6i8 POSTGRADUATE MEDICAL JOURNAL December I952

Carcinoma spreads from the penis to the inguinalglands by lymphatic embolism. This is fortunate,for the operation of amputation of the penis can,in consequence, completely excise the primarygrowth and thus secure the patient from any riskof local recurrence. If the inguinal glands havenot been involved the operation would cure thepatient, but if the inguinal glands are already in-volved the operation would at least save the patientfrom the horrors of a fungating growth of the penis.

BIBLIOGRAPHYCADE, S. (I939), Proc. R. Soc. Med., 33, 1509.COORAY, G. H. (I944), Indian J. Med. Res., 32, 7I.DEAN, A. L. (I950), 'A Text Book of Surgery,' edited by

Christopher. W. Saunders & Co., Philadelphia, p. 3x1i.B.

DAVIES COLLEY, cited by Pearce Gould.GALBRAITH, W. W. (1948), 'Textbook of Genito-Urinary

Surgery,' edited by Winsbury White. E. & S. Livingstone,Edinburgh, p. 609.

HILTON, cited by Pearce Gould.JACOBSON, W. H. A. (I893), 'The Diseases of the Male Organs

of Generation.' J. & A. Churchill, London, p. 707.LEHMANN, cited by Ngai.McCREA (1940), 'Diseases of the Urethra and Penis.' John

Wright & Sons, Ltd., Bristol, p. 271.NGAI, S. K. (1933), Amer. Y. Cancer, 19, 259.PAUL, M. (1929), Yournal of the Ceylon Branch of the Brit. Med.

Assoc., 26, No. 2, p. 13. tPEARCE GOULD, A. (I882), Lancet, May 2o, 821.THIERSOH, cited by Pearce Gould.WOLBARST, A. L. (I932), Lancet, i, 15o.WINDEYER, B. W. (I939), Proc. R.-Soc. Med., 32, 1504.WINSBURY WHITE, H. B. (1948), 'Textbook of Genito-

Urinary Surgery.' E. & S. Livingstone, Edinburgh.THOMSON-WALKER, J. (1936), 'Genito-Urinary Surgery.'

Cassel and Company,' Ltd., London.

SIMPLE OBESITYBy JOHN S. RICHARDSON, M.V.O., M.D., F.R.C.P.

Physician, St. Thomas's Hospital

The interest that our forebears had in obesitywas social rather than medical. It was displayedin its more flamboyant form by the voluptuariesof some of the ruling houses of Europe andpainters of the School of Titian and Rubens, whodelighted in mastering the shadows cast by massivefolds of flesh. It also appealed to the sportinginstincts of t4e inhabitants of this country wholove records that can be numerically expressed.The present desire of most people to avoid

obesity reflects not only an alteration in taste andthe present dictates of fashion, but also shows anawakening to some unpleasant realities. Insurancestatistics, largely those of the Metropolitan LifeInsurance Company of America, show that be-tween the ages of forty-five and fifty for everyIO lb. overweight there is roughly a io per cent.increase in the death rate over the average forthat age. This is largely a result of cardiovascularand renal disease, whilst fat diabetics have a verymuch poorer outlook than thin. Age certainlycontributes to the incidence of these disorders inthe obese, but the evidence of the dangers ofobesity is overwhelming. The problem is, there-fore, quite literally a vital one.

Physiological ConsiderationsPhysiologists have tackled it for many years from

numerous aspects and a great deal of work -hasbeen done. Nevertheless, it is fair to say that up

to now all metabolic studies have failed to showwhy some get enormously obese and others remainslim all their lives. It seems clear that in theobese food is no less efficiently absorbed than inthe normal. It is not converted into fat or storedmore easily, neither is it mobilized less easily, norburnt more economically. Recently Dodds (1950)reported some experiments by which he hasexamined this subject. He found that when somepeople whose weights have been constant overmany years were given double or treble theirnormal intake, they did not put on weight. Heshowed that in them this was not due to a failureof assimilation or digestion, but suggested thatsome studies that were being made in his depart-ment on their respiratory metabolism might showthat they responded to a high caloric intake by anincrease in their metabolic rate. The controlseries of those who got fat with this gross over-feeding showed no such increase in metabolism.These observations call to mind the theory of' Luxus Konsumption ' (Grafe and Graham, I9II;Grafe, I933) which has long been in disrepute,Wiley and Newburgh (93I) finding no evidenceto support it. Dodds (1950) made the novelsuggestion that the mechanism that keeps mostpeople's weight so remarkably constant was thegravitational pull of the earth, but he has so farbeen unable to devise experiments to test hishypothesis.

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Fluid RetentionThe emphasis that different workers place on

the importance of fluid retention in obesity variesconsiderably, but most are agreed that obesepeople tend to retain fluid more easily than slim.Greene (1950), -who stresses the importance offluid retention, has pointed out that pitting oedemain the legs is common in obese women in theabsence of renal or cardiac lesions, and oedemaonly appears when a considerable amount of fluidhas been retained.

It is possible that in some of these cases thewoedema is due to hypostatic causes and a poorvenous return, as pitting oedema, when theweather is hot or after standing, is sometimes foundin women with large legs, even if they are otherwiseslim.

It is commonplace to find that delay in apparentreduction in weight in a patient on a very lowcalorie diet is due to fluid retention (Newburgh,1942). Diuretics, long used in the treatment ofobesity, result in a very rapid fall in weight to theexpected weight level. This diuresis will occurspontaneously, but its delay may well discouragethe patient so much that the strict limitation offood intake is given up and the treatmentabandoned.

Extra-cellular fluid retention is not present inevery case of obesity, as Odier and Mach (1949),after measuring the extra-cellular fluid in 43clinically obese patients by the sodium thiocyanatemethod (Crandall and Anderson, I934), found itwas actually less than in the 20 controls of normalsize.McCance and Widdowson (I95I) have recently

devised a method of estimating the total body fat.They determined the extra-cellular fluid volumeand the total body water. The difference betweenthese figures was regarded as the cellular water;that in turn was assumed to be 67 per cent. of theweight of the cellular mass. The body fat wascalculated by subtracting the weight of the extra-cellular fluid, the cell mass and mineral from thebody weight. They found that both the extra-cellular fluid and the fluid mass, when expressedas a percentage of the body weight, were less inobese men and women than in the normal. Theyshowed, therefore, that obesity in their subjectswas due to an increase in fat and not to an increasein extra-cellular water or cellular mass, 67 percent. of which is intra-cellular fluid. The per-centage of fat was higher in normal women thanin men and was between 12.6 to 28.5 per cent.and 7.2 to 22.4 per cent. respectively. The obesewomen contained up to 58.I per cent. of fat.Hormones such as thyroxine, oestrogens and

certain adrenal steroids have an effect on fluid

balance, the last two leading to fluid retention andthe first to diuresis. These factors play an impor-tant part in endocrine disorders such as myx-oedema, the menopause and in some cases ofhyperfunction of the adrenal cortex or therapeuticover-dosage from desoxycorticosterone, but theirrole in simple obesity is at present believed to besecondary and of no great importance. The hor-mone that is probably of much more significancein fluid retention in obesity is the posteriorpituitary anti-diuretic hormone. Verney (I946)has shown that not only trauma but also emotionalstress, by acting on the hypothalamus, can leadto a release of the anti-diuretic hormone, withconsequent fluid retention. He suggested thatcircumstances in which sympathetic tone is lowin man might be favourable to the prolongedsecretion of the hormone.

It is felt that, while recognition of fluid retentionis of some importance in the management ofobesity, this importance should not be overstressed.

Adipose Tissue and its DistributionThere is no good evidence that the metabolism

of adipose tissue in the obese is in any way differentfrom that in people of normal weight (Newburgh,I944). Likewise, no anatomical abnormalitieshave been found in the structure of adipose tissue.Edwards (I95ib) has shown that fat spaces in thecells of fatty tissue in the obese are larger inproportion to the degree of obesity when this is of;.the simple type, but, when the case is one of lipo-matosis, fat spaces in the cells are of normal sizebut the cells are present in abnormal numbers.He has also done interesting work on the dis-tribution of subcutaneous fat (Edwards, 1950).He estimated this by measuring the thickness offolds of skin and subcutaneous tissue at 53 stan-dard sites over one side of the body in various agegroups and in the two sexes. The normal patternshows a sparing of the extremities with a greaterthickness over the shoulders and base of the neck,the pituitary hump, the back, abdomen and thighs.Sacral and adductor pads, pads over the lowerangle of the scapula, the so-called pituitary cape,and pads behind the knees are found in slim peopleand are variations of the normal fat pattern. Thisconstancy of pattern of subcutaneous fatty tissueis maintained in the obese and there is very littledifference in the fat pattern between them andthe slim. This is bof special interest, as the greatpopularity of the endocrine theories of obesity inthe past led to various descriptions of so-calledpituitary, adrenal, thyroid and hypogonadal bodyshapes. It has been realized for some years thatthese body patterns are found in many patients inwhom there is no evidence of any endocriiie dis-order and it is now recognized that they merely

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represent the different ways that people can getfat and are of little or no diagnostic significance.Edwards (I95ia) has shown that this pattern ofdistribution of subcutaneous fat is the same inpre-pubertal boys and girls, but that once pubertyis established differences develop. These are notof any very great degree and the chief differencein distribution is to be found in the legs, that have1.25 times as much fat in them in proportion tothe total fat in females as in males. Females ofaverage weight of all ages have approximately I.7times as great an average thickness of subcutaneousfat as have males.

Endrocrine GlandsThe belief in the simple relationship of the

endocrine glands to obesity, like other simpleconceptions of this problem, has not survived anincrease in knowledge, but it is unwise to assert,as some do, that their influence is entirely un-important. Simpson (1952) has recently sum-marized some of the evidence in favour of thethesis of an endocrine origin for obesity and drawsattention to Kendall's (I945) work on the adrenalsteroids. Kendall showed that Compound (A)(ii dehydrocorticosterone), when implanted intomice, produced an increase in weight, althoughthe animals were maintained on a standardizeddiet. When the carcases of these rats wereanalyzed the increase in weight was shown to bedue to fat and the body protein was reduced. Inorder to explain this, Kendall (I945) suggestedthat the action of certain adrenal steroids resultedin glucose derived from protein being convertedinto fat. Simpson (I952) points out that Kendall,by this experiment, has shown than an endocrinesubstance exogenously supplied can lead to anincrease in weight without the animal having anincrease in calories supplied to it.

Insulin plays a large part in fat metabolism.It allows the transformation of glucose into fattyacids and permits these fatty acids to be stored inthe fat depots of the body. When there is noinsulin in the body the conversion of dietaryglucose into fat is re4ced to io per cent. of thenormal rate (Stetten and Boxer, I944; Brady etal., I951; Chernick and Chaikoff, I951).The anterior pituitary gland has an effect on

body weight through the growth hormone. Young(195i) has shown that the administration of growthhormone to dogs, with or without insulin, resultsin the maintenance of their body weight whenthey were kept on a diet that was of insufficientcaloric value to do so. This was achieved by thedeposition of protein and the burning of fat withthe consequent production of more energy. Whenmore food was allowed to his animals both proteinand fat were stored. These recent observations

are of very considerable interest, but their relation-ship to the problems of simple obesity in clinicalpractice is still obscure.

HypothalamusThe original observation of Erdheim (I904) that

lesions of the hypothalamus rather than of thehypophysis lead to obesity received experimentalsupport in 1913 when Camus and Roussy showedthat hypophysectomy in dogs did not cause obesityunless the hypothalamus was also damaged.Hetherington and Ranson (I939), Brobeck et al.(I943) and, more recently, Kennedy (1950 and195I) have confirmed this by use of a techniquewhereby small electrodes are introduced into thehypothalamus and electrolytic lesions produced.The technique is a delicate one, as the hypothala-mus in a rat, the animal that is usually used, isonly 3 mm. across. Rats so treated all developedmarked obesity and this is the result of an enor-mouse increase in their appetite and not due toincreased absorption or utilization. Some ofKennedy's rats had weights that were doublethose of the controls and they contained as mnuchas 65 per cent. of fat. The animals showed noincrease in skeletal length and Kennedy suggeststhat this can be taken to show that the increase inweight was not due to any anterior pituitary factor.The figure of 65 per cent. is particularly interest-ing, as recently Widdowson and McCance (1951)have recorded the case of a woman of 25 stonewho, by their methods, was shown to containover 6o per cent. of fat.

Hetherington and Ranson (I939) and Brobecket al. (I943) found that when food was givenad libitum to their operated rats the amount ofincrease in weight was accounted for completelyby the amount of food eaten, but that in a smallproportion of the rats whose food was restr.;ctedafter operation there was a minor increase inweight over the controls, suggesting that in thema mechanism other than increased intake waspresent. This may be explained by the change inthe feeding habits of these animals that followsoperation and leads them to eat whatever is avail-able as fast as they can. Brobeck et al. (1943) haveshown that normal rats will convert glucose into fatat an accelerated rate if the animals are trained toeat their normal 24 hours' ration in a short time.Kennedy's observations on this alteration infeeding habits are of considerable interest. Hisanimals, like those of previous workers, showeda violent and voracious appetite even before theywere completely round from the anaesthetic.This voraciousness became less after the effectsof the operation had worn off, but they wouldstill eat two or three times as much as-the controls.Once their obesity was fully developed their food

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intake dropped and Kennedy found that some ofhis rats could maintain a weight of some 50 percent. above the normal for an indefinite periodwithout any significant increase in intake of food.This observation agrees well with those of clini-cians and dietitians who have frequently observedthat once patients have become obese they neednot eat more than a normal person in order tomaintain their weight and may in fact eat less, astheir activity is perforce reduced and their intakeis enough for their energy requirements.

Kennedy's rats showed a remarkable change intheir attitude to food once the period of gorgingwas over. The normal rat eats anything and theonly limiting factor seems to be its caloric require-ments. The hypothalamic animal, once it isobese, becomes discriminating. Kennedy showedthis by mixing kaolin with the feeds and, while thenormal animals ate an amount that would supplytheir caloric requirements, the obese animalsrefused to eat the mixture until they had used uptheir fats stores. If the ordinary unmixed dietwas restored to them the rats would again eatenormously until they were once more grosslyobese, just as they had after recovery from theoperation.

Dehydration will also reduce the amount thatoperated rats will eat, and their appetite at onceimproves when fluid is supplied to them. It thusseems that, in these animals, reduction in palat-ability of their food and the withholding of fluidcan both lead to a restriction in their appetite,but that once a desirable diet is restored they will*eat themselves into a state of obesity once more.

These findings throw light on clinical observa-tions of obese patients. It is generally agreed thatfluid retention and diuresis is responsible for thevery rapid changes in weight that are found insome obese patients. Kennedy suggests that thetemporary success of dehydration therapy may, inpart at least, be due to its anorexic effect. Certainit is that reducing regimes that rely on dehydrationwithout any attempt at producing permanentcontrol of the appetite are effective for only aslong as the patient remains on them. The reduc-tion of appetite in the obese rats when given un-appetising food also has its parallel in man. Veryfew people enjoy a reducing diet, however un-restricted their purse, and they will have to facethe fact that the success of the treatment willlargely depend on the reduction of their appetite,and that this will involve some loss of interest in-the delights of the table. If they remain on areducing diet for a sufficient length of time theirappetite and eating habits, as well as their interest-in food will change and it will be possible forthem to maintain a reasonable weight without-undue hardship. If they come off the diet too

soon they will, like the rats, begin to eat too muchof the food they like and again become obese.Patients have a harder time than the rats, as theirgift of free will makes the struggle to controltheir appetite their own, whereas the rat has hisfood problem settled for him under the con-ditions of the experiment. This is why it is usefulto have some patients under strict in-patientcontrol at the beginning of treatment. The rapidinitial reduction that is then possible and thediscipline that is forced upon them results inencouragement and eventually in an alteration ofappetite that may enable them to stick to theirdiet long enough to develop a change in eatinghabits.Kennedy has suggested that in his rats the

normal mechanism of appetite control is exercisedthrough the hypothalamus and results in theanimals eating only enough for their caloricrequirements. In those who have had an inducedhypothalamic lesion this control is absent orimperfect and such control as exists is suppliedat the cortical level and, as a result, the rat willnot eat unpalatable food. He tentatively suggeststhat the same m-y be true of man, lean peoplehaving a perfectly geared hypothalamic mech-anism, whereas those who tend to obesity have torely more and more on cortical control. Thistheory accords well with both experimental andclinical evidence and leads us to the considerationof the effects of disorders of the psyche on theproblems of obesity.

Psychological FactorsThe importance of psychological factors in the

production of obesity has been appreciated to anincreasing degree over the last decade and, asa result, this aspect of the subject has been studiedby those interested in pscyhosomatic medicine(Weiss and English, 1943; Dunbar, 1943) and bypsycho-analytical methods (Fenichel, I945). Bruch(I940) stressed the importance of psychologicalfactors in obesity in childhood and emphasized inparticular the lack of parental love that is some-times shown to these children. Their mothersunconsciously try to make up for their lack ofaffection by over-indulging and over-protectingthe child and the child himself may find solacefor the love he misses and gain a feeling of securityin over-eating.The success of the practical application of

Bruch's observations has been reported by severalauthors, and Macaulay (195i) has recorded a goodexample in an obese girl in whom he showed thatfluid retention was an unimportant factor. I haverecently been less successful with a young girl.She and her brother, aged thirteen and twelve,respectively, were quite amazingly alike in appear-

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ance, with a similar fat distribution and like firmconsistency of their adipose areas. They wereput on the same reducing diet, given the sameinstructions and exhortations and both attendedthe Dietetic Department of St. Thomas's Hospitalregularly. The boy lost weight rapidly and with-out apparent effort. The girl lost very little andsaid she was always hungry. It was quite obviousthat the boy was his mother's favourite and thatshe had little sympathy for or interest in herdaughter. All our efforts to educate the motherwere unavailing and every attempt to persuadethe girl to co-operate was met by a smiling, good-tempered but very definite assertion that shecould not stick to her diet, she did not like it andwas always hungry. This attitude is frequentlyfound in adults who eat to gratify not only theirappetite for food, but also to recompense them-selves for failures in life, for sexual frustrationsand the neglect of others. Some actually takepride in their obesity, as in it they find a distinctionthat is granted to them in no other way.

Fear, as in all human affairs, has a predominantplace in the production of obesity. Fear makesthe mother urge her child to eat so as to avoid thedangers of illness, and any falling off of his appetiteis regarded with horror. Fear of not gettingenough leads some patients who have been hungryin childhood to eat whenever there is a chance.Fear of social failure may result in a desire toavoid any situation that might result in humiliation,and over-eating is then used not only to compen-sate for other delights that are missed, but theresult-obesity itself-provides an excuse for notcompeting. Failure is thus us'ed by the patientin an attempt to avoid failure.There are several series of carefully studied

cases of obesity in which it has been found to becommonly associated with insecurity and tension.Schopbach and Matthews (I945) studied 50 cases,in all but six of whom psychogenic factors seemedclosely related to the onset of obesity. They werefor the most part suffering from mild anxietystates in which obsessional features were pre-dominant. A further 50 obese patients werestudied by Freed (i94'), who found good evidencethat anything that increased their emotional toneled to a coincident increase in appetite. Not onlyprolonged anxiety, but severe emotional traumaof a sudden and violent nature can lead to thedevelopment of obesity. Shorvon and Richardson(1949) reported three cases that, with many othersnot included in the report, illustrated the horrify-ing stresses to which these apparently placid andcertainly obese people had been subjected. Thepresence of powerful emotional factors in themwas originally suspected only when the patientsfailed to lose weight on dietary restriction under

satisfactory supervision. Excitatory abreactionswere induced by the ether technique and thepatients re-lived the original traumatizing situa-tion. The release of tension that followed thisresulted in loss of anxiety and in most cases anactual loss of weight of between i and 2 stones.After this treatment further attempts at reductionin weight were made using the dietary regime thathad previously failed but was now successful.

Obesity resulting from severe and suddenpsychological trauma was observed by Lichtwitz(1923) in the first and Gilbert-Dreyfus (1948) inthe second world war. It occurred in women whowere subjected to severe mental strain and resultedfrom bombing, imprisonment, death of a husbandor brother, or some other acute stress of war.Hochman (1938) reported six cases in whom

a shock, such as a death of a parent, had resultedin over-eating, and Greene (1946) recorded a caseirk whom great unhappiness led to obesity thatdisappeared when her life became smooth again,in spite of the fact that the patient gdve up herdiet at the same time.The discussion earlier in this short review will

have shown that there is a background of physio-logical observations that are consonant with thesepsychological ones. The work on the hypothala-mus in the production of obesity through alterationof appetite, and Verney's (1946) observations onthe effect of emotion acting through the hypo-thalamus on the anti-diuretic hormone may clearlybe relevant. Certainly in the field of practice thetreatment of obesity resolves itself into devisingmethods that will induce a control of appetitewith a consequent reduction of caloric intake.This is predominantly a psychological problemthat requires individual study in every case. Thesocial circumstances of the patient must beexamined, if possible modified, and the emotionalreactions of the individuals to their life situationmust be appreciated and help given on that levelwhen it can be. The attitude of the doctor andthe dietitian to the patient is all-important, andthe correct balance of encouragement and criticismmust be achieved.

SummaryWhile the proper treatment of obesity is at the

present time agreed by all to be the reduction ofcaloric intake, and this requires the control and, ifpossible, the alteration of appetite, the reason whymany people get obese and others always remainslim is by no means established. The answer doesnot lie in all cases in a simple statement that theobese eat too much and the slim too little, as Dodds(1950) has shown by the persistenice of slimness inhis subjqcts who were given two or three times

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their normnal caloric requirement. It seems theremust be some mechanism that normally maintainsthe body weight at a remarkably constant level, butthis is not as yet understood. Where obesity andslimness are undoubtedly related to caloric intake,and this is in the vast majority of cases, the theorythat suggests that appetite control may be a com-bined function of the hypothalamus and cortex isthe most satisfactory. Damage to or dysfunctionof the hypothalamus leaves only cortical control,and man being what he is, that control may breakunder various stresses and result in anorexia ormore often in over-eating.

BIBLIOGRAPHYBRADY, R. O., LUKENS, F. D. W., and GURIN, S. (i95i),

Science, 113, 413.BROBECK, J. R., TEPPERMAN, J., and LONG, C. N. H. (1943),

YaleJ-. Biol. & Med., is, 831.BRUCH, H. (1940), Amer. J. Dis. Child., 59, 739.CAMUS, J., and ROUSSY, G. (1913), C.R. Soc. Biol. Paris, 75,

483.CHERNICK, S. S., and CHAIKOFF, I. L. (igsi), Y. Biol. Chem.,

I88, 389.CRANDALL, L. A., JuN., and ANDERSON, M. X. (I934), Amer.

Y. Digest. Dis., I, 126.DODDS, E. C. (I950), Proc. Roy. Soc. Med., 43, 342.DUNBAR, F. (I943), 'Psychosomatic Diagnosis,' Hoeber, New

York.EDWARDS, D. A. W. (i930), Clin. Sci., 9, 259.EDWARDS, D. A. W. (I91ia), Proc. Roy. Soc. Med., 44, 904.EDWARDS, D. A. W. (Ig9ib), Clin. Sci., 10, 305 and 317.ERDHEIM, J. (I904), S.B. Akad. Wiss. Wien., 113, 537.FENICHEL, 0. (I945), 'The Psycho-analytic Theory of Neurosis,'

Norton, New York.

FREED, S. C. (I947), .7. Amer. Med. Ass., 133, 369.GILBERT-DREYFUS (1948), Pr. Mid., s6, 2z4.GRAFE, E. (I933), ' Metabolic Diseases and their Treatment,' Lea

& Febiger, Philadelphia.GRAFE, E., and GRAHAM, D. (i9iI), Ztschr. f. Physiol. Chem.,

73,'.GREENE, R. (1946), POSTGRADUATE MEDIcAL JoURNAL, 22, 169.GREENE, R. (I950), Proc. Roy. Soc. Med., 43, 344.HETHERINGTON, A. W., and RANSON, S. W. (1939), Proc.

Soc. Exp. Biol., N. Y., 41, 465.HOCHMAN, S. (1938), Med. Rec., N.Y., I48, Io8.KENDALL, E. C. (1945), Trans. Josiah Macy Foundation Con-

ference on ' Metabolic Aspects of Convalescence,' N.Y., iothmeeting, 8I.

KENNEDY, G. C. (I950), Proc. Roy. Soc. B., 137, 535.KENNEDY, G. C. (igsi), Proc. Roy. Soc. Med., 44, 899.LICIITWITZ, L. (I923), Klin. Wschr., 2, I255.MACAULAY, D. (I95I), Arch. Dis. Childhood, 26, 539.McCANCE, R. A., and WIDDOWSON, E.M. (I95I), Proc. Roy.

Soc. B., 138, II5.NEWBURGH, L. H. (I942), Arch. Intern. Med., 70, 1033.NEWBURGH, L. H. (I944), Physiol. Rev., 24, i8.ODIER, J., and MACH, R. S. (949), Praxis (Rev. Suisse Med.),

38, 834.SCHOPBACH, R. R., and MATTHEWS, R. A. (194S), Arch,

Neurol. Psychiat., Chicago, 54, IS7.SHORVON, H. J., and RICHARDSON, J. S. (I949), Brt. med.J.

2, 951.SIMPSON, S. L. (1952), Brit. Med. 3., i, 476i.STETTEN, DE W., JUN., and BoxER, G. E. (x%4), _. Biol. Chem..

156, 271.VERNEY, E. B. (1946), Lancet, ii, 739 and 78I.WEISS, E., and ENGLISH, 0. S. (I943), 'Psychosomatic

Medicine,' Saunders, Philadelphia.WIDDOWSON, E. M., and McCANCE, R. A. (I9Sx), Proc. Roy.

Soc. Med., 44, 903.WILEY, F. H., and NEWBtJRGH, L. H. (I93I),J. Clin. Invest.,

10, 733.YOUNG, F. G. (I9Si), Brit. med. _., ii, II67.

CONVULSIONS IN INFANCY ANDCHILDHOOD

By R. M. MAYON-WHITE, M.D., PH.D., M.R.C.P., D.C.H.Paediatrician, Ipswich Area, East Anglian Regional Hospital Board

To a mother the word 'convulsion' seems tomean almost any sudden temporary aberrationfrom what she believes to be normal childish be-haviour. The complaint of 'convulsions' in achild may cover simple starts and stares, cryingspells, tooth-grinding, colic pain, temper tantrums,epilepsy in any of its forms, nightmares in a schoolchild, or the Moro start reflex of a baby. The firsttask in such a case is to elucidate a description ofthe event and so define the term. For our presentpurpose no better definition could be found thanthat given by Hughlings Jackson: 'A convulsionis the product of sudden temporarv nervous dis-char Jackson was at pains to emphasize theimportance of each of the adjectives he chose.Some 50 years later the electroencephalogram,whilst increasing our knowledge of epilepsy,served to substantiate the validity of Jackson's

concept so that the definition serves equally welltoday.The definition ' sudden temporary nervous dis-

charges' adequately describes the observed phe-nomena of epileptic seizures; it may also be saidto cover the psychogenic discharges resulting inhysterical fits, breath-holding attacks and tempertantrums; it covers the state of increased irrit-ability of nerve cells during pathological alterationsof the physiological milieux interieur-tetany, forexample-or affected by toxins either endogenous(uraemia), exogenous (lead encephalopathy) orbacterial (tetanus). Without stretching the pointtoo far, even simple faints are covered by thedefinition, for the modern use of the term vaso-vagai syncope indicates that we recognize over-action of the parasympathetic as the aetiologicalfactor.

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Postgrad M

ed J: first published as 10.1136/pgmj.28.326.618 on 1 D

ecember 1952. D

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