14 POST GRADUATE MEDICAL JOURNAL January 1948

position of such nutrient arteries is reasonablypredictable.On the nerve a series of epineural vessels is

formed, whose branches pass into the perineuriumand, finally, there is produced within the fasciculia longitudinally disposed capillary plexus whichis continuous throughout the length of the nerveand is not dominated by local nutrient vessels.

Experimental. The intraneural plexus forms asystem which is normally reinforced by the localnutrient arteries, but which can function ade-quately in a given length of nerve even when thelocal branches are ligated.

Obliteration of epineural or intraneural vesselsproduces degeneration of varying degree depend-ing on the extent of vascular deprivation.The complete and intact system of vessels upon

and more particularly within the nerve is function-ally more important than any localized group ofnutrient vessels.

BIBLIOGRAPHY

ADAMS, W. E. (1942), J. Anat., Lond., 76, 323.ADAMS, W. E. (1943), J. Anat., Lond., 77, 243.ADAMS, W. E. and ROBINSON, W. (194I), Lancet, November

8th, p. 555.ATKINSON, M. (1941), J. Amer. Med. Ass., Ix6, I753.BACSICH, P. and WYBURN, G. M. (1945), J. Anat., 79, 74.DENNY BROWN, D. and BRENNER, C. (x944), Arch. Neur. &

Psychiat., 52, 1.LEWIS, T., PICKERING, G. W. and ROTHSCHILD, P. (1931),

Heart, 16, I.SEDDON, H. J. and HOLMES, W. (1945), Brit. J. Surg., 32, 389.SUNDERLAND, S. (1945), (a) Arch. Neur. & Psychiat., Chicago,

53, 91.SUNDERLAND, S. (1945), (b) Arch. Neur. & Psychiat., Chicago,

54, 280.SUNDERLAND. S. (1945), (c) Arch. Neur. & Psychiat., Chicago,

54, 283.

CONFUSIONAL STATES IN ACUTE DISEASEBy J. M. NAISH, M.D., M.R.C.P.Tutor in Medicine, University of Bristol.

Many a patient's battle to overcome an acutedisease is lost because, failing to stand the strainof the illness, he becomes delirious. The additionalburden thrown upon his body by restlessness, fear,and failure to obey those trying to help, is sufficientto tip the balance against him. The problemwhich such cases present is a common one, and,lying in the no-man's-land between generalmedicine and psychiatry, does not receive theattention which it needs.

Classical DeliriumThere is nowhere any sharp dividing line be-

tween the full-blown picture of severe deliriumand the mild nocturnal confusion of thought sofrequently found in ill people.Many patients, particularly the elderly, become

confused when their illness is at its height. Thisconfusion and lack of grasp, always at its worstnocturnally, may lead them to get out of bed inthe belief that they should be going out to work,or to put their shoes on beneath the sheets to keeptheir feet warm. They are often shamefaced in themorning and attribute their experiences to a baddream.

Fully developed delirium leads to well-definedphysical and mental changes in these patients, andthese should be kept clearly in mind.

The physical manifestations are restlessness, in-somnia, incontinence and anorexia; examinationusually shows some pyrexia and tachycardia, afurred tongue and slurring of the speech.The mental changes vary from one moment to

the next. The changing form of the mentalpicture is perhaps the most typical finding indelirium and is due to the extreme suggestibilityof delirious people whose moods and behaviourare swayed both by their physical surroundingsand their attendants. The prevailing deliriousmood, however, is one of fear and horror; theirspeech abounds with talk of struggles, crises andbankruptcy. Restless activity and complete in-somnia dominate the picture.The delirious are not only prone to invent, or to

elaborate the truth in a broken sort of way, butthey misinterpret their present surroundings andinstructions. Essentially, this inability to interpretor understand the present has the same roots-failure of memory, concentration, and mentalgrasp-as the tendency to invent the past. Theycan only do the simplest and shortest test problemsbecause they cannot hold their brains to the taskfor more than a few moments at a time. It istrue to say, however, that some delirious patientscan, by a superhuman effort of will, achieve mentalclarity when circumstances urgently demand it.

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Yet another characteristic of delirious people istheir reference to ideas of persecution. A patientmay blame his wife, his children and the corpora-tion for his sleeplessness, though there is no ordernor reason in such accusations.

Disorders of sensation and perception occur fre-quently; visual hallucinations are the mostcommonly experienced, but occasionally voices areheard or creeping sensations felt beneath the skin.The classical features of delirium then are,

restlessness, insomnia, a fearful mood, confusionof thought and grasp, memory defect, confusedparanoid ideas, hallucinations, and a mental statewhich is liable to change not only from day to daybut from hour to hour.

Atypical Forms of Delirium(a) Hallucinating

This form of delirium is, of course, mosttypical of alcoholic poisoning. The chief featuresof delirium tremens are visual hallucinations, fearand ceaseless motor activity, but in this as in otherintoxications, notably those produced by bella-donna or bromide, hallucinations may dominatethe picture. Such a state may be difficult todistinguish from the acute onset of psychoticmania.

(b) Amnestic (Korsakow's Syndrome)Patients may develop a form of mental distur-

bance during the course of an acute disease inwhich, at first sight, mental confusion does notappear conspicuous, and from which the ceaselessmotor activity, so typical ofmost forms of delirium,is absent or slight. Though they appear rational,such patients confabulate, invent fairy tales whichare spoken as the truth, confuse the past with thepresent, have no memory for recent events, andobstinately hold wrong ideas of their position inspace. More careful appreciation shows that theyhave, in fact, a severe defect of memory and aconsequent deterioration of intellect. Beingreally unaware of themselves and their surround-ings, they are completely disorientated.

(c) Delirious StuporMany infections, typhoid fever for example, are

so overwhelming that the activity of delirium ismasked by toxic stupor, which is also the case whenacute vitamin deficiencies develop in the courseof fevers or gastro-intestinal disturbances.

The Aetiology of Toxic Confusion andDeliriumNo direct pathological cause has been found for

the gross disturbances of cerebral function whichoccur in most intoxications. When the brain or itscoverings are affected by an inflammatory process

such as encephalitis, meningitis, or an abscess, thecause of mental confusion is not far to seek; and,when acute vitamin deficiencies produce not onlywell-defined confusional states but also demon-strable vascular changes and alterations in cellstructure within the brain, it may then be saidthat a specific aetiology has in these cases beendiscovered. As a rule, however, workers in thisfield have had to postulate some unknown dis-turbance of cerebral nutrition or blood supply tocover their ignorance of the real pathology.One concept has helped us to explain the

fundamental similarity between the toxic psychosesproduced by different poisons or infections. Thereis a threshold for toxaemia in each individual overwhich mental confusion will develop. Thenoxious dose from some infections and somepoisons is obviously greater than from others, butthe stage at which mental confusion developsdepends primarily on the constitution of thepatient. Furthermore, the exact form which atoxic psychosis takes depends far more on thehereditary and psychological make-up of thepatient than upon the nature of the toxic process.The psychosis is, therefore, determined bothquantitatively and qualitatively by the character ofthe patient.

Nevertheless, it is true that certain toxaemiasgive rise more often than not to a particular type ofpsychosis. Typhoid causes lethargy and amuttering delirium. Streptococcal septicaemiaoften leads to seeming mental clarity but hallucina-tions occur.

Confusional States of Specific AetiologyWater DepletionThis causes intracellular dehydration, a process

which probably does not spare the cerebralneurones. Confusion begins to appear whenthere is a bodily water deficit of about five litres,that is, under temperate climatic conditions afterabout four days of complete water deprivation.The onset of the full psychotic picture may besudden, violent reactions occur, and hallucinationsare common.

Because people deprived of water suffer fromintolerable thirst, it is unlikely that confusionalstates purely due to dehydration should occur inordinary practice. Many ill, confused patients are,however, also suffering from a water deficit andthis should be made good by pressing fluids bymouth, or if necessary by intravenous infusion ofglucose saline.

Salt DepletionThis lowers the osmotic tension of the extra-

cellular fluids and so leads to extracellular de-hydration and interference with cellular nutrition.

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Apathy, lassitude and exhaustion, gradually de-velop and later give way to a stuporose confusionalstate. Such mental confusion is often seen inpatients who have lost large quantities of salt bysweating, vomiting, or diarrhoea, as in pyloricstenosis, ulcerative colitis and Addison's disease.

In many diseases and post-operative statespatients suffer from unsuspected salt depletion.This may lead to a mental confusion which inter-feres with the management of their original disease.If the urine is not unduly dilute, salt depletionshould be suspected when the urinary chloride ex-cretion is under 2 gm. per litre as estimated byFantus' simple method. If vomiting or anorexiais present, extra salt must be given by the in-travenous infusion of isotonic saline (0.9 gms.NaCi per Ioo cc.). In other circumstances thesalt may be given by mouth in the form of sodiumchloride in cachets.

AlkalosisThe mental confusion which sometimes occurs

in patients suffering from pyloric stenosis is nodoubt chiefly attributable to salt deficiency, butsimilar symptoms may be met with in patientswith peptic ulcers who have taken large quantitiesof alkalis by mouth. The diagnosis must be con-firmed biochemically and acid-forming salts (acidsodium phosphate 2 gms. in cachets four-hourly ormore frequently) given.Cerebral AnoxaemiaThis occurs in patients after a severe

haemorrhage, an haematemesis for example, aftercarbon monoxide poisoning, and in patients withcongestive heart failure. Hallucinations are notcommon, but severe mental confusion, mis-interpretation of surroundings, fearful dreams andrestlessness, make up the clinical picture. Rest-lessness, in those whose life depends on adequaterest, may be a symptom very difficult to controland to treat, and may, in fact, be the prime causeof death. As with the anoxaemia of high altitudes,the mental confusion is often tinged with aneuphoric and fatuous mood.

Cerebral anoxaemia due to heart failure canrarely be modified unless the cardiac conditionimproves. In most cases the anoxaemia is due tothe stagnation and deoxygenation of blood in thecerebral tissues, but in the presence of pulmonaryoedema an anoxic factor may also be present sothere is a clear indication for the immediate andthorough administration of oxygen through aB.L.B. mask.The immediate treatment by blood transfusion,

wherever and whenever practicable, of haemor-rhage sufficient to cause mental confusion isdoubly important because there is a danger that

such patients, if left exsanguinated for long, maydevelop permanent damage to nervous tissue.This happens in post-haemorrhagic amaurosis.

HypoglycaemiaHypoglycaemia, such as occurs after an over-

dosage of insulin may, before the onset of coma,lead to mental confusion, restlessness, failure ofmemrry and judgment.Acute Vitamin Deficiencies

(a) Cerebral Beri-Beri (Wernicke's Encephalo-pathy). Since 1938 it has been suspected thatWernicke's encephalopathy was due to a nutritionaldeficiency, probably of thiamine, associated withalcoholic or neoplastic cachexia.

It remained for a large human experiment toprove the case and this was provided by the con-ditions under which the Japanese kept AlliedP.o.W.s in the Far East. Thanks to the in-telligence and awareness of imprisoned medicalofficers, not only was a severe outbreak of en-cephalopathy recognized at once, but the thera-peutic efficiency of thiamine in these early caseswas proved beyond all doubt. The outbreak ofcerebral symptoms also coincided with the peakincidence of classical beri-beri amongst theprisoners.

Since the development of cerebral beri-beri waswatched .carefully from its very outset in thesepatients, the symptomatology differs somewhatfrom that of cases previously described in theliterature. Early cases were recorded, and re-covered patients were able to recall something oftheir sensations during the onset and recoveryperiod. It is worth while then, since this en-cephalopathy, though not common, may be metwith as a complication of many diseases, to recallthe cardinal features of cerebral beri-beri, asdescribed by observers in the Singapore camps.

Cerebral beri-beri occurred chiefly in those withsevere diarrhoea (which impairs the synthesis andabsorption of thiamine from the gut) or in thosewith febrile condition (in which the body's demandfor thiamine is enormously increased). Theearliest symptoms were anorexia, apathy and in-somnia, followed by nausea and vomiting. Re-covered patients stated that at this stage all sensa-tions were dull and toneless. Later these de-veloped visual disturbances such as diplopia,blurring or failure of vision, and mental changessuch as disorientation and amnesia, accompaniedperhaps by hallucinations or excitement, butusually ending in fatal cases with stupor.Occasionally in fulminating cases severe mentalsymptoms developed at the outset. The most fre-quent physical abnormalities were nystagmus, ex-ternal rectus fatigue and signs of classical beri-

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January 1948 NAISH : Confusional States in Acute Disease 17

beri. Peripheral neuritis was nearly alwayspresent. Other clinicians have stressed the fre-quent finding of pupillary abnormalities in thiscondition. The classical pathological lesions otcerebral beri-beri were multiple haemorrhages inthe corpora mamillaria, around the aqueduct ofSylvius, in the posterior corpora quadrigeminaand in the thalamus. Microscopically, thesehaemorrhages were seen to have come fromcapillaries irregularly dilated, thickened and de-formed. Chromatolysis of ganglion cells and pro-liferation of the glia occurred in the affected areas.

In clinical practice, cerebral beri-beri may bemet with in any condition producing severediarrhoea, vomiting or cachexia, particularly ifaccompanied by fever. It is most often seen insevere chronic alcoholism or as a terminal eventin patients with carcinoma of the stomach. Itdoes also occur in conditions of better prognosis,such as hyperemesis gravidarum, perniciousanaemia or ulcerative colitis. For reasons not wellunderstood, it may occur as a complication insevere liver disease. Once a fatal disease and nowcurable, it must be recognized and treated in theearliest stages for the best results. Any patientdeveloping mental confusion and ocular abnor-malities in the course of other general diseases,should be treated as a case of cerebral beri-beri,20-50 mg. of thiamine hydrochloride should begiven intramuscularly at once and 20 mg. per diemsubsequently. Dehydration should be correctedand as appetite returns a diet should be givenwhich contains plenty of animal protein, yeast andMarmite. Patients who develop the Korsakow'ssyndrome during the course of cerebral beri-berimay be left with a permanent memory defect, andmay never regain mental normality.

(b) Nicotinic Acid Deficiency Syndrome. Joliffeet alia (I940) described a syndrome developing inelderly patients ill from a variety of generaldiseases which was characterized by disorienta-tion, stupor, cog-wheel rigidities of the extremitiesand the occurrence of uncontrollable grasping andsucking reflexes. The patients improved whentreated with 300 mg. of nicotinic acid daily intra-venously, and many of them recovered, though asimilar group treated with thiamine did no betterthan a control group. The pathological basis ofthis type of cerebral disturbance has not, so far,been adequately studied. It seems probable, how-ever, that it may be the result of acute nicotinicacid deficiency, just 'as pellagra is chiefly the resultof chronic nicotinic acid deficiency. Certainly, illpatients who become disorientated and developgrasping and sucking reflexes for which no im-mediate organic cause can be found, should betreated by large doses of nicotinic acid parenterally.

The therapeutic effect should be obvious withintwo to three days.

Often patients develop symptoms and showsigns which are suggestive, but not diagnostic, ofacute hypovitaminosis B. In view of the risk ofpermanent sequelae in untreated cases it may bejustifiable to treat such doubtful cases withparenteral thiamine and nicotinic acid.

Case RecordA woman aged 51 with no previous history of

dyspepsia, suffered a moderately severe haema-temesis. When seen the next day she did notappear unduly exsanguinated or shocked and wascheerful. Her spleen was palpable about Il in.below the left costal margin. Two days later, herhaemoglobin being then 70 per cent. of normal, shebecame mentally confused, drowsy and finallystuporose. On examination there was generalizedmuscular rigidity; no grasping or sucking reflexeswere present. Cerebrospinal fluid was normal.On account of these findings, and because adiagnosis of hepatic cirrhosis with bleeding oeso-phageal varices seemed a possibility, she was givennicotinic acid Ioo mg. and thiamine hydrochlorideio mg. intramuscularly daily. Within 48 hoursshe had recovered consciousness, appetite andwell-being. Later she successfully underwent anoperation for splenectomy during which hercirrhotic liver was seen.

Confusional States due to Specific PoisonsMorphiaMorphia addicts, who are deprived of their drug

by an acute illness, often develop great restless-ness, insomnia and confusion. Tremors andtwitchings are usually present.Belladonna

Excitement, pressure of ideas, restlessness,tremors, complex repetitive movements, andhallucinations associated with tachycardia, dilatedpupils, a dry mouth and a dry red skin, make afairly distinct clinical picture. The condition mustbe treated symptomatically as there is no effectiveantidote. If restlessness passes into violence,chloroform or ether may be used to control thespasms.

LeadChronic plumbism may lead to a wide variety

of mental disturbances which may first appearwhen an acute disease or carcinomatous meta-stases cause bony decalcification and consequentliberation of stored lead into the blood stream.Organic neurological signs or convulsions usuallyoccur. The treatment is to give large quantities of

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alkalis, calcium lactate and milk by mouth in anattempt to fix the lead in the bones.

BromidesBromism may lead to mental confusion, in-

tellectual deterioration, memory loss and distanthallucinations. Organic neurological signs, suchas dysarthria, depression of deep and superficialreflexes, and tremors may be present. Unless thecondition is thought of and an enquiry made intothe drugs which a patient has been taking, themental confusion may be ascribed to some othercause and specific treatment not begun at once,with disastrous permanent results. A blood bro-mide level of Ioo mg. per Ioo ml. or over isdiagnostic. The best treatment is to give largequantities of fluids and of sodium chloride bymouth.

AlcoholDelirium tremens has been produced experi-

mentally in human volunteers by the daily con-sumption of a litre of whisky. The occurrence ofdelirium was not prevented by nutritional supple-ments or daily injections of thiamine. It wastherefore the direct result of alcoholic poisoning.The clinical features are those of classical delirium,but the vivid visual hallucinations and the constantsemi-purposeful movements are peculiar. It hasalways been said that if tachycardia, cardiac dila-tation and failure develop during delirium tremens,the prognosis becomes very bad. These are, how-ever, but the cardiac manifestations of hypovit-aminosis B and should be treated promptly withthiamine.

Confusional States of Doubtful AetiologyDiabetic coma is always and uraemia usually

associated with dehydration. The mental con-fusion which develops in such cases may be due tocellular dehydration.Confusional States Associated withOrganic Intracranial LesionsInflammatory brain lesions in particular are

liable to be complicated by acute confusional states.The first consideration in any patient who developsconfusion or delirium early in the course of a fevershould be to exclude meningitis or other treatableintracranial conditions.

Mental confusion is a particularly troublesomefeature of severe head injuries. The temporaryabolition of such symptoms by the intravenous in-jection of hypertonic glucose solution, or the intro-duction of a saturated solution of magnesium sul-phate into the rectum, is evidence that cerebraloedema is their cause. Subdural haematomataoften cause fluctuating mental symptoms. Cerebral

tumours may present with symptoms of generaldisease and a variety of mental disorders.

Confusional States of Unknown AetiologyAs has already been suggested, it is the patient's

own physical and mental constitution whichchiefly determines whether or not a toxic psychosisdevelops in the course of an acute febrile illness.Advanced age or cerebral atheroma are two of themore obvious constitutional defects predisposingto mental confusion.

Pneumonia, malaria, typhoid, typhus, ful-minating exanthemata and the septicaemias arethe most important of the fevers in which deliriumcommonly occurs. It may also occur in destruc-tive liver disease. Malaria is important as a causeof delirium, because the diagnosis is often missedand life-saving treatment delayed. It should notreally be considered in the same breath as the otherfevers in that organic cerebral changes, destructionof neurones in the areas supplied by cerebralcapillaries blocked with cellular debris, are usuallyfound and in that organic neurological disturbancessuch as convulsions, aphasia or hemiplegia occur.Drugs in common use today which may give

rise idiosyncratically to confusional states are thesulphonamides.The General Treatment of Confusional

StatesThe treatment of delirium is vital because the

patient's ability to fight his original disease dependsso much upon his getting over the mental dis-turbance without too great a loss of energy. Thegeneral practitioner or physician sees such casesand has to treat them, but the textbooks to whichhe has access give little advice on the subject.Often there is not much which can be done in suchcases, but there is always a great deal which oughtnot to be done. Some treatments may be triedwithout harm, others must be abjured completely.Principles of Treatment

I. Seek out and treat, if present, any conditionsuch as salt depletion or hypovitaminosis whichare known to cause mental confusion.

2. Treat the underlying disease adequately.3. The patient should be nursed and managed

by those skilled in managing the unmanageable.Care and tact reduce a patient's restlessness, butsilly interference or attempts to bully him willproduce violent reactions. Those who are knownto irritate him when sane should not be allowed toapproach him when delirious.

4. Make the patient's surroundings simple andeasy to understand. The wards of a generalhospital with their bustle and noise are unsuitable.A quiet, partially darkened room, where he should

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January 1948 CRITCHLEY: Speech Iterations I9not be alone, is the ideal. Once the patient hasbeen moved to suitable surroundings, do not movehim again or in any way ask his confused brain tounderstand any but the simplest things.

5. Hydrotherapy. Great restlessness may belessened by the application of wet packs or byimmersion in a bath. The former is generallybetter because it is less disturbing.

6. Diet. Readily assimilable carbohydrate foods,preferably in fluid or semifluid form, are the easiestto give. The caloric intake should be about2,500 C. daily. If such high carbohydrate feedinghas to be continued for more than three days, or ifthe patient has been starved previously, thiamineand nicotinic acid should be given parenterally asprophylaxis.

7. Drugs. The less of these the better. Givethem not at all or infrequently. If you have to usethem, see that the dose is adequate, the aim beingto produce quietness and sleep. Hyoscine hydro-

bromide 0.5 mg. is not too much. The elderlyand sufferers from delirium tremens respond wellto hyoscine. Paraldehyde 12-20 ml. is safe.Morphia in doses of 20-30 mg. may be given if theco-existing disease provides no contraindication.It should be remembered, however, that certainpatients do not tolerate morphia or hyoscine.When confronted with a patient who becomes

mentally confused or delirious during the courseof another illness, the first aim of the physicianshould be to exclude or treat organic cerebraldisease, gross alterations in the cell en-vironment, deficiency states, or drug intoxications.Only then should he regard the case as one oftoxic psychosis to be treated symptomatically.

BIBLIOGRAPHY

CURRAN, D., Encycl. Med. Practice, 10, 316.DE WARDENER, H. F., and LENNOX, B. (I947), Lancet, I, II.JOLIFFE, N. et alia (1940), J. Am. Med. Assn., 114, 307.SPILLANE, J. D. (1946), 'Nutritional Disorders of the Nervous

System.' Edinburgh. Livingstone.

'SPEECH ITERATIONS('TING A IING' PHENOMENON)*

By MACDONALD CRITCHLEY, M.D., F.R.C.P.Neurologist, King's College Hospital; Physician, National Hospital, Queen Square.

Like an Englishman abroad who rings thechanges in his conversation on the few phrases ofwhich he is the master, so in the same way wemeet patients who reiterate certain words, phrasesor sentences to the exclusion of all others. Therebywe are reminded not only of our traveller, but ofsome animal cries and infantile babbling-monotonous repetitions which constitute the wholeof the subject's vocalization.The circumstances under which we encounter

these speech iterations are very diverse; some ofthe cases are frankly psychotic, others are neuro-logical problems. Sometimes they obviously forman aphasic disturbance-a disorder of language. Inother cases the defect is one of articulation orspeaking. At other times it is difficult to decide,and possibly a disorder both of speech and ofspeaking coexists. With others again the defectis plainly the result of a thought disorder upon aconceptual plane higher than the zone of language.

Years ago Gairdner applied the term ' barrel-organisms' to all these various kinds of speech

* Being a paper read at La Salpetriere, Paris, onNovember 12th, I947.

iterations. The term is not a very satisfactoryone for the recurrent vocalization is neither amelody nor a theme. More often it is merely aphrase, or maybe a single word. One might,perhaps, use the term ' ting a ling phenomenon,'after the music-hall song which was familiar lastcentury.t

t She only answered 'ting a ling'To all that I could say.

She seemed to live on ' ting a ling'By night as well as day.

When I asked her if she'd marry meAll that she could say

Was ' ting a ling a ling ting,Ting a ling a ling ting

Ting a ling a lint ting tay.'English folk music embodies a number of meaningless

phrases of dubious etymology. Ranging from the old-time ' Hey nonny nonny ney ' and ' Fol-de-rol,' etc., wecome to the 'Tick-a-tang' and the 'Tararaboomdeay'of two generations ago, the 'Yip I addy I ay I ay' andthe ' Hitchy-koo ' of the first war and the various non-sense syllables of the Hill Billy songs we hear today.Perhaps these are melodious phrases easy to sing; moreprobably they represent broken-down sense words ordilapidated speech.

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