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or November, he ha,s given notice to the InsuranceCommittee in writing of his desire to transfer, whereuponhe will be entitled to transfer as from the end of March,June, September, or December next following, but suchtransfer can be effected only if the new doctor agrees toaccept him. If our correspondent tries to take advantage ofthis regulation, his present doctor will probably tell him thathe must wait until his old doctor has been back for a year.The protection of practices scheme is supposed to

apply in exactly the same way to private patients, butthese do not hold medical cards and when applying fortreatment they often omit to explain that they are reallypatients of an absentee doctor.

MEGALOBLASTIC ANÆMIA IN CHILDREN

ANÆMIA with high colour-index and large red-blood cellsdoes occur in infancy and childhood, but the frequenciesof its causes are quite different from those in adultlife. The commonest cause in childhood is nutritionaldeficiency, either primary or secondary to cceliac disease ;Blackfan and Diamond 1 have seen it in acute infectionsin infants with temporary achlorhydria ; haemolyticsyndromes, like erythroblastosis fcetalis and familialacholuric jaundice, and leukaemias are not uncommoncauses. There has been much argument about theincidence of true pernicious anaemia before adult lifeand the evidence has been reviewed by Peterson andDunn.2 They point out that the following criteria areessential for establishing the diagnosis of perniciousanaemia in childhood : macrocytic anaemia, gastricachlorhydria resistant to histamine stimulation, megalo-blastic change in the bone-marrow, a specific responseto liver treatment, and the necessity for continuedtreatment to prevent a relapse. Examined by this strictstandard, every case but two reported up to 1942 failedto qualify ; not a few had free HC1 in the gastric juice,others showed no relapse after liver treatment was

stopped, some were clearly nutritional cases, and in

many the evidence was inadequate or rested primarilyon post-mortem changes. .

Pohl 3 described the case of a girl of 13 years who wasstudied for 4 years and presented all the features ofpernicious anaemia ; Dedichen 4 reported a macrocyticanaemia in a child of 13 months in whom repeated relapseswere observed over a period of 3 years whenever livertreatment was stopped. Peterson and Dunn describea case of their own, in a child of 13 months who wasadmitted because of diarrhoea and pallor ; the red-cellcount was 810,000 per c.mm., haemoglobin 2 g. per100 c.cm., colour-index 0-82, white cells 62,000 per c.mm.,with 90% lymphocytes and 8 %

" smudges," and reticulo-cytes 14%. It is not surprising that pernicious anaemiadid not figure in their original differential diagnosis ;_the child was transfused and not given liver until 3months later, when it produced a surprisingly good effect.The patient relapsed several times ; during her fourthrelapse, 31/2 years later, the bone-marrow proved to bemegaloblastic ; gastric achlorhydria had been notedpreviously. It was found that the girl had an iron-deficiency, and when this was remedied she improvedremarkably and the blood-count became normal. Ninemonths later a mild normochromic anaemia was remediedby increasing the dose of liver extract ; the white cellswere then normal and with normal distribution. Thatsuch an extraordinary case should be reported as per-nicious ansemia emphasises the diagnostic difficultiesthat arise in children ; yet, apart from the absence ofmacrocytosis and the curious lymphocytosis, the caseconformed to all the criteria given above, and the lackof macrocytosis is attributed to the iron-deficiency.1. Blackfan, K. D., Diamond, L. K. Atlas of the Blood in Children,

London, 1944.2. Peterson, J. C., Dunn, S. C. Amer. J. Dis. Child. 1946, 71, 252.3. Pohl, C. Mschr. Kinderheilk. 1940, 84, 192.4. Dedichen, J. Acta med. scand. 1942, 111, 90.

Davis 5 has described 3 cases of macrocytic anaemiain children. The first was in an underdeveloped girl of13 years who had a megaloblastic marrow and, at first,free acid in the gastric juice ; she was treated, but 3years later was seen in a relapse when she had achlor-hydria and responded to a purified liver extract usedfor treating pernicious anaemia ; it is clear that had shebeen seen for the first time at the age of 16 she wouldhave been regarded as a case of pernicious anaemia. Hissecond patient was a boy of 14 years who had achlor-hydria and megaloblastic marrow; a purified liverextract was ineffective, but proteolysed liver -by mouthand a crude liver extract parenterally produced a

remission after which no further treatment was needed.The third patient, a girl of 3 years, resembled the second,but gastric acid secretion was present. Neither of thesepatients would be classified as pernicious anaemia.

Recently Zuelzer and Ogden 6 in Detroit have drawnattention to a macrocytic anaemia in infants aged up to18 months that they found to be quite common, andthey give details of 25 cases. The bone-marrow, aspiratedfrom the femur, was typically megaloblastic, gastricachlorhydria was present in some ; the anaemia wassevere and clinically the patients had pallor, fever,vomiting, diarrhoea, and sometimes petechiæ. All

except 5 of the infants responded rapidly to liver extractor to folic acid, and so far these have not relapsed; the5 exceptions died from complications, mostly infective.From all this evidence it can be deduced that a macro-

cytic anaemia with megaloblastic change in the bone-marrow is fairly common in infancy and childhood. Itshould be distinguished from other forms of macrocyticanaemia, since most of the patients respond to liverextracts ; ordinary crude extracts should be used andnot the purified extracts specially designed for thetreatment of pernicious anaemia, like Anahaemin’ ;Zuelzer and Ogden’s results suggest that it will beworth while to try folic acid for these patients. It isdoubtful whether true relapsing pernicious anaemia ofadult type does, occur before puberty, and the outlookfor the children who seem to have the disease is relativelygood, since they nearly all show a lasting response toliver, and if they weather the original crisis they willrecover permanently. It seems reasonable that the name" megaloblastic anæmia," which describes the maindiagnostic features of the disease without confusing itwith pernicious anaemia, should be adopted.

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MECHANISM OF PAIN

IN his founder’s lecture at the annual congress of theChartered Society of Physiotherapists on Sept. 14,Prof. G. W. Pickering spoke of the pain mechanism inman as consisting of three essential parts : the sensorynerve-ending or receptor, the nerve-nbre or conductor,and the brain or cortical analyser. Receptors were verynumerous in the skin and liberally provided irl the deepfascial and muscular structures, but rather few in thesubcutaneous tissues. The parietal layers of the serousmembranes were well supplied, but the visceral layersand the viscera themselves not at all, though perhapsthere was some evidence that the pains of -angina andpeptic ulcer do arise directly in the organs concerned.Periosteum and ligaments were sensitive, spongy boneslightly so, compact bone and joint surfaces insensitive ;arteries possessed more receptors than veins, and themeninges were profusely studded with them, whereasthe brain itself had none.The tissue changes which produced excitation of these

receptors might be physical, a deformation of surface

producing alteration iri configuration and tension ;or chemical, like the pain of claudication due to theaccumulation of metabolites in muscle-fibres, peptic-5. Davis, L. J. Arch. Dis. Childh. 1944, 19, 147.6. Zuelzer, W. W., Ogden, F. N. Amer. J. Dis. Child. 1946, 71, 211.