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Springer, Ninfa ralurninoNutrition and Mental Retardation. An tnnotateclBibliography, 10611-1970.Michigan Univ., Erin 7rbor. Inst. for the Sturlv ofMental Retardation.70f-In.

Institute for the Study of :40.tal Retardation,University of Michigan, 611 Church Street, AnnArbor, Michigan 4R104. (S1.D0 per copy)

FOPS Price `fir -S0. Fs hC-3 1.29*Annotated Bibliograrhies, Health Fducation,*Mentally Handicapped, *Mental Retardation,*Nutrition, *Nutrition Instruction

APSTRACTThis annotated bibliography is primarily orgati7ed

for nutritionists. It presents selected articles published from 1°r4to the present. All aspects of nutrition in mental retardation arecovered excenting inborn errors of metabolism. Sections are includedon (1) nutrition, birthweicht, and mental retardation; (2)

nutrition, growth, and mental retardation: (4) malnutrition: and itseffects on nervous system development; (4) nutrient metabolism andmental retardation; and (r) techniques in feeling and therapeuticnutrition for the mentally letardel. (T11

an annotated bibliography

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NUTRITION AND MENTAL RETARDATION

AN ANNOTATED BIBLIOGRAPHY1964 - 1970

NW. Saturnino Springer, Ph.O., Program Director for NutritionInstitute for the Study of Mertal Retardation

The University of Michigan

For sale by the institute for the Study of Mental Retardation

the University of Michigan, 611 Church Street, Mn Arbor.

Michigan 4810 - Price ovie dollar

3

CONTENTS

(ReferencePREFACE

Number)

1 - 11

12 - 14

35 - 55

GENERAL

NUTRITION, DIRTHWEIGHT, AND MENTAL RETARDATION

NUTRITION, GROWTH AND MENTAL RETARDATION

MALNUTRITION AND ITS EFFECTS ON NERVOUS SYSTEM DEVELOPMENT

NUTRIENT DEFICIENCY

Multiple Deficiencies in Humans 56 - 110

Multiple Deficiencies in Animals 111 - 168

Vitamin and Mineral Deficiencies

Thiamine 169 - 181

Folic Acid and Vitamin a12

182 - 1;)

Other Vitamins 200 - 210

Minerals 211 - 215

NUTRIENT INTOXICATION 216 - 232

NUTRIENT METABOLISM AND MENTAL RETARDATION

CARBOHYDRATES AND PROTEIN 233 262

VITAMINS, MINERALS, AND WATER 263 - 276

NUTRIENT METABOLISM IN DOWN'S SYNDROME 277 - 287

TECHNIQUES IN ruci4t AND THERAPEUTIC NUTRITION FORTHE MENTALLY RETARDED 288 - 333

PREFACE

This Annotated Bibliography on Nutrition and Mental Retardation has beenprepared and organized primarily for nutritionists. It is intended as an in-troduction for nutritionists specializing in mental retardation, and as a sourceof research topics. This does not, however, preclude its use by professionalsfrom other disciplines who wish information on the significance of nutrition Inthe field of mental retardation.

The Annotated Bibliography presents selected articles published from 1954to the present. The selections cover all aspects of nutrition in mental re-tardation excepting inborn errors of metabolism. References on inborn errorsof metabolism have been excluded from this bibliography since reports on thistopic alone would constitute a separate volume.

The first section, GENERAL, contains articles explaining the role of thenutritionist in facilities serving the mentally retarded. In addition, it in-cludes articles dealing ith the broad problem of malnutrition. The secondsection, NUTRITION, BIRTHWEIGHT, AND MENTAL RETARDATION, emphasizes the impor-tance of nutrition in achieving normal weight at birth, and cites reportswhich implicate prematurity or low birthweight as a possible cause of mentalretardation. The section on NUTRITION GROWTH AND MENTAL RETARDATION includesreports on the physical growth and other anthropometrit measurements of thementally retarded. The fourth section, MALNUTRITION AND 11$ EFFECT ON NERVOUSSYSTEM DEVELOPMENT, offers voluminous references reflecting the growing inter-est on this topic. Malnutrition may result from a deficiency or an excessiveintake of nutrients. The section has, therefore, been divided into NUTRIENTDEFICIENCY and NUTRIENT INTOXICATION. The tomer is divided into three sub-headings. The subheading Multiple Deficiencies in Humans includes studiesshaking the effects of malnutrition on the rental development of children axialso contains reviews of studies dealing both with humans and with animals.On the other hand, Multiple Deficiencies in Animals deals strictly with Stu-dies on an experimental basis. Vitamin and Mineral Deficiencies have f6therbeen subdivided for specific vitamins whenever the number of references issufficient to justify a separate section. It incorporates studies on bothhumans and animals. NUTRIENT INTOXICATION underscores the teratogenic effectsof excessive intakes of certain n.arlents. The section on NUTRIENT METABOLISMIN MENTAL RETARDATION contains few references on protein and vitamin metabol-ITT,. Those on carbohydrate metabolism stress risk factors involved in dia-betes and hypoglycemia. VITAMINS, MINERALS AND WATER deals with the problemof electrolyte balance and the possibility of brain damage due to hypereatre-mia during infancy. A separate subsection on NUT TENT METABOLISM IN DOWN'SSYNDROME Is given because of the number of reports published on this topic.References published prior to 1964 are included it the section TECHNIQUES INFEEDING AND THERAPEUTIC NUTRITION FOR THE T4NTALLY RETARDED due to the growinginterest in this topic by nutritionists working In the clinical setting. In-

5

eluded also are references that make use of nutrient modification of the dietIn the treatment of epilepsy and other conditions associated with mental retar-dation. Also included are articles which Indicate successful nutrient supple-mentation of diets for the mentally retarded.

Grateful acknowledgement is due Barbara Davis and Robert Thompson fortheir technical assistance and above all to Margaret Joseph for her invaluableeditorial skills and perseverance which made possible the completion of thisproject.

This publication was supported in part by grant number 923 from the Maternaland Child Health Service of the Health Services and Mental Health Administration.

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June, 1970

GENERAL

AMERICAN ACADEMY OF PEDIATRICS, COM-MITTEE ON INTERNATIONAL CHILDHEALTH. Malnutrition in the

World's Children. Pediatrics, 4,1(1)031, 1969.

The article discusses the extentand occurrence of protein-caloriemalnutrition in the world's chil-dren and makes recommendations forUnited States assistance in solvingthis problem. (1)

BERG, A.D. Malnutrition and Nation-al Development. Foreign Affairs,46(1):126, 1967.

The economic costs of the physicaland mental retardation caused bymalnutrition, and their effects onnational economics are discussed.Research and programs for Increas-ing the world'a protein supply aredescribed. The need for an inter-disciplinary approach to the malnu-trition problems is emphasizel. (2)

CULLEY, W.J. Nutrition and MentalRetardation. IN: Carter, C.H.,ed. Medical Aspects of MentalRetardation. Springfield, Illin-ois, 88, 1965.

A review of the nutritional aspectsof mental retardation: effect ofprotein, calorie and vitamin defic-iencies on mental development; andthe nutritional problems of the men-tally retarded child. (3)

M1LL1E, H.M. and REEVES, M. TheBattle Against Mental Retarda-tion: file Dietitian's frarr.Hospitals 38:101, 1914.

A description of the role of thedietitian in the infant and matern-lty care team is given. (4)

JOURNAL OF TROPICAL PEDIATRICS, 14

(3):149, 1968. Nutrition In Ma-,ternal and Child Health (WithIlecial Reference to the Western)'aCl/TC).

The monograph reviews nutrient defi-ciencies; infant and maternal feed-ing practices; and suggested im-provements, as they exist in theWestern Pacific. A guide for thetreatment of malnourished children,plus recipes, based on South Pacificfoods, for ififants, toddlers,school children and populations ingeneral is included. Sugge.-;Ions fornutrition educatloa are given. (5)

LELAND, H. The Relationship Ue-tween "Intelligence" and MentalRetardation. American Journal ofMental Deficiency, 73:533, 1969.

The author points out the interrela-tionships between the biomedicaland social aspects of an crvinism;and the importance of a classifica-tion system oriented towards treat-ment of disorders. (6)

NUTRITION REVIEWS, 27:39, 1969. TimeEconomics of Malnutrition.

Discussion is given of economiccosts involved in malnutrition Inunderdeveloped countries. Halm,'tritIon leads to physical and men-tal impairments which lead to furthen economic costs. (7)

PHILLIPS, m.1;. Nutrition Opportun-,sties in Specialized HealthAreas. Journal of the AmericanDietetic Association, 54):3148,1969.

7

The article focuses on health pro-grams, funded by the Children's Bur-eau, to meet needs of low-incomefamilies. Health Services for Chil-dren and Youth Projects are descri-bed In addition to programs especi-ally for the mentally retarded andUniversity Affiliated Centers. Therole of nutrition within these pro-grams Is defined with an explana-tion of the functions of nutritionpersonnel; their academic experi-ence qualifications for positions;specialized training programs de-signed to prepare kdividuals forsuch positions; and sources of in-formation regarding establishedprograms. (8)

STEVENS, H.A. "....The Field is

kich...and Ready for Harvest..."American Journal of Mental Derr-clency, 70(1)14, I965.

A broad discussion on mental retar-dation Includes: possible Intellec-tual function of the mentally retar-ded; biomedical aspects; culturalfamilial mental retardation; educa-tional and social work problems;manpower needs; and evaluation ofprograms and services. (9)

THARD, J. Cultural Deprivationand Mental Handicap. Nursing Mirror, 1211t1j)10-, 1969.

A brief discussion is presented onthe effect of poor social and environmental conditions, including mal-nutrition, on the developing child.

(10)

UABARCER, 8. Role of the Nutrition-ist or Dietitian in Clinic Ser-vices for the Mentally Retarded.Mental Retardation, 3(5):25,1965.

The role of the nutritionist ordietitian is outlined. Included Isinformation on services performed,data collection, and nutritionalcounseling. (II)

NUTRITION DIRTHWEIGHTMENTAL RETARDATION

ABRAMOWICZ. M., and KASS, CM., Path-ogenesis and Prognosis of Prema-turity.. New England Journal ofMediclre, 275(19):1053, 1966.

Although perinatal death, cerebralpalsy, mental retardation, andother neurolocicel disorders occurmore frequently In infants of lowbirth weight (.c2500 gm), the effectof low birth weight has not beenestablished. Spastic symmetricalcerebral palsy is more common inprematures. Although reports ofthe association of rental retarda-tion with prematurity have been con-flicting, it does appear that a sig-nificant owner of very underweightinfants are mentally retarded andhave other abnormalities. (12)

BREWER, T., Human Pregnancy Nutri-tion: & Clinical View. Obstt.t-

rics and Gynecology, 31(4):605,1967.

Tie necessity of adequate pregnancynutrition is discussed and an ade-Cuate prenatal diet described. Whenmaternal nutrition is adequate, thefetal nutrition is more likely tobe adequate and prematurity ratesmay be lower. (13)

SWISH MEDICAL JOURNAL, 2(5406):401, 1964. low Pirth Weight and

ILLe.11ittat

1066 children weighing less than 4pounds at birth were admitted to 19premature baby units IA Britain be'twten October 1951 and June 1952and were followed. It was concludedthat if a premature baby escapesCongenital defects the intellectualdevelopment le normal, espec-tally if birthweight exceeds 3 lbs.

(14)

AND

BULLARD, D.M., Jr., GLASER, H.H.HEAGARTY, M.C., and PIVCHIK, E.C.Failure to Thrive in the "He lec-ted Child". American Journal ofOrthopsychlat.y, 37(4):680, 1967.

Feliure to thrive, of non-organiccauses, is discussed. Investiga-tions have noted parental neglectand vario.:s forms of maternal depri-vation in these children. The needfor direct observations of feedingpatterns and nutrient intake, andevaluation of the child and parentsin the home are discussed. (IS)

CYURCHILL, J.A., NEFF, J.W., andCALOWEIL, U.F. Girth Weight andIntelligence. Obstetrics and Gy-necology, 2fr3):245, 1966.

A study to determine the relation-ship between birth weight, intelli-gent), and social class. Signifi-cant reduction In Intelligenca oc-curred in low birth weight group;no effect of social class found.

(16)

CHURCHILL, J.A. The Relationship.Bet'ieen Intelligence and birth=wei ht in Twins. Neurology, 15t):341, 1965.

SO sets of twins were compared forthe relationship between birthwtightand WISC IQ. The lighter memberswere found to have lower IQ's. (In)

((MORO, S.M. Prevention of Prema-turity the Sine Qua Non for Re-duction in Mental Retardation andOther Neurologic Disorders. TheNew England Journal Of Medicine,271(0:243, 1964.

The identification of the high riskpatient followed by special care isnecessary to prevent prematurebirths and, thus, lower the perina-tal mortality rates. It was feltthis would also lower tie high mor-bidity and its accompanying mentaland physical injuries. Identifica-

tion of various high risk patientsIs discussed. (!8)

CREERY, R.D.G. The Infant of LowBirthweight. Nursing Mirror, 125(3):12, 1967.

Although the premature and the

"small for dates" infants are simi-lar In that both have low birth-weight, their management and prog-nosis are appreciably different. Re-cently it has become known thatonly about two-thirds of low birth-weight infants are premature. Therest are "small for dates" due tointra-uterine growth failure. Un-

less the diagnosis is in questionor the clinical condition is severe,the "small for dates" infant does

not have to be transferred to a spe-cial baby care unit. They usuallydo not have respiratory and centralnervous system problems; however,they do develop hypoglycemia and hy-pothermia and do warrant special

care. Early tube feeding is probab-ly indicated in many premature anddysmature infants. (19)

GORDON, H.H. Some Biological As-

pects of Premature Birth. IN:

Askin, J., Cooke, R., and Haller,J.A., Jr., eds. A Symposium on

the Child. Baltimore: Johns, Hop-kins Press, 233, 1967.

The use of rigidly scheduled feed-ing at 3 hour intervals for prema-ture Infants is questioned by dataon self-regulated feeding for 20

thriving premature infants. (20)

HARMELING, J.0., and JONES, M.B.

Birth Weights of High SchoolDropouts. American Journal ofOrthopsychiatry, 38:63, January,1968.

Study on all Negro population ofhigh schools in Gainesville, Flori-aa to determine if any significantdifference in birth weight existsbetween high school cl.'op-outs and

their classmates. The Diop-outs hadthe lowest average birthweight bysex and in total. The Slow Learnerswere in middle group, the Normalsin the highest birth weight cate-gory. (21)

HEIMAR, C.B., CUTLER, R., and FREED-MAN, A.M. Neurological Sequelaeof Premature Birth. AmericanJournal of Diseases In Children,108(2):122, 1964.

The incidence of neurological abnor-malities was observed in a group of319 prematurely born children in

the birth weight range of 775-2,100gm. Results indicated the highestincidence of neurological abnormal-ities was in the lowest birth weightgroup, that in the weight range un-der 1,250 gm. (22)

JACOBSON, H.N., REID, 0.E. A Pat-tern of Comprehensive Maternaland Child Care. The New EnglandJournal of Medicine, 271(6):302,1964.

Improved medical care for impover-

i:hed mothers and young children isnecessary to lower the prematurityrates and hence the mortality andmorbidity rates. A three fold pro-gram is outlined to help attainthis goal. (23)

10

KATZ, C.N., and TAYLOR, P.M. Theincidence of Low Birthweight inChildren with Severe Mental Re-tardation. American Journal ofDiseases of Children, 114(1):80,1967.

The incidence of low birthweight a-mong 573 institutionalized severementally retarded children was veryhigh and could not be accounted forsolely by socioeconomic factors.The cause of mental retardation wasunknown for 369 patients who weretermed the undifferentiated group.The incidence ,f birthweight below5.5 pounds was. 25 percent for thetotal mentally retarded populationand the undifferentiated group, ascompared to 7 percent for the gen-eral population. This study agreeswith othr,r studies that showed anassociation between prematurity andmental retardation. (24)

KING, L.S. Intrauterine Malnutri-tion. Journal of the AmericanMedical Association, 191(13):1077, 1965.

A discussion of the effects of in-trauterine malnutrition, outliningthe physical and mental subnormali-ties generally found. (25)

LESLIE, L. Prematurity as an Eti-ologic Factor in Cerebral Dyl:function. Archives of PhysicalMedicine and Rehabilitation, 47

(11):711, 1966.

In an attempt to understand the sig-nificance of prematurity, its inci-dence Is reviewed in both the nor-mal population and those having cer-ebral dysfunction. Various pre-na-tal and neonatal factors predis-posing the premature Infant to dis-turbances of the central nervoussystem are discussed; perhaps the

11

most Important correlate of prema-

turity is the neonate's susceptibility to trauma. Other anatomicand physiologic handicaps of the

premature infant are difficulties

in regulation of body temperature,respiratory immaturity, and suscep-tibility to infection, any of whichcould have an effect on the centralnervous system. (26)

LIGHT, I.J., BERRY, H.K., and SUTH-ERLAND, J.H. Amino Aciduria of

Prematurity. American Journal

of Diseases of Children, 112(3):229, 1966.

Aromatic amino acid metabolism ininfants born at the Cincinnati,Ohio General Hospital between Feb-

ruary 2 and July 20, 1965, weighingless than 2268 gm. were studied.

Vitamin C supplementation to theirdiet helped in controlling serum

tyrosine levels. (27)

NAYLOR, A., and MYRIANTHOPOULOS, N.The Relation of Ethnic and Sel-ected Socio-Economic Factors to

Human Birth Weight. Annals of

Human Genetics, 31(1):71, 1967.

Data from the Collaborative Studyon Cerebral Palsy, Mental Retarda-tion and Other Neurological and

Sensory Disorders of Infancy andChildhood were used to determine re-lationships of ethnic and selectedsocio-economic factors to human

birth weight. Foreign or rural

birth of the mother, presence of

the husband in the household, andlow density (number of persons per

room) have a positive effect onbirth weight in all 3 ethnic groups:Negro, Puerto Rican, and Caucasian.

(28)

RILEY, R.L., LANDWIRTH, J., KAPLAN,S.A., and GOLLIPP, P.J. Failureto Thrive: An Analysis of 83 Ca-ses. California Medicine, 108-

17:32, 1968.

Children with a diagnosis of fail-ure to thr;va from unknown causewere investigated. With 1/3 of theminadequate home environment was a

causative factor. Organic disease,low birth weight, congenital anoma-lies leading to feeding difficul-ties, and mental retardation wereother causes or influences on the

failure to thrive. Association be-tween mental retardation and poorgrowth are discussed. (29)

ROBOR, I.R., W., WU, P.Y.K. ,

METCOFF, J., VAUGHN, M.A. and

GABLER, M. Th. Effects of Earlyand Late Feeding of IntrauterineFetally Malnourished Infants.Pediatrics, 42(-271:16171568.

Observations suggest that early (4hour) feeding of infants with intra-uterine fetal malnourishment andbirth weights below 2,040 gm. mayenhance glucose hcceostasis in ear-ly neonatal life and prevent neona-tal symptomatic hypoglycemia. (30)

SINCLARI, J.C., and CALOIRON, J.S.Low Birth Weight and Post NatalPhysical Development. Develop-mental Medicine and Child Neur-ology, 11:314, 1969.

Some newborn infants of low birthweight tend to retain height andweight deficits. The prognosis forgrowth appears to be poorer for theterm infant with low birth weightthan for the preterm low birthweight infant. Cellular basis ofgrowth retarding influences are dis-cussed. (31)

12

SMALLP1ECE, V., and DAVIES, P.A. Im-mediate Feeding of Premature In-fants with Undiluted Breast Milk.Lancet, 2(7374):1349, 1964.

A series of 111 infants seen duringa period of 17 months in one hospi-tal was used as cases in a study todetermine the effects of early feed-ing In the possible control of hypo-glycemia and hyperbilirubinemia. Itwas concluded that early f4cdingwas Justified for the prevention ofhypoglycemia, hyperbilirubinemIa,and neurological damage. (32)

STRUTHERS, J.N.M., and KEAY, A.J.

Early or Late Feeding of Prema-ture Infants. Nursing Times, 61(47):1577, 1965.

Sixty-five rewborn infants weighingless than 4 1/2 pounds were studiedfor effects of early or late firstfeedings. There was a higher inci-dence cf signs of respiratory dis-tress syndrome and a higher biliru-bin level for late feeders. Vomit-

ing was more frequent for early

feeders. No significant differencein mortality was found. It was sug-gested by this study that early

feeding may have some advantageover delayed feeding. (33)

WALKER, J. Pregnancy and PerinatalAssociation with Mental tibrior-

FlaTit77-17T: Meade, and

F, A.S., eds. Genetic andEnvironmental Factors in HumanAbility. New York: Plenum Press,1966.

Risk pregnancies and perinatal fac-tors are discbssed in terms of

their association with mental sub-normality. In considering prematur-ity the general health and physiqueof the mother is more important

than the nature of the pregnancy.

Poor environmeots associated withpoor nutrition may lead to stuntedgrowth, poor obstetric performance,and low birth weight. 04)

I 3

NUTRITION, GROWTH, AND MENTAL RETARDATION

BAILIT, H.L., and IJHELAN, M.A. SomeFactors Related to Size and In-

telligence In An InstitutionalMentally Retarded Population.Journal of Pediatrics, 71(6):897,1967.

Anthropometric measurement of 77institutionalized mentally retardedcases, aged 6 to 25 years, showedthem to be smaller in every measure-ment than a control population. An-

thropometric measurements includedheight, head length, blacromial di-ameter, bi-iliac diameter, weight,sittinc height, bicristal diameter,head breadth, bigonial and blzygo-mattc measurement, chest breadth,and chest depth. Birth weight wassignificantly related to IQ and

ieng91 of institutional stay. Therewas a positive correlation betweenage at admission and IQ. Those hea-vier at birth were larger, more In-telligent, and. had significantlylarger anthropmetric measurementsin 6 of 11 parameters. (35)

BOHMVANNI, A.M. Control or Growthand Development.IN: Askin, J.A.,Cooke, R.E., and Haller, J.A.,Jr., eds. A Symposium on theChild. Baltimore: Johns HopkinsPress, 255, 1967.

Since growth and development can beaffected by factors in the externalenvironment such as emotional dis-turbance and inadequate nutritionas w..,11 as by factors in the inter-nal environment such as major dis-turbances in chemical composition,genetic factors, the central ner-vous system, pituitary activity,the functioning of the thyroid hor-mone, and endocrine secretion, anappreciation of the psychopathologyof disease can provide increased un-derstanding of the usual control ofhuman growth. (36)

CHEEK, D.B., and COOKE, R.E. Growthand Growth Retardation. AnnualReview of Medicine, 15:357, 1564.

A detailed discussion of the sub-ject is presented and basic informa-tion concerning cell number, cellsize, and body composition is inclu-ded. Growth retardation informationdealing with malnutrition, inade-

quate oxygenation, central nervoussystem disturbances and altered min-eral metabolism effects are given.

(37)

CRAIG, J.O. Growth of Mental Defec-tives. Developmental Medicineand Child Neurology, 8(1):87,1966.

The confusion caused by existingsystems of classifying mental retar-dates on physical growth patternsinto different diagnostic categor-ies of retardation was discussed.it was suggested that the number ofclasses for categorizing mental re-tardates should be reduced to a fewwell-defined groups. (38)

CRAVIOTO, J., BIRCH, H.J., DeLICAR-DIE, E.R., and ROSALES, L. The

Ecology of Infant Weight Gain ina Pre-Industrial Society. ActaPaediatrlca Scandinavica, 56:71,1967.

The paper reports the results of anecological longitudinal study of

weight gains made during the first6 months of life by all childrenborn in a representative Central

American village in the course of a19 month period. (39)

EI.MER, E., GREGG, G.S., and ELLISON,P. Late Results of the "Failureto Thrive" Syndrome. ClinicalPediatrics, 8(10:584, 1969.

Non-organic failure to thrive Is ex-plained as resulting from poorchild care. Emotional deprivationinfluences pituitary functioning tocause growth failure. Studies on 15children and their families demon-strated "catch-up growth" as a re-sult of therapeutic intervention.Intellectual growth was found to

parallel physical development as

damage during infancy is not alwaysreversible, and many such childrenexhibited mental retardation in la-ter life. (40)

FRANKEL, J.J., and LARON, Z. Psy-chological Aspects of PituitaryInsufficiency in Children and Ad-olescents with Special Referenceto Growth Hormone. Israel Jour-nal of Medical Science, 4:953,1966.

Thirty -nine children and adoles-cents, aged I to 20 years, with pi-tuitary insufficiency were assessedby means of a battery of neuropsy-chological tests to determine pos-sible correlates with the state ofendocrine deficiency. Results re-

vealed a lower intellige,--.e quo-

tient for the group as a whole, aswell as for a variety of clinicalsubgroups, when compared with the

normal population. There was alsoa distinct deficiency in visuomotorfunctioning. An attempt is made toexplain these findings on the basisof prenatal or postnatal lack of ac-tive growth hormone, with resultantInfantile hypoglycemia, an acceptedcause of mental and motor retarda-tion. (41)

GRAHAM, G.G. Effect of Infantile

Malnutrition on Growth. Federa-

tion Proceedings, 26(1)039,1967.

Longitudinal studies of 53 severelymalnourished children show that aninadequate diet can have marked ef-fects on subsequent growth, especi-ally growth of the head. In gen-

eral, the head circumference andheight were significantly below the50th percentile values even afterresumption of proper diet. (42)

JOURNAL OF THE AMERICAN MEDICAL AS-SOCIATION, 209(11):1712, 1969.

Nature, Nurture, and Stature.

An investigation with underdevelop-ed and emotionally deprived infantsdemonstrated that improved diet re-sulted in 1-7.pid growth Increasesand weight gain. Other changes werenot made to the physical and emo-tional environment of these child-ren, therefore, indicating that ne-glect of proper feeding was themain cause of the under-development.

(43)

KERR, G.R., CHAMOVE, A.S., and HAR-LOW, H.F. Environmental Depri-vation: Its Effect on the Growthof Infant Monkeys. Journal ofPediatrics, 75:833, 1969.

Monkeys reared either in partial ortotal social isolation for periodslonger than three months, were com-pared to control animals. This ex-periment suggests that social stim-ulation is not necessary for normalgrowth. In children with "depriva-tion dwarfism", inadequate food in-take should be regarded as the pro-bable cause of growth failure. (44)

KERR, G.R., ALLEN, J,R., SCHEFFLER,G., and WAISMAN, H.A. Malnutri-tion Studies in the RheUT671-Rey. I. Effect on Physicaltrowth. the American JournalZIT7TTnical Nutrition, 23(6):739,1970.

In an attempt to define the courseand sequelae of malnutrition in oneprimate species, exact degrees ofprotein--, or total, calorie malnu-trition were produced and investi-gated In infant rhesus monkeys. Da-ta led to the conclusion that chil-dren with edema or emaciation mayshow only subtle signs of malnutri-tion; correct diagnosis may not beconsidered in children in whom thequality of ingested protein resultsIn growth failure without the moredramatic clinical evidence of mal-nutrition. (45)

KOMROWER, G.M. Failure to Thrive.British Medical Journal, 2(5421):1377, 1964.

Possible causes of developmental re-tardation are outlined including:insufficiency of diet, inability toeat and digest food properly, im-paired absorption, inability to me-tabolize properly, and the inabili-ty to properly utilize nutrientswhich have been metabolized. Recom-mended tests and treatments are al-so outlined. (46)

KRIEGER, I. Head Circumference, Men-tal Retardation and Growth Fail-ure. Pediatrics, 37(2):384 ,

Twenty-three Infants with growthfailure without organic disease and28 infants with idiopathic growthfailure were evaluated in regard tostature, head circumference, height,age, and mental retardation show-ing no correlation between headsize and mental retardation. (47)

G

LOWRY, G.H., BACON, G.E., FISHER, S.and KNOLLER, H. Fasting GrowthHormone Levels in Mentally Retar-ded Children of Short Stature.American Journal of Mental Defi-ciency, 73(3):474, 1968.

Fasting serum growth hormone assayswere obtained on 46 mentally retar-ded children with short stature.The etiology of the stunted growthassociated with mental deficiencyremains speculative, but it appar-ently is not related to decreasedgrowth hormone levels in the fast-ing state. (46)

MARSHALL, W.A. Growth in MentallyRetarded Children. Developmen-tal Medicine and Child Neurol-ogy, 10(3):390, 1968.

Mental retardation is not pathogen-ic to abnormal growth; rather ,

small or excessive stature may bedue to the same cause as the low in-telligence. Some studies have er-roneously correlated mental retar-dation and growth abnormalities byregarding mental retardation as acomplete diagnosis and ignoring un-derlying pathology. Valid compari-sons between retarded and normalpopulations can be made only if thephysical growth of both groups issubject to the same genetic andneuro-endocrine handicaps. (49)

MOSIER, H.D., Jr., GROSSMAN, H.J.,and DINGMAN, H.F. PhysicalGrowth in Mental Defectives. Pe-diatrics, 36(3):465, 1965.

Anthropometric studies were done on2,472 mentally defective resident

patients at Pacific State Hospital.Ten body dimensions were obtainedand the presence or absence of sec-ondary sex development was recorded.Tables of means and standard devia-tions for each measure by sex, IQ,age, and diagnosis were given. (50)

O'CONNELL, E.J., FELDT, R.H., and

STICKLER, G.B. Head Circumfer-ence, Mental Retardation, and

Growth Failure. Pediatrics, 36(0:62, 1965.

This study supports the use of headcircumference measurement in sus-

pecting mental subnormality in chil-dren. (51)

POZSONYI, J. and LOBE, J. Growth inMentally Retarded Children. Jour-nal of Pediatrics, 717):865,1967.

Investigation of the linear and

skeletal development of 958 mental-ly retarded or non-mentally retard-ed children found that 2 groups ofmentally retarded children with noknown organic encephalic disorderwere equal in growth to children ofnormal intelligence which indicatesthat mentally retarded children arenot necessarily physically retarded.Stunting occurred most markedly inmongolism, metabolism disorders,

and low birth weight groups. (52)

PRYOR, H.B., AND THELANOER, H.E.Growth Deviations In HandicappedChildren: An AnthropometrlcStudy. Clinical Pediatrics,

6(8):501, 1967.

Comparison of the anthropometricmeasurements of 678 handicappedchildren with those of 12,000 normalchildren, ages 1 to 15 years, revea -ed revealed deviations from the nor-mals In all the handicapped cases ex-cept those with a mild neurolooic de-ficit. Results indicated that

growth is adversely affected mostseverely in cases with Down's syn-drome followed by those with mul-tiple congenital anomalies. Leastaffected groups were those with cer-ebral palsy from birth injury andthose with severe hypoxia after nor-mal gestation. Those with onlyneurological deficit showed no de-viation from normals. (53)

RUNDLE, A.T., ..1c1 SYLVESTON, P.C.

Endocrinological Aspects of Men-tal Deficiency: IV. Growth andDevelopment of Young Females. Am-erican Journal of Mental Defici-ency, 69:635, 1965.

104 physically healthy female men-tal defectives, ages 7 to 20 years,were examined. Gross body measure-ments, (standing and sitting height,biacromial diameter, and bi-iliacwidth), indicated physical under-development of the females, but theannual percentage increase was sim-ilar to normal American girls. (54)

TANNER, J.M. Galtonian Eugenicsand the Study of Growth: The Re-lation of Body Size, Intelli-gence Test Score, and SocialCircumstances in Children andAdults. Eugenics Review, 58122, 1966.

Studies indicate that body size andmental ability increase in smallfamilies, in favorable occupationalor socioeconomic classes, and inpeople who migrate either away fromoome or upwards in social classes.In children of school age there isa correlation between intelligencescores and body size, this contin-ues at a diminished rate to matur-ity. (55)

17

MALNUTRITION AND ITS EFFECTS ONNERVOUS SYSTEM DEVELOPMENT

NUTRIENT DEFICIENCY

Multiole Deficiencies In Humans

ADAMS, R.N. Cultural Aspects of In-fant Malnutrition and Mental De-veloo7ent. IN: Scrimshaw, N.S.

and Gordon, J.E.. eds. Malnutri-tion, Learning, and Behavior.Cambridge: MIT Press, 465, 1968.

Tnis paper discusses a broad frame-work, embracing the full adaptive

cycle, that studies investigatingthe relationship between infant mal-nutrition and mental developmentshould be based on. This resultsin expanding the scope of the re-

search with a final goal of a bet-ter adaptation of man to the world.

(56)

BABSON, S.G., KANGAS, J., YOUNG, N.

and BRAMHALL, J.L. Growth and

Development of Twins of Dissimi-

lar Size at Birth. Pediatrics,

33(3):327, 1964.

Sixteen pairs of dissimilar sized

twins at birth, with a median age

of 8 1/2 years were investigated.

There were highly significant dif-ferences in height, head circumfer-ences and weight; significant dif-ferences in intelligence and lan-guage comprehension and expression;and no significant differences in

articulation, oral structures, oraldiadochokinetis or auditory acuity.

(57)

BARAITSER, M.E. The Effect of Under-Nutrition on Brain-Rhythm Devel-opment. South Africa Medical

UKFr1D, 43:56, 1969.

Evidence is presented to validatethe hypothesis that electroencephal-°graphic rhythms are affected by

early malnutrition. (58)

BARNES, R.H. Earle e,alnutrition andEchcvioral Cevelc.)ment. Food andNutrition News, 39C5-7 1967.

Studies on malnourished children byCravioto and by Stock and Smytheare d.scribed. The specific contri-butions of nutrition and those ofsocial stimulation to mental devel-opment can not, as yet, be separa-ted. (59)

BARNES, R.H. Malnutrition in EarlyLife and Mental Development. NewYork State Journal of Medicine,65:2816, 1965.

Evidence from animal and human stu-dies shows that in acute stages ofmalnutrition, behavioral abnormali-ties and low scores in psychologi-cal development tests are evident.Age of onset and type of malnutri-tion influence recovery. (60)

BEUKERING, J.V. Uldernutrition Dur-ing Infancy and the Effect ofBrain Growth and Intellectual De-velopment. South Africa MedicalJournal, 41:1179, 1967.

A brief letter questioning the val-idity of Cie work of Stock andSmythe in South Africa is provided.

(61)

BIRCH, M.G. Field Veasurement in

Nutrition, Learning, and Behav-ior. IN: Scrimshaw, N.S. andGordon, J.E., eds. Malnutrition,Learning, and Behavior. Cam-bridge: MIT Press, 497, 1968.

Some of the specific questions tobe answered regarding malnutritionand mental development are dis-

cussed. Quantitative determinationsc4 the frequency and extent to

which malnutrition affects learn-

ing and behavior; the relative sig-nificance of malnutrition among

other causative factors; the ages

when malnutrition has most effecton mental development; and the mech-anisms by which malnutrition exertsits action are included. Tests mustbe developed to measure, sensitive-ly, behavioral differences, and,

yet they must be relatively insensi-tive to cultural differences be-

tween populations. (62)

BOTHA-ANTON, E., BABAYAN, S., and

HARFOUCHE, J.K. Intellectual De-velopment Related to NutritionStatus. Journal of Tropical Pe-diatrics, 14(3):112, 1968.

A group of children, who had beenundernourished before 18 months,

had significantly lower IQ's than

an adequately nourished group at

the age level of 4 to 5 years withno evidence supporting an originaldifference in IQ. (63)

BRITISH MEDICAL JOURNAL, 1(5588):333, 1968. Nutrition and the De-veloping Brain.

Studies on infants with brain dam-age resulting from improper nutri-tion, both before (chronic) and Im-mediately after (acute) birth arediscussed. Neither hypernatremia,nor hypoglycemia are prevalent cau-ses of neonatal brain damage; how-ever, they are only 2 of possiblenutritional disturbances. Detectionof persistent difficult behavior ininfants, proper diagnosis of the

malnutrition, and subsequent treat-ment are required of pediatricians.

(64)

BRITISH MEDICAL JOURNAL, 1:651,

1964. Nutrition of the Brain inInfancy.

Discussion of several studies on

malnutrition and brain developmentis presented. It was concluded thatit would be very difficult to provethe effects of malnutrition in ear-ly infancy, and the ethical consid-erations of any prospective studiesare mentioned. (65)

BROWN, R.E. Decreased Brain WelihtIn Malnutrition and its Implica-tions. East Afric Medical Jour-nal, 42:584, 1965.

Review of 1100 autopshs of Ugandanchildren, aged from birth to 15years. Those with a history of mal-nutrition showed significant reduc-tion in body and orain weight. Im-

plications of findings are dis-

cussed. (66)

BROWN, R.E. Organ Weight in Malnu-trition with Special Referenceto Brain Weight. DevelopmentalMedicine and Child Neurology,8(5):512, 1966.

Heart, liver, spleen, brain, andbody weights from autopsies of

1,094 Ugandan children up to 15years of age were investigated. Thechildren were divided into 2 groupson the basis of whether or not theywere undernourished. The weightswere compared with those from chil-dren of comparable age in othercountries. (67)

CABAK, V. and NAJDANV1C, R. Effect

of tiodernutrition in EarlYCIPFWI Physical and Mental Develop-ment. Archives of Disease In

rfiTTdhood, 40(213):532, 1965.

1 9

The records of 36 children who wereadmitted for malnutrition to theHospital for Sick Children in Sara-jevo, Yugoslavia, between 1951 and1957, and later discharged, were se-lected to compare their presentbody weight, height, and Binet- Si-mon IQ as adapted by Stevanovic tothose for normals. A correlationwas sound between deficit in admis-sion weight and present IQ. (68)

CANOSA, C.A. Ecological Approach tothe Problems of Malnutrition,Learning, and Behavior. IN:

Scrimshaw, N.S., and Gordon, J.

E., eds. Malnutrition, Learning,and Behavior. Cambridge: MITPress, 389, 1968.

The paper reviews some of the com-plexities and the planning aspectsof field studies dealing with mal-nrltion, learning, and behavior.It is based on a prospective long-term study that began in 1964 atthe institute of Nutrition of Cen-tral America and Panama with fieldoperations in Guatemala. The mainindependent variable is the nutri-tional state of pre-school childrenwith mental development as the de-pendent variable. The study at-tempts to improve understanding ofthe relationships between malnutri-tion, learning, and behavior. (69)

CHAMPAKAM, S., SRIKANTIA, S.G.,and GOPALAN, C. Kwashiorkor andMental Development. AmericanJournal of Clinical Nutrition,21:844, 1968.

Study of nineteen children success-fully treated for kwashiorkor. Re-ductions in intelligence and inter-sensory organization were found,particularly in the younger agegroup. The retardation was notice-able mainly with regard to percep-tual and abstract abilities. (70)

CHANDRA, R.K. Nutrition and BrainDevelopment. Journal of Tropi-cal Pediatrics, 10(2):37, 1964.

The author reviews some studies onnutritional deficits and their ef-fect on intellectual developmentand stresses the need for more re-search in this area. (71)

CHURCHILL, J.A., AYERS, M.A., andCALDWEIL, D.F. Intelligence ofChildren Whose Mothers Have Bi-iary Tract Disease. Journal ofthe American Medical Association,201(6):482, 1967.

A prospective, longitudinal studyof children born of mothers with bi-lary tract disease found that theirIQ was lower than the IQ of matchedcontrols. Malabsorption of fats,particularly linoleic acid, may in-terfere with the lipid supply essen-tial for fetal brain development.

(72)

COURSIN, D.B. Effects of Undernu-trition on Central Nervous Sys-tem Function. Nutrition Reviews,

131337617965.

The literature on the effects of un-dernutrition on the central nervoussystem is reviewed, and suggestionsfor further research are made. (73)

COURSIN, D.B. Undernutrition andBrain Function. Borden's Reviewof Nutrition Research, 26(1),1965.

This paper presents a discussion ofthe extent of undernutrition in de-veloping countries and its effecton mental capacities. Informationon normal development of the brain;the spectrum of mental retardation;the clinical symptoms of severe un-

2 0

11

dernutrition; and the biochemicalmechanism abnormalities in protein-calorie undernutritlon is included.

(74)

CRAVIOTO, J., DeLICARDIE, E.R., andVEGA, L. Amino Acid-Protein Mal-nutrition and Mental Development.IN: Nyhan, W.L., ed. Amino AcidMetabolism and Genetic Variation.New York: McGraw-Hill, 449,1967.

The relationship between neurointe-grative behavior and nutritionalstatus was examined in 2 groups ofchildren (ages 6 to II years) ofthe same ethnic backgru,dd. Aminoacid-protein malnutrition was de-fined, retrospectively, as a signi-ficant diminuation of height. ThereIs evidence of delayed neurointeora-tive development in malnourishedchildren. (75)

CRAVIOTO, M., BIRCH, J.G. and GAONA,C.E. Early Malnutrition and Aud-itory - Visual Integration in

School-Age Children. Journal ofSpecial Education, 2:75, 1967.

A study of the ability of malnour-ished and normal groups of childrento integrate visual and auditory in-formation. (76)

CRAVIOTO, J. and ROBLES, B. Evolu-tion of Adaptive and Motor Beha-vior During Rehabilitation fromKwashiorkor. American Journal ofOrthopsychiatry, 36(3) 449, 1965.

The psychological test performanceduring rehabilitation of a group of20 infants and pre-school childrensuffering from severe protein-calo-rie malnutrition was studied by theGesell method as soon as they hadbeen cured of any acute infectiousepisode and/or electrolyte distur-

bance, and afterwards at intervalsof 2 weeks during their stay in thenutrition ward. As the patients re-covered from malnutrition: the dif-ference between chronological ageand developmental age in the fieldsof adaptive, motor, language, andpersonal-socio behavior was foundto decrease except in the group ofchildren whose chronological age onadmission was below 6 months. (77)

CRAVIOTO, J., and DeLICARDIE, E.R.Intersensory Development ofSchool-Age Children. IN: Scrim-shaw, N.S. and Gordon, J.E., eds.Malnutrition, Learning, and Beha-vior. Cambridge: MIT Press,252, 1968.

The relationship between neuro-in-tegrative function and malnutritionIn a group of children In a Guata-malan village was studied. Theshortest children were assumed to

have experienced malnutrition as

they showed a lag in development ofintersensory competence. This wasnot the case with urban childrenstudied who were assumed not tohave suffered malnutrition. The re-sults of an investigation of audi-tory-visual capacity of children ina Mexican village are described.Height was once again used as a cri-terion of evidence of malnutrition.The taller group performed betterthan the shorter. (78)

CRAVIOTO, J., DeLICARDIE, E.R., andBIRCH, H.G. Nutrition, Growth,and NeuroIntegrative Development:An Experimental and EcologicStudy. Pediatrics, Supplement 2,38:319, 1956.

A study using height as a measureof pre-school nutrition was conduc-ted on poor rural children. resultsshowed a positive correlation be-tween height and intersensory Inte-grative ability. The study was re-

21

peated on a group of upper classchildren whose heights were unlike-ly to have been affected by malnu-trition. Here differences in heightwere not related to intersensoryIntegrative competence. (79)

DAIRY COUNCIL DIGEST, 19(3)03,1968. Malnutrition in Early Lifeand Subsequent Mental Perfor-mance.

Current concepts of brain develop-ment are discussed, and studies in-vestigating the relationship of nu-trition to human and animal behavi-or are described. (80)

DAYTON, D.H. Early Malnutrition andHuman Development. Children:71rTZ), 1969.

Studies describing the nutritionalstatus of children in various areasare discussed. Studies on mentaldevelopment and the efferlts of mal-nutrition are provided, and infor-mation on methods of nutritional as-sessment is discussed. (81)

EICHENWALD, H.F. and FRY, P.C. Nu-trition and Learning. Science,163:610i, 1969.

This is a broad discussion of thephysiological, socio-economic, andpsychological factors surroundingnutrition and learning. (82)

FRISCH, R.E. Present Status of theSupposition That Mainutritiorl

Causes Permanent Mental Retarda-tion. American Journal of Clin-ical Nutrition, 23(21:189, 1970.

The author reviews many of the stu-dies dealing with malnutrition andmental retardation, as well as one

study investigating the effects of

social-environmental factors on men-tal development. She concludes thatthe evidence is not yet sufficientto support the supposition that mal-nourished children will be perman-ently mentally retarded. (83)

GRAHAM, S.G. Effect of InfantileMalnutrition. Federation Proceed-ings, 26(1):1, 1967.

A longitudinal investigation was

carried out on 53 severely malnour-ished children. The earlier in lifethe deficits occur, the more severeand permanent the stunting ofgrowth, particularly growth in oeadsize. The older the infant when de-prived, the longer the period of un-dernourishment he can tolerate without permanent stunting. (84)

GRIEVE, S., JACOBSON, S., and PROC-TOR, N.S. A Nutritionalhlifist-pathy Occurring in the Bantu on

the Witwatersrand. Neurology,17:1205, 1967.

A series of 61 cases of a nutrit1on-al ryelJpathic syndrome is descri-bed. Two autopsies are describedin detail, and the main pathologi-cal feature in both is degenerationof the lateral pyramidal tracts. A

low Intake of protein, fats, andvitamins, and often excessive alco-hol intake, cal be Implicated inmost cases. (85)

GYORGY, P. arlitth:SafortearLdtfi-.

tamln A Malnutrition in South'.east Asia. Federation Proceed*TiliT71113):9k9, 1968.

Dietary analysis and supptements-Lion were stJdied. Because some de-ficiency symptoms are irreversible,prevention is of paramount impor-tance and nutrition education is es-sential. (B6)

22

HUGHES, E.A., STEVENS, L.H., andWILKINSON, A.W. Some Aspects ofStarvation in the Newborn EltmArchives of Disease in Childhood,39(208):598, 1964.

Nitrogen, potassium and sodium bal-ance studies were made on 2 newborninfants under starvation. Both in-fants showed remarkable capacitf toresist starvation. (87)

MEDICAL WORLD NEWS, 8(1l):60, 1967.Better Diet for Brighter Minds?

Human studies in South Africa, Mex-ico, and Nazi consentration campsindicate that undemqtrition beforethe age of 4 has intellectual andemotional effects; however, the ma-ture brain can be rehabilitated af-ter starvation. Discussion is pres-ented on enriched food products asa method to combat malnourishment.Fish protein ncentrates are des-

cribed. (88)

MEDICAL WORLD NEWS, 9(37):91, 1968.Deadline for Saving StarvedMinds.

Studies show that early malnutri-tion results in Impaired learningability and that the time availablefor the nutritional rescue of stun-ted minds Is less than 6 monthsfrom birth. Cell division in the hu-man brain continues until 6 monthsof age; therefore, early good nutri-tion is the key to a normal comple-ment of brain cells. (89)

mONCKEBERG, F. Effect of tally Maras'mic MainutrifT5r r subsequentPhysical Devel-opment. IN: Scrimshaw, H.S.,

and Gordon, J.t., eds. Malnutri-tion, Learning, and Behavior.Cambridge: MIT Press, 269, 1968.

23

Studies on children indicate thatearly malnutrition tends to res-trict expression of the genetic po-tential for development, both phy-sical and psychological. The effects of socioeconomic factors aredifficult to separate from nutri-tional influences. (90)

MORAN, R.E. Possible Causes of Men-tal Retardation in Puerto Rico.Presented at the g:th Annual Con-vention of the American Associa-tion on Mental Deficiency, May10, 1966, Chicago, Illinois.

Various etiological factors accoun-ting for mental retardation are dis-cussed. Malnutrition as a result ofpoverty is given a major role. (91)

NAM, R.L. Malnutrition: ProbableCause of Fetal Growth Retarda-tion. Archives of Pathology, 79

Ti17284, 1965.

The study compares organ strctureof prenatally retarded infants withorgan structure of children dyingof post natal alimentary malnutri-tion. Results showed that bothgroups had abnormal amounts of cut-aneous fat. While liver and spleenwere disproportionately small,brain, pancreas, heart, lungs andkidney were nearest to normalweight. Malnutrition, therefore,May be a major factor in some casesof antenatal growth retardation.Placental abnormalities suggest acause. (92)

NATURE, 221:808, 1969. The Develo-ping Brain.

The process of myelination seems tobe a "once and foe all" event, andtherefore is a vulnerable period ofdevelopment; for even mild undernu-trition can permanently affect mye-lin deposition in the brain. (93)

NUTRITION REVIEWS, 26(7):197, 1968.Undernutrition in Children andKITiTiTWilt Brain Growth and In-tellectual Development.

The article presents a review ofthe longitudinal study conducted byStock and Smythe in South Africa.Evidence is presented that severeundernutrition during the first twoyears of life is associated with abrain size and an intellectual de-velopment below average. Furtherstudies are necessary to separatenutrition from other possible caus-ative factors. (90

PLATT, B.S., and WIECLER, C.F. Pro-tein-Calorie Deficiency and the

Central Nervous S stem. Develop -men ne and Child Neuro-

logy, 9(1):104, 1967.

Poor educational performance and re-duced brain weight are tie° resultsof malnutrition in childhood. (95)

POLLITT, E. Ecology, Malnutrition,snd Mental Onvelopment. Psychoso-matic Medicine, 31:193, 1969.

The author points out two major dif-ficulties in malnutrition and Intel-ligence studies: obtaining adequatehistory, and separating nutritionalcomponents from biological and soc-ial variables. (96)

RAJAIAKSHMI, R. The PsycholcolcalStatus of Unde7=RMIledged Cat-drenReared at Home arrefin an Or-phanage in South India. -IndianJournal of Mental Retardation,1(2):53, 1963.

Children living in an orphanage inSouth India and children living intheir own homes in a small village

near the orphanage were tested forpsychological performance. the re-

sults showed that nutritional im-provement alone does not restorenormal psychological functioning inchildren whose social and culturalenvironment Is totally lacking in e-motional and psychological stimula-tion. (97)

RANDAL, .i. Hunger: Does It CauseBrain Damage? Think, 32:2, 1966.

Discussion is given of early malnu-trition and mental retardation, andthe role of amino acids in brain de-velopment. (98)

READ, M.S. Malnutrition and learn-ILI, American Education, 5:10 ,

1t

Malnutrition and its extent in the

United States is described. Animaland human studies investigating therelationship between malnutritionand mental abilities are discussed.The influence of other variablessuch as parental, social and envir-onmental are postulated. (99)

SACHDEV, K.K., MANCHANDA, S.S., andLAI, H. The Syndrome of Tremors,Mental Regression, and Anemia inInfants and Young_ChIldren: AStudy of 102 Cases. Indian Ped-iatrics, 2:239, 1965.

Complex nutritional factors, ratherthan specific vitamin deficiency,appears to be at the rota of thissyndrome. (100)

SCOTT, K.E., ant! USHER, R. Cpiphy-seal Del/12mo in Fetal Malnu-Tilinn4neroore. New EnglandJournal of Medicine, 210:822,1964.

2

X-ray films of the knees were takenIn 30 malnourished newborn infantsand in 18 normally nourished con-trols of the same gestational age.

The results indicated that fetal

malnutrition is accompanied by a de-lay in epiphysial development. (101)

SCRIMSHAW, N.S. Infant Malnutritionand Adult learning. Saturday Re-view, 84:614, 196E.

The paper presents a review of theanimal and human studies investiga-ting the effects of malnutrition onphysical growth, learning, and beha-vior. (102)

SC.:I/641N, N.S. and GORDON, J.E.

Malnutrition, learning, and Beha-vior. Cambridge: MIT Press,

MIL

The book reports the pro:eedings ofan international Conference on Mdi-nutrition, learning, and Behavior.

It was attended by medical, biologi-cal, and social scientists 'of 38

countries. Both animal and Edman

studies investigating malnutritionand physical and mental developmentare presented, and the consequencesof nutritional deficiencies in the

young child on later mental func-tions are discussed. (103)

SCRIMSHAW, N.S. Malnutrition, Learn-ing, and Behavior. American Jour-nal of Clinical Nutrition, 20:

493, 1967.

A general discussion of the interre-lationships tetwten malnutrition,learning, and behavior is given.

(104)

STOCK, M.B., and SMYTHE, P.M. Under-nutrition During infancy, and

Subsequent Brain Growth end In-

tellectual Development.. IN:

Scrimshaw, N.S. and Gordon, J.E.,eds. Malnutrition, learning, andBehavior. Cambridge: MIT Press,

278, 1968.

The results of an 11 year study on20 Cape Coloured children, whowere grossly undernourished in in-

fancy, is reporte.d. Evidence indi-

cates that severe undercutrition du-ring the first 2 years of life,

when brain growth is most active,results in a permanent reduction ofbrain size and a restricted intel-

lectual development. (105)

STOCK, M.S., and SMYTHE, P.M. The

Effect of Undernutrition DurriiInfancy on Subsequent BrainGrowth and intellectual Develop-ment. South Africa Medical Jour-nal, 0:1027, 1967.

Smaller head tircumfarence, abnor-

mal electroencephalographic patternsand impairment of visual ....rception

was found in a group of malnourishedAfrican children. (106)

WINICK, M. Malnutrition and Brain

Development. The Journal of Pe-

diatrics, 74(5):667, 1969.

A broad survey of studies, oealingwith the effects of malnutrition onthe developing brain, are described.Both animal and human studies inves-tigating physical and chemical

brain growth are shown, as well as

studies dealing with the developmentof brain function. (107)

WINICK, M. and ROSSO, P. .lead Cir-

cumference and Cellular Growth

of the Brain in Normal and Mar-asmic Children. Journal of Pedi-atrics, 74:774, 1960.

The relationship between !iead cir-cumference and cellular growth ofthe brain is examined In normal andmalnourished children in the firstyear of life. The data support thevalidity of .sing changes in head

circumference as a measure of post-natal brain growth. (108)

WiNICK, M. and ROSSO, P. The Effectof Severe Early Malnutrition onCellular Growth of the HumanBrain. Pediatric Research, 3:181,TIE57

In ten "normal" brains, obtainedfrom well-nourished Chilean chil-dren who died accidentally, weight,protein, and DNA and RNA contentwere all normal when compared withthose values derived from similarchildren in the United States. Innine infants who died of severe mal-nutrition during the first year of

life, there was a proportional re-

duction in weight, protein, and RNAand DNA content. These data are

slAilar to previous data in animalsand demonstrate that in children,Severe early malnutrition can re-

sult In curtailment of the normalincrease In brain cellularity withincrease In age. (109)

WITKOP, C.J. Genetics and Nutri-

tion. Federation Proceedings,1b11):148, 1967.

Similar biochemical findings existin histidinemia, phenylketonuria,and kwashiorkor. It is suggestedthat investigations be done to com-pare the mental retardation result-ing from protein malnutrition withthe type of mental retardation re-sulting from histidinemia and phen-ylketonuria. (110)

2(3

Multiple Deficiencies in Animals

BAR%ES, R.H., MOORE, A.U., REID, I.

m. and POND, W.G. Effects of

Food Deprivation on GehavicralPatterns. IN: Scrimshaw, N.S.,and Gordon, J.E., eds. Malnutri-tion, Learning, and Behavior.Cambridge: MIT Press, 203, 1968.

The results of animal studies on

pigs and rats investigating the ef-fects of food deprivation on behav-ior are described. Differences warenoted between behavioral changescaused by simple food restrictionof normal diet, and those causedby a protein deficient diet. Thereappeared to be no relationship be-t^een the extent of behavioralchange and the stunting of bodysize in animals deprived in early

life. (Ill)

BARNES, R.N. Exerirental Approach-es to the Study of Early Malnu-trition and Mental Development.Federation Proceedings, 2b(1T:

1144, 1967.

Certain types of nutritional depri-vation imposed early in life areshown to affect learning capacity.

(112)

BARNES, R.M., CUNNOLD, S.R. eAd 21M-MERMA4, R.R. Influence Of Nutri-tional Ceprivations Early.

Life _on learning Behavior ofRats as Measured h) Performancein a Water Maze. Journal of Nu-trition, 19:399, 1966.

Learning behavior was studied inrats that were subjected to differ-ent forms of nutritional deprive-lion in early life. Kale rats thatwere deprived both before and afterweaning made significantly rt.re er-

rors than the normal controls. The

animals that here deprived pre-nean-Ing or post-weaning alone gave in-termediate results. No significantdifferences were found among femalerats subjected to the same treat-ment regimens. (113)

BARNES, R.H., MOORE, A.U., REID, 1.M. and POND, W.G. Learning Ee-

halor follo4ing Nutritional Ce-privations in Early Life. Jour-nal of the American Dietetic As-sociation, 51(1):14, 1967.

The results of animal studies inves-tigating the relationship of malnu-trition and learning behavior aredescribed. Pigs, malnourished in

early life, .re unable to extin-guish a condi:ionec response, al-though both the malnourished andcontrols were able to develop thisresponse at the same rate. Rats,nutritionally deprived during nur-sing, made significantly more er-rors than controls in a water mazetest. Rats deprived during the post-weaning period as *Ill as duringnursing made the most errors. (114)

BARNES, R.N., MOORE, A.U. and POND,W.G. Behavioral Abnormalities inYoung Adult Pigs Caused by Malnu-

trition in Early Life. JoJrnal

of Nutrition, 100(41-1149, 197D

Baby pigs were malnourished for a

period of 8 weeks by restricting

protein or caloric intake with the

Objective of studying behavioral

changes that remained long after nu-

tritional rehabilitation bad been

Achieved. the nutritional conditionwhich caused the greatest change inbehavioral development resulted

from feeding a diet very low in pro-tein from the third through tte ele-venth week of life. (115)

BENTON, J.W., MOSER, H.W., DODGE, P.R. and CARR, S. Modification ofthe Schedule of Myelination in

the Rat by Early Nutritional De-rivation. Pediatrics, 38(5):1, 19 .

Nutritional deprivation during thefirst 21 days in newborn rats pro-duced a decrease in myelination.Brain weight, total brain lipids,cholesterol, and phospholipids weredecreased 80 percent in the depri-ved group. (116)

BROWN, A.L. and GUTHRIE, N.A. Ef-

fect of Severe Undernutrition inEarly Life Upon Body and OrganWeights in Adult Rats. Growth,32:113, 1968.

Male rats subjected to severe under-nutrition from two days followingbirth until 3, 5, 7 and 9 weeks ofage were subsequently fed an ade-quate diet until reaching adult ageof 19 weeks. Body weight and weightsof liver, kidneys, heart and brainof all deprived groups were signifi-cantly lower than controls andweights of animals deprived for 9weeks were lower than other deprivedgroups. (117)

CALDWELL, D.F. a..d CHURCHHILL, J.A.

Learning Ability ire the Progenyor Rats A4ministered a Protein

Varalaliiir-GTWITUIrre=ndHalf of. Gestation. neurology,

71795, 1967.

A group of ten pregnant rats werefed a protein deficient diet, withvitamin supplement, during it sec-ond half of gestation. Resultsshowed that subjects receiving theProtein deficient diet had longer,%eriods of gestation, weighed lessat birth and weaning, and had a

higher preweening mortality rate.

In learning ability, the controlrats were significantly better in

both tests. (118)

CHASE, M.P., DORSET, J. and ?IMAM,G.M. The Effect of 111122111112a

on the Synthesis of a Myelin Li-Lid.. Pediatrics, 40(4MT,1967.

The hypothesis that the period of anactive myelin formation is both a

cricial and a vulnerable time forthe developing central nervous sys-tem was strengthened when rats sub-jected to nutritional deprivationfrom bith to 21 days of age had a

decreased synthesis of suifatidewhich was not corrected by refeed-ing. Malnutrition produced a signi-ficant decrease of brain weight ,

brain lipid, and body weight. Re-

feeding resulted in a rapid gain ofbody weight but a slower gain ofbrain weight and lipids. (119)

CHASE, H.P., LINDSLEY, W.F., Jr.,and O'BRIEN, D. Undernutritionand Cerebellar Development. Mao

ture, 221:554, 1969.

The purpose of this study is to astcertain whether malnutrition has

any regionally specific effect oncell growth. Rats were undernour-ished by creating nursing litters

of 1E animals to one mother. Body

and total brain weight were signifi-cantly lower in undernourished ani-mals. DNA was significantly lower- -wholly as a result of the differ-ence In cerebellar DNA content.The effects of undernutrition canbe interpreted as less protein and%Pallet cells in the cerebrum, butwith no difference in cell numbers.

(120)

CHOW, 8.F., BLACKWELL, R.Q. andSHERWIN, R.W. Nutrition and Ce-yelopment. Borden Revie;7771N-tritioet Research, 29:25, 1968.

The effects on animals of maternaldietary restricitions are described.It was concluded that both fetaland neonatal undernutrition perman-ently affect the offspring, andthat maternal nutrition In the tat

influences both the fetal 'nd neo-natal nutrition. (121)

2S

COLLIER, G.H. and SQUIBB, R.I. Mal-nutrition and the Learning Capa-city of the Chicken. IN: Scrim-

shaw, N.S. and Gordon, J.E., eds.Malnutrition, Learning. and Beha-vior. Cambridge: MIT Press,

236, 1968.

No abnormal motivation or learningresponses were found in chickens

placed on a protein deficient dietfor the first two weeks after hatch-ing, and then re-fed and examinedfrom 6 weeks onward. (122)

COWLEY, J.J. and GRIESEL, R.D. TheEffect on Growth and Behavior -3TRehabilitating First and SecondGeneration Low Protein Rats. An-

1741-8eravlor, 14:506, 1966.

Two experiments are described in

which rats fed on a low protein di-et were rehabilitated on a labora-

tory diet containing a higher per-centage of protein. The retardationin the growth and developrwt be-came more marked as successive gen-erations cf rats were reared on thela: protein diet. It is concluded

that a low protein diet fed to one) eneration of rats affects the

growth and development of the next

generation; this seems to be due,

at least in oart, to a deficiencyin the nutrients received from themother during the foetal period.

(123)

COWLEY, J.J. Time Place and Nutri-tion: Some Observations from Aimal ftwThlies7 IN: Scrimshaw, N.

T. and Gordon, J.E.. eds. malnu-trition, Learning, and Behavior.Czmbridge: MIT Press, 218, 1968.

Rats fed on a low protein diet af-ter weaning showed no 119Rificantchange in problem kolving behavior

2t,

from controls. If rats and theiroffspring were retained on the diet,the problem solving ability of suc-ceeding generations was increasing-ly affected. Protein synthesis wasstimulated by supplementing tl.K.se

rats with Clanabol. These rats

showed some imorovement in problemsolving and appeared to be "more

purposive" than controls. It was

also noted the.' rats, mice and ham-sters restrict their food intakewhen moved from one territory to an-other. Analogies between these ob-

servations and the human situationwere made. (120

CULLEY, W.J. and MERTZ, E.T. Effectof Restricted Food intake on

Growth and Composition of Pre-weanln Rat Brain. Proceedingso the Sod-AT-Tor ExperimentalBiology and Medicine, 118(1):233,1965.

The incorporation of non-lipid sol-ids, cholesterol, phospholiplds,and cerebrosides into the brain wasreduced by restricting food intakeof rats from 5 until 20 days of age.

(125)

CULLEY, W.J. and LINEBERGER, R.O.

Effect of Undernutrition on theSize and Composition_ of the RatBrain. Journal of Nutrition, 96

ni-U75, 1968.

Studies with ra s indicated that

the ability of the rat brain to re-cover from undernctrition is estab-lished somewhere betweeo 11 and 17days of age. The effects of the re-stricted feeding were greatest in

the cerebellum and least in the

ports medulla. (126)

DAVISON, A.N. The influence of Nu-tritional Disorders on the LipidComposition of the Central Ner-

revs System. Proceedings of theNutrition Soci-ly, 27(i):83, 1968.

Research investigating the relation-ship between malnutrition and lipidcomposition of the brain is dis-cussed. Evidence Indicates that per-manent effects may be produced onlyduring a vulnerable period of devel-opment. More :nvestigations areneeded to relate this to intellect-ual performance. (127)

DAVISON, A.N. and DCBBING, J. Nye-lination as a Vulnerahle PeriodIn Brain Development: The Foetusand the Newborn. British MedicalBulletin, 22(l):40, 1966.

The deposition of myelin as a crit-ical process in the later phase ofbrain development Is discussed. The"vulnerable" period in human myelindevelopment is Probably between theseventh intrauterine month to thefirst few months of postnatal life.

(1281

OICKERSON, J.W.T. and DOSSING, J.Prenatal and Postnatal Growthand Development of the e, +oral

Nervous System of the Pig. Pro-ceedings of the Royal boclety ofLondon, 166(1005):384, 1967.

The growth and maturation of thecentral nervous system of pigs wasstudied by quantitative chemicalmethods. The most rapid period ofgrowth was from about 6 weeks be-fore birth to about 5 weeks after-

wards. This study shows that thetame when the spinal cord and thebrain, or the cerebellum in parti-cular, may be most susceptible to

insult Such as undernutrition Is de-terminable. (129)

DICKERSON, J.W. and WALMSLEY,The Effect of Undernutrition and---ra---erTTgrtrithesequatiOP onthe Growth and Composition of

the Central Nervous System ofthe Rat. Brain, 90:897, 1967.

Weanling rats were undernourisheduntil they were 11 weeks old. Someof them were then allowed unlimitedaccess to food for one, two or

eight weeks. The effect of undernu-tritIon and subsequent rehabilita-tion on the weight of the brain,and on the weight and "thickness"of the spinal cord was studied. Thebrain and the c'rd were analysedfor total N, total P, ONA-P andcholesterol. (13U)

DOBBINL, J. Effects of ExperimentalUndernutrition on Development ofthe Nervous System. IN: Scrim-shaw, N.S. and Gordon, J.E., eds.Malnutrition, Learning, and Beha-vior. Cambridge: MIT Press, 181,1968.

The effect of undernutrition on thebrain lipids of pigs is described.in rehabilitated pigs, the brainsare smaller and they seem to be un-dermyellnated. The total number ofcells is permanently reduced. Re-sult. of rat experiments supportdata that the effects of undernutri-tion on the brain depends on thetiming of the undenutrition in re-lation to the period of fastestbrain growth. (131)

DOSSING, J. The Effect of Undernu-trition on Myelinati)n in theCentral Nervous System. Biologic

Nesmatorum. 911-6):132, 1966.

Three separate animal experimentssupport the hypothesis that undernttrition, if sufficiently severe andoccurring during critical periods,can affect myelination. (132)

30

DOBBING, J. and WIDDOWSON, E.M. TheEffect of Undernutrition and Sub-sequent Rehabilitation on Myelin-ation of Rat Brain as Measuredby its Composition. Brain, 13$

(2):357, 1965.

The effect of undernutrition andsubsequent unlimited nourishment onmyelinatIon of the brains of 200rats was investigated. The studyclearly showed the ability of theadult brain to synthesize largequantities of cholesterol during re-habilitation after a period of un-

dernutrition. (133)

FRANKOVA, S. and BARNES, R.H. Ef-

fect of Malnutrition in Ea Tylife on Avoidance Conditioningand Behavior of Adult Rats.Journal of Nutrition, 96(0:485,1968.

Rats, undernourished both beforeand after weaning, showed behavior-al disturbances but did not differsignificantly in learning rates

from controls. Animals restrictedIn the preweaning period only didnot show signs of these disturban-ces. (130

FRANKOYA, S. and BARNES, R.H. In-

fluence of Malnutrition in EarlyLife on Exploratott Behavior ofRats. Journal of Nutrition, 96111-7477, 1968.

Investigations of rats indicated

that undernutrition in the firstweeks of life may cause a long termdecrease of exploratory drive, des-pite rehabilitation with a satisfac-tory diet fed ad libitum from 21

days of age. this effect was foundto be greater in males than females.

(135)

FRANKOVA, S. Nutritional and Psy-

chological Factors in the Devel-opment of Spontaneous Behavior

In the Rat. IN: Scrimshaw, N.S.and Gordon, J.E., eds. Malnutri-tion, learning, and Behavior.

Cambridge: MIT Press, 312, 1968.

Investigations on rats to study theeffects of undernutrition and the

effects of stimulation on the deg-ree of spontaneous activity of theanimals are reported. A reduced cal-oric intake in the early stages ofdevelopment results in decreasedspontaneous activity, but the ef-fect may be modified appreciably bystimulation. (136)

GEISON, R.L. and WAISHAN, H.A.fects of Nutritional Status onRat Brain Maturation as Measuredby Lipid Composition. Journal

of Nutrition, 100(3):315, 1970.

Alteration of the rate of growth ofsuckling rats prcduces changes inthe concentrations of several brainlipid components ( galactolipid,cholesterol, plasmalogens) andchloroform-methanol extractaEle pro-tein (proteolipid protein). The re-

sults suggest thet the rates of li-pid accumulation in suckling ratsare related to the body and braingrowth. (137)

GRANDEE, O.M. and HOWARD, E. Malnu-trition In Infancy and Brain Ot-velopeent. Journal of Pediatrics

75:732, 1969.

The importance of regional determin-ation of DNA in the brain, and theneed to clarify the function?! sig-nificance of these alterations inbrain composition Is discussed.

(138)

31

GUTHRIE, H.A. and BROWN, H.L. Ef-

fect of Severe Undernutrition inEarly Life on Growth Brain Sizeand Composition in Adult Rats.Journal of Nutrition, 94:WIT1968.

A study was undertaken to determinethe effect of varying periods of un-dernutrition in postnate life on

the size and chemical coopositionof the brain in rehabilitated adultanimals. Undernutrition during suck-ling caused a degree of stunting ofbody size that was only partiallyreversed by nutritional rehabilita-tion. Brain size and brain DNA weredepressed by undernutrition in thepreweaning period but were not af-fected further by depi'vatIon inthe postweaning period. (139)

HOWARD, E. and GRANOFF, D.H. Effectof Neonatal Food Restrictions inMice on Brain Growth, DNA, andCholesterol. and on P.Jult Delay-ed Response Learning. Journal orNutrition, 95:111, 1968.

This study was designed to examinethe long-term effects of a limitedperiod of nutritional restrictionon ultimate brain size and function-al capacity. At 9 months, body,cerebral and cerebellar weightswere reduced in the males by 17, 7and 14$, respectively, below C001

trol values. Total DNA was reducedIn in the cerebrum and 22$ in thee.erebellum. Cerebral cholesterolwas reduced slightly. Despite thesebrain changes, the restrictedgroups showed no lasting impairmentIn voluntary running, in learning aLashley type III maze, or a visualdiscrimination with escape from wa-ter as a reward. (140)

HURLEY, L.S. The Consequences of Fe-tal impoverishment. Nutrition To-day, 3(4):2, 1968.

The role of nutritional factors onprenatal development is discussedin general. Specific investigationon the offspring of zinc and mangen-ese deficient animals during preg-nancy are described. (141)

McCANCE, R.A. Some Effects of Un-dernutrition. Journal of Pedia-trics,CM:1008, 1964.

Experiments investigating the ef-

fects of undernutrition, as well asundernutrition and rehabilitation,on pigs, nulnea pigs and rats aredescribed. (1421

KEDOVY, H. New Parameters in Neona-tal Growth--Cell Number and CellSize. Journal of Pediatrics, 71

1-371159, 1967.

Studies in the rat fetus show that

early malnutrition interfered withcell division, and later malnutri-tion caused a reduction of indiv-idual cell size. If the number ofcells in the brain is decreased,mental retardation can be anticipa-ted; however, If the cells are onlydecreased in size, an increase ingrowth may catch up to normal site.

(143)

MILLEN, J.V. and WOOLIAM, D.H.M.Maternal Nutrition in RelationUp_ Abnormal fetal Development.Proceedings of the Nutrition So-

19(1):1, 1960.

A review of research Investigatingthe relationship between maternalnutrition and fetal abnormalitiesis provided. (144)

MOUREK, J., HIHVICH, W.A., mYSLIVE-CEK, J. and CALLISON, D.M. TheRole of Nutrition in the Develop-ment of Evoked Cortical Respons-es in Rats. Brain Research, 6:241, 1967.

Maturation of evoked cortical re-sponses to visual and auditory stim-ulation was Investigated In normalas well as in acute and chronicallystarved rats. Some probable mech-anisms of these changes are dis-cussed. (145)

NUTRITION REVIEWS, 27:146, 1969.

Celiularity of Rat Adipose Tis-sue In Relation to Gro.lth, Star-vation, and Obesity.

There are indications that the cell-ularity of adipose tissue can bepermanently modified only duringthe early life--i.e. nutritional in-fluences during this time may be ex-tremely important. Certain metabol-ic processes in adipose tissue seemto be a function of cell number andnot cell size. (146)

NUTRITION REVIEWS, 22(8):244, 1964.Diet, Development and intelligene.

Second generation fAts fed a margi-nal African type diet showed retar-ded growth and development and poor-er Intelligence test scores thandid control rats. (147)

NUTRITION REVIEWS, 23:211, 1965.

Early Weaning, Diet *Ad Intellisgehte.

Rats weaned at 15 days of age to astock ration showed a poorer abili-ty to master and to remember a mazethan those weaned at 30 days. When

rats %fere weaned at an earlier ageto a high fat diet they respondedto the maze test as well or betterthan those weaned at the later date.

(148)

NUTRITION REVIEWS, 25:334, 1967.

Underfeeding and Brain Develop:ment.

This is a review of a study onyoung rats that were selett;v?ly un-dernourished in total quantity offood, but not in quality. Brain

weight was reduced in the deprivedrats, and brain total lipid, phos-pholipid, and cholesterol were re-duced by the same relative amountsas brain weight. (1119)

NUTRITION REVIEWS, 25:185, 1967.

Undernutrition and Developmentof the Central Nervous Systemin the Pig.

A review of a study on growth of

spinal cord and brain regions in un-dernourished and control groups ofpigs. (ISO)

OGATA, K., K1DO, H., ABE, S., ROWS-AWA, Y. and SATAKE, M. Activityof Protein Synthesis of the

Brain of ProteinDeficient Pats.IN: Scrimshaw, N.S. and Gordon,J.E., eds. Malnutrition, learn-ing, and Behavior. Cambridge:MIT Press, 131, 1968.

The incorporation of C1 k-leucine in-

to the total protein by gray mattersli:es and by a cell-free S12 frac-

tion tonsisting of microsownes andcell sap from adult rat brain cor-tex was unaffected by deprivationof dietary protein for 7 days. (151)

OLEWINE, D.A., BARROWS, C.H., Jr.

and SHOCK, N.W. Effects of Redu-ced Dietary Intake on Random andVoluntary Activity In Male Rats.Journal of Gerontology, 19(TT7230, 1964.

Weanling rats subjected to 50 per-cent dietary restriction showed areduction in total random movements,an increase in voluntary wheel ac-tivity and increased activity be-

fore presentation of food as com-pared with controls. These effectswere reversible. (152)

PLATT, B.S. and STEWART, R.J. Ef-

fects of Protein-Calorie Defici-ency on Dogs. 1. Reproduction,Growth and Behavior. Developn.en-tal Medicine and Child Neurology,10:3, 1968.

Dogs maintained from weaning on di-ets of low protein value grow slow-ly and develop changes in theirbones, brains and behavior. Many ofthe abnormalities of gait, growthand electroencephalographic patterndisappear when the deficient ani-mals are given diets of high pro-tein value. (153)

PLATT, B.S. and STEWART, R.J. Ef-

fects of Protein-Calorie Defici-ency in Dogs. 2. MorphologicalChanges in the Nervous System.Developmental Medicine and ChildNeurology, 11:174, 1969.

The morphological changes observedin the dogs are discussed in rela-tion to clinical signs described inmalnourished children. It is sug-gested that malnutrition during in-trauterine and early postnatal lifemay lead to irreversible -hangeswithin the central nervous vstem.

(154)

34

RAJALAKSHMI, R., GOVINDARAJAN, K.,

and RAMAKRISHNAN, C. Effects ofDietary Protein Content on Vis-ual Discrimination, Learning andBrain Biochemistry in the AlbinoRat. Journal of Neurochemistry,12 4):261, 1965.

Groups of albino rats, aged 1 month,6 months and 12 months were main-tained on protein deficient dietsfor 4 to 6 months. They were test-ed psychologically, then killed,and the brain was analyzed chemical-ly. They were found to performless well on visual discriminationlearning than controls, and some

enzymes and amino acids levels werelow. (155)

SCHAIN, R.J., CARVER, M.J., COPEN-HAVER, J.H. and UNDEROAHL, N.R.Protein Metabolism in the Devel-oping Brain: Influence of Birthand Gestational Age. Science,156(3777):984, 1967.

Brain synthesis decreases with agein young animals primarily in thefirst days of life. Whether this

decrease is due to gestational age

or to birth itself is unclear. Ex-

periments with newborn pigs suggestthat birth factors result in a

sharp decrease in amino acid incor-poration into brain protein, irres-pective of gestational age. (156)

SERENI, F., PRINCIPt, N., PERLETTI.L. and SERENI, L.P. Undernutri-tion and the Developing Rat

Brain. Biologic Neonatorum, 10Tg7i54, 1966.

Acetylcholinestera,,e activity, nor-epinephrine concentration, and 5-OHtryptamine concentration in rat

brain were significantly lowered byundernutrition during the sucklingperiod. Undernutrition caused a

slowing of body weight and brain

weight, growth affecting most those

r_

rats subjected lo undernutritionfor 35 days. (157)

SHERWIN, R.W. Perinatal Nutritionas a Developmental Determinant.Nutrition News, 30(0:13, 1967.

The effects on rats of manipulationcf the maternal diet during gesta-tion and/or lactation are discussed.Data showed the inadequacy of bodyweight as an index of functional de-velopment. (158)

SIMONSON, M., SHERWIN, R.W., HANSON,H.H. and CHOW, B F. Maze Perfor-mance of Offspring of UnderfedMother Rats. Federation Proceed-ings, 27:727, 1968.

Progeny of mother rats on 50% diet-ary restricition during gestationand lactation were fed ad libitumafter weaning. They had means ofrunning time and errors double thatof controls during the first trialon an elevated multiple T maze.Thereafter they required moretrials to reach a certain criterionand made more errors. (159)

SIMONSON, M., SHERWIN, R.W., ANIL-ANE, J.K., YU, W.Y. and CHOW, B.F. Neuromotor Development, in

Progeny of Underfed Mother Rats.Journal of Nutrition, 98(1):18,1969.

Offspring of mother rats, subjectedto 50% dietary restrictions duringgestation alone or during gestationand lactation, displayed delays ofup to two weeks in neuromotor devel-opment. Lesser delays occurred withthe less dietary restricted rats.Abnormal activity occurred withboth types of progeny, but weightdeficits did not occur with thoserestricted during gestation alone.

(160)

SIMONSON, J., YU, W., ANILANE, J.

K., SHERWIN, R. and CHOW, B.F.

Studies of Development in Pro-geny of Underfed Rats. Feder-atiun Proceedings, 26:519, 1967.

Progeny of rats on 50% restricteddiets during gestation and lacta-tion demonstrated physical develop-ment, initiation of movement and

response to stimuli later than con-trols but at a lower body weight.Movements requiring extensive coor-dination showed the longest delay

and did not occur at a lower bodyweight. (161)

STEWART, R.J.C. and PLATT, B.S. Ner-vous System Damage in Experimen-tal Protein-Calorie Deficiency.IN: Scrimshaw, N.S. and Gordon,J.E., eds. Malnutrition, Learn-ing, and Behavior. Cambridge:MIT Press, 168, 1968.

Nervous system changes in protein-calorie deficient pigs are descri-bed, as well as nervous system chan-ges in dogs born to protein depriv-ed mothers. (162)

WINICK, M. Food, Time, and CellularGrowth of the Brain. New York

Journal of Medicine, 69:302,

1969.

A general restatement of his arti-

cle in Nutrition Review, July,

1968 is given. (163)

WINICK, M. Nutrition and Cell

Growth. Nutrition Review, 26:

195, 1968.

Discussion of the use of DNA con-tent to measure brain cell numberand weight; and the variation in

growth for different regions of thebrain is presented. (164)

r

WINICK, M., FISH, I. and ROSSO, P.Cellular Recovery in Rat TissuesAfter a Brief Period of NeonatalMalnutrition. Journal of Nutri-tion, 95(1+):623, 1968.

Rats undernourished for the first 9days of life and then adequatelyfed until weaning, did not show areduction in cell number in variousorgans. This indicates that optil.umfeeding, begun during the period ofactive cell division, will correctcellular deficiencies caused by mal-nutrition. (165)

WINICK, M. and NOBLE, A. CellularResponse in Rats During Malnutri-tion at Various Ages. Journalof Nutrition, B9(3):300, 1966.

Studies on rats show that cellulareffects of malnutrition depend on

the growth phase at the time of mal-nutrition. Early malnutrition im-pedes cell division which is irre-versible. Later malnutrition causesa reduction in cell size but can becorrected with adequate feeding.

(166)

ZAMENHOF, S., VAN MAF1HENS, E. andMARGOLIC, F.L. UNA (Cell Number)and Protein in Neonatal Brain:

Alteration by Maternal DietaryProtein Restriction. Science,160(3825):322, 196117

Female rats were maintained on 8 or27 percent protein diet by a pair-feeding schedule for 1 month beforemating and throughout gestation.The brains of newborn rats from fe-males on the 8 percent protein dietcontained significantly less DNA,nd protein compared to the progenyof the females on the 27 percentdiet. This quantitative alterationin number, as well as the qualita-tive one (protein per cell), mayconstitute a basis for the frequent-

ly reported impaired behavior of

the offspring from protein deprivedmothers. (167)

ZIMMERMAN, R.R. Effects of Age, Ex-perience and Malnourishment onObject Retention in Learnhalet.Perceptual Motor Skills, 28:867,1969.

Repeated presentation of 100 6-trialproblems produced significant reten-tion of individual object discrimin-ations in both 25-month-old and 6-month-old infant monkeys. Depriva-tion in the form of malnutrition of6-month-old monkeys produced superi-or performance in intraproblemlearning and subsequent retention,but the retention loss remained con-stant. (168)

fli

Vitamin and Mineral Deficiencies

Thiamine

ALLSOP, J. and TURNER, B. Cerebel-lar Degeneration Associated withChronic Alcoholism. Journal of

Neurological Science, 3:238,

1966.

The neuropathological details of 7autopsied cases are presented. The

changes of Wernicke's encephalo-pathy were found in all but onecase. The significance of this par-ticular syndrome in relationship toatrophy of the vermis is discussedin the light of cerebellar physiol-ogy. It is concluded that chronic

alcoholism may be associated withthis form of cerebeliar degenera-tion. (169)

COLLINS, G.H. An Electron Microsco-pic Study of Remyeiination in

the Brainstem of Thiamine Defici-ent Rats. American Journal of

Pathology, 48:259, 1966.

A report on the process of remyelin-ation in a chronic lesion in vita-min deficient rats in a restrictedarea in the central nervous system.The observations suggest that remye-lination in the central nervous sys-tem is not restricted to a singlepattern, but may be accomplished ina number of ways dependent upon thegeometric features of the lesion aswell as, perhaps, metAbolic condi-tions at the time. (170)

COLLINS, G.H. Glial Cell Changesin the Brainstem of Thiamine De-ficient Rats. American Journalof Pathology, 50:791, 1967.

3 ri

A study of the brainstems of thia-mine deficient rats reveals a ser-ies of alterations involving glialcells, which ran be related to thefurther development of tissue break-down. An attempt is made to corre-late this data with biochemicaldata which suggest that oligodendro-cytes, with their high transkelot-ase activity, would be the most pro-bable tissue element affected bythiamine deficiency. This, however,is not conclusive. It is apparentthat glial cells are affected be-fore other tissue components. Themechanism whereby these changes mayaffect other parenchymal elementsis discussed. (171)

FRANTZEN, E. Wernicke's Encephalo-pathy: 3 Cases Occurring in Con-nection with Severe Malnutrition.Acta Neurologica Scandinavica,42:426, 1966.

The symptoms of Wernicke's encephal-ography are described and the aeti-ology and pathology discussed.Three case histories of patients ad-mitted to the department of neurology with symptome of W.e. are re-ported. Two of the patients werechronic alcoholics, while the thirdhad been on hunger strike formonths. The results of clinical

neurological investigation supple-mented by electro-encephalographyand air encephalography are report-ed. (172)

GREENHOUSE, A.H. and SCHNECK, S.A.Subacute Necrotizinq Encephalomy-elopathy. A Reappraisal of the

Thiamine Deficiency Hypothesis.Neurology, 18:1, 1968.

Subacute necrotizing encephalomyel-opathy is a disorder of early infan-cy with htstopathologic findingswhich closely resemble Wernicke'sdisease. A defect in metabolic pro-cesses involving thiamine utiliza-tion seems a more likely etiologicexplanation for this syndrome. (173)

LOPEZ, R.I. and COLLINS, G.H. Wer-

nicke's Encephalopathy. A Compli-cation of Crironic Hemodialysis.Archives of Neurology, 18:248,1968.

This is a report of a patient suf-fering from central pontine myelino-sis in association with Wernicke'sencephalopathy, along with chronicrenal failure. Thiamine deficiencywas suspected 35 one of the etiol-ogical conditions in this case.

Many other complicating factorswere present. (174)

MANCALL, E.L. and McENTEE, W.J. Al-terations of the Cerebellar Cor-tex in Nutritional Encephalopa-/i. Neurology, 15(4):303, 1965.

A case study of an 18-year-old boy,severely undernourished and havingthe pathological alterations of Wer-nicke's encephalopathy, was presen-ted. The undernourished state wasdue primarily to a partial intesti-nal obstruction resulting from con-genital duodenal bands. Since the

patient was a non-alcoholic it wasconcluded that the cerebellar dis-order was due to nutritional deple-tion rather than a direct toxic af-fect of alcohol. (175)

NEWMAN, A.J. Suspected Thiamine De-ficiency in Pigs. Veterninary Re-cord, 84:577, 1969.

Three case reviews of pigs exhibit-ing recumbency, irregular breath-ing, apparent blindness, and the in-ability to walk properly are given.The only consistent feature of thethree cases was a movement betweenfarms and a change of diet. Admin-istration of thiamine brought rapidimprovement. A possible explana-tion is that a disturbance in themetabolism of nutrients may destroyor inhibit available thiamine.

(176)

NUTRITION REVIEWS, 27:54, 1969.

Early Brain Stem Lesions in Thia-mine Deficient Rats.

The early lesions of acute thiaminedeficient rats show swelling ofglial cell cytoplasm which is coin-cident with the onset of neurologi-cal signs. Of 68 thiamine defici-ent rats 37 exhibited neurologicalsigns of deficiency, and 32 had dem-onstrable lesions. (177)

PENA, C.E. Wernicke's Encephalo-pathy. Report of Seven Caseswith Severe Nerve Cell Changesin the Mamillary Bodies. Ameri-can Journal of Clinical Patholo-gy, 51:603, 1969.

Among 92 cases of Wernicke's ence-phalopathy received, 7 were foundthat exhibited unusual changes ofthe neurons of the mamillary bodies.Whether the changes are due to ax-onal injury, to transynaptic degen-eration, or to a direct metaboliceffect on the neurons, secondary tothiamine deficiency, still remainsto be determined. (178)

38

ROd:ATSON, D.M., WASAN, S.M., and

SKINNER, D.B. Ultrastructural

Features of Brain Stem Lesions

of Thiamine Deficient Rats. Amer-ican Journal of Pathology, 52:

1081, 1968.

The lesions of acute severe thia-mine deficient rats were studied byelectron microscopy. It is suggest-ed that the failure of active trans-port results from interference cf

production of chemical energy by

thiamine dependent enzymes involvedin carbohydrate metabolism. (179)

TELLEZ, I. and TERRY, R.D. Fine

Structures of the Early Changesin the Vestibular Nuclei of theThiamine Deficient Rat. AmericanJournal of Pathology, 52:777,

1968.

The effect of thiamine deficiencyon the fine structure of the later-al vestibular nucleus was investi-gated. Material from 9 control ratsand 6 thiamine deficient rats withacute central nervous system symp-toms were studied with the electronmicroscope. (180)

YONEZAWA, T. and 1WANAMI, H. An Ex-perimental Study of Thiamine De-ficiency in Nervous Tissue, Us-ing Tissue Culture Technics.Journal of Neuropathology and Ex-perimental Neurology, 25(3) 362,1966.

In vitro studies of thiamine defi-ciency in nervous tissue of rats

and mice are reported. The general-ized degeneration seen with high an-timetabolite concentrations may re-sult from the inhibition of all theoxidative reactions in which thia-

mine pyrophosphate is involved. Fur-thermore, the severe myelin degener-

ation may result from the inactivation of transketolase in the myelin-

forming cells. (181)

I9

Folic Acid and Vitamin B12

ARAKAWA, T., MIZUNO, T., HONDA, Y.,TAMURA, T., SAKAI, K., TATSUMI,S., CHIBA, F. and COURSIN, D.B.Brain Function of Infants Fed OnMilk From Mothers With Low Serumrotate Levels. Toholc, Journal ofExperimental Medicine, 97:391,1969.

Brain function of exclusivelybreast fed infants from 3 to 6

months old was examined by electro-encephalography. Infants of motherswith low serum folacin valuesshowed a definite delay in matura-tion patterns of the brain function.

(182)

ARAKAWA, T., MIZUNO, T. and SAKAI,K. Electroencephalographic Fre-quency Patterns of Rats TreatedWith Aminopterin in Early Infan-cy, iohoku Journal of Experimen-tal Medicine, 97:385, 1969.

The aim of the present study is toexamine the effect of folic acid de-ficiency upon the maturation of

brain function of rats in early in-fancy. Folic acid deficiency was in-duced by injection of aminopterinto dams and offspring soon afterbirth. The maturation of the brainwas evaluated by frequency analysisof electro2ncephalograms. Resultsshowed definite differences fromanalytic patterns of the EEG. (183)

FLEMING, A.F. and DADA, T.O. FolicAcid and Neurological Oisease.Lancet, 1(7428):97, 1966.

Seven of 15 consecutive Nigerian pa-tients with neurologic disease hadlow serum folic acid activity. Theserum folic acid range was low tointermediate in 12.3 percent of 228Nigerian blood donors and in none

40

of 50 healthy Europeans. Folic acidsupplements are likely to be usefuladjuncts to vitamin B preparationsfrequently prescribed to patientswith neuropathies. (1814)

GORDON, N. Folic Acid Deficiencyfrom Anticonvulsant Therapy. De-velopmental Medicine and ChildNeurology, 10(4):497, 1968.

Folic acid deficiency may resultfrom treatment with various antiep-ileptic drugs. This seems morelikely to be due to an interferencewith folic acid metabolism than todefective absorption. Seventy-twopatients on such treatment were stu-died. The possible results of thisdeficiency are discussed with par-ticular reference to the role of

folic acid in protein synthesis.

(185)

HERBERT, V. Inborn Errors in FolateMetabolism--A Cause of Mental Re-tardation? Annals of InternalMedicine, 68:956, 1968.

A possible link between defectivefolate metabolism and mental retar-dation is discussed. It is sugges-ted that serum folate level deter-mination be done on all congenitalcases of mental retardation. (186)

HUNTER, R. and MATTHEWS, D.M. Men-tal Symptoms in Vitamin-8-12 Def-iciency. Lancet, 2(7415):738,1965.

A wide variety of psychiatric mani-festations of vitamin B-I2 deficien-ri may precede anemia or gross neur-ological signs by months or years.Routine screening tests for 8-I2 de-ficiency were recommended in psychi-atric practice. (187)

KAUL, K.K., PRASAN, N.G. and CHOWD-HRY, R.M. Further Observationson the Syndrome of Tremors in In-fants. Indian Pediatrics, 1:219,

clinical study of sixteen Infantspresenting with the characteristicfeatures of the syndrome of tremorsconsisting of delayed development,mental retardation, skin pigmenta-tion, anaemia and tremors, is pre-sented. A similar clinical pictureresulting from vitamin B12 deficien-

cy and megaloblastic anaemia, hasbeen reported by some workers. Ourprevious as well as the present ob-servations indicate that the syn-

drome is not the result of vitaminB12

deficiency or of megaloblastic

anaemia. (188)

McNICHOLL, 8. and EGAN, B. Congen-ital Pernicious Anemia: Effects

on Growth, Brain, and Absorption

of 812'Pediatrics, 42(1):11 WT

1968.

Congenital pernicious anemia fromvitamin B

12deficiency affects

growth and development. Case re-

ports of 3 children with megaloblas-tic anemia at 1 year of age demon-strated a deficiency of gastric in-trinsic factor. Spinal cord andcerebral lesions may also occur inthe vitamin B

12deficiency of con-

genital pernicious anemia; the factthat the IQs of the patients wereabout 70 suggests that minor cere-bral damage may have occurred. (189)

MEDICAL WORLD NEwS, 800:40, 1967.Lack of B-Complex Vitamin Threa-tens Mother and Fe:us.

Although severe folic acid defici-ency in pregnancy is associatedwith maternal megaloblastic anemia,

the presence of lesser degrees offolic acid deficiency in 22 percentof 250 pregnant women indicates

that this deficiency may be associa-ted with placental abruptlon, mis-carriage, and congenital defects.

(190)

MILLER, D.R. Serum Folate Deficien-cy in Children Receiving Anti-Convulsant Therapy. Pediatrics,11(3):630, 1968.

The occurrence of subnormal serumfolic acid levels among 37 randomlyselected epileptic children (ages 5to 20 years) treated with antl-con-vulsants was 51.2 percent; slight

macrocytosis was found in 18.8 per-cent. The etiology of decreased fo-late levels in patients receivinganti-convulsant medication is un-

known, but the drug eficacy may

depend on drug-induced folate defi-ciency. (191)

PANT, S.S., ASBURY, A.K. and RICH-ARDSON, E.P., Jr. The MyelopAthyof Pernicious Anemia. A Neuro-

pathological Reappraisal. Acta

Neurologica Scandanavica, 44:1,

1968.

The neuropathological changes in 41cases of myelopathy associated withpernicious anemia, representing 40

years of experience at the Massa-chusetts General Hospital were re-evaluated. Observations suggest

that the largest nerve fibers with

the thickest myelin sheaths are

most vulnerable to the deficiencystate. (192)

REYNOLDS, E.H., CHANARIN, I., MIL-

HER, G. and MATTHEWS, D.M. Anti-Convulsant Therapy, Folic Acid

and Vitamin B12

Metabolism and

Mental Symptoms. Epilepsie, 7(4):261, 1966.

Evaluation of 62 epileptic patientsIndicates that anticonvulsant medi-cation has antifolate activity

which in turn causes megaloblasticanemia and perhaps a variety of or-ganic neurological disorders inclu-ding mental retardation and psychi-atric disorders. (193)

REYNOLDS, E.H., PREECE, J. and CHAN-ARIN, I. Folic Acid and Anticon-vulsants. Lancet, 1:1264, 1969.

There were significant differencesin values for folacin in serum andcerehrospinal fluid between 60 epil-eptic patients treated with anticon-vulsant drugs and controls. Fola-

cin values in different mental dis-orders are tabulated. (194)

REYNOLDS, E.H., CHANARIN, 1., andMATTHEWS, D.M. NeuropsychiatricAspects of Anticonvulsant Meglo-blastic Anemia. Lancet, 1(7539):394, 1968.

A 20-year-old girl with epilepsycontrolled by phenytoin and primi-done developed a drug-induced mega-loblastic anemia. Successful treat-ment of the anemia with folic acidwas associated with an increase infit frequency and an improvement inher mental state. (195)

STONE, M., LUHBY, L., FELDMAN, R.,GORDON, M. and COOPERMAN, J. Fo-lic Acid Metabolism in Pregnancy.American Journal of Obstetricsand Gynecology, 99(5):638, 1967.

Studies of folic acid metabolism in250 unselected pregnant women re-vealed that folic acid deficiency;(1) was present in 22 percent, (2)

could be present without overt meg-aloblastic anemia, (3) increased in

severity at or near term, (4) in-

creased in complicated pregnancies,

and (5) could be of significance Ininfant growth and development. Fo-

lic acid deficiency has been sug-gested as a cause of fetal brain

damage, mental rer.rdation and re-tarded growth and development. (196)

TORRES, I., SMITH, W.T. and OXNARD,C. Degeneration of the Peripher-al and Central Nervous System inVitamin B

12Deficient Monkeys.

Experientia, 25:273, 1969.

This is a further study based onthe findings of Oxnard and Smith,(Nature, 210, 507, 1966), regardingneurological degeneration in vita-min B

12deficient monkeys. There

was degeneration found, and the ap-

pearance of regeneration was obser-ved in a group of monkeys treatedto reduce the B12 deficiency. (197)

WALKER, F.A., AGARWAL, A.B. and

SINGH, R. The Importance of theFalsely Positive Reaction. Jour-nal of Pediatrics, 75:344, 1969.

Infants with failure to thri,e andwho present false positive test forketone and acetoacetic acid in theurine nay have a treatable metabo-lic disorder. A case of a child withvitamin B

12deficiency is presented.

(198)

WOODWARD, J.C. and NEWBERNE, P.M.The Pathogenesis of Hydrocepha-lus in Newborn Rats Deficient inVitamin B

12 .Journal of Embryol-

ogy and Experimental Morphology,17(0:117, 1967.

The hydrocephalus ,- _ is caused infetal rats by maternal deficiencyof vitamin B

12was not influenced

by addition of X-methyl folic acid

or choline chloride added to thematernal diet. (199)

Other Vitamins

ARAKAWA, T., MIZUNO, T., AND CHIBA,F. Frequency Analysis of EEG'sand Latency of Photically Induc-ed Average Evoked Responses In

Children With Ariboflavinosis.Tohoku Journal of ExperimentalMedicine, 94:327, 1968.

Frequency analysis of electroenceph-alograms and estimation of the aver-age latency of photically inducedevoked responses were carried outon children aged 8 to 9 years withor without ariboflavinosis associa-ted with low serum folate levels.

(200)

BOWER, B.D. Pyridoxine, Tryptophan,and Epilepsy. Developmental Med-icine and Child Neurology, 7(1):

73, 1965.

Pyridoxine deficiency (a result ofan abnormal diet) has long been sus-pect as a cause of cryptogenic epi-lepsy. The history of this defici-ency, the measurement of its occur-rence with the tryptophan-load test,and the therapeutic application ofpyridoxine were reviewed. It was

concluded that the tryptophan test,as commonly used, examines only apyridoxine-dependent pathway (an in-born error of metabolism) and thatpyridoxine has not been demonstra-ted to be highly effective in thetreatment of epilepsy. (201)

DREYFUS, P.M. Nutritional Disordersof the Nervous System. Part I --

Specific Vitamin Deficiencies.Lippincott's Medical Science, 17(3):44, 1966.

Influences of vitamin deficiencieson the nervous system are discussedin terms of various nutritional syn-dromes. (202)

EBERLE, E.D. and EIDUSON, S. Effectof Pyridoxine Deficiency on Aro-matic L-Amino Acid DecarboxylaseIn the Developing Rat Liver andBrain. Journal of Neurochemistry,15:1071, 1968.

Maternal pyridoxine deficiency be-gun 2 weeks before mating and con-tinued throughout pregnancy and thenursing period resulted in dimin-ished weight gains in the brain,the liver and the body in the first16 days of life, as well as loweredlevels of the aromatic 1-amino aciddecarboxylasc in both brain and

liver tissue. (203)

FRATTA, I., ZAK, S.B., GREENGARD ,

P. and SIGG, E.B. Fetal Deathfrom Nicotinamide Deficient Dietand its Prevention by Chlorproma-zine and Imipramine. Science,145(3639):1429, 1964.

Fetal death and resorption causedby a nicotinamide deficient dietfed to pregnant rats can be preven-ted by administration of eitherchlorpromazine or imipramine. Theresults demonstrated that in ani-mals fed the deficient diet the fe-tuses failed to survive and the ni-cotinamide adenine dinucleotide con-centration was low; however, treat-ment with chlorpromazine or imipra-mine reversed these effects. Higherconcentrations of nicotinamide ade-nine dinucleotide were responsiblefor the survival of the fetuses.

(204)

FRENCH, J.H., GRUETER, B.B., DRUCK-MAN, R. and O'BRIEN, 0. Pyridox-ine and Infantile Myoclonic Sei-zures. Neurology, 15(2):101,1965.

4 3

The effects of pyridoxine on theelectroencephalogram, kynureninaseactivity, and clinical picture of15 children with Infantile spasmswere investigated. The data indica-ted the necessity for employing pyr-idoxine therapy In neonatal convul-sions which have not responded to

anticonvulsants. (205)

HOWELL, J.M. and THOMPSON, J.N. Ob-servations on the Lesions in Vit-amin A Deficient Adult Fowlswith Particular Reference to

Changes in Bone and Central Ner-vous System. British Journal ofExperimental Pathology, 48(4):450, 1967.

Nine cockerels and nine hens werefed hatchery diets free of vitaminA but supplemented with retinoicacid. They were made deficient in

vitamin A by discontinuing the sup-plement and the deficiency signswere described. (206)

McK1BBIN, B. and PORTER, R.W. TheIncidence of Vitamin C Deficien-CIrTtier. Develop-mental Medicine and Child Neurol-ogy, 3:338, 1967.

Cases with meningomyelocele have ahigh incidence of vitamin C defici-ency. Twenty-five cases with men-ingomyelocele were compared with 16cases with orthopedic problems, butwithout neurologic diseases. The

stress of repeated operative proce-dures in cases with meningomyelo-cele may deplete body stores of vi-tamin C. All cases with meningomye-locele should be on replacement vi-tamin C therapy. (207)

PILLAY, V.K. Acre:ephalosyndacttly.In Singapore. A Study of Five

Chinese Males. Journal of Boneand Joint Surgery, 46:94, 1964.

This syndrome is noted by: high,short, broad skull; crowded teeth;syndactylism of hands and feet; men-tal retardation; but, no reductionin life span. Etiology: Syphilis,

rickets, or other vitamin deficien-cies; disturbances of endocrinefunction; and, injury at birth haveall been attributed to this condi-tion. (208)

SOULAYROL, R., MESDJIAN, E., LOB,H., TASSINARI, C.A. and ROGER, J.The Tryptophan Loading Test in

Epileptic Children. Epilepsia,6(4) :310, 1965.

The Wachstein and Gudaitis trypto-phan loading test was performed on138 (120 mentally retarded) chronicepileptic children, 2 to 20 yearsof age, before and during treatmentwith vitamin B

6.Non-convulsive gen-

eralized epilepsy was seen especial-ly in the vitamin-deficient group,and grand mal seizures were morefrequent than tonic seizures. Fol-

low-up studies after vitamin B6

therapy showed a correction in themetabolic disturbance with reversalto a negative tryptophan loadingtest but with little, if any, ef-

fect on the clinical or electroen-cephalographic manirestations of

epilepsy. (209)

STEWART, C.N., BHAGAVAN, H.N. andCOURS1N, D.8. Effect of BiotinDeficiency on Escape and Avoid-ance Learningin Rats. Journalof Nutrition, 88:427, 1966.

4 41

Biotin deficient rats exhibited im-parted avoidance learning. Escapelearning was not affected, whichsuggests that the impaired avoid-

ance learning was not due to motorimpairment. Behavioral ano biochem-ical evidence suggest that the ef-fects of the deficiency may be onthe central nervous system. (2(0)

45

Minerals

EVERSON, G.J., SHRADER, R.E. andWANG, T.I. Chemical and Morpho-logical Lhanges in the Brains ofCopper-Deficient Guinea Pigs.

Journal of Nutrition, 96:115,1968.

The histological findings of thebrain, cord, and nerve of copper-deficient guinea pigs at birth andthe distribution of phospholipidsin a small number of control andcopper-deficient animals at birthand 63 days of age were investiga-ted. Cerebellar folia were missingor malformed in some of the copper-deficient animals at birth andthroughout the brain there was un-derdevelopment of myelin. (211)

EVERSON, G.J., TSAI, N.C. and WANG,T.I. Copper Deficiency in theGuinea Pig. Journal of Nutri-

tion, 93:533. 1967.

Copper deficiency was investigatedin the guinea pig because this spe-cies undergoes considerable myelin-ation in utero. Brain abnormalities

and aneurisms were observed amongthe progeny cf female guinea pigson a copper deficient diet. (212)

O'DELL, Q.L. Trace Elements in Em-bryonic Develooment. federation1)roteedings, 22(1)099, 1968.

Deficiencies of essential mineralsin the maternal diet causes damage

to the developing embryo, but thenature and severity of the damagevaries from element to element. A

relatively narrow ((Weal range ofnutrient intake results in dAdnai-iRS. The efft.11A of cobalamin, cog'per, time and iron deficiencies arediscussed. (213)

OLNEY, J.W. Brain Lesions, Obesityand Other Disturbances in MiceTreated with Monosodium Glutam-ate. Science, 164:719, 1969.

In newborn mice subcutaneous injec-tions of monosodium glutamate indu-ced neuronal necrosis on several re-gions of the developing brain, in-

cluding the hypothalamus. (214)

O'NEAL, V.M., PIA, G.W., FOX, h.R.

S., GIBSON, F.S. and FRY, B.E.,Jr. Effect of Zinc Deficiencyand Restricted Feeding on Pro-tein and Ribonucleic Acid Metab-°list' of Rat Brain. Journal ofNutrition, 100:V9-17 1970.

Experiments were performed on youngrats to support evidence that malnu-trition during Infancy inhibits max-imum mental development of the in-dividual. Tests indicate zinc is

necessary for optimal synthesis ofRNA and protein which is Importantto brain metabolism. kestricted-fedand zinc deficient rats grew veryslowly, and data showed a function-al deficiency of zinc in these ratseven when zinc content in the brainwas normal. Results show the rela-tionship of malnutrition to metabol-ic processes of the brain to be as-sociated with aspects of mental per-formance. (215)

NUTRIENT INTOXICATION

ADAMSONS, K., Jr. and JOELSSO4, I.The Effects of Pharracolic Ac-ents Upon the Fetus end Nc,rborn.Amarican Journal of Obstetricsand Gynecology, 66(3):437, 1966.

The most corcronly used drugs in ob-stetric practice are revic,ed. The

effects of administration of agentsincluding vitamin K, proteins andthose resulting in fetal goiter aregiven. (216)

AMERICAN ACADEMY OF PEDIATRICS, COM-MITTEE ON NUTRITION. The Rela-

tion Bet..;een Infantile Hypercal-cerla end Vitamin O--PublicHealth Irplications in No,thcrica. PediatriCT7TarilgY71967.

Excessive Intake of vitamin 0 may

produce hypercalcemia with serioussequellae. The mild form of infan-tile hypercalcemia, which is readi-ly reversible with conservativetherapy, consists of azotemia andfailure to thrive. The more severeform, which probably has its onsetin utero, includes a characteristic"elfin" facies, rental retardation,and supravalvular aortic stenosis.

(217)

SAANES, A.C. The Fetal Environrant:

OrL.Ds and Chemicals. IX: Barnes.A.C., ed. Intra-Uterine Develop*rent. Philadelphia: Lea and Feb'iger, 962, 1968.

It is difficult to establish sped'fie causal relationships betweenteratogenesis and Chemical agents

administered to pregnant but

it is probable that S070 chileiren

with defects due to chemical con-tact during the intrauterine periodare being produced at all tires.lead, vitamin K and nicotine, amongother drugs and chenicais are asso-ciated with teratongenesis in hum-ans, and human fetal graAl. and id-velopment have been advt.:rsely affec-ted by exposure to them. (218)

BRADY, J.P. and WILLiAmS, H.C. met-nesiul Intoxication in a Pre-a-turc Irzant. PediatriTT,71Yrir:100, 1667.

A mother treated with magnesium sul-fate for pre-colampsia gave birthto a premature infant with toxic ef-fects of motor and respiratory par-alysis caused by hypermasnesemiawhich were immediately reversed by4,wering the serum magnesium level.

(219)

COCHAANC, V.A. Overnutrition in

Prenatal and Neonatal Life: A

Problem? Canadian Medical Asso-ciation Journal, 93(17):893,1965.

Clinical and biochemical disordersoccurring in the newborn which arete:ated to the excessive ingestionof calories, fat, protein, vitz,ItSand minerals before and after birthwere outlined. Particular refer-ence Is made to the ingestion of nu-tritional substances during pr,:irart-

cy in aMOurai that are relativelyinnocuous to the mother but may beharmful to the infant In utero,(2:0)

COLEMAN, E.N. Infantile Hypercal-cemia and Cardiovascular Lesions.Archives of Disease in Childhood,

40(213):535, 1965.

A report concerning cardiovascularlesions in patients suffering from

infantile hypercalcemia indicates

that congenital endocardial fibroe-lastosis and the myocardial lesionof fibrocystic disease of the pan-creas are related to vitamin D.

(221)

FORBES, G.8., CAFARELLI, C. and MAN-NING, J. Vitamin 0 and Infan-tile Hypercalcemia. Pediatrics,42:203, 1968.

Does the hypercalcemia syndrome rep-resent a form of hypersensitivityto vitamin 07 Twelve cases recent-ly observed showed no history of ex-cessive intake of vitamin O. A caseof excessive intake of vitamin 0was observed and described. (222)

K1MBROUGH, R.D. and GAINES, T.8. Ef-

fect of Organic Phosphorus Com-pounds and Alkylating Agents onthe Rat Fetus. Archives of Envi-ronmental Health. 16(6):805,

1968.

The organic phosphorus compounds,parathion, dichiorvos, and diazinonare somewhat teratolenic in rats

when given in a single dose intra-

peritumeally on the eleventh day ofgestation. the chemica:s were givenin large enough dosage to cause poi-soning symptoms in the dams.Decrea-

sed body weight of the fetus ap-pears to be the most sensitive indi-cator of toxicity. (223)

KOCMMAR, D.M. Studies of Vitamin A-Induced Teratogenes s: 1IYectson Embryonic Mesench)me andipl-OleTium, anTSFT7i&rporalon of

M-Thymid the . Teratology, 1(3):

29. 1968.

The teratogenic action of hypervit-aminosis A was studied experimental-ly with rat embryos, and congenitalmalformations associated with theexcess vitamin were noted. All

treated embryos were growth retard-ed, had abnormal dorsal curvatures,protusion of the mesencephalon, de-creased somite number, and cellulardisorganization. (224)

K1CHHAR, D.M., LARSSON, K.S. and 80-STROM. H. Embryonic Uptake ofS35-Sulfate: Change in Level Fol-lowing Treatment with Some Tera-togenic Agents. Biologia Neona-torum, 12(1):41, 1968.

Effects of teratogenic procedures,namely hypervitaminosis A, trypanblue and cortisone administration,on 535 - sulfate uptake in earlymouse embryos were investigated.

(225)

MANIOS, S.G. and ANTENER, I. A Stu-dy of Vitamin D Metabollso In Id-iokathic Hypercalcemia of infan-cy.. Acta Paediatrica Scandinavi-ca, S5(6):600, 1966.

Effects are cited from tests on amarkedly elevated serum vitamin Dactivity in 2 uniovular female sib-lings with a severe form of idiopa-thic hypercalcemia. Data suggests agenetically determined defect in

the degradation of vitamin D. (226)

MEDICAL WORLD NEWS, 8(10)016, 1967.Placenta is NO Barrier to Mostof Agents.

Excessive vitamin D administrationin pregnant women may result in ab-normalities of the major blood ves-sels. mental retardation, and fail -ire of growth. Excessive vitamin K04, result in hemolytit anemia andkernicterus. (227)

45

NORA, J.J., NORA, A.M., SOMMERVILLE,R.J., HILL, R.M. and McNAPARA, D.G. Maternal Exposure to Poten-tial Teratogens. Journal of theAmerican Medical Association,202(12):1065, 1967.

In children born with anomalies it

was found that each mother had beenexposed to potential teratogenic a-gents at some time during pregnan-cy. No statistical difference wasfound between children with anoma-lies horn to mothers exposed duringthe first trimester and those ofmothers exposed later in pregnancy.Prescription drugs, including ex-cessive vitamin intake, constitutedthe majority of exposures. (228)

PERSSON, B., TUNELL, R. and EKENG-REN, K. Chronic Vitamin A Intox-ication During the First HalfYear of life. Acta PaediatricatilWainavica, 54(I):49, 1965.

A study of chronic hypervitaminosisA effects In infants under 6 monthsof age was reported. Noted were: (1)anorexia, (2) pronounced craniota-bes and occipital edema, (3) antra-cranial pressure, and (4) irritabi-lity. All cases were cured relative-ly fast once vitamin A was discon-tinued. (229)

SMIRKEY, N.C. The innocent Child.Journal of the American MedicalAssociation, 196(5)0418, 1966.

Several fetal and post-natal drugreactions are considered. Excessivevitamin K, given tq a mother justprior to birth, may result in jaudice, kernicterus, mental retarda-tion, spasticity and even death.

(230)

SIMMONS, R.L. and HAWKINS, B.W. Idi-opathic Hypercalcemia of Infancy.Texas State Journal of Medicine,

61(5):407, 1965.

A case of idiopathic hypercalcemiawas reported along with a resume ofpertinent aspects of the disease.The condition may have been causedby an !nborn error of metabolismwhich created a hypersensitivity tosmall doses of vitamin O. (231)

TUNNELL, R., ALLGEN, L.G., JAILING,8. and PERSSON, B. ProphylacticVitamin: A Ooze in Sweden. ActaPaediatrica Scandinavica, 54(1):61, 1965.

A study concerning the prophylacticdosage of vitamin A and the pos-sible risk of hypervitaminosis Awas reported. (232)

43

NUTRIENT METABOLISM AND MENTAL RETARDATION

CARBOHYDRATES AND PROTEIN

ANDERSON, J.M., MILNER, F.D.G. andSTRICH, S.J. Effects of NeonatalHypoglycemia on the Nervous Sys-tem: A Pathological Study. Jour-nal of Neurology, Neurosurgery,and Psychiatry, 30(4):295, 1967.

The n °cropsy findings of three un-

treateo and three treated infantswith hypoglycemia were compared todemonstrate that untreated hypogly-cemia during the first week of lifeis an important cause of brain dam-age. The pathogenesis of brain dam-age from neonatal hypoglycemia isdiscussed. (233)

BRIG, M.A. and 002IEN, J.C. Carbo-hydrate Metabolism in Kwashior-

kor. Lancet, 2(7410:662, 1965.

A study investigated the biochemi-cal mechanism involved in the dis-

turbance of glucose utilization inkwashiorkor. The kwashiorkor pa-

tients were found to have slightlyreduced fasting blood-sugar and di-minished glucose tolerance. Fastingplasma insulin was low and patientshad diminished adrenocortical func-tion. It was suggested that the dis-turbance' in blood-glucose regula-tion could be explained by insulinhypersensitivity and poor pancrea-tic response to Intravenous glucose.

(234)

BLATTNER, R.J. Central Nervous Sys'teat Damage and Hypoglycemia.Journal of Pediatrics, 72(6):904,1968

early diagnosis and treatment of

Congenital hypoglycemia Is Impera-

tive in order to preclude the pot,sibility of severe, irreversible

brain damage resulting in mental

retardation and cerebral palsy. Um-

corrected and even delayed correc-tion of neonatal hypoglycemia isoften fatal. (235)

CHANTLER, C., BAUM, J.D. and NORMAN,D.A. Dextrostix in the Diagnosisof Neonatal Hypoglycemia. Lancet,

2(7531)0395. 1967.

"Dextrostix" (Ames Company) was suc-cessfully used as a screening testto detect hypoglycemia. (236)

CLINICAL PEDIATRICS, 6(2):94, 1967.Hypoglycemia in Infancy. Apprai-sal of the Problem, Methods ofInvest; ation and Possible Assoc-iation of Cataracts.

Three Children demonstrating di-verse aspects of the problem of hy-poglycemia were presented. There

may be a causative association be-tween hypoglycemia and cataractsand hypoglycemia and brain damage.Hypoglycemia is found in several

clinical syndromes including hypo-

pituitarism and growth hormone def-iciency, galactosemia and glycogenstorage disease. (237)

COMM, J.T., GRUNT, J.A. and BRANDT,I .K. NevroSrtdrot4eortatalit-poglycemla. New England Journalof Medicine, 275(5): 236, 1966.

Clinical Vtures and evaluationsof therapy are presented on threeinfants with a neonatal hypoglyce-mia syndrome of unknown etiology.Cortisol was used with success on 1

case, a, zinc glucagone and diaoxide were effective In 2 cases.

(238)

50

COX, M. and DUNN, H.G. IdiopathicHypoglycemia and Children of LowBirth Weight. Developmental Med-icine and Child Neurology, 9(4):430, 1967.

Of 500 infants with a birth weightbelow 4 1/2 pounds, 9 had idiopath-ic neonatal hypoglycemia, and 3 hadidiopathic hypoglycemia after theneonatal period. Fourteen otherchildren wits idiopathic hypoglyce-mia after the neonatal period wereincluded in the study. The outcomewas significantly more abnormal inthe children with hypoglycemia dur-ing or after the neonatal periodthan in other children of low birthweight withoqt hypoglycemia. (239)

CREERY, R.D.G. Hypoglycemia in theNewborn: Diagnosis, Treatment,and Prognosis. DevelopmentalMedicine and Child Neurology, 8(6):746, 1966.

Hypoglycemia is a significant haz-ard to the nervous system. Seriousbrain damage results when it is as-

sociated with cerebral birth injury.

(240)

EHRLICH, A.M. and MARTIN, J.M. Tol-butamide Tolerance Test and Plas-mai-Insulin Response in Childrenwith idiopathic Hypogitsemia.Journal of Pediatrics, 7I(4):485,

1967.

Fifteen children with Idiopathic hy-poglycemia were differentiated fromten normal children by means 00 thetolbutamide tolerance test. the in-sulin-glucose ratio after intraven-ous tolbutamiee and oral glucose ad-ministration shows that childrenwith Idiopathic hypoglycemia havehyp_rinsulinism, which may be theImportant pathogenetic factor inthis disorder. (241)

$1

FISHMAN, R.A. and RASKIN, N.H. Ex-

perimental Uremic Encephalopathy.Permeability and Electrolyte Me-tabolism of Brain and Other Tis-sues. Archives of Neurology, 17111710, 1967.

Acute uremia produced a generalizedincrease in permeability of the

blood brain barrier in a radioiso-tope study of nephrectomized an-imali. This non-specific increasedpermeability in uremia may allowentrance of toxic compounds intothe brain and thus explains the cen-tral nervous system signs of uremia.

(242)

GELLER, H., CHANEY, R. and EYMAN. R.Liver Function and Serum ProteinStudies on Mentally Retarded In-dividuals. American Journal ofMental Deficiency, 72(4):554,1968.

This study was undertaken becauseof the presence of abnormal "liverfunction tests" in a significantnumber of mentally retarded patientswho had been a "control group" inan Investigation of hepatitis at

Pacific State Hospital. It was con-

cerned with determining the rela-

tionship of such tests to institu-tionalization or to biochemical ab-normalities inherent in retarded in-dividuals. (243)

HAWORTH, J.C. and McRAE, K.N. TheNeurological. and DevelopmentalEffects of Neonatal Hypoglycemia:A Follow -Up of 22 Cases. Canad-ian medical Association Journal,

92(16):661, 1965.

Twenty-two infants in Whom hypogly-cemia (blood sugar less than 20 mg./100 ml.) was noted during the firstfew lays of life were followed-upwhen 6 to 30 months of age. this

preliminary study suggests that Ay-poglytemla associated with neurolo-

gical symptoms In the newborn per-iod carries a poor prognosis with

respect to permanent neurologicaldamage. Asymptomatic hypoglycemiamay have a relatively good progno-sis. (244)

HUNTER, A. Perinatal Events and Per-manent Neurological Sequalae.New Zealand MedicAl Journal, 68:108) 1968.

The preliminary results of a pros-pective survey of the developmentof infants who had been at riskfrom hypoxia and biochemical distur-bances in the neonatal period aregiven. Significant neurologicalsigns including cases of mental de-fect, cerebral palsy and epilepsywere found In 22.5 percent of thoseseen at follow up. (245)

JORDAN, W.R. The Pregnant Diabetic.Southern Medical Journal, 60(11):1213, 1967.

A review of 105 pregnant diabeticsshowed that although the diseaseposed a problem, careful attentionpaid to medical and obstetrical com-plications improved the fetal sur-

vival rate. Problems encounteredand treated included: need for In-

creasing insulin dosage, lower ren-al threshold, developing acidosis,

tendency towards toxemia, possiblecatastrophic effect of relativelyminor intercurrent disease, and pre-cipitous fall of insulin require-ments at the termination of pregnan-cy. (246)

LANCET, 1(7538):349, 1966. Carbohy-drate Metabolism in the Newborn.

Insulin secretion Is low and gluecase tolerance reduced during thefirst postnatal days. Infants pre-dominantly affected by symptomatichypoglycemia include: svall-for-dates, premature, smaller of twins,

and infants with respiratory dis-tress or symptoms of cold exposure.In all these categories the liverglycogen is low. (247)

LONG, W.N. and HOLZMAN, G.B. Haz-

ards to the Fetus from MaternalDiabetes. IN: Long, W.N. andHolzman, G.8., eds. Intra-Uter-ine Development. Philadelphia:Lea and febiger, 427, 1968.

Respiratory distress syndrome asso-ciated with prematurity is the lar-gest cause of death of newborns ofdiabetic women. Infants with diabe-tic mothers have problems associa-ted with ketoacidosis, excessivesize, growth retardation because ofmaternal vascular disease, and/orcongenital malformation. (248)

MED1ZAL WORLD liEqS, 8(20):37, 1967.Hormone Shot Saves Diabetics'Babies.

Treatment with epinephrine immedi-ately after birth aids infants ofdiabetic mothers to avoid brain da-mage and respiratory distress cau-

sed by Insulin build up and de-pressed sugar levels. (249)

NAEYE, R.L. Organ Compositicn in

Newborn Parabiotic Twins with

tipaglycemliTPecilitries,1110h11. 1964.

A quantitative histological examin-ation of p:stmortem material takenfrom each meolber of ten pairs ofmonovular twins with placentaltransfusion syrWromo was performed.There was a disproportionate reducetiOn in the site of liver, pancreas,and fetal adrenal cortex in donortwins. Donor malnourished twinswere on the arterial side whereasthe recipient twins were on the ven-

ous side. (250)

52

NIELSEN, J. Diabetes Mellitus in

Parents of Patients with Kline-

felter's Syndrome. Lancet, 1

(7450:1376, 1966.

Eight (32 percent) of 25 patientswith Klinefelter's syndrome werefound to have near relatives withdiabetes mellitus. Of the patients'parents, 8 percent of the fathersand 12 percent of the mothers haddiabetes (at least 5 times the ex-pected incidence) indicating a pos-sible correlation between diabetesmellitus and Klinefelter's syndromewith a higher risk of sex chromo-some nondisjunction in the off-

spring of parents with diabetesmellitus. (251)

PATERSON, P., PHILLIPS, L. and WOOD,C. Relationship Between Maternaland Fetal Blood Glucose DuringLabor. American Journal of Ob-

stetrics and Gynecology, 98(7):

938, 1967.

Tests conducted with 21 pregnantwomen demonstated that glucose le-vels of maternal and fetal blood

have a close relationship during

labor. The glucose concentration

1

in the umbilical venous blood wasnot significantly greater than thatin fetal blood. (252)

PEDERSEN, L.M., tYPSTRuP, I. and rE..

DERSEN, J. Congenital Malforma-

tions In Newborn infants of Dia-betic Woven. Acta aediatricaScandinavica. Supplement 159,40.

1965.

A consecutive series of t53 newbornInfants (bIrthwelght 1,000 g. or ow-ver) of diabeti' mothers, born InRigshospltalet, Copenhagen, betweenJanuary 1, 1962, and September 30,1963, was contrasted with a control

series of 1,212 infants (birth-

weight 1,000 g. or more) of nondia-betic mothers, born in the same de-partments bet%een the autumn of

1959 and the spring 1960. Congeni-tal malformations were found in 6.4percent of the diabetes group andin 2.1 percent of the control group.

(253)

PILDES, R.S., FORBES, A.E. and CORN-BLATH, M. Studies of Carbohy-drate Metabolism in the NewbornInfant. IX. Blood Glucose Levelsand Hypoglycemia in Twins. Pedi-

atrics, 4D(1):69, 1967.

Carbohydrate metabolism and clin-ical studies on 100 pairs of twinsshowed a relationship between birthweight and blood sugar levels andno relationship between first orsecond bor.-4, or sex and blood sugar

levels. The relationship betweenhypoglycemia and mental retardationcould not be determined from thisdata but the pc ,ability makes hypo-glycemia a disorder that should bevigorously searched fnr and treated.

(254)

REISNER, S.M., FORBES, LE., andCORNBLATH, M. the Smaller of

Twins and typoglycemia. Lancet,

1731177115.

Neonatal symptomatic hypoglycemiahas been presented in the smallermember of 11 sets of twins. Hypo-

glycemia is proposed as a possibleetiological factor for the mental

subnormality and slow developmentin the smaller twin as compared to

the larger sibling. The smallertwin Is thought to be an example ofintrauterine malnutrition with thelarger twin as a natural controlduring the period of gestatlo

1 55)

ROSENBAUM, A. and Churchill, J.A.S.Neuropsychologic Outcome of Chil-dren Whose Mothers had Proteinur-la During Pregnancy. Obstetricsand Gynecology, 33:118, 1969.

A study of proteinuric mothers andthe effects on offspring as to neur-ologic and psychologic deficits areexplained. (256)

ROSENBLOOM, A.L., SMITH, D.W. andCOHAN, R.C. Zinc Glucagon in Id-iopathic Hypoglycemia of infancy.American Journal of Diseases ofChildren, 112(2):107, 1966.

Two male infants with idiopathic hy-poglycemia were successfully treat-ed with zinc glucagon. Frequentfeeding is a necessary part of man-agement of other hypoglycemic syn-dromes presenting excessive insulinproduction or decreased glycogenrelease. (257)

RUSNAK, S.L. and )RISCOLL, S.G. Con -genital- Spinal Anomalies in In-fants of Diabetic Mothers. Pedi-

atrics, 35(6):09, 191r--

Three cases of agenesis of the low-er spine in infants of mothers whohad diabetes mellitus were present-ed. A relationship between the an-omalies and maternal diabetes mel-litus was suggested. The effect ofinsulin was considered as a pos-sible etiologic factor. (258)

WAXOH, 1., REISS, M. and HikIMAH, J.

investiganetabtioo-lism In MthSA!JYj2WAei__IVrients. American Journal Of Meretai Deficiency, 69:319, 1964.

the investigation of basal metabol-ism is o.ot easily done on mentallyretarded children because of theirinability to it quietly for a suf-

ficient period while being testedby the standard apparatus. The au-thors tell of an "open system" for

measuring metabolism which does notrequire mouth pieces, etc., andconsequently does not upset the

children. (259)

WHITEHEAD, R.O. Biochemical Testsfor Assessing Subclinical Nutri-tional Deficiency. Clinical Pe-diatrics, 6(9):516, 1967.

Possible uses, potential difficul-ties, and types of biochemical

tests for assessing nutritionalstatus are presented. (260)

WHITEHEAD, R.G. Biochemical Testsin Differential Diagnosis of Pro-tein and Calcrie Deficiencies.Archives of Disease in Childhood,42(225):479, 1967.

Serum protein, the amino acid ratio,and the hydroqproline index wereused to differentiate between nutri-tional marasmus and two types of

kAashiorkor. (261)

WILSON, J.S.P. and VALLANCE-DWIN, J.Congenital Deformities and insul-in Anta onism. Lancet, 2-0175r70, 19 .

Increased antagonism to insulin as-sociated with plasr.3 albumin wasfound in 13 of 14 mothers whosechildren had spinal deformities, 15of 18 mothers whose children hadupper -lint deformities, and 14 of

Sp controls. (262)

5

r

VITAMINS, MINERALS AND WATER

SRUCK, E., AL L, G. and ACETO, T.,

Jr. 7Hrany_of Imi'ents wi,h Fy-:ertonic De'lydnation D.. to Di-

errhca. Arerican Journal of Di-seases of Children, 115(3) 281,1508.

A controlled study of 59 infants(including 5 mental retardates)with dehydration compared electro-lyte solution with electrolyte freesolution for rehydration. Althoughit takes longer for total correc-

tion of the electrolytes, a poly-ionic solution with 10 percent glu-cose is recomnended for therapy ofhypertonic dehydration in children.

(263)

CANELAS, H.M. DeASSIS, L.M. and De-JORGE, F.E. Disorders of Paene-slum Metabolism in Epilepsy.Journal of Neurology, t:euro-Sur-gery and Psychiatry, 28(4)078,11)65.

Eighty-three epileptic patients andthirty-four mtntal patients (mostlyschizophrenics) were studied andtheir blood and cerebrospinal fluidmagnesium levels compared. Hyponag-neseria was found in the intersei-zure oeriod of the epileptics andthe terebrospinal fluid level washigh. The ',erebrospinal :luid and

bioNi magnesium levels increased af-ter complete crisis elicited throughelectroshock in the rent11 patients.

(260

DODGE, P.R. Sore Com7ents crS.--.r.u:dte of t^,Lrrhea

tno Electrolyte Disturbanc:s. IN:Eichenwald, ri.f., ed. Tne Pre-vention of rental ReturdetionThrough Control of Infectious Di-seases. Washington, 0.C.: U.S.Government Printing Office, 285,1568.

The neurological sequeiae that re-sult from diarrhea and electrolytedisturbances include convulsions,rental retardation, and death.3rainswelling and convulsions can be theresult of hyponatreria t-d bodyfluid hypotonicity following irpro-per fluid therapy. In a serves of

53 infants with acute infections diarrhea, seizures did not c:cur

the infants were rehycrated. ;.z.-ny of the neurological seeuelee -.aybe from Improperly treated cCrov,;-

sloris, (265)

Fl%:ERC, L. S:3-2 7`o_c'ts

:o 17eter .1e-ers.t ti-e irai1

burin: Itfec.io:s 1110as_.Eienerwaid, x.r., ed. Tro Prevention of Men:al ReardationThrough Control of Infectious Di-seases. Washington, D.C.: U.S.

Government Printing Office, 273,ISM

Wetpr and electrolyte metabolism. ofthe brain is considered in relationto treatrent for centrel nervous sy'stem infections and the ofeventi:,1of mental retardation caused by ir.*fection treatment. Specific conc!^Lions and treatment are describec.

(260

FRIEDEN, E. Ceruloplasmin, a Link

Between Copper and Iron Metabo-lism. Nutrition Reviews, 28:87,1970.

There is now ample evidence thatthe copper protein of serum, cerul-oplasmin, is the molecular link be-tween copper and iron metabolism.it has been shown both in vivo andin vitro to be directly Involved iniron mobilization, the rate of for-mation of Fe(111)-transferrIn andultimately hemoglobin biosynthesis.While the precise mechanism of thiseffect is not known, It appears tobe directly related to the ferrox-idase activity of this serum enzyme.

(267)

MACAULAY, D. anti WATSON, 11. Hyper-natremia in infants as a Causeof Brain Damage. Archives of

Disease in Childhood, 42(225):485, 1967.

Of 122 children with hypernatremiain infancy, who were followed upI 1/2 to 8 years after initial pre-sentation, 100 gave no history ofantecedent nervous disease. Ofthese, 16 were thought to have Sut-tained brain damage, apparentlyfrom the hypernatremia. Preventionof hypernatremia is a better ap-proach to treatment than managementof the established condition. (268)

MtKIBBIN, B., MILANO, P.A. andDUCKVORt14, T. Abnormalities In

Vitamin C Metabolism in spina Bi-fida. Developmental Medicine andChild Neurology, Supplement No.

'SAO, 196B.

A high incidence of vitamin C unset-oration in children with meningooylocale has already been reported.

these results were obtained by theusual vitamin C saturation test,

but since this investigation is notentirely reliable, confirmation wassought using an alternative investi-gation, namely the urinary excre-tion of parahydroxyphenylacetic ac-id. This is an intermediary in ty-rosine metabolism and is excretedin excess in the absence of vitaminC. Abnormally high levels werefound in 75% of the children, whichcorresponds with the number of ab-normalities found in the earlier in-vestigations. Possible reasons forthe results are discussed. (269)

MORRIS-JONES, P.M., HOUSTON, I.B.,

and EVANS, R.C. Prognosis of theNeurological Complications ofAcute Hypernatremia. Lancet, 2(7530:1 385, 1967.

16% of a series of 50 cases ofacute hypernatremia had a neurolog-ical syndrome which included convul-sions, muscular hypertonicity, anddepression cf consciousness. Datasuggest that serum osmolality maybe the most significant factor. It

was suggested that, in some instan-ces, convulsions were caused bytransient cerebral edema ratherthan by infarction or hemorrhage,aid nay therefore, be preventableby improvement of the regimen of re-hydration. (270)

ROSTAFINSKI, M.J. A Case of BrainDamage Due to Dehydration. Vir-ginia Medical Monthly, 91:75,1964.

Brain damage occurs in three maintypes resulting from dehydrationfrom acute diarrhea. A case studyis cited In which the patient suf-fered from hypertonic dehydrationand it was assumed brain damage otturfed from intracerebral hemorrha-ges. the history and literatureshowed that the earlier the patientSuffering from diarrhea associatedwith acute dehydration receives med-ical help, the greater the chance ofpreventing brain damage. (271)

SEGAR W.E. Chronic Hyperosmolal-la. American Journal of Dis-

eases of Children. 112(4):318,1966.

A 10-year-old microcephalic boy hadan absence of thirst, an inabilityto maximally concentrate urine, anda defective osmoregulation result-ing in chronic hyperosmolality. Theinitial treatment after 24 hourswas intravenous fluid therapy. The"osmostat" abnormality may be a de-fect in hypothalamic secretion ofantidiuretic hormone. (272)

SHIMIZU, M. Ceruloplasmin as a Con-trolling fa,.tor of the Hematopol-elitlystel. Birth Defects Or-iginal Article Series, 4(2):49,1968.

Intramuscular injections of cerulo-plasmin, folic acid, and vitamil812

in combination daily for 16

weeks to rabbits produced slgoif-leant Increases In plasma erythro-Ooletin as measured by erythrocyticIncorporation of radioircn in ratsgiven pooled plasma from the treat-ed rabbits. (273)

SNODGRASS, J. typernatraemia and

Brain Darla e. Lancet, 1(7535):,186- 1968.

Brain damage from hypeinatremla isd .cribed; mortality is estimatedas 10'-151; and morbidity includesepilepsy and retardation. (274)

WADA, T., SAKURADA, S., O1KAWA, K.,FURUKOHRI, T. and MURAHOTO, Y.Pathobiochemical Studies on Epil-epsy. Daily Variati,n of BloodComponents with Special Refer-ence to Serum Electrolytes. Psy-chiatria et Neurologia Japonica,66(8):1, 1964.

Endocrine-metabolic aspects, espec-ially those in the serum electro-lytes, were studied in both refrac-tory and well-controlled epilepticcases. The findings may indicatesome unstable pathophysiclogicalconditions of refractory epilepsy.

(275)

WADA, T., SAKURADA, S., FURUKOHRI,T., SASAKI, J. and SHIBUKI, K.Patho-biochemical Studies on Epi-lepsy. Part II. Diurnal Rhythmof Urinary 17-0KCS, Ha, K, and

Ca excretion. Psychiatria etNeurologic& Japonica, 66(8):6,1964.

Diurnal - rhythms of 17-0HCS-, kla-K-and Ca-excretion in the urine werestudied in order to iniostigate ep-ilepsy from the viewpoint of endo-crine and electrolyte metabolism.In 17 epileptics, most of the casesshowed more or less distorted excre-tion rhythms. The diurnal rhythm ofthe steroid or electrolytes seemedto be controlled by the autochthon-ous and endogenous rhythmic activi-

ty of the living body itself. Theauthors presumed that the epilep-tics may have a biochemical dysfunc-tion of the central nervous system,particularly of the limbic systemand the dienceohalon. (276)

NUTRIENT METABOLISM IN DOWN'S SYNDROME

APPLETON, M.D., HAAB, W., CASEY, P.J., CASTELLANO, F.J., SCHORR, J.M., and MIRAGL1A, R.J. Role ofVitamin A in Gamma Globulin Bio-syntheses and Uric Acid Metabo-lism of Mongoloids. AmericanJournal of Mental Deficiency, 69(3):324, 1964.

A study was made of the effect ofserum vitamin A concentration on pu-rine metabolism, and its possiblerelationship to the production ofnormal gamma globulin . It-was con-

cluded that there is a possiblecause and effect relationship be-

tween low serum vitamin A levelsutilized as a measure cf absorptionand purine metabolism, specificallywith regard to the biosynthesis ofgamma-globulin . (277)

CHAPMAN, M.J., DONAGHUE, E.C., SAG-GERS, B.A., and STERN, J., Par-otid Saliva Sodium in Down's Dis-ease. American Journal of MentalDeficiency, 11(3)085, 1967.

Analysis of sodium concentration inparotid salivary secretions andsweat demonstrated that the contentin saliva was 2 1/2 times higher in33 cases with Down's syndrome thanit was in 33 severe mental retar-dates of other etiology or in 17normal adults. Inability of the sal-ivary glands to reabsorb sodium inDown's syndrome cases may be a mem-brane manifestation of the general-ized defect seen In trisomtc cells.

(278)

COBURN, S.P., LUCE, M.W., and MERTZ,E.T. Elevated Levels of SeveralNitrogenous Nonprotein Metabol-ites in Mongoloid Blood. Amer-

ican Journal of Mental Defici-ency, 69(6):814, 1965.

A study was made of the relativeconcentration of certain major ni-trogenous nonprotein constituentsin the blood of mongoloids. It washypothesized that the increased lev-el of nitrogenous nonprotein sub-stances may be due to an increasedrate of nitrogen metabolism. (279)

CULLEY, W.J., GOYAL, K., JOLLEY, D.H., and MERTZ, E.T. Caloric In-take of Children with Down's Syn-drome (Mongolism). Journal of Pe-diatrics, 66(4)1772, 1965.

A study was made of caloric intakeamong 23 mongoloid children with anage range of 5 to 11 years. Mean in-take for boys was 1,814.0 caloriesand for girls, 1,555.0 calories. Fi-nal results indicated body size ra-ther than age, was a better indica-tor of caloric needs, and heightwas a more convenient means of es-timating need than weight or body

surface. (280)

GRIFFITHS, A.W., and BURMAN, J.

Dark Adaptation in Mongols. Jour-nal of Mental Deficiency Research,11(2):23, 1967.

Dark adaptation was found to be im-paired significantly in 7 healthymongoloid cases when compared to 7non-mongolu:1 controls. A popularhypothesis is a disorder in vitaminA metabolism, influential to darkadaptation, existing In mongoloids.Several facts support this includ-ing decreased levels of serum vita-min A and analogous defects foundin mongoloids and in animals depri-ved of vitamin A during development.

(281)

1

is

If

I;

McCOY, E.E., ROSTAFINSKY, M.J., andFISHBURN, C. The Concentrationof Serotonin BFFrareTerrinDown's Syndrome. Journal-of KO=tal Deficiency Research, 12(1):

18, 1968.

Platelet and whole blood serotoninwas found to be low in patientswith Down's syndrome, but plateletbinding of serotonin was not signi-ficantly lower which suggests thatdecreased serotonin synthesis ac-

counts for the low values. It is

theorized that a block of serotoninsynthesis exists in mongoloids at

the metabolic stage where trypto-phan is hydroxylated to 5-hydroxy-

tryptophan. (282)

MARGOLIS, F.J., NAGLER, R.C., andHOLKEBOER, P.E. Short-term Fluor-ide Excretion in Young Children.American Journal of Diseasesof Children, 113(6):673, 1967.

A study of fluoride excretion fol-lowing known fluoride intakes in 24institutionalized mongoloid bcys

showed that a single daily dose of

fluoride is retained in the body aslong as multiple doses in water.

(283)

MISUNSKY, A., MARKS, V., and SAMOLS,E. insulin and Glucose Response

to Gluca on in Down's Spokane.Lancet, 2 7525 :1093, 1967.

Sixteen children (5 normal, 5 men-tally retarded, and 6 mongoloid)aged 20 months to 6 years, who werefor 4 months on high carbohydratediets of 1,000-2,000 calories /day,

were studied for their response toglucagon. Previous data indica-

ting that glucagon promotes insulinsecretion and that such action isless effective in children than in

adults were confirmed. (284)

9

NELSON, T.L. Milk Precipitin Dis-ease in Mongoloids and Other Men-tally Retarded Persons. Mind OverMatter, 9(2):413, 1964.

Twenty mongoloids (ages 8-45 years),closely matched with a non-mongo-loid control group and a non-retard-ed group, were studied to determinemilk precipitins. The results ofthe precipitin determinations indi-cated a significantly high inci-dence of precipiting and hemagglu-tinating antibodies to milk in the

mongoloid group. (285)

NELSON, T.L. Spontaneously Occur-ring Milk Antibodies in Mongol-

oids. Journal of Diseases ofChildren, 108(5):494, 1964.

The similarity of the recurrent res-piratory symptoms In mongoloidswith the milk precipitin syndromeof Heiner was evaluated for mongo-loids, non-mongoloid retardates,and normal controls. There was adiscussion on possible mechanismsof the increased milk antigen stim-ulation among mongoloids. (286)

REISS, M., WAKOH, T., and HILLMAN,J.C. Endocrine Invests ationsInto Mongolism. American ournaof Mental Deficiency, 70(2):204,1965.

Data were presented on the energymetabolism of mongoloids, both wak-ing and sleeping; on the serum PBI

levels and thyroid 1131

uptake in

the resting state and after pljec-tion of TSH; on urinary 17 ketoster-oids and 17-hydroxy-corticosteroidsIn the resting state and on the

urinary 17 OCHS response to metopi-rone. Pre-natal endocrine,environ-ment of the mongoloid child may beinstrumental to development of ab-normalities in this syndrome.Chromo-soma! deviations during develoomentof Down's syndrome is questioned.

(287)

TECHNIQUES IN FEEDING AND THERAPEUTIC

NUTRITION FOR THE MENTALLY RETARDED

ADAIR, R. Home Care and Feeding ofa Mentally Retarded Child. Jour-nal of the American Dietetic As-sociation, 36:133, 1960.

A report is presented by a nutri-tionist mother on feeding tech-niques for the severely retarded 5-year-old child. A basic premise as-sumes nutritional requirements of anormal child and procedures beginat this point. Relaxed feedingsgive best results, and a child'swheelchair (same height as a highchair) adds convenience in feedingsto both mother and child. Dietaryallowances may be supplemented; forexample, by ascorbic acid added to

milk while the child passes througha phase of dislike for citrus fruitand Juices. Feeding schedule andpreparation methods are describedalso. (288)

AMERICAN JOURNAL OF OCCUPATIONALTHERAPY, 7(5):199, 1953. Feed-ing Suggestions for the Trainingof the Cerebral Palsied.

Difficulties encountered in feedingtechniques for cerebral palsiedchildren are handled, beginningwith a program for the therapist.Awareness of a child's mental andmotor capabilities is stressed andinitial objectives are cautioned tobe kept simple to assure success.Procedures in feeding are suggestedto parents noting the importance ofcare and the approximation of nor-mal conditions. Requirements forself-feeding are Included, and foodand utensil suggestions are de-tailed. (289)

ARNOLD, C.B. Feeding Suggestions.American Journal of OccupationalTherapy, 16(6):290, 1962.

Mentally retarded children with sev-ere handicaps are described as har-ing individual needs in the area offeeding training. Equipment suchas sturdy furniture and feeding dev-ices are detailed for use :n an in-stitutional setting. Also, for useby ambulatory and bed patients, aresuggestions on the positioning of achild for feeding and other helpfulfeeding techniques. (290)

ARNOLD, C.B. Feeding Suggestionsfor the Severely Retarded Childin the Institution. AmericanJournal of Occupational Therapy,16:290, 1962.

The institutionalized, severely retarded child present' feeding prob-lems which should be considered Inthe layout of an institution andthe types of furniture and equip-ment chosen for it, (291)

BABCOCK, S.D. and DRAKE, M.E. A Stu-dy of the Behavioral Changes ofSixty Institutionalized FemaleRetardates During a Three MonthCourse of Treatment with Monosod-ium Glutamate. Training SchoolBulletin, 611(2):49, 1967.

Supplementing the diet of 30 insti-tutionalized mentally retarded fe-males with monosodium glutamate inthe form of 1-Glutavite appeared tobenefit some states of learning andsocial readiness, particularly so-cial contact. (292)

60

11

1 i

1

is

11

11

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I

1

I 1

11

BERANT, M. and JACOBS, J.A. A "Pseu-do" Batt'red Child. Clinical Pe-diatrics, 5(4):230, 1966.

The case of a 2-year, 8-month-oldretarded child who was admitted to

the Hadassah University Hospital inJerusalem, Israel, for tender swel-ling of both legs, left shoulderand left arm was presented. Fromthe laboratory and clinical data itwas concluded that the patient wassuffering from multiple nutritionaldeficiencies, the dominant diseasebeing active scurvy, with severeiron and folic acid deficiencies.Treatment consisted of ascorbic ac-

id, oral iron, multivitimln prepar-ations, and a blood transfusion.

(293)

BERMAN, H.H. and NOE, O. An Evalua-tion of the Nutritive SupplementDietall. American Journal of

Mental Deficiency, 62:657, 1958.

An experiment on mentally retardedchildren with severe feeding diffi-culties is described. Patients ina controlled ward environment re-

ceived Dietall (precooked powderedingredients supplements, as did

other patients having no special en-vironmental provisions. Dietall wasfound reliable for fast nutritionrehabilitation, and friendly feed-ing procedures encouraged increasedfood intake and body weight gain.

(294)

BERNSTEIN, N. Rehabilitating a

Child with a Severe Feeding Prob-lem. Journal of the American Di-etetic Association,,36031, 1960.

A case study of a 3 1/2 year oldChild with retarded growth due toinsistent refusal to eat is given.The child could not relate to pea -

pie and reacted by refusing all

food. A program was initiated toencourage eating, and ward staff co-

operated by limiting food as direct-ed by the nutritionist who spentmealtime alone with the child. Thisstudy shows the necessity of manydisciplines to accomplish goals inrehabilitation. (295)

BLANCHARD, I. Developing Motor Con-trol for Self Feeding. CerebralPalsy Journal, 27(5):9, 1966.

A step by step method of teachingself-feeding to cerebral palsiedchildren is reviewed. initially thechild is spoonfed with gradual suc-cession toward self-feeding. Fre-quent progress checks are viewed ne-cessary to avoid regression. (296)

BOSLEY, E. Development of Suckingand Swallowing. Cerebral PalsyJournal, 26(6) :l4, 1965.

Exercise on chewing, sucking, andswallowing reflexes is consideredvaluable to speech development ofthe cerebral palsied child. Suckingis noted as important throughoutthe period of speech development.

(297)

BOSLEY, E. Teaching the CerebralPalsied to Chew. Cerebral PalsyJournal, 27(4):8, 1966.

This review stresses the importanceof considering each part of theChewing process separately in teach-ing cerebral palsied children ,to

chew. Coordinating muscles andJoints is mentioned as a controlfor drooling and as an aid tospeech. Beneficial mouth exercisesare also mentioned. (298)

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CHILDREN'S BUREAU PUBLICATION No.

450, U.S. Department of Health,Education and Welfare, 1967.

Feeding the Child with a Handl-

SAP:

This pamphlet explains proceduresfor teaching self-feeding to handi-

capped children. It is a guide to

parents to help the child learn tochew, swallow, control tongue, etc.Diagrams of modified feeding equip-ment are shown, menus meeting dailynutritional requirements are given,and suggestions about managing time,energy and money are stated. (299)

DANES, B.S. and BEARN, A.G. The Ef-fects of Retinol (Vitamin-A Alco-hol) on Urinary Excretion of Mu-copolysaccharides In the HurlerS ndrome. Lancet, IMPT:TOW,-1967.

Daily amounts of 10,000 to 100,000IU retinol (vitamin-A alcohol) In-

creased urinary excretion of muco-polysaccharides In 6 cases (ages 6months to 11 years) with Hurler'ssyndrome. No signs of vitamin A in-toxication were seen. increased ex-

cretion of mucopolysaccharides overprolonged periods might decreasethe severity of disease In caseswith Hurler's syndrome. (300)

DEKABAN, A.S. Plasma Lipids in Epi-leptic Children Treated with theHigh Fat Diet. Archives of Neur-ology, 15(2):177, 1966.

High fat diet treatment of 11 chil-dren (ages 1 to 6 1/2 years) with

frequent and uncontrollable sei-

zures eliminated the attacks com-pletely in 5 and reduced them by 60-80 percent in 4. Case histories aregiven for 4 cases (2 with border-line intelligence and 1 with an IQ

of 61). (301)

DODDS, J.M., ed. Proceedings of theRegional Workshop on Nutritionand Feeding the Handicapped. Den-ver: University of ColoradoPrinting Service, 1969.

This is a compilation of the paperspresented on January 19-23, 1969 du-.ring a workshop which was sponsoredby the John F. Kennedy Child Devel-opment Center, and also by th,1 Mat-

ernal and Child Health Service, theHealth Services and Mental HealthAdministration, the Public HealthService, and the Department of

Health, Education and Welfare. Theworkshop's goal was to teach skillsto dietitians and nutritionists tobe used in diagnosing nutrition pro-blems. Speakers included physi-cians, nurses, occupational thera-pists and a speech therapist amongothers. (302)

EDWARDS, M. and LILLY, R.T. OperantConditioning: An Application toBehavioral Problems in Groups.Mental Retardation, 4(4):18,1966.

Mealtime behavior was modified sat-isfactorily in a group of 26 assaul-tive, retarded females who were cho-sen to undergo operant conditioningtraining. (303)

ENDRES, J. and THAMAW, A. New Per-spectives in Applied Nutritionfor Mentally Retarded Children.Mental Retardation, 7(1174471969.

A well planned feeding situationfor the mentally retarded child hasimplications for the physical, psy-chological and social developmentof the child. The feeding programof the Child Development Day Activi-ty Center, St. Louis University, St.Louis, Missouri, is explained as anexample of the effectiveness of

such a program for total develop-ment of retardates. (304)

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FILIPPI, B. Antibiotics and Congen-ital Malformations: Evaluationof the Teratongenicity of Antibi-otics. IN: Woollam, D.H.M., ed.Advances in Teratology) vol. 2.hew York: Academic Press, 239,1967.

The teratogenic effects on rat em-bryos of tetracycline and a penicil-lin-streptomycin complex both withand without vitamin replacement wasstudied. Vitamin supplements wereused because it is known that vita-min deficiency can be caused by an-tibiotics and that congenital mal-formations appear in embryos whenmaternal vitamin deficits occur.

(305)

GERTENRICH, R.L. A Simple AdaptableDrinking Device for Mental Retar-dates Lacking Arm-Hand Control.Mental Retardation, 8(3):51,1970.

A drinking device consisting of acup placed in a ring attached to abar, In a manner allowing the ringto swivel freely, aided retardatesin consuming liquids. The devicefunctioned best when attached to awheel chair, and all but the veryyoung and most severely retardedsucceeded in using the apparatus.

(306)

GREENBERG, L.H. and TANAKA, K.R.Hereditar Hemol tic Anemia Due

to Glucose- -Phosphate Dehydroge-nese Deficiency. American Jour-nal of Diseases of Children, 110(2):206, 1965.

This is a case report of an infantwith hereditary hemolytic anemia.The child was maintained on folicacid treatment. Improvement in thechild was said to have been due to

spienectomy and oral folic acidtherapy. (307)

HALL, M.E. Two Feeding Appliances.American Journal of OccupationalTherapy, 5(2):52, 1951.

Two feeding appliances, used at

Children's Hospital School, Balti-more, Maryland, are diagrammed and

explained. Designed for cases of

severe lateral immobility, both dev-ices involve a tray which may beraised to almost mouth level. Onedevice incorporates handles which

the patient grasps to move an at-tached spoon in a scooping motionbehind food In the tray. (308)

HENK1N, R.I. Impairment of Olfac-tion and of the Tastes of Sourand Bitter in Pseudohypoparathy -

roidism. Journal of Clinical En-docrinology and Metabolism, 28

(5):624, 1968.

Elevated thresholds for sour andbitter taste and for olfaction werefound in nine mentally retarded pa-

tients (ages 13 to 26) with pseudo-hypothyroidism. Abnormal hard pal-ates appeared to be responsible forthe defective sense of taste. (309)

HENRIKSEN, K. and DOUGHTY, R. Decel-erating Undesired Mealtime Beha-

vior in a Group of ProfoundlyRetarded Boys. American Journalof Mental Deficiency, 72:40,

1967.

Four profoundly retarded young boys,considered to be the least capablein eating habits of their cottage,

were placed at a special training

table. Five specific forms of eat-ing misbehavior were significantlyreduced in frequency by differen-tial movement interruption, verbal

castigation, and facial disapproval.Proper eating habits were encourag-

ed by verbal and facial approvaland pats on the back. (310)

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HOLSER-BUEHLER, P. The BlanchardMethod of Feeding the CerebralPalsied. American Journal of Oc-cupational Therapy, 10(1):31,1966.

The Blanchard spoon feeding methodwhen used with the cerebral palsiedcan lead to better use of the basicreflex behavior of the lips, tongue,and throat. Such a program, as des-cribed, can result in shorter feed-ing time, less wasted food, elimina-tion of coughing, choking and gag-ging, happier patients and more ef-fective management by parents andpersonnel working with children whohave feeding problems. (311)

HOUZE, M., WILSON, H.D. and GOODUL-LOW, H.D.L. Treatment of MentalDeficiency with Alpha Tocopherol.American Journal of Mental Defic-iency, 69(9) 328, 1964.

The effect of large doses of vita-min E (alpha tocopherol) on the in-tellectual performance of 3 agegroups of 20 mental retardates (6

patients under 10 years of age, 6between 10 and 13, and 8 over 13years of age) was investigated. As

early as 2 weeks following treat-ment, some Intellectual and behavi-oral improvement was observed by

the teachers in half of their sub-jects. A group of 7 phenylketonur-ics also were treated. (312)

JOHNSON, J. and JENNINGS, R. Hypo -

calcemia and Cardiac Arrhythmias.American Journal of Diseases ofChildren, 115(3):973, 1968.

A 5 1/2-year-old mentally retardedcase with rickets due to vitamin Ddeficiency had a complex cardiac ar-rhythmia which responded to oral vi-tamin replacement. Mental retarda-tion and blindness created a feed-ing problem which in turn produced

the deficiency in vitamins and cal-cium. Treatment with oral vitamin(10,000 units/day) and a high cal-cium diet produced a normal sinusrhythm. (313)

KAUFMAN, M. Fare and Feeding forPatients with Arthritis. Ameri-can Journal of Occupational Ther-apy, 19(5):281, 1965.

Information is provided to assistarthritic patients in activities re-lated to food preparation and self-feeding. Prescribed diet modifica-tions, nutritional requirements,and false information are describedextensively. (314)

LONGFELLOW, L.A. Effects of FoodDeprivation on Temporally SpacedResponding in Moderately Retard-ed Children. Dissertation Ab-stracts, 288(7):3075, 1968.

Food deprivation was effectivelyused to motivate bar pressing behav-ior in 3 non-verbal mental retar-dates. Special food providing a bal-anced diet was given as a reinfor-cer at spaced intervals. (315)

LUCCI, J.A. Gaily Living Achieve-ments of the Adult TraumaticQuadriplegic. American Journalof OcCupational Therapy, 12(3):144, 1958.

An investigation of the case re-cords of 107 male adult traumaticquadriplegic patients was conductedto determine the achievements they

had acquired in a group of selectedactivities of daily living, duringthe rehabilitation process. The eat-ing activity necessitated assist-

ance in food preparation and de-

vices such as plate guards, utensilhandles, and drinking tubes. This

activity, although the most complex

6 4

In necessitating preparatory assist-ance, ranked first in the abilityof the patient. (316)

LUCKEY, R.E., WATSON, C.M. and MUS-

ICK, J.K. Aversive Conditioningas a Means of Inhibiting Vomit-

Rumination. AmericanJournal of Mental Deficiency, 73(1):139, 1968.

Mild electric shock was applied toa severely retarded 6-year-old boyto inhibit vomiting and ruminating.

(317)

MILLICHAP, J.G., JONES, J.O. and RU-DIS, B.P. Mechanism of Anticon-vulsant Action of Ketogenic Diet.American Journal of Diseases ofChildren, 07(6):593, 1964.

Seventy-five young, female, albinomice were used to investigate theanticonvulsant effect of the ketoge-nic diet as compared with that ofacetazolailde in children with pe-tit mal epilepsy. The results ofthe mice experiment were confirmedby the clinical study which suggest-ed that the mechanism of action ofthe ketogenic diet is independentof acidosis and ketosis but may becorrelated with changes in the bal-ance of electrolytes. (318) ,

MITCHELL, P. Buccinator Apparatusto improve Swallowing. PhysicalTherapy, 47(12):1135, 1967.

A description is given of a buccina-tor apparatus developed to aid andimprove the swallowing of some men-tally retarded persons. (319)

MORRISON, D., MEJIA, B. and MILLER,D. Staff Conflicts In the Use ofOperant Techniques with AutisticChildren. American Journal of Or-thopsychiatry, 38(4):647, 1968.

Food, used as a reinforcer in oper-ant conditioning of a child, causedconflicts among personnel. Some

viewed this experiment as scientif-ic methodology; others as-a-"last-

resort". Ward and research s'caff

found themselves acting emotionallyrather than rationally, and the

need for communication to solve dif-ficulties was stressed. (320)

PITTS, J.L., WHITE, B.O. and COATES,M.L. An Approach to Meeting theNutritional Needs Among Tube-FedMentally Deficient Children. Am-

erican Journal of Mental Defici-

ency, 65:489, 1961.

Sustagen, a powdered, whole food

preparation mixed with water, was

given to a group of severely retard-ed children instead of their previ-ous multiple daily gavages. Admin-istered through an indwelling cathe-ter the approach alleviated prob-

lems and lessened dangers associa-ted with multiple gavage feedingsby non-professional personnel. No

complications emerged and generalconditions of the group improved.

(321)

FOWELL, M. An Analysis of Behaviorsto Promote Independent FeedingSkills. IN: Nursing in Mental

Retardation Programs. Children'sBureau: 4th National Workshopfor Nurses in Mental Retardation,89, 1967.

6i

Self-feecIng must be programmed bythe nurse, in its simplest form,

for the mental retardate. Handlingthe child learning self-feeding in-volves: observation, interviewing,idenLIfication of the problem, plan-ning, intervention and evaluation.Familiarity with family and the

child's history is needed in addi-

tion to repetition and reinforce-ment when working with the mental-ly retarded child. , (322)

REGER, R. and DAWSON, A. Useful Ad-aptation Devices for Quadri212.-

gics. American Journal of Occu-pational Therapy, 15(5):205,1961.

A metal band with spoon or fork at-tached is pictured and explained.The device makes it possible for a

patient with flaccid paralysis ofthe hand to feed himself. (323)

SNOW, R., SACKS, M.O. and CORNBLATH,M. Ketotic Hypoglycemia in .a Rus-sell Dwarf. Journal of ?ediat-tics, 69(1)02101966.

A Russell dwarf Witt, recurrent hypo-glycemic selzureswas found to haveketotic hypoglycemia. The patienthad a reduction of 'seizures on a re-gimen of low fat, Nigh carbohydratediet, and anticonvuhants. (324)

SPRADLIN, J.E. The Premack Hypothe-sis and Self-Feeding by Profound-ly Retarded Children. ParsonsState Hospital and Training Cen-ter, Parsons, Kansas, 196'. (A

case report) i

A profoundly retarded preadolescentgirl is taught self=feeding with aspoon. Training steps are outlined.

(325)

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WALKER, G.H. Nutrition in MentallyDeficient Children. Journal ofThe American Dietetic Associa-tion, 31:494, 1955.

Special diets and feeding methodsare frequently necessary for thementally retarded child; especiallyfor the child with cerebral palsy,the mongoloid, the epileptic, andthe cretin. (326)

WHITE, J.C. and TAYLOR, D.J. Nox-ious Conditioning as a Treatmentfor Rumination. Mental Retarda-tion75717W7 1967.

Electric shock was administered totwo ruminators with subsequent de-crease in the behavior. The useful-ness of shock in treating such beha-viors is discussed. (327)

WHITNEY, L.R. Behavioristic Nursing.90th Annual Meeting of the Ameri-can Association on Mental Defici-

ency, Chicago, Illinois, 18,

1966. (Paper.)

Strengthening and weakening the be-haviors of retardates to achieve in-dependent skills in daily living,as a nursing responsibility, Is dis-cussed. Behavior is defined, andchanges are induzed by changes inenvironmental conditions. A proce-dure for strengthening and maintain-ing self-feeding skills is mention-ed, and techniques of shaping andfading are described. (328)

WHITNEY, L. Operant Learning Theory:A Framework Deserving Nursing In-vestigation. Nursing Research,15(3):229, 1966.

66

This is a review of literature nnoperant learning and its Imp' ca-tions to nursing. An explanation ofterms is given as well as mentionof the situations in which operantlearning deserves nursing attention.Operant learning and the mentallyretarded child is stressed. (329)

WHITNEY, L.R. and BARNARD, K.E. Im-

plications of Operant LearningTheory for Nursing Care of theRetarded Child. Mental Retarda-tion, 4(3):26, 1966.

Effective operant conditioning of amental retardate to spoon-feed her-self is described. Positive and neg-ative reinforcement was used. Oncespoon-feeding was learned, systema-tic reinforcement was withdrawn andextinction occurred. Relearning pro-gressed rapidly and training ofcounselors was undertaken to avoidextinguishing in examiner's absence.

(330)

WOLFSON, I.N., FLACK, K.E. and WEST,L. Special Diet for Feeding Ad-vanced Spastics and Low GradeMental Defectives who PresentFeeding Problems. American Jour-nal of Mental Deficiency, 58:465,

1954.

The feeding of severe spastic pa-tients is aided by a powdered dietformula, Dietall, that is mixedwith water and served as a cereal.

Nutritive value proved satisfactoryin patients given this formula dur-ing a two year experimental program.General physical conditions of pa-tients improved; they received eas-ily controlled nourishment; and Di-etall is economical financially,as well as time and labor saving,in the preparation and serving offood. Advanced patients rejectedthe formula and associated it withlow grade patients. (331)

Z1CKEFOOSE, M. Feeding the Childwith a Cleft Palate. Journal ofthe American Dietetic Associa-tion, 36:129, 1960.

A study of feeding problems of chil-dren with a cleft palate revealedthat most of them, with the aid ofparental ingenuity, have little ser-ious difficulty In feeding. Food in-take patterns of these children areoften similar to those of otherchildren. Suggestions about food

preparation and feeding techniquesare also explained. (332)

ZIMMERMAN, M.E. Analysis of AdaptedEquipment. American Journal ofOccupational Therapy, 11(4):229,

1957.

Stress is placed on knowing the ana-tomy and kinesiology of body partsbefore one can assess feeding sug-gestions for mentally retarded andhandicapped patients. An explana-tion of basic body motions, in addi-tion to an analysis of materialsbest suited to feeding device con-struction, is prtivided. A tablegives evaluations of the biodynam-ia of eating motions, mcthods andde ' .As used, equipment, and typesof sod most suitable for handicap-ped patients. (333)

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