclinical examination. The main difference betweena superior medical opinion and one which is lessvaluable, is not that the one man necessarily knowsso much more than the other, but that he is wiseenough to make a more careful and more accurateexamination of his cases.

The RelationOF

MEDICINE TO THE NATURALSCIENCES.

A Presidential Address delivered to the Science Masters’Association on Jan. 5th, 1925,

BY SIR BERKELEY MOYNIHAN, BART.,K.C.M.G., F.R.C.S. ENG.,

PROFESSOR OF CLINICAL SURGERY, UNIVERSITY OF LEEDS.

[IN the earlier sections of his address Sir BerkeleyMoynihan traced from prehistoric times, throughGrecian and Roman civilisation, the concept anddevelopment of the scientific idea-" the idea that theworld in which we live is governed by laws, that thelaws can be formulated by a close observation of theirmethods of working and by their failures to work, andthat by experiment the processes by which they workcan be tested." He then showed how the science ofthe Greeks from the first to the last was the child ofMedicine ; Hippocrates was the true originator ofinductive logic, but his followers for centuries addednothing to the science or the art of medicine, beingonly concerned with following uncritically theteachings of the master. He alluded to theone great exception to an acquiescence in tradi-tion which marked five centuries-namely, thefamous anatomical work done at Alexandria. Latercame the experimental work of Galen, the parentof the deductive method, and he with Hippocratesruled the science of medicine until at the Renaissance,Bologna, Padua, and Salerno became centres for thestudy of medicine. There followed a great develop-ment of natural science largely due to medicine, which,said Sir Berkeley Moynihan,

" has in truth provedbhe fairy godmother of many of the natural sciences,"For Copernicus, whose views were later confirmed byGalileo, was a medical man, and William Gilbert, the

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