6 AMENTIA IN RELATION TO CEREBRAL DISEASE AND ABNORNIALITrY

lar need, and also attempts at desensitizationby specific therapy, whether by means ofprotein extracts or bacterial vaccines. I nmany cases considerable benefit has beenobtained by the method of general desetnsi-tization by various forms of protein shock,the method commonly used comprising in-jections, intramuLscular or intravenous, ofsuch substances as peptone, milk, anti-typhoid vaccine, anid recently the use oftuberculin. IntramuscuLlar irnjection of thepatient's owIn blood in quantities varyinigfrom I to 5 c.c. at weekly intervals, is ameasure which I have found of conisiderablebenefit to many cases in the out-patienitdepartment, when for various reasons ad-missioni of the patient for prolonged inves-tigation was impracticable. This has theadvantage of an extremely easy techniqtue,and I have never seetn any unpleasant reac-tionls or other untoward effects. Of a fairlylarge number of patients so treated a suffi-cient proportion have undoubtedly improvedto an extent which has encouraged me topersist in the treatment. I believe that goodresults have also been obtained by intra-venous injection of sodium iodide in normalsaline. Apart from these special points,treatment on the general lines indicated inmost textbooks is of importance. Attentionto diet, regulation of the bowels and theregular administration by the mouth ofiodide of potassium with tincture of stra-monium are among the routine measureswhich do unidoubtedly afford considerablerelief. For the actuaal distress of the severeattack injections of adrenalin are probablythe most effective and best known remedy,but it should be remem-nberied that very uIn-pleasant and even alarminig symptoms ofgiddiness, faintness and even syncope haveoccasionally followed the use of this drug.The combination of atropin with adrenalinis said to lessen the risk of occurrence ofsuch symptoms. As an alternative toadrenalin the nexx synthetic preparationiephedrin has been found of considerableuse, and has the advantage thal it may be

given by the mouth in closes of hialf agraini.

Attention has beeni called by Scott [5 l, tothe value of X-rays in the treatmenit ofasthma, beneficial results having been ob-tained from applications onice or twice aweek with a small dosage over a largeradiation field. Accor-ding to his experiencethis seems to offer conisiderable possibilitiesfor- futtire research.

REFERENCES.El] FREEMAN, J. Proc. Roy. Soc. Meti.. vol. xiii, parts

1-2, 1919-20, p. 129.[2] VAN LEEUWVEN, S. "Allergic Diseases," 1925.[3] STARLING, E. H. "Principles of Human Physio-

logy," 1926, Fourth Edition, p. 889 ct seq.[4] SAMSON- WN'RIGHT. "Applied Physiology," Oxford,

1926.[51 ScoTT, S. G. " Radiolog,y" (Jont',,. Rad(liol. Soc.. of

V. Aimierica), October, 1927; Bi-it. M1cd. Jour,it,London, 1926, i, 939.

AMENTIA IN RELATION TOCEREBRAL DISEASE AND

ABNORMALITY.,By E. W. NEILL HOBHOUSE,

M.D., M.R.C.P.,

Assistant Physician, Royal Frec Hospital, and(u West Eiid.Hospital for Nervous Diseases; Phtysician to Oult-Paitientls,

Vlictoria Hospital for Childlren.

I MUST begini by admitting freely to yotuthat I ani not speaking as a specialist orexpert itl the scientific aspect of mental(leficiency. I am attempting to speak on thesubject from a different point of view ; todiscuss the aspect of mental arrest orimpairment which is met with by thenieurologist in the cases which are brotughtto a clhildren's hospital or a niervous hospital,or seen inl consultationi. I think that thispoint of viexv is wvorthy of some considera-tion, because a very large number of thesechildren are brought to the neurologist, andbecause the element of amentia which ispresent is one of the most important factorsin the treatment of these patients, whatever

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the actual sytnptoms mlay be wlich haveattracted the attention of the parents. Myobject will merely be to describe some typesof cerebral disease or abnormality whichare likely to involve some element ofamentia, and to discuss the bearing of thelatter on prognosis and treatment.

I should like to make a few remiarks inexplanation and defence of the rather un-scientific attitude which I shall take up witliregard to classification. You are all -aareof the fundamental distinction, in theory atany rate, between amentlia and tlemiefnttit,dependent on the question of whether thedefect was due to a failure of developmentor to a deterioration of faculties alreadydeveloped. In adolescents and adults Ithink that this is a distinction of greatimportance, and that every effort should bemade to keep it clearly in mind. For thisreason I view with misgiving the recentlegislation which has widened the scope ofthe Mental Deficiency Act so as to includesufferers from epidemic encephalitis.Nevertheless, in children one has to admitthat it is often absolutely impossible toestablish any hard and fast distinctionbetween these two types of defect, becauseone has no means of determining how mucharrest or retardation there has been, or howmuch is to be accounted for by subsequentdeterioration. Take as an instance anepileptic boy of 9 with an intelligencedefect; how is one to estimate, in 'theabsence of a reliable medical history, theextent to which his mental faculties mayhave developed in the first instance ? Fromthe fact that " the age is early " one may beinclined to class him as an ament; from thefact that he is now deteriorating one is givenequally good grounds for regarding him asa dement.

Still more emphatically must one pointout the limitations of the attempted distinc-tion between primary and secondaryamentia, when these terms are applied tochildren who suffer from some form ofcerebral disease. I personally do not hesitate

to say that in the present state of our know-ledge this distinction cannot be made, andthat to make it involves the begging of someunsolved questions. The reason for this isthat the whole problem of the xtiology ofinfantile cerebral disease is in the melting-pot at the present moment; tliere are manyconflicting opinions and but few establishedfacts. There are a number of morbid con-ditions which a few years ago were confi-dently classified as " primary "-attributed toagenesis or true developmental failure--buton the aetiology of which no such unanimityprevails to day. Perhaps the best instanceof them is porencephaly. Porencephaly isa condition in which cavities, sometimes ofconsiderable size, are found in the cere-bral hemispheres. It is found in post-lnortem examinatiois, sometimes of casesshowing no definite abnormality during life,but more often of cases which show signsof lesion of the cortico-spinal tracts, or ofmental defect, or of both. Until fairlyrecently it was assumed on all sides that thiswas a prenatal defect; it was described bysome authorities as being due to a primaryagenesis, and by others as the result ofthrombosis or embolism during intra-uterinelife. In many books you will find referenceto primary porencephalic amentia. At thepresent day, largely as the result of theresearches of P. Schwartz, of Frankfort,the view that porencephaly is a primarydefect is by no means universally held,though it has its adherents. Schwartz hasbrought forward a considerable amountof evidence in support of his contention thatporencephaly is an entirely secondary con-dition, is in fact the end-result of venoushemorrhages from tributaries of the vein ofGalen, which takes place during delivery orshortly after. From this it will follow thatanyone who, like myself, regards the hypo-thesis of Schwartz as at any rate more con-vincing than any other, will look on anamentia associated with porencephaly, or a

diplegia associated with porencephaly, asbeing par excellence a secondary condition ;

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8 AMENTIA IN RELATION TO CEREBRAL DISEASE AND ABNORMALITY

one who does not share this conviction willcontinue to speak of a primary porencephalicament. I merely mention this as a goodexample; similar doubts may be raised aboutalmost any other morbid cerebral conditionin early life. The point which I want tostress is simply that at the present state of ourknowledge the -etiology is a matter of opinionand not of fact, and that it is unscientific toembark confidently on the diagnosis ofprimary amentia in individual cases. Thatthe majority of them are primary is likely,because the preponlderance of the hereditaryfactor points to a germinal defect, butclinical data are insufficient for the differen-tiation of all but a few of them, and eveni themorbid histology of some of them is soobscure that microscopical examination ofthe brain does not fully establish the natureof the condition. I think that it is within theexperience of most of us to have found somedefinite indication of cerebral disease in thepost-mortem examination of a case whichwe had preeviously regarded as a "simpleprimary ament." In the cases -vhich I shalldiscuss I shall treat mental deficiency entirelyfrom the symptomatic and practical point ofview, without much reference to its exactorigin.The type of child -which concerns us most

is that which is roughly classed as itnfantilespastic paralysis. Patients beloniging to thisgroup (it is merely a group and not a disease-entity) present a problern of far greaterimportance than do the other types to whichI shall refer, because in them the questionis not merely one of diagnosis, classificationprognosis, but of the possibility of active,effective treatment. Furthermore, the esti-mation of the degree of mental defectpresent in these children is of tlle greatestpractical importance to the neurologist,because it is the factor above all otherswhich stands in the way of the treatmenitwhich is necessary for recovery of the motor-disability.

Inifantile spastic paralysis is the resuLlt ofa lesion of the cortico-spinal tract which

constitutes the upper motor neurone. Thelesioni is typically in the cortex, or the whitemnatter of the subcortical region. Theparalysis occurs as either a hemiplegia or adiplegia; the latter group is commonlyreferred to as Little's disease.The wetiology is a much-disputed subject

which does not closely concern us at theinoment. I will just mention the threeprincipal views which are held on the usualmnode of their origini; I think that all willagree that each of these causes is responsiblefor somlte of them, but opinionis differ as toxvhich is the cause of the majority. Theyare regarded as: (i) Primary degenerationof the cerebral nieurones (Collier) ; (2) resi-dual effects of meningeal hemorrhage, andparticuilarly of the superior longitudinalsinus (Adie) ; and (3) residuLal effects ofintracerebral haemorrhage, particularly oftributaries of the vein of Galen (Sclhwartz).The symptoms presenited by inifanits wvho

ate affected by lesionis of these kinds willof course vary according to the exact siteof the disease or damage. The symptomsreferable to the pyramidal tracts will be veryslight at birth and in the first few months,because the infanit's pyramidal tract isincompletely developed, and its movementsare dominated by lower centres. Later oni,a child with a pyramidal lesion will developspasmn in the affected limb, and will tendnot to develop new voltunitary movemenitsin it. Within wide limits, those in whomthe cortex is inivolved tend to suffer fromfits anid mental impairmlent, while thosewhose lesionis are subcortical suffer fr-om agreater degree of spastic .Weakness.Now the prognosis in these children

depends uponl the extent to which thev willreact to treatmenit, and the only effectivetreatment is the initiationi of active imove-ments. To get this done, various meastiresar-e uisually niecessary which are perfectlysimple but require a good deal of persever-ance. For instanice, in a hemiplegia thesound arm is tied up, so that if the childwants to handle anythinig it mLst do it with

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the stiff one. The normal infant does wantto handle things, and its instinctive desireto do so is made use of in this way, and ina great proportion of them a very goodultimate result may be obtained. But theinfant who has suffered extensive damage inthe cortex, particularly of the frontal lobes,may suffer friom some degree of amentia inaddition to the motor disability. In this casethe normal instinctive activities of the infant-almost ceaseless during the waking state-are replaced by a state of apathy which is anabsolute bar to the initiation of active move-ment; you may tie up the sound arm, butthe child will merely lie with both armsimmobile. For all these children, amentsor otherwise, the process of learning is goingto be more difficult than for normal ones,and in later years all new functions must betaught them with a good deal of patienceand perseverance. But this is of no availunless there is a will to learn, and if thechild's attitude is one of apathy or nega-tivism the improvement cannot be achieved.For this reason the prognosis in a case ofinfantile hemiplegia or diplegia dependsupon the presence or absence of associatedamentia, and not nearly so much on thecondition of the affected limb. The pro-gnosis in a very large number of thesecases, when there is not an appreciabledegree of mental impairment, is really quitegood, so that the determination of the mentalstate is very important; it constitutes aquestion about which you will always bepressed by the parents when you see thesechildren in the course of practice, and theproblem which you will then be confrontedwith is precisely that which I want to discussat some length now.

Tlhe first point to remember is this; ingiving a prognosis of this kind you are notestimating the child's intelligence at themoment, but trying to arrive at some idea ofwhat it may be in-the future. In the simpleprimary aments the degree of intelligenceremains roughly constant; a child which hasthe characteristics of an inbecile at the age

of 4 is likely to have them to a fairly similardegree at 8. As a result of this we havegot into the habit of talking of the condi-tion as a permanent one, and of basing theprognosis simply on the results of mentaltests at a given moment. In general, I thinkthat prognoses made in this way, by experi-enced observers, turn out to be right in aremarkably high percentage of cases, as faras simple primary aments are concerned.But I am firmly convinced that when we aredealing with children who are suffering froma cerebral lesion--particularly a residual one-this is very far from being the case, andthe more experience I have of these childrenthe more am I confirmed in this opinion.Except in cases of gross idiocy, I do notbelieve that when you see a diplegic or

hemiplegic child in the first three or fouryears of life, you can do any more than saythat the mental development is retarded atthe moment, a fact which is probably obviousto all unbiased observers, though not alwaysto the parents. You know that the childhas leeway to make up, and will need a gooddeal of help in doing so, but I would cautionyou against prophesying as to how much itwill do so, until you have observed for aconsiderable period the way in which itresponds to your efforts to further its deve-lopment. If you proceed as if you weredealing with a simple primary ament, andsay that the child will or will not attainthe mental development of a more or lessnormal individual, I think that you willbe embarking on a venture which may leadto a good deal of trouble for yourself, andperhaps some risk of interfering with thechild's chances ofrobtaining suitable treat-ment. I am ready to admit that I am unableto diagnose permanent mental defect in thesechildren, with any certainty, in infancy andearly childhood. I am very much inclinedto doubt whether anyone else can do so, asit is so often my experience to be consultedabout a child of 8 or ro who still has somedegree of paresis, and to hear that a diagnosisof melntal deficiency has been made by a

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10 AMENTIA IN RELATION TO CEREBRAL DISEASE AND ABNORMALITY

competent observer in earlier years, thoughno evidence of it has remained. Thesechildren, I may remind you, will be treatedby the general practitioner rather than themental expert, and they are at least as impor-tant to you as the more typical forms ofamentia; this is my excuse for going intosome detail about them.

If one considers the clinical characteristicsof these children, some of the reasons whyone can foretell so little about their mentalpossibilities become obvious. They have amotor disability, by which movement isrendered difficult or impossible in somepart of them. It is not only the gross move-ments which are hampered; complicatedvoluntary movements such as those involvedin speech are affected. Moreover, one ofthe most important functions of the cortico-spinal tracts is inhibition of superfluousmovements which in the infant have beenperformed by lower centres. Consequentlya fairly common symptom is hyperkinesisin some form or other, particularly grimac-ing. There may be some stiffness of thepharyngeal muscles, so that the childdribbles. So that you may be confrontedwith a child of about 3 who does not talk,grimaces, and dribbles. If you meet withthis combination in a child whose motorsystem is normal, further investigation willusually show evidence of mental defect.But if you find that there is a pyramidallesion, whether hemiplegia or diplegia, thenyou must discount all these purely motordisturbances as evidences of mental impair-ment, because you cannot tell whether thefailure to speak is due to an intelligencedefect, a failure to register impressions, orwhether it is merely that the child has. notyet overcome its mechanical difficulties inarticulation.Now when you come to estimate the intel-

ligence of a small child, almost all the testswhich you use involve some motor functionin their performance; you are left withalmost nothing else. But you generally canform some idea of the amount of interest

that the child takes in his surroundings, byobserving the response to visual, auditory,and tactile stimuli as shown by movementsof eyes or some part which is not spastic. Astate of apalhy, in which there is no desire towatch or handle objects, is the principal ifnot the only symptom which you may regardas really ominous. But even this must beinterpreted with a certain amount of caution;do not attach too much significance toapathy until you have found out whetherthe child is apathetic under favourable con-ditions. The majority of these children arelate in reaching the so-called milestones ofinfancy and childhood; they are late insitting up, crawling, &c. A very importantpart of the treatment both of the mental andthe physical disability consists in correctingor compensating this delay in adopting newpositions. For instance, a child of 15 monthswho has never done anything but lie on itsback may present the appearance of extremeapathy, but as soon as you do what shouldhave been done long before, but very often isnot done, and get it into a sitting posture bythe use of pillows, a chair with a bar, orsome other means, it may rapidly acquire aninterest in its surroundings and begin to doa lot of things which it could not do whilelying down. If there is no response aftera number of montlhs to your efforts to stimu-late the sensori-motor reactions while keep-ing the child in a position which will givehim a fair chance, then you are justified ina strong suspicion that permanent mentaldefect is present.What I have said so far applies mainly

to infants and children of the pre-schoolage. To summarize: When there is a

spastic lesion one should be very chary ofdiagnosing mental defect in the sense of a

perlmanent condition (i.e., of a kind whichwill come under the M.D. Act); this canonly be done with certainty by observingover a long period the extent to which thechild's interest can be aroused when suit-able conditions are provided. It is of thegreatest importance that this should be done

_._

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AMENTIA IN RELATION TO CEREBRAL DISEASE AND ABNORMALITY 11

early. Too often one finds that it has beenpostponed and that the child has lain inertfor months or years. I am used to hearingtwo phrases, sometimes attributed to thedoctor; that the child" needed rest," and that" they thought that it would grow out of it."They do not need rest, they need activityand interest. They do not often grow outof it spontaneously, but ale apt to deteriorateif left to their own devices.The next point to consider is the mental

state of these children at a later age, say 5to o. It is at this stage that the questionoften comes to a head, because the childhas now reached the school age, and thequestion of educability arises. At this periodone can attempt to form some more definiteideas about the prognosis, but still tliere area number of pitfalls. In the first place donot judge by appearances. Tile silly, inanelook, and the indistinct " mouthing" articu-lation, whicli give an appearance of mentalvacuity, are often really the effects of dysar-thria, and the child has good powers ofunderstanding and talks quite good sense.In the second place, if you are going toapply mental tests, put your watch in yourpocket. The standardized time-limits,which are I think justified in the resultwhen applied to ordinary aments, have noplace here. The child is running its race insplints, and is not going to achieve anythinglike normal reaction times. Such tests asability to interpret pictures, tell the time bythe clock, tell you something about thestreet he lives in, are the most valuable, forthey are the tests that give you evidence asto whether he is registering and retainingimpressions.Now as to this question of "educability,"

which is very likely to be the point on whichyou will be consulted.

Let me remind you that the child willcome under the scope of the M.D. Act if it" appears to be permanently incapable ofreceiving proper benefit from the instructionin ordinary schools." This classification,intended for and admirably suited to the

primary aments, raises considerable diffi-culties when applied to cerebral diplegics.The majority of them are unable, I think,to obtain proper benefit in tliem, and aremoreover liable to develop unsatisfactorilyif thrown among normal children. Thereason of this is that they are under thesecircumnstances so liable to suffer from thevery thing that it is most important toprotect them from; a sense of inferiority.If the child does this, half the battle is lost;it becomes discouraged and diffident, avoidseffort from fear of failure, and tends torecede into itself and live in phantasy.There is also a tendency to compensate inother ways, and the fact that some of thesechildren develop unpleasant traits, such asspitefulniess and cruelty, is due far more, Ibelieve, to their very niatural sense ofinferiority than to the actual cerebraldamage itself. For these reasons one isanxious to get them out of the ordinaryschools. But I personally am very reluctantto admit that in the majority of cases the"inability to profit" is permanent, and Ithink that doubtful cases should not becertified. And if they are sent to specialschools for ment;ll defect the disadvantagesare nearly as great. They are amongchildren, the great majority of whom arenever going to make much progress, whoare, to put it unscientifically, "duds"; afair proportion of them are also mischievousand generally unpleasant. This does notconstitute an environment which will helpthe child to overcome the handicap withwhich he started. When it can be done, Ithink that far the best thing is to get thechild into a special school for cripples, andoverlook as far as possible the mental dis.ability. In private practice, the ideal toaim at is to get these children educated bya tutor or governess in groups of three orfour. Mind and body require to bedeveloped simultaneously, and special atten-tion should be paid to handicrafts and suchactivities. I think if you follow such casesin your practices up to the years of adoles-

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12 AMENTIA IN RELATION TO CEREBRAL DISEASE AND ABNORMIALITY

cence, you will often have occasion to beglad that you saved one of these children inearlier years from certification as feeble-minded.There is one imlportant point w\hich I

purposely did not mention until now, thesignificance of fits. This is a very difficultquestion, on which opinions seem to differa good deal, and I can only give you myexperience. Of the cases which I have seen,the great majority, both of those who havedone well later and those who have donebadly, have had fits in infancy. And of theminority who have not to my knowledgehad fits, not all have made good progress.So I am not able to draw any prognosticsignificance from fits occurring during thefirst eighteen months. As you know, quiteapart from the presence of cerebral lesions,fits in tiny children mean rather little, andfits in older ones or in adults mean rather alot. But of the cases I have seen who havemade good mental progress up to andbeyond puberty, very few have had morethan an occasional fit after the fourth orfifth year. The onset of measles, or a fall,or an unduly exciting occasion, mayperhaps be a legitimate stimulus to accountfor a fit, but if convulsions or lapses ofconsciousness occur during the child'snormal activities, on more than a few oc-casions after the age of 4, I personally donot regard the prognosis as at all favourable.Fits also influence the progress in anotherway, and I believe it is an important one.In order to control them one must givecertain drugs. These drugs are usually"sedative," intended to diminish mentalactivities. The ones usually given certainlyhave a deleterious effect on the child'smental progress. I think that a great dealof the retardation of many of these childrenis due to the prolonged use of bromide,given in large doses over a long period,sometimes necessarily, but I think usuallyunnecessarily. On this point I know thatopinions differ, but I have entirely given upthe use of miassive doses of bromide, and I

mnake it my object to find the smallest doseof whatever drug 1 am using whicli willkeep the child- more or less free of fits; Iwould rather- that the child had a fit or twoin thle year than that it spent the yeardrenched with bromide. And in themajority of cases that are going to do at allwell, I generally find that small doses willdo this. I always try first to see what canbe done with a drug which I find perfectlyharmless, borax. Of course it is not nearlyso effective as the others, but in a mild caseit may be enough for a long time, and it is a

,reat advantage to the child to escape themore potent drugs. If this does not controlthe fits, I add bromide, in small doses suchas iij gr. to vj gr. t.d.s. I seldom go higherthan this; if it fails I go on to luminal fora few weeks and tlhen back to the borax.I am fully convinced in my own mindthat children make better mental progresson this treatment than if they are keptperpetually under the influence of bromide.

Before leaving this subject I should liketo say a word about the question of givinga prognosis, which is so very important toyou in general practice, because I havefound so often that the parents have beenresentful with or have lost confidence intheir doctor because of what has been fore-told, or more often not foretold, about thesechildren. Do not tell them that the childwill "grow out of it," or words to thateffect. Tell them that the brain is damaged,but that the mind is capable of beingdeveloped to a considerable extent; thatthere is a very good chance of the childbecoming a normal member of society, butone who is not going to be suitable for hardbrain work. If in the course of time youfind that the child is not progressing, and isclearly an ament, tell them so, graduallyperhaps, but at any rate let them know itfrom you rather than discover it in spite ofyou. Otherwise there is always a tendencyfor them to think that if you had known itearlier something more might have beendone,

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Epilepsy.-Of all the mentally retardedchildren which are commonly seen by theneurologist, epileptics are probably the com-inonest. I do not want to say much aboutthem, 'but to point out that, as we see tlhemin early life, they do not make up an entity,bult ar-e merely a mlixed group of a wholenumber of conditions exhibiting a commonisymptom. Some will turn out normal in theenid, others will be cases of chroniic idiopathicepilepsy, others no doubt have cerebral birthlesions of which there are no physical signs.But in early childhood one cannot distin-guish these types from one another. Themain characteristic of the mental impairmnentis usually an extreme lack of attention of aparticular sort. It is not real apathy, thechild is always taking notice of something,but it is impossible to get him to keep hisattention on any one thing for any length oftime. Consequently many of them seemfairly normal in the pre-school age, but assoon as lessonis begin they fall behind theirfellows and are always getting into trouble.In my experience the greater number ofepileptics slhowing slight ameintia (one is butlittle concerned with the grosser cases ofimbecility) are those who have few definitefits but fairly frequent " absences," momeni-tary lapses of attenition without any muscular-relaxation or loss of consciousness. A childof this kind often has a true fit every now andagain, perhaps when he is cotnvalescing from afever or gets unduly excited. This is a type ofpatient which will ofteni be brought to you,not so much for treatment as for adviceabout the sort of life he should lead. Thouglhthe pr-ognlosis is niot very good, taking thesepatients as a whole, yet it is worth doingwhat you can as long as the amnentia is inild,as some of them do itliprove. The first thinigis to get the parents' attention directed awayfrom the fits, and oIn to the mental develop-mnent, which is an aspect of the case that hasoften escaped them. Make them realize thathe will want more teaching, not less, than anormal child, but that it will lhave to be donequietly and patiently. Get thein to keep tlle

child occupied, particularly in such ways aslearning to mnake things, or nature study.Secondly, try to control the fits with thesmallest, niot the largest dose of drugs thatwill do it. Finally, see that the child is notprevented unnecessarily from doing things.A few pursuits, such as ridinig a bicycle, orswimming alone, must obviously be for-bidden, but they cani do nearly all the thingsthat another child does, and are much thebetter for it. Watch the result of your treat-ment for a year or so with an open mind.You will have a fair number of cases whosemental retardation does not turn out to bepermanent; on the other hand, when you dofind that it is progressive, you will do wellto recogniize that the prognosis is unfavour-able, anid adrnit

(To be continted).

THE CANARY ISLANDS ASA HEALTH RESORT.

By GEOFFREY LUCAS,B..., M.D.,

Residentt Physicict i, Munideslcy Sanatorium.

I-r has always been a source of wonder to methat the Canary Islands have not becomemore popular as a health resort, moreespecially of late, since I have become moreintimately acquainited with them personallyin search of health.

I can only think that the bogy of the Bayof Biscay exercises a terrorizinig effect upotnthe travelling public, but, as I will showlater, this drawback miiay be obviated.The Canary Islanids are the niearest resort

to the British Isles where one is certaini ofwarmth, sunshine and dryness during thewinter months.The group consists of seven larger islands

a'tnd several smaller ones. They are distantr-ouighly I,700 miles from England. Theyare situated between the latitudes 27' 4' and290' lnorth anid longitudes I3' 2' aind

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