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49 dose of nicotinic acid can be reduced to 500 mg. given in divided doses. Later the oral administration -of 25 mg. thrice daily should suffice for maintenance. If there are signs of peripheral neuropathy, and perhaps if there are not, thiamin should be given as well ; an amount equal to one-tenth the nicotinic acid is a convenient dose. Dr. H. M. SINCLAIR (Oxford) discussed those-peripheral neuropathies which are believed to be caused by nutri- tional deficiency, and said that at least four vitamins had been incriminated : A, E, BI and riboflavin. Mellanby first showed 16 years ago that degeneration of nerves in the central and peripheral systems was caused by deficiency of vitamin A in animals. Later it was suggested that such deficiency in man might produce nerve degeneration, and therefore such condi- tions as xerosis conjunctivas, night blindness, retrobulbar neuritis; neuritis of beriberi, and subacute combined degeneration of the cord. The belief that the epithelial metaplasia of vitamin-A deficiency is due to nerve degeneration has now been disproved by Sauer. Hart showed that bony overgrowth in animals in vitamin-A deficiency could cause blindness, and Mellanby that it could also produce deafness. This bony overgrowth has recently been studied by Wolbach and Bessey, who have concluded that vitamin-A deficiency causes skeletal growth to stop but that the central nervous system and other soft tissue continue to grow ; they believe therefore that the nervous lesions of vitamin-A deficiency are wholly mechanical in origin. Evans and others showed that deficiency of vitamin E in animals caused degeneration in muscle and later other authors suggested that nerve degeneration was also produced. This led Bicknell and Wechsler independently to test, upon various neuromuscular disorders, vitamin E with or without the vitamin-B complex. Encouraging or disappointing results have been obtained by many clinicians in the last two years, and the weight of evidence is now strongly against vitamin E having any beneficial effect on such disorders ; in fact the four papers in which estimations of creatine or creatinine in urine have been done have all shown no effect of such therapy on this biochemical disorder. The most important vitamin from the point of view of peripheral neuritis is vitamin Bl. Much of the early work on deficiency of this vitamin in animals is untrustworthy because the effects of in- anition or deficiencies of other vitamins were not properly controlled. Recently several groups of workers in America have studied the histological changes in vitamin- B, deficiency with great care. For instance, Swank has shown that in pigeons acute deficiency produces opisthotonos with- only a few or no. degenerating fibres in peripheral nerves or the central nervous system ; on the other hand, chronic deficiency produces first locomotor ataxia due to proprioceptive loss, and then leg weakness with degeneration of peripheral nerves. The axon is first involved at its most distant point, degeneration progresses centrally and the myelin sheath degenerates later ; the largest fibres are affected first, and the smallest are usually untouched. Swank believes that the heemorrhages found in the lower parts of the brain are secondary to degenerative changes in the neurones surrounding blood-vessels and are caused by accumulation of acid metabolites. Since, according to Walshe and to Vedder, polyneuritis gallinarum is analogous to human beriberi, it is legitimate to apply these results obtained on animals cautiously to man. Unfortunately there is little clear-cut evidence of the r6le of vitamin BI in human multiple symmetrical neuritis, partly because a diet is unlikely to be deficient only in vitamin Bi, and partly because vitamin B1 stimulates appetite and therefore it is difficult to be sure that therapy has been confined to that one vitamin alone. In recent experiments in which human volun- teers have been placed upon diets deficient in vitamin Bl, neurasthenia but not neuritis has been produced ; it is probable from animal work that such experiments have not been sufficiently chronic. One of the most satisfactory methods of assessing deficiency is to estimate vitamin BI or its phosphorylated form (cocarboxylase) in blood, and results of these estimations obtained in Oxford were communicated to the Neurological Congress just before war broke out. It seems likely that nutri- tional, alcoholic ’and gastrogenous polyneuritis are accompanied by deficiency of vitamin Bi, and that the same is true of some cases of diabetic and of gestational polyneuritis. The neuritis that may accompany dosage with some sulphanilamide derivatives seems to be closely associated with conditioned deficiency of vitamin B1; but diphtheritic, arsenical and other toxic forms have no direct relation. - However, just’ as deficiency of vitamin BI produces neuritis by interfering with the utilisation of pyruvate in, neurones, so many of the toxic forms may be produced by a similar biochemical lesion ; arsenic, for instance, is known to interfere with the oxidation of carbohydrate in a similar way to defici- ency of vitamin B,. But other important factors may come into the picture : for instance, arsenic and alcohol interfere with the conversion in the liver of vitamin Bi to its coenzyme form. During the siege of Madrid some neuromuscular conditions arose from malnutrition, and Grande classified these in five groups: paraesthesise; paraesthesiae with causalgia; retrobulbar optic neuritis ; funicular myelopathy; and cochlear neuritis. These syndromes were often accompanied by the skin manifesta- tions of pellagra. The diet however was not especially low in vitamin-Bl> and biochemical evidence from the utilisation of lactate indicated that there was no parti- cular vitamin BI deficiency. In fact Grande doubts whether vitamin BI played a part in any of these condi- tions, which however could be cured by giving yeast. There is no doubt that other as yet unidentified members of the B complex play a part in causing nerve degenera- tion ; the work of Moore, of Landor and Pallister, and of Wilkinson has shown the importance of this complex in the aetiology of retrobulbar neuritis. The most likely cause of this is deficiency of riboflavin. In the discussion the CHAIRMAN mentioned his observations on scurvy in the last war amongst Bulgar prisoners, and also suggested that attention should be paid to trace elements.-Dr. FBANEMN BICKNELL was unwilling to accept the biochemical evidence against the r6le of vitamin E in neuromuscular disorders, and Prof. E. J. BIGWOOD stressed the importance of multiple vitamin deficiencies.—Dr. HUGH STANNUS thought the encephalopathic states described by Dr. Syden- stricker were probably not uncommon in this country, and he again emphasised the variability of symptoms. Reviews of Books Post-Natal Development of the Human Cerebral Cortex Vol. II. Cortex of the one-month infant. J. LERoy CONEL, professor of anatomy, Boston University School of Medicine. London: Humphrey Milford, Oxford University Press. Pp. 144. 46s. 6d. THIS is the second monograph of a series designed to trace the postnatal development of the architecture and morphology of the neurones in the human cerebral cortex. The first volume, published in 1939, dealt with the cortex of the newborn infant. The present study is based on an examination of five normal brains obtained at the first month, using the same technical methods as before. Comparison with the newborn shows a slight gain in the total depth of the cortex in most parts of the cerebrum, affecting the deeper laminse rather than the superficial. Definitely formed Mssl bodies and neurofibrils are restricted to the giant pyramidal cells of the precentral gyrus at this time, being best seen in the hand region. There is little gain in development in the occipital lobe. Among the primary receptive areas the somaesthetic is by all criteria more advanced than the visual, acoustic or hippocampal areas. Such observations have an evident bearing on changes in behaviour of the growing infant, and it will be interesting to see how neuronal development shapes towards the twelfth and eighteenth months. Histological criteria leave open the question of function, but the observation of J. R. Smith that the electro- encephalogram records the first appearance of waves at the age of one month seems to agree with the present evidence on the initiation of mature stages in the neurones at this age. The work is superbly illustrated with 108 plates of camera-lucida drawings of Cox- Golgi preparations as well as macrophotographs and low-power microphotographs.
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49

dose of nicotinic acid can be reduced to 500 mg. givenin divided doses. Later the oral administration -of25 mg. thrice daily should suffice for maintenance.If there are signs of peripheral neuropathy, and perhapsif there are not, thiamin should be given as well ; anamount equal to one-tenth the nicotinic acid is a

convenient dose.Dr. H. M. SINCLAIR (Oxford) discussed those-peripheral

neuropathies which are believed to be caused by nutri-tional deficiency, and said that at least four vitaminshad been incriminated : A, E, BI and riboflavin.Mellanby first showed 16 years ago that degenerationof nerves in the central and peripheral systems wascaused by deficiency of vitamin A in animals. Laterit was suggested that such deficiency in man mightproduce nerve degeneration, and therefore such condi-tions as xerosis conjunctivas, night blindness, retrobulbarneuritis; neuritis of beriberi, and subacute combineddegeneration of the cord. The belief that the epithelialmetaplasia of vitamin-A deficiency is due to nervedegeneration has now been disproved by Sauer. Hartshowed that bony overgrowth in animals in vitamin-Adeficiency could cause blindness, and Mellanby that itcould also produce deafness. This bony overgrowthhas recently been studied by Wolbach and Bessey,who have concluded that vitamin-A deficiency causesskeletal growth to stop but that the central nervoussystem and other soft tissue continue to grow ; theybelieve therefore that the nervous lesions of vitamin-Adeficiency are wholly mechanical in origin. Evans andothers showed that deficiency of vitamin E in animalscaused degeneration in muscle and later other authorssuggested that nerve degeneration was also produced.This led Bicknell and Wechsler independently to test,upon various neuromuscular disorders, vitamin E withor without the vitamin-B complex. Encouraging ordisappointing results have been obtained by manyclinicians in the last two years, and the weight of evidenceis now strongly against vitamin E having any beneficialeffect on such disorders ; in fact the four papers in whichestimations of creatine or creatinine in urine have beendone have all shown no effect of such therapy on thisbiochemical disorder. The most important vitaminfrom the point of view of peripheral neuritis is vitaminBl. Much of the early work on deficiency of this vitaminin animals is untrustworthy because the effects of in-anition or deficiencies of other vitamins were not properlycontrolled. Recently several groups of workers inAmerica have studied the histological changes in vitamin-B, deficiency with great care. For instance, Swankhas shown that in pigeons acute deficiency producesopisthotonos with- only a few or no. degenerating fibresin peripheral nerves or the central nervous system ;on the other hand, chronic deficiency produces firstlocomotor ataxia due to proprioceptive loss, and thenleg weakness with degeneration of peripheral nerves.The axon is first involved at its most distant point,degeneration progresses centrally and the myelinsheath degenerates later ; the largest fibres are affectedfirst, and the smallest are usually untouched. Swankbelieves that the heemorrhages found in the lower partsof the brain are secondary to degenerative changes inthe neurones surrounding blood-vessels and are causedby accumulation of acid metabolites. Since, accordingto Walshe and to Vedder, polyneuritis gallinarum isanalogous to human beriberi, it is legitimate to applythese results obtained on animals cautiously to man.Unfortunately there is little clear-cut evidence of ther6le of vitamin BI in human multiple symmetricalneuritis, partly because a diet is unlikely to be deficientonly in vitamin Bi, and partly because vitamin B1stimulates appetite and therefore it is difficult to besure that therapy has been confined to that one vitaminalone. In recent experiments in which human volun-teers have been placed upon diets deficient in vitaminBl, neurasthenia but not neuritis has been produced ;it is probable from animal work that such experimentshave not been sufficiently chronic. One of the mostsatisfactory methods of assessing deficiency is to estimatevitamin BI or its phosphorylated form (cocarboxylase)in blood, and results of these estimations obtained inOxford were communicated to the Neurological Congressjust before war broke out. It seems likely that nutri-tional, alcoholic ’and gastrogenous polyneuritis are

accompanied by deficiency of vitamin Bi, and that thesame is true of some cases of diabetic and of gestationalpolyneuritis. The neuritis that may accompany dosagewith some sulphanilamide derivatives seems to be closelyassociated with conditioned deficiency of vitamin B1;but diphtheritic, arsenical and other toxic forms haveno direct relation. - However, just’ as deficiency ofvitamin BI produces neuritis by interfering with theutilisation of pyruvate in, neurones, so many of thetoxic forms may be produced by a similar biochemicallesion ; arsenic, for instance, is known to interfere withthe oxidation of carbohydrate in a similar way to defici-ency of vitamin B,. But other important factors maycome into the picture : for instance, arsenic and alcoholinterfere with the conversion in the liver of vitaminBi to its coenzyme form. During the siege of Madridsome neuromuscular conditions arose from malnutrition,and Grande classified these in five groups: paraesthesise;paraesthesiae with causalgia; retrobulbar optic neuritis ;funicular myelopathy; and cochlear neuritis. Thesesyndromes were often accompanied by the skin manifesta-tions of pellagra. The diet however was not especiallylow in vitamin-Bl> and biochemical evidence from theutilisation of lactate indicated that there was no parti-cular vitamin BI deficiency. In fact Grande doubtswhether vitamin BI played a part in any of these condi-tions, which however could be cured by giving yeast.There is no doubt that other as yet unidentified membersof the B complex play a part in causing nerve degenera-tion ; the work of Moore, of Landor and Pallister, andof Wilkinson has shown the importance of this complexin the aetiology of retrobulbar neuritis. The most likelycause of this is deficiency of riboflavin.

In the discussion the CHAIRMAN mentioned hisobservations on scurvy in the last war amongst Bulgarprisoners, and also suggested that attention should bepaid to trace elements.-Dr. FBANEMN BICKNELL wasunwilling to accept the biochemical evidence againstthe r6le of vitamin E in neuromuscular disorders, andProf. E. J. BIGWOOD stressed the importance of multiplevitamin deficiencies.—Dr. HUGH STANNUS thoughtthe encephalopathic states described by Dr. Syden-stricker were probably not uncommon in this country,and he again emphasised the variability of symptoms.

Reviews of Books

Post-Natal Development of the Human Cerebral CortexVol. II. Cortex of the one-month infant. J. LERoyCONEL, professor of anatomy, Boston University School ofMedicine. London: Humphrey Milford, Oxford UniversityPress. Pp. 144. 46s. 6d.

THIS is the second monograph of a series designed totrace the postnatal development of the architecture andmorphology of the neurones in the human cerebralcortex. The first volume, published in 1939, dealtwith the cortex of the newborn infant. The presentstudy is based on an examination of five normal brainsobtained at the first month, using the same technicalmethods as before. Comparison with the newbornshows a slight gain in the total depth of the cortex inmost parts of the cerebrum, affecting the deeper laminserather than the superficial. Definitely formed Msslbodies and neurofibrils are restricted to the giantpyramidal cells of the precentral gyrus at this time,being best seen in the hand region. There is little gainin development in the occipital lobe. Among theprimary receptive areas the somaesthetic is by allcriteria more advanced than the visual, acoustic orhippocampal areas. Such observations have an evidentbearing on changes in behaviour of the growing infant,and it will be interesting to see how neuronal developmentshapes towards the twelfth and eighteenth months.Histological criteria leave open the question of function,but the observation of J. R. Smith that the electro-encephalogram records the first appearance of wavesat the age of one month seems to agree with the presentevidence on the initiation of mature stages in theneurones at this age. The work is superbly illustratedwith 108 plates of camera-lucida drawings of Cox-Golgi preparations as well as macrophotographs andlow-power microphotographs.

50

British Encyclopaedia of Medical Practice ,

Surveys and Abstracts 1941-42 ; cumulative supplement1941-42. Editor: Sir Humphry Rolleston, Bt., MDCamb., FRCP. London: Butterworth and Co. Pp. 432and 289. 32s. 6d./ together.OF these two supplements one contains critical

reviews of medical progress and abstracts of currentmedical periodicals all over the world ; the other bringsthe’ original volumes up to date with a cumulativeselection of new material. In this way each annualsupplement replaces the one before it ; the latestsupplement, read alongside original articles justpublished, is intended to provide a complete descriptionof each disease as understood today. This intention isexcellent and on the whole well fulfilled. Subjects receivenotice in proportion to the advances made in theirstudy so that it is not surprising to find much abouttropical diseases, malaria, leprosy, amcebiasis andcholera, and never a word on migraine, constipation orsciatica; and little new knowledge has been foundworthy of note under the heading of cancer, comparedwith the facts lately accumulated about poison gases,drug addiction and blood transfusion. The criticalsurvey of general medicine has been written by Prof.W. E. Hume, that of general surgery by Prof. G. GreyTurner. Effort syndrome receives special attention andDr. William Evans in a chapter on cardiovasculardisease again stresses the importance of X-ray examina-tion ; he is convinced that cardioscopy is the surestmeans of discovering or confirming the presence of anearly mitral lesion. Sir Arthur Hurst describes giardialinfections, colovesical fistula in diverticulitis and thepathogenesis of the sprue syndrome. In surgery,shock and compression and blast injuries receive themost attention. Dr. F. A. Knott admits that shock isnot a readily recognisable clinical entity, but gives astimulating review of blood transfusion in its treatment.Sir Harold Whittingham surveys- aviation medicine andDr. W. Gunn summarises acute infection. Col. L. W.Harrison’s account of venereal diseases is particularlyfull and instructive. But the surveys in part i do notoffer anything of such outstanding importance as theaccount in part 11 of the sulphonamides and recentdevelopments in drug therapy by Prof. W. J. Dilling.In the next edition penicillin will presumably occupymore than the single page allotted to it here, thougheven this brief résumé will whet the appetite. In part ain abstracts of published work fill over 300 pages ofclose print; they are arranged in alphabetical order andwell indexed.

Food and Beverage Analyses(2nd ed.) M. A. BmiDOES, MD, FACP ; M. R. MATTICE, MS.London : Henry Kimpton. Pp. 344. 208.

The authors of this book have set themselves " toprovide analytical data, on the largest possible numberof food factors " but no figures seem to have been includedfor characteristically Chinese, Indian, Malayan or Africanfoods, many of which are available. Actually the authorshave limited themselves to European and particularlyAmerican foodstuffs. Even this, however, was a Hercu-lean task and published work has been closely scrutinised,full weight being accorded to British and Continentalauthorities. For many of the proprietary foods theauthors have relied upon the makers’ data, though theyhave analysed ’a few themselves ; nevertheless the bookis essentially a compilation and its scope may be gaugedfrom the fact that the protein, fat, carbohydrate andcalories of 97 cheeses are given in table 17, and the sametable opens with: abalone, abalone canned, acido-philus milk com., agar-agar, ale yeast, dried, alewives,alfalfa bread, algae, Hawaiian (Limu eleele, Limu lipoa),alimentary pastes, and so on. Data for availablecarbohydrate, fibre, purines, minerals (including bromine,iodine and sulphur), acidity in terms of pH, organicacids and metabolic reaction have all received fullconsideration and the vitamins are strongly represented.From the English point of view, the arrangement of themain table of protein, fat and carbohydrate valuesis unfortunate for the figures are not given per oz. oreven per 100 g., but per portion and this portion is of

course a variable quantity. The authors give thearguments for this method of presentation, but it is

t. difficult to see why they were swayed by them. The) opening chapters on the proteins, fats and carbohydrates2 are general, elementary and rather misleading. Thus.

the chapter on the -carbohydrates closes with the state-L

ment that " Bananas, chestnuts, and potatoes are parti-cularly rich in starch." But what about biscuits, bread

j and rice ? The wealth of data contained in the book3 is really extraordinary, however, and no doubt it will

have its uses.

i Dermatologic Therapy in General PracticeL (2nd ed.) MARION B. SULZBERGER, MD ; JACK WOLF, MD.

Chicago : Year Book Publishers ; London : H. K. Lewis.Pp. 632. 3 ps.IF the title of this work implies that it deals entirely

with the treatment of skin diseases, it is misleading, formost of the diseases are described in full and one of thebest features of the book is the space given to differentialdiagnosis. Even if, as the authors insist, diagnosis isof first importance in skin disease, treatment based onthe form of the lesion may be tried, and often helps toalleviate symptoms pending a definite diagnosis. Minutedetails of therapeutic procedure have been given and thework is crammed with useful hints and tips. The practi-tioner is advised to use few local remedies-say eight-and to understand their proper application thoroughly :this is golden advice. It should be a rule never to changea remedy if the case is progressing favourably, and totell a patient how to apply local therapy is not enough-he must be shown. If the library of the family doctorwere to be restricted to- one book on skins, this volumewould be a safe choice.

Antenatal and Postnatal Care

(4th ed.) FRANCIS J. -BROw, MD, DSe Aberd, FRCSE,FRCOG. London : J. and A. Churchill. Pp. 592. 24s.

THIS comprehensive work on antenatal care hasbecome a popular standard textbook for MB, MD andMRCOG examinations, as well as a stand-by for registrarsand first assistants. Every general practitioner whodoes obstetrics will find it useful. The fourth editionhas been completely revised, and obsolete or unnecessarymatter eliminated. Most of the new work in it relatesto recent advances in the- physiology and pathology ofthe togaemias and hyperemesis, the treatment of habitualabortion by endocrine therapy and the use of radiologyin obstetric diagnosis and prognosis, with special referenceto pelvimetry and cephalometry. The chapters on thediseases and disorders of the various systems in pregnancyare comprehensive and lucid. No-one has done morethan Professor Browne to preach the gospel of improvedantenatal care or its effect on reducing maternalmortality, and foetal and neonatal morbidity.

Myself, My Thinking, My ThoughtsK. W. MONSARRAT, FRCSE. Liverpool and London:University Press of Liverpool. Pp. 140. 78. 6d.

PSYCHOLOGY, says Mr. Monsarrat, is the title that isgiven to what is said about " thinking " and " knowing."It is because psychology could be thus defined until ahundred years ago that it came so much closer to meta-physics-and to an arid epistemology than to the studyof human beings as we know them in their daily lives.Mr. Monsarrat’s thoughtful treatise is written in a greatscholarly tradition, but it has little value for the psy-chologist and the physician, impatient of psychologicalstudies that do not help them directly to understandhuman conduct. There is a fundamental issue dividingMr. Monsarrat’s approach from that of current psycho-logical schools. Taking the Cartesian anirmation as hisstarting-point he examines his habits of thought minutely,chiefly by the methods of introspection and analogy.His style is fine and candid, as all good philosophicalwriting should be. In the first part dealing with" thinking," chapters are devoted to ideas, rememberingand reasoning, images, and the problem of the relation-ship of energy to mind. In the second part Mr. Mon-sarrat aims at a general and consistent conception ofthe world and its troublesome affairs.


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