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destruction of the other hemisphere does not producethis result. Visual records of only one side are usedin symbolic association. Yet the inactive side isas well developed as the other, and must have been" irradiated equally with the active." This wouldleave some record in the cells of the inactive side, ,anengram which would be opposite in sign and wouldform a mirrored pattern. May it not be, then. Dr.Orton asks, that while normally only one of thesepaired engrams is in activitv, in these abnormal casesunder consideration the habit of suppression of theother engram has not been established and hence thedifficulty in differentiating between p

" and q,"and " d " and " b," " was " and saw," and thetendencies to mirror-reading and mirror-writingwhich he found in his cases to be characteristic of thecondition ? The theory is fascinating, but .not quiteconvincing, apart from the difficulty of proving it,which is as great as in the case of the theory it isproposed to supplant. The possibility of its truthdepends upon the correctness or otherwise of Dr.Orton’s claim that the " tendency to reversal in the i

direction of reading " is the cardinal factor of the I,condition. The confusion of letters like " p

" and"

q " is one which probably few children escape at

an early stage, and mirror-writing has been a wellrecognised curiosity of development, usually of shortduration, in many normal children, and of longerduration in some feeble-minded children. Thesefacts may seem to support Dr. Orton’s theory thatthe condition which he names strephosymbolia is aphysiological variant, but mirror-writing does notappear to have been a factor in some recorded casesof word-blindness. He admits that only one of his15 cases " fits the measure " of Hinshelwood’s con-genital word-blindness, and his estimate that 2 percent. of school-children are affected with strepho-symbolia confirms the suspicion that he includes casesthat do not even approximate to word-blindness,which has in England been estimated to occur in1 out of 2000 children. The mirror-engram theoryalso fails to explain the difficulty with other lettersand words, a difficulty which Dr. Orton somewhatcursorily sets aside as of slight importance. Certainnew training methods based upon the theory are

being carried out upon some of the children ; theresults of these, when they are available, should beof much interest.

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PSYCHOLOGY OF ANÆSTHESIA.

IN a lecture recently delivered at the Royal DentalHospital 1 Dr. Dudley Buxton discussed the psycho-logical aspects of anaesthesia, a matter as obscureand little studied as it is practically important. Ifthe essential causes of difficulties and dangers thatarise both in early and in late stages of narcosiswere better understood it would probably be foundthat the root of the trouble is often psychologicaland not physical. Every anaesthetist is familiar withsome of the phenomena that may arise throughwhat is spoken of as the " mental " or

" psychological"disposition of his patient. The anaesthetist knowsthat an abnormal reflex activity even during deepnarcosis, or an extraordinary amount and degree ofexcitement in the light stages, may characterise theunconscious state of the " temperamental " patient.In other subjects of the same kind narcosis mayleave a peculiar and abiding effect, so that for weeksor months after its induction the patient’s ordinarysleep is attended by vivid and distressing dreamswhich were first originated by the inhalation of ananaesthetic. Dr. Buxton alludes to the well-knowninstances in which shock, even fatal shock, hasoccurred at the beginning of an administration, evenbefore any anæthetic at all had been inhaled by theapprehensive subject. It is verv plain, therefore, thatwhat is called the " psychological " side of anaesthesiahas a direct and powerful influence on the effects ofanaesthetic administration, and this influence ispossibly even more determinant when a local

’ British Dental Journal, 1928 : XLIX. 405.

analgesic is employed than when there is unconscious-ness. It is, however, the play of the " psychological’’factor during unconsciousness that is so interesting,so dominating, and, further, so hard to investigate.Animal experimentation is here likely to be of littleguidance as to human behaviour, for we are dealingwith that very part of the organism in which thehigher is most differentiated from the lower animal.Subjective evidence, too, is only partially reliable,for the memory of what has taken place when thebrain was still under narcotic influence is necessarilyimperfect. ____

IS THERE A RACHITOGENIC DIETARY FACTOR ?

’ WE are accustomed to think of rickets as a deficiencydisease brought about by a lack of vitamin D or by aninsufficiency or unbalance of the calcium and phos-phorus in the diet. E. Mellanby (1925,1 1926 2)believes that there is, in addition, a substance,occurring chiefly in cereals, the presence of whichrenders the foodstuff containing it actively rickets-producing, and that when the substance has beenremoved the same diet has no ill-effects. P. M.Holst (1927 3) adduces evidence in support of

Mellanby’s idea. He shows that rats develop ricketswhen they are fed on an exclusive diet of oats oryellow peas, or wheat or rye, or barley or maize, orpolished rice. Pure starch does not produce theeffect ; rats are able to live on it for some time, anddevelop only an osteoporosis. An addition of caseinand lard makes the animals live longer and, grow.and r:ckets is not produced, but when the casein andlard are added to the diet of pure oats or other purefoodstuffs rickets is not prevented. Holst foundthat he could extract the rachitogenic substance byboiling oatmeal with a dilute solution of hydrochloricacid ; the extract, when filtered and neutralised andgiven to rats, in a daily dose corresponding to15-20 g. of oatmeal produced rickets in rats on thepure starch diet. The substance is organic since theash of oats does not possess the rickets-producingpower ; it is dialysable and can be precipitated withalcohol, but Holst’s results are not entirely in agree-ment with Mellanby’s as to the physical and chemicalbehaviour of the rachitogenic substance.

Recently A. F. Hess and M. Weinstock (19274) havemade the startling suggestion that cow’s milk containsa rachitogenic substance and that the more of themilk an infant receives the more likely it is to developrickets. Much in their paper is unsupported asser-tion ; they state, for instance, that an infant of sixmonths, receiving a quart of milk, is more likely todevelop rickets than one of the same age receivinga pint, but they bring no figures in support of thestatement, nor do they dispose of the objection thatan infant of six months, receiving only a pint ofmilk would be under-caloried. Rickets is a diseasewhich requires active growth, in order to show itselfin a florid form, and growth is unlikely to be activeif the supply of calories is much too low. As todetails, Hess and Weinstock start with the premissthat human milk is more preventive of rickets in thehuman infant than is cow’s milk, because they havefound that in new York, in March, all bottle-fedinfants, unless they have received some specialspecific therapy, are suffering from some degree ofrickets. Only one-half to two-thirds of the breast-fedinfants are found to suffer in this way. Hess andWeinstock, therefore, set out to discover whetherthe difference is due to the superiority of human milkin the antirachitic factor. When they tested the eantirachitic value of cow’s milk and of humanmilk on rats, they found that 20-25 c.cm. of the formerwere needed to prevent rickets, while 25-30 c.cm. ofhuman milk were needed. This result showed thatthe human milk tested was of very poor antirachiticpotency for rats, whereas Hess and Weinstock make

1 Med. Res. Council Special Report Series No. 93.2 Proc. Phys. Soc.. Jour. Physiol., 1926, lxi.

3 Jour. of Hygiene, 1927, xxvi.. 437.4 Amer. Jour. Dis. Child., 1927, xxxiv., 845

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the assertion that breast milk is of high antirachiticpotency for infants. They therefore conclude that" the high protective value of human milk in infantilerickets cannot be ascribed to its content of the anti-rachitic factor." If it were due to abundance ofthe antirachitic factor, they argue, rickets wouldhave been prevented in rats, in a smaller dosagethan that found necessary. When they made

experiments on rats with the cream of cow’s milk,they got into yet more difficulty. They used 20 percent. cream and top-third milk, but they did notget as good results with the top milk as with thecream, although the doses of fat given were supposedto be identical. From this slender piece of evidenceHess and Weinstock conclude that there is an actualrachitogenic factor in the skim fraction of the topmilk, which offsets the antirachitic value of thecream contained in it, and presumably accountsfor the inferiority of cow’s milk to human milk forthe prevention of rickets in human infants. The

animal experiments are very few in number, and ifsuch an important conclusion was to be drawn fromthem it would have been advisable to supply actualestimates, showing that the same amount of fat wasgiven to both sets of rats.The conclusions which Hess and Weinstock draw

may be correct, but evidence is lacking that theirwhole premiss, that human milk is so much superior,is not false. They tell us that all the infants oncow’s milk and a large proportion of those on breastmilk get rickets. Some breast milk is thereforesuperior to cow’s milk as an antirachitic for infants,but some from their own admission, is not. Clinicalevidence should certainly have been included to showthat the breast milk tested on rats was derived fromthe mothers of non-rachitic infants, and not from themothers of rachitic ones, who admittedly existed inthe community in large numbers. Hess is too wellknown a pediatrician for this communication to bedisregarded, but the reasoning is difficult to follow,and some of the necessary data have not beenpublished. The evidence offered is certainly notsufficient at present to warrant the inclusion of milkamong the substances which contain a positiverachitogenic factor, but evidence seems to be accumu-lating that cereals do contain such a factor.

NORMAL VARIATIONS IN THE CEREBRO-SPINAL

FLUID.

IT must be admitted that the examination of

cerebro-spinal fluid is often disappointing. Thepathologist feels that he should be able to do morewith what has been so hardly won ; was not the firstclinical sample obtained by laminectomy ? The

specific changes are rather few, and if -%ve agree thatthe fluid varies within the limits normally stated,many organic lesions of the central nervous systemseem to leave it unaffected by their presence, andtherefore of but little use in diagnosis. Greaterprecision is desirable if possible, and Dr. Axel Neel’ zhas therefore done a service in analysing 6000 succes-sive cases in which the C.S.F. was examined. Hefinds-and most pathologists will agree with him-that the normal maximal number of cells per cubicmillimetre is not, as conventionally stated, five, butis in fact not more than one. Moreover, his 800normal cases never showed a total albumin value(as estimated by the Brandberg-Stolnikow-Bisgaardmethod) exceeding seven, and it rarely exceeded six.In order to count cells with such accuracy, a chamberof exceptional depth and area is necessary to obviateerrors of multiplication. Dr. Neel claims that he was unaware of the clinical diagnosis until after the examination of the fluid ; but he was, perhaps, alittle fortunate in never coming across those specksof dust, epithelial cells, or even red blood cells, or

blood leucocytes from needle trauma which worryother pathologists, and might have ruined his series. He finds the gold-sol test of no differential value I

1 Münch. med. Woch., April 27th,

here again most observers will agree with him.Pandy’s test, in which C.S.F. is dropped into saturatedaqueous phenol, he regards as the most reliablecrude test for excess globulin. He rightly insists thatmuch useful information may be lost by failing to doaccurate counts and accurate albumin estimations.Particularly is this true in the differential diagnosisbetween hysteria and organic lesions of the centralnervous system. It is remarkable what a large pro-portion of syphilitic patients without clinical nervouslesions fall just outside normal values both in cellcount and albumin content. Of late there has beena tendency among physicians to demand quantita-tive instead of qualitative estimations of C.S.F., andthere is no great difficulty in meeting the demand.There is, however, no Fuchs-Rosenthal countingchamber. of adequate dimensions on the Englishmarket at present. Dr. Neel’s chamber has doublethe usual volume.

____

IMPACTION OF THE WISDOM TOOTH.

I THE reason why the third molar tooth is so aptto lead to trouble in the lower jaw is that the mandibleis rarely large enough to accommodate this tootheven when it is normally situated, and the lack ofroom leads frequently to its misplacement. When

the eruptive impulse results in impaction againstthe tooth in front, infection in the bone and softtissues is likely to ensue, and the position of the toothfavours the spread of such infection along cellularplanes backwards, downwards and upwards, intodangerous areas. The lay public is so readyto attribute any pain or swelling of the upper orlower jaw in adult life to a wisdom tooth, however,that practitioners are apt, after glancing into anapparently normal mouth, to search for less obvioussources of pressure or inflammation. In the lowerjaw especially, however, attempted eruption of thethird lower molar can give rise to most unpleasantresults, and superficial inspection without a radiogramis not sufficient to exclude its presence in an abnormalor impacted situation. The dangers of neglect totake a radiogram are exemplified by two cases

recently described by E. Polloson and M. Dechaumein the Presse Médicale.1 The first case was that ofa girl of 18, who had a large swelling at the angle ofthe jaw accompanied with much pain. The con-

dition had existed for over a year. There was nohistory of inflammation and the growth, at first soft,had become progressively harder. A surgeon diag-nosed a periosteal sarcoma of the mandible; heoperated and removed a large mass of fibrous tisssuewhich, when examined microscopically, showed nosigns of malignancy. The wound healed well, butthe swelling soon returned, increased in size andinvaded the mouth, leading to trismus. Radium wasapplied intrabuccally but with no result beyondthat of causing ulceration of the mucosa followed bythe establishment of a discharging sinus at the baseof the coronoid process. The surgeon advised a

further operation of a more extensive character,but, fortunately for the patient, at this stage a

radiogram was taken. The alveolar plates of themandible were seen to be expanded and lying betweenthem was a deformed, unerupted third molar. In themaxilla, on the same side, both the second and thirdmolars were misplaced, so that normal eruption wasimpossible. It was evident that the swelling andtrismus were due to infection round these teeth.The patient came under the care of Prof. Tixier, whooperated and with much difficulty removed theimpacted teeth. The trismus and swelling speedilysubsided, though some permanent deformity remained.The second case recorded was equally instructive.A woman of 58 had suffered from excruciating attacksof facial neuralgia on the left side for over 20 years.The slightest draught brought on an attack and thepatient spent most of her time in bed in a warm

atmosphere. In 1924 the neuralgia became more1 A propos des accidents graves liés a l’éruption vicieuses de

la Dent de Sagesse, Presse Médicale, April 11th.