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Causative factors of mental retardation.
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Content
CAUSATIVE FACTORS OF MENTAL RETARDATION
A Project
Presented to
the Faculty of the School of Education
University of Southern California
In Partial Fulfillment
of the Requirements for the Degree
Master of Science in Education
by
Edwin D. Krutoff
June 1^51
UMI Number: EP46414
All rights reserved
INFORMATION TO ALL USERS
The quality of this reproduction is dependent upon the quality of the copy submitted.
In the unlikely event that the author did not send a complete manuscript
and there are missing pages, these will be noted. Also, if material had to be removed,
a note will indicate the deletion.
Dissertation Publishing
UMI EP46414
Published by ProQuest LLC (2014). Copyright in the Dissertation held by the Author.
Microform Edition © ProQuest LLC.
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unauthorized copying under Title 17, United States Code
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S- < z L ) f \ 5^5 F*TV* ■ 'J
a
This project report, written under the direction
of the candidate’s adviser and approved by him,
has been presented to and accepted by the Faculty
of the School of Education in partial fulfillm ent of
the requirements for the degree of M aster of
Science in Education.
Date.
dviser
Dean
TABLE OP CONTENTS
CHAPTER PAGE
I. INTRODUCTION ......... ........ 1
Problem ................ 1
Purpose ................ 1
Review of literature ......... 2
Outline of causative factors ..... ! { -
II. CAUSATIVE FACTORS BEFORE CONCEPTION . . . 8
X-ray ................. 8
Alcohol 9
Lead poisoning ••••..•••••• 12
III. CAUSATIVE.FACTORS AFTER CONCEPTION . . . 13
Smoking ................ 13
Sulfanilamide l i { .
Hh blood factor 15
Infectious disease in the mother . . . l6
IV. BIRTH FACTORS AS CAUSATIVE FACTORS . . . 18
Asphyxia or cyanosis ......... 20
V. CAUSATIVE FACTORS AFTER BIRTH ...... 2 [ j .
Encephalitis lethargies ........ 2 l | _
Polioencephalitis ........... 2I 4 .
Syphilis........... 2 i [ .
CHAPTER PAGE
Measles • 25
Whooping cough. ........... 25
Nutrition .............. 26
Vitamin ......... 27
VI. RESEARCH OH THE ELECTRIC ACTION OP THE BRAIN 30
Carbohydrates ............ 30
Phosphocreatine . ........ ..... 32
Glutamic acid ............
Acetylcholine ............ 33
Benzedrine . . ............. 1^2
VII. PSEUDO-PEEBLEMINDEDNESS........... .. i j . 6
BIBLIOGRAPHY"......... J ^ - 9
CHAPTER I
INTRODUCTION
The study of the causes of mental retardation
draws heavily upon all of the life sciences. This project
could have been written or approached from any one of them.
The problem was attached from the physiological standpoint.
How does the body function abnormally to cause brain damage
and/or mental retardation? Also, if the scientists know
what causes the abnormality, what have they done to stop
it from occurring again?
This is not a work feasible for the pen of any
one man or any one project. All this work tries to do is
to familiarize the reader with a few of the many organic
or physiological reasons which in the light of recent re
search may be factors in causing mental retardation. The
work does not try to show that only one factor by itself
causes all mental retardation, but that a combination of
many factors each doing a little damage, can cause more
than any one single factor.
An important prerequisite of teaching mentally
retarded children is that the teachers should know some of
the organic causative factors for their malady, and that
is the reasonfor this project. The sociological causative :
2
factors are of major importance also, but are not included
in this project.
The’quoted material of this project was taken
mainly from scientific periodicals of various medical
association journals, also from journals of chemistry,
psychology and psychiatry. There are only a few good books
on the subject and the best of these are "Children with
Mental and Physical Handicaps"-*- by J. E. Wallin, and also
by the same author, "The Education of Handicapped Children"2
which is a little dated.
The outline of the causative factors include only
the environmental causes. The hereditary causes were left
Out as much as possible. In this project heredity means
that which is transmitted by the genes from parents to
offspring. Environment means any factor -which affects the
formation of: 1. Genes (egg and sperm cells) before concep
tion, 2. The embryo of fetus before birth, or 3. The child
or adult after birth. Heredity is the raw material and
- * • J. E. Wallin, Children with Mental and Physical
Handicaps (Prentice-Hall, Inc; Hew York, 1949)
2 J. E. Wallace Wallin, The Education of Handi
capped Children (Houghton Mifflin Company: Hew York, 1924)
3
anything that shapes or molds that material is environment.
In this sense, if the child is mentally retarded because of
the raw material or the heredity given him, little can be
done to correct it in the retarded person, or to stop it
in his offspring except through possible sterilization.
On the other hand, when dealing with the environmental
conditions causing retardation, it is possible for the
researchers to either stop the environmental conditions
from occurring, or after it did occur to find some remedy
to cure the malady. These factors can be physical, phy
siological, psychological and social, but mainly the phy
siological factors are included in this paper.
The outline of the causative factors which
follows is a short survey of the subject including the
factors which are discussed in the project and many which
are omitted for various reasons.
OUTLINE
of
ENVIRONMENTAL CAUSATIVE FACTORS OF MENTAL RETARDATION
I. Before conception (union of sperm and egg)
A. Parental toxieations by poisons
1. Alcohol
2. Nicotine
5. Lead
4. Mercury
5. Arsenic
6. Iodine
7. Alkaloids
8. Opium
9. Morphine
10. Ether
B. X-Rays
C. Atomic radiations
II* After conception (union of sperm and egg) before birth
A. Maternal dysfunction
1. Diseases of an infectious nature
a. Typhus
b. Typhoid fever
c. German measles (2nd & 3rd months)
$
d. Malaria
e. Cholera
f. Syphilis
2. Toxins in the blood stream
a. Lead poisoning
b. Micotine
c. Other poisonous drugs esp. alcohol
d. Poisons used in abortions
e. Rh factor
5. Hutritional deficiency
4. Endocrine system or ductless gland
dysfunction.
5. Reproductive system pathological
B. Child, fetus, or embry dysfunction
1. Hemorrhages of intracranial or super
ficial blood vessels
2. Membranes congested around brain
3. Endocrine or ductless gland dysfunction
4. Injury by violent blows or falls
C. Birth troubles
1. Forceps injury brain
2. Anesthetic improperly used
3. Prematurity or precipitated delivery
4. Difficulty or prolonged birth
6
a. Suspended breathing
(1) Suffocation or oxygen defi
ciency in blood of child.
5. Abortions
a. Use of drugs
b. Use of instrument incorrectly
III. After Birth (chiefly in early years)
A. Infectious diseases (Chief cause)
1. Cerebrospinal meningitis
2. Encephalitis lethargica (sleeping
sickness)
5. Polieneephalitis lethargica
4. Chronic rheumatic infection
a. Causes chronic encephalitis
5. Lesser causes
a. Measles
b. Whooping cough
c. Diptheria
d. Scarlet fever
e. Other childhood diseases
B. Brain pathology (disease)
1. Brain lesions
2. Brain infections
3. Faulty circulation of brain
7
4. T;umors
C. Glandular dysfunctioning (possibly hereditary)
1. Hypothyroidism (deficiency of Thyroid
activity)
2. Hypopituitarism (deficiency of Pituitary
activity)
3. Defects of thymus gland, gonads
D. Nutritive disorders of Malnutrition
1. Protein not digested or metabolized
a. Usually a specific protein break
down
(1) Phenylpyruvic acid
(2) Cholesterol
(5) Glutamic acid
2. Fats not digested or metabolized
a. Usually a specific fat break down
or overproduction in a certain
tissue
3. Long continued and severs epileptic
seizures
4. Head injuries through falls or blows
CHAPTER II
CAUSATIVE FACTORS BEFORE CONCEPTION
Can genes (characteristic carriers) in the eggs
and sperms of the parents actually develop incorrectly be
cause of the environmental conditions the parents place
upon themselves? Also after the sperm and egg are fully
formed, can the genes be affected by environmental condi
tions so as to produce an abnormal child? If the answer to
these questions are "yes”, there is a possibility that
environmental conditions can cause mental retardation before
conception.
Much experimentation has been done in X-Rays on
the reproductive cells. Miller^ in 1927, was the first to
demonstrate experimentally on the fly (Drosophilia) that
permanent changes in heredity can be artificially induced
by the X-Ray. In other experiments by Miller^ the sperm
cells were changed by high and low temperatures, colchicine,
and mustard gas. In some cases the changes continued from
generation to generation.
^ H. J. Muller, ”Artificial Transmutation of the
Gene,” Science ;84-7, June 22, 1927
2 Ibid. . . PP. 84-7
There have been reports^ that many chemicals as
lead, mercury, arsenic, ether, morphine, opium, alkaloids,
iodine, etc., can affect the genes of the parents reproduc
tive cells.
Alcohol. Stockard, Craig and Papanieolau4 experi
mented on guinea pigs who were known to be fertile by pre
vious experiments. These male and female guinea pigs in
haled alcoholic fumes from one to three hours a day, for
six days a week. These guinea pigs were experimented with
for periods of a few months to five or six years. Then
they proceeded mating an alcoholic male with a normal female
and vice versa, and then with both being alcoholics. The
offspring of the alcoholics were found to be inferior in
fourteen or fifteen qualities compared with the non-alco
holic guinea pigs, as failure to conceive, late prenatal
deaths, early prenatal deaths, in size of litter, mortality,
average weight at birth, at one month and at three months,
and abnormalities. Among the abnormalities were absence of
one eye, absence of both eyeballs, opaque cornea, opaque
lens, cataract and paralysis agitans. No defects of this
kind were found in the non-alcoholic group. Greater defects
3 Gerrit P. Frets, Alcohol and Other Germ Poisons
(The Hague: Martinus Nijhoff, 1931)
^ J. E. Wallace Wallin, The Education of Handi
capped Children (Houghton Mifflin Company: New Iork,' 1324)
ppSM
10
were seen when giving alcohol to the female, and the in
juries could be seen through several generations.
Pearl^ did the same experiment with domestic fowls
but did not find the loss of weight or mortality, and con
cluded that ’ ’ The offspring of the alcoholized are as a class
indubitably differenciated from the offspring of the non-
alcoholies.”
Ivamow^ experimented with the sperm of different
animals as a dog, rat, rabbit, guinea pig, and sheep, by
putting them in alcoholic solutions of not more than 1%
before combining them with.the egg for fertilization, and
found the offspring to be normal. But when Stockard placed
the eggs of fish shortly after fertilization in the same
solution monstrosities resulted.
Arlitt and Wells7 administered alcohol in the food
of rats for two or three months, and found degeneration in
the testicles, while other organs were unaffected. The rats
spermatozoa showed many degrees of abnormality and finally
the testicles stopped their formation altogether causing
sterility.
5 J. E. Wallace Wallin, The Education of Handi
capped Children (Houghton Mifflin Company: Hew York, 1924)
pp 295
6 Ibid*, pp 296
7 Ibid., pp 296
Hodge and Ptarrenger^ experimented with dogs and
Laitenan9 experimented with guinea pigs and they found a
large proportion of stillborn and defective young when they
were given alcohol during pregnancy.
Nicloux and Renault® found alcohol in the human
testes and ovaries in the ratio of two to three and three
to five as compared with the blood. Lancereaux10found that
alcohol paralyzed the ova and produced ovarian degeneration.
Thirty-seven of thirty-nine chronic alcoholics showed tes
ticular degeneration in an experiment of Weichselbaum^.
Lonnett- * - 2 reported that 107 English women dying of
alcoholism, before the age of twenty-nine, had twenty-nine
vigorous children previous to becoming alcoholic. After
they became alcoholic, these women had six children all of
whom were delicate or deformed. Laitenan- 1 - 3 reported on
twenty-thousand Denmark children. The percentage of mis
carriages was 1.07$ among total abstainers, 5.26$ among
moderate drinkers, and 7.11$ among heavy drinkers. The
weight averages of the children of the drinkers was less
8 J. E. Wallace Wallin, The Education of Handi
capped Children (Houghton Mifflin Company: New York, 1924)
pp 296
9 Ibid., pp 296
10 Ibid. pp 296
11 Ibid. pp 296
12 Ibid. pp 296
12
than the non-drinkers. Alcohol is definitely a possible
cause of mental retardation.
13
Lead Poisoning. Cole and Baehhuber gave lead
acetate to male rabbits and cocks. The litters of the
rabbits given lead acetate weighed less and had a higher
mortality than the rabbits on a normal diet. The eggs of
the poisoned cocks developed less frequently than the ones
fertilized by normal males, and besides the mortality was
higher both before and after hatching.
In the making of pottery a lead type of soil is
used, therefore, people making pottery would be a good
study as to the effeet of lead on them. Rennert*^ records
frequent abortions, deaf-mute, and macrocephalics of mothers
employed in the pottery works in Germany. If both parents
were working with the lead, the fetus and the continuance of
pregnancy was affected ninety-four time out of one hundred,
and when the mother alone was working it was ninety-two times
and the father alone it was sixty-three times. Also in this
experiment, it was shown that the lead may pass from the
mother’s blood to the fetus and it also was found in the
mother’s milk.
^ J.. E. Wallace Wallin, The Education of Handi-
• capped Children (Houghton Mifflin Company: Hew York, 1924)
pp 297
14 Ibid., pp 297-8
CHAPTER III
CAUSATIVE FACTORS AFTER COHCEPTIGI
After the union of the sperm and egg, when the
egg cell divides to form the embryo, does the mother’s bad
health, drinking and smoking harm the child? The placenta
of the mother is connected with the umbilical cord of the
embryo. There is no direct connection between the blood
vessels of the mother and the child. They only lie side by
side, thus no blood of the mother goes into the child. But
the embryo gets food by absorption of diffusion through the
walls of the mother’s vessels into the embryos blood system.
Some scientists believe that all poisons are filtered out
at this point and only the food gets through. Other scien
tists disagree on this point and base their conclusion on
experiments in the order of the following.
The absorption toxins from maternal toxemias does
not come to a complete halt at the portal of the pla
centa. When the pregnant mother is alcoholized or
nicotinized, the embryo shares in the intoxication.
Experiments have shown that the rate of the heart beat
of the fetus is speeded up when the mother smokes.
The average increase in one experiment was five beats
a minute. Unborn babies smoke when their mothers
smoke, and go on a ’ ’binge*’ when their mothers are ”on
a 3ag.” 1
J. E. Wallin, Children with Mental and Physical
Handicaps (Prentice-Hall, Inc: Hew York, 1949) p. 213
34
Heekel^ showed sulfanilamide in the blood of the
fetus within 5 minutes after it was given to the mother for
treatment of a disease. What would have happened if the
fetus was allergic to the sulfanilamide is open to specula
tion. In this case a good size molecule goes straight into
the fetus.
Sontag^ reported instances of impaired postnatal
development in children born to mothers who were emotionally
disturbed during pregnancy. He believes that the developing
fetus was adversely influenced by the physiological disturb
ances of the mother.
The parents do not realize that the effect of the
poison on themselves is different than the effect on the
fetus. The embryo is growing at a tremendous rate and any
thing which inhibits or in any way complicates the growing
process can easily do damage at this crucial growing point.
During, this period, the organs of the fetus, as the heart,
liver,’ and brain, are literally being chemically manufac
tured. What the injection of poisons in the embryo and
fetus can do, can readily be seen.
2 George D. Heckel, nChemotherapy During Pregnancy
Danger of Fetal Injury from Sulfanilamide and Its Deriva
tives,” Journal of the American Medical Association. :1314-
1316, October 18, 1941
® Lester W. Sontag, "Some Psychosomatic Aspects of
Childhood,” The Nervous Child, 5:296-304, October, 1946
Rh blood factor. In 1940, the Rh blood factor was
discovered by Landsteiner and Wiener and was named after the
monkey which they experimented on, the rhesus monkey. Re
search was done by Yannet and Lieberman4 by a so called iso
immunization method. They came to these conclusions:
Rh iso-immunization demonstrated that a pregnant
woman whose red blood cells do not contain the Rh
factor may be sensitized by the Rh factor present in
the red blood cells of the fetus. As a result of the
maternal sensitization, the fetus may be seriously
affected.5
Yannet and Lleberman found many cases of recurrent
miscarriages and stillbirth related to this process. Levine®
and his eo-workers experimented with the mentally retarded
to find out if this condition was prevalent in many of these
people. They found the following:
In a preliminary study it was found that the in
cidence of Rh negative mothers of an unselected group
of undifferentiated idiots and imbeciles was signifi
cantly random selection..This indicated that possibly
the Rh iso-immunization may have etiological signifi
cance in a certain proportion of the eases.5
4 Herman Yannet and Rose Lieberman, ’ ’ The Rh Factor
in the Etiology on Mental Deficiency,” The American Journal
of Mental Deficiency. ;133-7, October, 1944
5 Ibid., p. 135
6 Ibid., p. 135
i6
Infectious disease in the mother* Any disease in
the mother probably can send poisons in the blood and even
tually the poisons can do damage to the fetus as typhus,
typhoid fever, German measles, malaria, cholera, and
syphilis. Few will disagree that these diseases will cause
damage to the fetus but whether it causes mental retardation
is another question.
Swan and Black? have listed many defects in child
ren which they were born with, when their mothers had German
measles (Rubella) during the second and third months of
pregnancy. They found many children had the following:
unable to walk at correct age, lessened control of micturi
tion and defecation, difficulty in feeding, miscarriage,
lymphadenitis, eye defects, deaf-mutism and speech defects,
cardiac defects, microcephalism, death, etc., when their
mothers had this disease.
Syphilis can also be a damaging disease. If the
mother has the disease during pregnancy much damage can be
done to the fetus. First, the reproductive system of the
mother can be pathogenic or damaged, so the fetus will not
develope correctly or the disease can actually affect the
? C. Swan, A. L. Toslevin and G. H. Black, ’ ’ Final
Observations on Congenital Defects in Infants Following In
fectious Diseases during Pregnancy, with Special Reference
to Rubella” Medical Journal of Australia 2:889-808,
December 28, 1946.
fetus by direct damage. The child can be born malformed if
this be the case. Damage can occur to the brain and thus
cause mental retardation.
CHAPTER IV
BIRTH FACTORS AS CAUSATIVE FACTORS
There are many factors during birth that can cause
mental retardation. Faber1s^- research on this subject is as
follows:
Cause Ho. of Cerebral Damaged
Children
Anesthetics
Hitrous Oxide 22
Chloroform 4
Ether 8
Spinal 1
Sedation
Unspecific “shots” 5
“Pills and specific barbaturates 5
Sedation, heavy (judged by effect
on mother) 6
Induced Labor
Oxytoeial 2
Castor Oil 1
Quinine 1
Breech Presentation 9
^ Harold K. Faber, “Cerebral Damage in Infants and
in Children; Some Observations on Its Causes and the Possi
bilities of Its Prevention” American Journal of Diseases of
Children. :l-9, July 1947
Delivery, Abnormal Total 22
Prolonged 7
Dry 4
Version 2
Precipitate 5
Cesarean 3
High Forceps 1
Abnormalities of Cord Total 6
Very Tight about Heek 4
Prolapse 1
Very short 1
Placental Separation (Bleeding) 15
Toxemia 10
Oversized Infant 9
Premature Rupture of Membranes 5
Maternal Trauma (Falls, Automobile Accident) 5
Rh Incompatibility 5
Premature Labor Pains 4
Attempted Abortion 2
Cardiac Decompensation, Maternal 2
Infectious Diseases, Maternal 6
(Pneumonia, Influenza, sore
throat, rheumatic fever,
syphilis) one each.
20
Many doctors2 have pointed out the inadvisability
of using nitrous oxide in child birth and yet it is still
being used. Proof has been given in many articles that
more children have cerebral damage after its use as com
pared with other anesthetics. The use of morphine by the
mother (twilight sleep) affects the fetal brain by de
pressing the breathing center and thus may cause asphyxia
or anoxia during birth.
Asphyxia or Cyanosis. Asphyxia can be simply de
fined as the stoppage of breathing and pulse, caused by a
deficiency of oxygen. In prolonged births the child might
not be getting sufficient oxygen from the mother and not
being able to use his own lungs to get oxygen, thus turning
a bluish color (cyanosis). This lack of oxygen is a very
important factor in the child’s life, either fatal, during
birth, or after birth, as it had been shown that oxygen is
essential for the existence and functioning of the brain.
If oxygen is not obtainable by the brain, the cells will
die as to the amount of oxygen that is lacking, causing all
types of brain dysfunction. One of these brain dysfunctions
£ Harold K. Faber, ’ ’ Cerebral Damage in Infants
and in Children; Some Observations on Its Causes and the
Possibilities of Its Prevention” American Journal of
Diseases of Children. :l-9, July,--1947
21
may be mental retardation, as once a nerve cell dies the
body will not grow another.
Clifford3 studied the effect of asphyxia on the
newborn infant and came to these conclusions after studying
thirty-six cases selected from one hundred and sixty-four
cases. ’ ’ Asphyxia is responsible for over one-half of the
live-born infants deaths in the new born period.” The brain
in ten patients had the arachoidal and cerebral vessels en
gorged and tortuous. In six cases the arachnois was bulging
due to a great increase in the amount of clear cerebrospinal
fluid surrounding the medulla. The brain softened also.
The fundamental effect of asphyxia is the production of an
increased hydrogen ion concentration that causes the success
ive stages of stimulation discharge of energy, paralysis in
nerve cells and produces loss of tone and dilation of the
smooth muscle of the blood vessels allowing the escape of
plasma and red blood cells.”
Winde4 stated, ’ ’ Like our experimental animals, by
no means all asphyxiated human infants have permanent mani-
^ Stewart H. Clifford, ’ ’ Effects of Asphyxia on the
Newborn Infant” Journal of Ped.. 18:567, 1941
4 William Winde, ’ ’ Structural and Functional Altera
tions in the Brain Following Neonatal Asphyxia” Psychosomatic
Medicine. 6:155, April, 1944
22
1 festations of nervous disease, however, the possibility of
inferior mentality, diminished learning ability or simple
mental dullness as sequelae of anaxia at birth should not
be dismissed lightly."
CHAPTER V
CAUSATIVE FACTORS AFTER BIRTH
The main causes in the early years are cerebro
spinal meningitis, encephalitis lethargiea, poliencephalitis
lethargiea, chronic rheumatic infection, and syphilis.
Encephalitis lethargiea. This disease is caused
by a virus which attacks the sleep center of the brain and
thus causes the victim to sleep. Reduction of weight and
atrophy of the brain can result in causing mental retarda
tion.
Polioencephalitis. This is a disease caused by a
very small, tough, virus. This virus is most likely the
same one that causes poliomyelitis which attacks the spinal
cord but in this case it attacks the brain. As polioence
phalitis means an infection in the gray matter of the brain
the encephalitis lethargiea may also be classified under
this disease and can cause cerebral palsy and mental re
tardation.
Syphilis. This is a contagious venereal disease
produced by a threadlike micro-organism called nspirocheata
pallida or treponema pallidum.” If the disease reaches the
brain much damage can be done. According to the amount of
damage to the brain, the persons intelligence will be
lessened.
Chronic rheumatic infections, and cerebrospinal
meningitis can also do damage to the brain by their bacter
ial action and thus cause mental retardation.
Measles. Many doctors have reported that measles
caused brain damage. Amongi the doctors who have reported
more than one case of brain injury caused by measles are:
Heal and Applebavm. 1 who found twelve cases, Musses and
Hauser2 who found ten cases, and Ferraro and Scheffer3 who
found fourteen cases, all of extreme damage to the brain
caused by measles.
In Milwaukee, there were 15,000 eases of measles
in 1931-1932. Thirteen cases were studied by Peterman and
Fox^. After extensive research they came to these conclu
sions: ”The measles encephalitis complications appear to be
a definite clinical entity. The complications occur in
.young children usually between two and eight years of age.f J
1 Josephine B. Heal, Emanuel Applebaum, nEncepha
litis Associated with Measles”, Bull. Hew York Acad. Med.
3:414 June, 1927
2 J. H. Musser, G. H. Hauser, "Encephalitis as a
Complication of Measles”, Journal of American Medical
Association, 90:1267, April 21, 1928
cz
Armando Ferraro and F. H. Scheffer, "Encephali
tis and Encephalaomyelitis in Measles: A Pathologic &eport
of Six Cases”, Arch. Neurol. and.Psvchiat..25:748 April 1931
^M. G. Peterman and 1. S. Fox, "Encphalitis as a
Complication of Measles” American Joumal of Diseases of
Children. 46:512, 1933
25
Dr. Faber® stated,"that the early giving of
ganima globulin can prevent the migration of measles and
brain deterioration.”
Whooping cough (Pertussis). In 1942 Lurie and
Levy® published a research study on thirty-four children in
a child guidance home. These thirty-four children who
suffered such attacks of whooping cough during the first two
years of their lives and in whom there appeared to be a
definite relationship between the neurologic sequelae of
whooping cough and the behavior disorders and personality
changes, were tested. Seventy per cent of these were rated
below average in intelligence as a result of said attacks.
Lurie and Levy stated that they believed that ^neurologic
sequelae of whooping cough in young children may be a factor
in the development of a social or abnormal behavior in later
life.B
In 1948, a later research study was performed by
Levy and Perry? of the V/ashington State Institution. They
5 Harold K. Faber, nCerebral damage in Infants and
in Children: Some Observation on the Causes and the Possibi
lities of Its Prevention1 1 , American Journal of Diseases of
Children. :l-9, July 1947
® L. A Lurie and S. Levy, Personality Changes
and Behavior Disorders of Children Following Pertussis,”
J ournal of American Medical Assn.120:890-4. November 21,1942
? Sol Levy and H. A. Perry, American Journal of
Mental Deficiency. 42:217, January, 1948
26
selected one thousand inmates, each having a complete data
or history on their development and health. The inmates
were also given questionnaires and from these, Levy and
Perry established one hundred and twenty-eight cases of
whooping cough. Of the one hundred and twenty-eight cases,
twenty cases or 15.6$ thereof showed a definite causal re
lationship between the whooping cough and intellectual re
tardation. The said twenty eases were those believed to
have only whooping cough and no other causal factor. If
another causal faetor was found, the inmate was excluded
from the study. From the 15.6$ studied, 14.3$ of them had
whooping cough between the ages of two and five years, while
only 1$ had it after the age of five years.
Faber8 thinks that much of the damage to the brain
could be stopped if early vaccination against whooping cough
could be given, and should a child contract the disease,
there should be early hospitalization and oxygen given.
Nutrition. Kugelmass9 and his associates performed
a research study on the effect of better nutrition on the
® Harold K. Faber, ’ 'Cerebral Damage in Infants and
in Children: Some Observations of Causes and the Possibili
ties of Its .Prevention” American Journal of Diseases of
Children. :l-9, July, 1947
8 Isaac N. Kugelmass, L.C. Poull, and E.L.Samuel,
"Nutritional Improvement of Child Mentality,” American Jour
nal of Medical Sciences. 208:631-5, November, 1944
27
I. Q. of the mentally retarded and on normal persons. A
group, malnourished at the time of the first test and well
nourished at the time of the second test, showed a rise of
ten points for the retarded group and a rise of eighteen
points for the normal group, in contrast with an average of
no change in points for the group continuing malnutrition.
Vitamin. Poe^-O and associates made a research on the
effect of B-complex on intelligence of rats in which a split
litter technique was used, that is a litter from one mother
divided into two parts. From eighty-nine rats, forty-two
were made deficient in the B-complex vitamins from the ages
of two weeks until six weeks, and the other forty-seven were
given a normal diet. At the seventh week of age, the rats
were trained in a water maze and further tested when they
reached the age of three months. The results showed that
normal rats were superior to the vitamin deficient rats in
all learning situations and also in all other tests made.
If young rats are fed a B-complex deficient diet,
they are inferior to-normal rats not only immediately
after period of deficiency but also when they have
reached maturity, il
3-0 F. E. Poe, A. Wood, C. F. Poe and K. L.
Muenzing, ’ ’ The effect of Vitamin B Complex Efficiency upon
. the Acquisition of a Maze Habit in White Eats1 1 University
of Colorado Studies. Boulder, Colorado, 23:147-158, 1936
11 Loc. cit
28
Harrell'*-2 reported on an experiment in an orphan
age with vitamine on one hundred children. They were
paired child to child as to height, weight, age, sex, edu
cational achievement, length of residence, and intelligence
test score. The children in the orphanage had almost the
same kind of environment, as they ate together, slept in the
same room, and played together. One group was given two
milligrams of thiamine per day over a period of one year and
the other group was given a placebo ( a pill with no thera-
putic use). At the end of one year many differences were
shown, such as visual acuity, reading, memorizing new mater
ial, code substitution, and educational achievement, between
the two groups. At the end of the first year and for a
period of one year thereafter, twenty pairs of children were
reversed, the children who had been receiving thiamine in
the first year were placed on the placebo and the others who
had not were placed on the diet. At the end of the second
year both groups were given tests again. It was found that
in most instances the one who had been receiving thiamine in
the first year, but placebo in the second, was surpassed by
his paired companion who had not received thiamine in the
first year and had in the second year. In everyone of
12 Euth P. Harrell, -Effect of Added Thiamine on
Learning (Teachers College Contributions to^Education, Ho.
877. Hew York: Teachers College,Columbia Universityl943,p55
29
eighteen tasks the ones receiving surpassed in gains
those who did not receive it, even though the groups were
matched child for child. The intelligence test showed that
the group gained more in scores hut statistically it was
not significant. Hearing was the same for both groups.
Over all ’ the tests, the B^ group showed a gain from 7$ to
87$, and as an average the Bi group gained 27$ over the
controlled group.
CHAPTER VI
RESEARCH OH THE ELECTRIC ACTION OF THE BRAIN
Carbohydrates are broken down in the digestive
system to small sugars (glucose, mannose and fructose, etc.
and then sent by way of the blood system to all parts of
the body or to the liver to be stored. Glucose and a
little mannose are used as fuel by the brain. Animals^
who had their livers removed showed a lack of sugar in the
blood system. The animals thus developed mental confusion,
delirium, sensations of hunger and convulsions. But with
an injection of glucose or mannose the animals improved
quickly. Fructose is most likely converted in the liver to
glucose, and thus used in the brain. While using the glu
cose in the brain, much oxygen must be used which also
comes through the blood system.
Glucose----Lactic Acid plus energy to do work
Lactic Acid plus Oxygen Glucose
For some reason if the child is not getting
sufficient food, or the food is not being digested, or
something is wrong with the blood system leading to the
brain, so the food can’t get there, the brain cells will
B. Harrow, Textbook of Biochemistry. (Philadel
phia) B. Saunders Co., 1947, pp 536
31
wither and possibly die. If a brain cell once dies, the
cell can never be remade by the body and the more cells that
die, the more mentally retarded the child will become.
In order for a chemical reaction to take place in
the body, there must be protein chemicals to aid the re
action. These chemicals are not used in the reaction them
selves, but must be there for the reaction to take place.
These protein substances are called "enzymes1 *. The chem
ists can use heat and pressure and many other devices to
cause a reaction, but the body relies on the protein chemi
cals.
How does the brain send out electrical impulses?
If that eould be realized, possibly mentally retarded per
sons could be aided. Are some mentally retarded children
sick because of the fact that their bodies are unable to
make certain chemicals essential to correct brain function?
Are certain brains malfunctioning chemically, and are they
able to be aided by the administration of certain chemicals?
In 1930, Kirch2 worked on a problem of ho?/ nerve
cells chemically give off electrical impulses. Since the
ordinary nerve cell in the human and in most animals, give
off a small amount of electricity, it was almost impossible
2 B. Kirch, "Yon Phosphageir in Elekrichen Organ
von Torpedo" Biochemistry. 225:183-192, 1930
32
for Kirch to experiment with them. He decided to experiment
on a fish which protects itself by having a powerful organ
which could kill other animals by means of its electric-
sting. He used a fish called "Electrophorus Eleetricus"
electric eel, whieh averages between 400 and 600 volts each
sting. Some were known to give as high as 800 volts. After
experimenting, Kirch found a substance in the electric organ
of the fish called "Phosphocreatine".
In 1932 Quastel and Wheatley2 showed that a pro
tein breakdown "Glutamic Aeid" was being used as a fuel by
the brain. This was the first time that it was shown that
carbohydrates (sugar) are not the only fuel used by the
brain. Proteins are broken down in the digestive system to
small proteins called "amino acids" which are the building
blocks of the proteins of the body. Thereafter the amino
acids go to the cells or to the liver to be converted into
a different amino acid, but only one of the many amino acids
was found to be used as fuel by the brain.
In 1936, Weil and Malherle4 repeated the previous
experiment with reference to which amino acids are used as
2 .Quastel and Wheatly, Biochemistry J ournal. 29:
1620, 1932
^ Malherbe H. Weil, "Studies on Brain Metabolism:
Mechanism of Glutamic Acid in Brain", Biochemistry Journal.
30:665-676, 1936
33
fuel by the brain. Their conclusions were as follows:
It is very improbable that the amount of
glutamic acid supplied to the brain is sufficient
to be of importance as a fuel comparable with
carbohydrates. The peculiar position of glutamic
acid among the amino acids suggests that it ful
fils a specific function in connection with carbo
hydrates metabolism.5
Nachmansohn was sent to the United States by the
Dazian.Foundation to do research on electrical impulses.
In 1945, Nachmansohn6 using an electric eel showed that
phosphoereatine, discovered by Kirch, was the source of
energy for the electric reaction, When phosphorus is re
leased from a compound, energy is given off. Thus the phos
phorus released from the phosphocreatine gives the energy
for this reaction. Nachmansohn^ concluded that without the
acetylcholine and even with the phosphoereatine the impulse
was not given off. He showed that both the energy (the
phosphoereatine) and the acetylcholine had to be present to
make the impulse.
5 Ibid., pp 665-676
6 Cox B. T. Nachmansohn, C. Coates and A. L.
Machado, ”Aetion Potential and Enzyme Activity in the Elec
tric Organ of Electrophorus Eleetricus: II Phosphoereatine
as Energy Source of the Action Potential”, J ournal of Neuro-
Phvsiology. 6:585-396, 1943
* 7 Cox R. T. Nachmansohn, A. L. Machado, ”The Form
ation of Acetylcholine”, J ournal of leurophysiology. 6:397-
403, 1943
8 Ibid., pp 397-403
8 ^
Nachmansohn0 while experimenting found out that
floride enhanced the formation of acetylcholine. Also he
learned that copper, iodine, and iodoacetie acid have a
strong effect to stop the production of acetylcholine.
Iodine is taken by many mothers for thyroid gland treatments
during the child1 s fetal development. Could this contribute
to development of mentally retarded children?
Nachmansohn9 then used glutamic acid (an amino
acid) in his experiments, to see the effect of it on the
production of acetylcholine. He also experimented with
citric acid found in oranges and lemons. This is what he
found.
Chemicals Used Increase in Acetylcholine
Natural Glutamic Acid Four times as much
Alanine Two
n n n
Methionine Two
! ! M i t
Glutamide Two
« » ! n
Succinic Acid Two
n H n
Citric Acid Four to Six times as much
8 Ibid.. pp 397-403
9 John D. Nachmansohn, H.M. John and H. Waelsh,
"Effect of Glutamic Acid on the Formation of Acetylcholine"
J ournal of Biological Chemistry. 150:486, 1943
SIMPLIFIED IDEA
Acetylcholine
i
i
i
V | /
Broken down Acetylcholine f Electricity
Phosphoereatine
i
■
i
i
Citrii Acid
i
Glutamic Acid
i
Choline Aeetylase
i
i
i
■
i
i
i
- * ■
Acetylcholine
Nachmansohn believed that glutamic acid and citric
acid are enzymes in the making of acetylcholine. He-^ also
found another enzyme in the production of acetylcholine
called "choline acetylase".
Price-1 - - * ' showed that people suffering from a cer
tain type of epilepsy, petit mal, can be greatly aided by
giving them glutamic acid. There are abnormal electrical
waves that are given off by the brain during an attack which
can be shown on an electroencephograph (an instrument to
measure electric brain waves). The lack of glutamic acid
may cause an inadequate amount of acetylcholine, thereby
resulting in the abnormal electrical waves.
Zimmerman^ experimented with white rats, and
found that glutamic acid enhances the learning in a simple
maze. He added 200 mg of glutamic acid to the diet of
normal white rats for two weeks and continued it during the
periods of learning. He found that the rats who were given
- * - 0 d. Nachmansohn, A. L. Machado, "The Formation
of Acetycholine. A New Enzyme. Choline Acetylase." Journal
of Neurophysiology. 6:397-403, 1943
^ J. C. Price, H. Waelsch and F. J. Pulman, "dl-
'Glutamic Acid Hydrochloride in Treatment of Petit Mal and
Psychomotor .seizures," The Journal of American Medical
Association 122 No. 17:1153-5, August 21, 1943
l 2
F. T. Zimmerman and S. Ross, "Effects of Glu
tamic Acid and Other Amino Acids on Maze Learning in the
White Rat" Arch. NeuroPsychiat 51:446-451, May, 1944
37
glutamic acid learned much faster than the rats not given it.
Albert-*-^ then accomplished an experiment on rats
which included tests of increasing hardness. An apparatus
was used consisting of a circular cage with a series of
floor plates to he stepped upon by rats in order to secure
food. The rats passed gradually from a simple level (single
plate to ten or more plates)• The last plate accomplished
by each rat was the score given it.
Intelligence Glutamic Acid None
of Plates (9 rats) (8 rats)
1 ................. 0...................4
2 .........................1......................... 2
3 ...... *...... 7.................. 2
4 ..................0...................0
5........................1.........................0
Eight rats were given a normal well balanced diet,
and nine rats were given a well balanced diet plus 200 mg
average of glutamic acid. In the normal group four rats had
the intelligence of only two plates, while in the glutamic
acid group, eight rats had the intelligence of three plates.
"Results show glutamic acid does cause white rats
13
Kathryn Albert and C. J. Warden, "The Level of
Performance in White Rats." Science 100:476, November 24,
1944
38
to advance further in a series of increasingly difficult
problems. "-1 - 4
Glutamic acid on human subjects. In 1946, Albert-^
and associates reported on the effect of glutamic acid on
mentally retarded subjects. Eight mentally deficient indi
viduals were alternately given glutamic acid tablets Q.5gm
or a placebos (tablets of no therapeutic use) eighteen times
a day. Some started with placebos and others with glutamic
acid tablets and each was given to patients for a month or
more.
Before getting the tablets, each person was tested
with the Stanford Binet, Form L and the I. Q*s ranged from
22 to 73. A battery of almost every type of test which
could be given to these people were given.
Results of Four Patients-1 -®
First Patient:
1. Given glutamic acid for 2 months
a. Gained 1 year and 5 months in M. A.
14 Ibid., p 476
Kathryn Albert, Paul Hoch and Heinrich laelsch,
"Preliminary Report on the Effect of Glutamic Acid Admini
strated in Mentally Retarded Subjects" J ournal of Kervous
and Mental Diseases 104:263-74
16 Ibid.. p270-274
39
2. Few months after stopping of treatment
a. Back to original I. Q.
Second Patient:
1. Given placebos
a. Ko mental change
2. Five months of glutamic acid
a. 15 point rise in I. Q.
3. Stoppage of tablets
a. Lost 13 points in I. Q.
Third Patient:
1. Given glutamic acid for two.months
a. 13 point rise in I. Q.
2. Two months after stopping treatment
a. Lost 13 points
Fourth Patient:
1. Given placebos
a. One month no mental change
2. Given glutamic acid for two months
a. Gained equal to previous 7 years
b. 5 point I. Q. gain
Patients who, before administration of
glutamic acid appeared to be dull, inattentive
and easily fatigued, became more alert, attentive
and persistent in trying to accomplish the tasks
put before them. During administration of glu
tamic acid, they behaved in a manner which
suggests an improved emotional regulation. It
seemed to us that the performance of total
personality, rather than some circumscribed in
tellectual functions showed .improvement.
Glutamic acid was administered to subjects
with secondary mental deficiency. A significant
rise of mental age was found during the administra
tion of the amino acid. During the successive
placebos period, the patients I. Q. dropped back
to the level maintained before glutamic acid
administration. I®
Albert1^ and Zubin watched the electric shock and •
glutamic acid given to patients. Memory impairment, and
more or less severeconfusional state, are known to occur in
a large number of patients, after electric shock treatment.
Glutamic acid in the amount of a 10% solution was .admini
stered intravenously at the height of their confusion
(usually after 6 to 12 electric shock treatments). Albert
and Zubin believed it shortened the period of confusion and
memory impairment and in some patients an immediate definite
improvement in intellectual performance was shown.
The effects of the oral administration did not
show any toxic symptoms. Intravenously the glutamic acid
17 Ibid.. p 274
18 Ibid.. 263-74
19 Ibid., 270-74
ip.
can be toxie if a dilute solution of over 10$ is used and
if given faster than about Ice per minute.
In 1947, Zimmerman^® and his associates finished
a research with glutamic acid upon the intelligence in
children and adolescence.
pi
Conclusions dravrn:
1. Glutamie acid accelerates mental functioning
in human subjects.
2. The acceleration is general and is not restric
ted to segments of the intelligence and persona.1-
ity of individuals.
S. The greatest improvement in intelligence and
performance test scores occur within 6 months of
treatment, after which acceleration is diminished
and appears, to be approaching a ceiling after one
year of therapy.
Gain of Twenty-three Mentally Retared People
1. 10 gained 12 or more I. Q. points
£0 Frederic T. Zimmerman, Bessie P,. Burgemeister
and Tracy J. Putnam, t t Ceiling Effect of Glutamic Acid upon
Intelligence in Children and Adolescents,” American J ournal
of Psyciatry, CIV:593-99, April, 1948
21 Ibid.. pp 593-99
k2
2. 12 Gained 6 points
3. 8 gained 0 to 6 I. Q. points (1 gained 0)
A Stanford Binet group test was used together
with a battery .of projection, performance and I. Q. tests.
Actually 51 different tests were used. Genuine improvement
in reflective pattern, performance was shown.
i
Benzedrine. Since the mentally retarded persons
'usually are featured by psycho-motor retardation and apathy,
scientists used a drug known as f , Benzedrine, ! or Beta-phenyl-
isopropylamine to overcome to some degree these features.
If they could do so, then they would test and see what
effect it had on the intelligence, performance and improve
ment in speech correction. Now what are the effects of
benzedrine?
1. Affects the sympathetic system peripherally by
release of smooth muscle spasm and produces a rise
in the arterial blood pressure.
2. Centrally it may produce sensations of exhila
ration restlessnessj bringing relief from fatigue
and counteracting drowsiness by prolonging and
increasing the activity of the central nervous
system.
Is it possible that benzedrine could increase the
activity of the central nervous system of the mentally re-
l f - 3
tarded person? Moskowitz22 experimented with the effect of
benzedrine on mentally retarded subjects.
The cases were divided into four parts:
1. Mental Deficiency uncomplicated
2. Mental Deficiency associated with focal
Neurological signs
3. Mental Deficiency associated with focal
endocrine signs
a. Obesity, amenorrhea
4. Mental Deficiency associated with severe be
havior problems: motor hyperactivity, asocial
tendencies, etc.
Moskowitz used twenty-three cases of I. Q.’s
ranging from forty-three to seventy-five I. Q.'s, and ages
from twelve to twenty-six years. He evaluated by means of
intelligence tests, the improvement made in speech correc
tion, and performance ability. Of the tv/enty-three only
three showed striking improvements. The three that showed
improvement were in the mental defects uncomplicated. The
following is a ease study of one of the three children who
22 Harry Moskowitz, "Benzedrine Therapy for the
Mentally Handicapped"', American J ournal of Mental Deficiency
XLY:593-9 Aprii, 1948
V i-
improved • The child had a small sella turnia, and an aunt
in an insane hospital. Before Benzedrine therapy, education
was of no avail. After taking thirty mgms benzedrine daily,
speech correction became available, more alert and observant,
also functioned at a higher level and could show pictures
of one-syllable words and recited and wrote them. The
average improvement of the group was about 13%. In many
cases there was such great improvement that the pills were
called nThe Talking Pills”. The I. Q.fs did not change but
remained the same. The tests of ability show average In
crease of one and a half years after three months of benze
drine administration. In ~22% of cases, improvement was
noted, also increased alertness and response to the environ
ment, but learning capacity and performance ability did not
increase appreciably. Sixty-five per cent showed no im
provement that could not have been obtained by extensive
educational measures. Those most affected v/ere of normal
weight and height for their age. The farther away from the
normal, the less the drug aided.
In selected cases of uncomplicated oligo
phrenia.;, prolonged administration of benzedrine
sulphate raises the ability of the central nervous
system of-the .mentally handicapped to the point
where educational training can be utilized,
resulting in-greater performance ability. The
l\S
selection of .these . cases may. be correlated with
somatic factors and body measurements and response
to adrenaline injection. 23
23 Harry Moskowitz, wBenzedrine Therapy for the
Mentally Handicapped” American Journal Of Mental Deficiency.
XLV:595-9, April, 1948
CHAPTER VII
PSEUDO-FEEBLMIHDEDHESS
A theory has been presented in the last few years
which is worthy .of mention. Arthur-*- described a classifi
cation as follows:
1. Those with special disabilities that have been
confused with poor general ability.
2. Those with delayed speech that extended far
beyond normal limits, but did not prevent development of
non-verbal abilities.
3. Individuals who had had severe early illness
that delayed but did not prevent mental development.
4. Individuals with brain injury that interfered
with some kinds of intellectual activity but not with others.
5. Individuals with physical handicaps such as
impaired vision and hearing, and the like, that interfered
with academic-learning, and: with success on some scales for
measuring intelligence. Such individuals often find their
way to an institution for the feebleminded because an in
correct diagnosis was made by the community in which the
\
Grace Arthur, r j State Public School., Owatonna,
Minn." American Journal of Mental Deficiency. 52:137-142,
1947
i i - 7
child lived before institutionalization.
The following are quotations from a few articles
on the subject of pseudo-feeblemindedness:
Many children whose behavior suggests a lack
of native mental endowment are suffering from
specific disability of impaired hearing. The
child with a profound hearing impairment is rarely,
mistaken for feebleminded. But the child with
less severe impairment, whose acuity is better for,
low-than_mid-and high frequency sounds, is fre
quently mistaken for feebleminded. Tests of
visual and auditory acuity should be completed
before psychometric evaluation.2
True and false mental deficiency can be dis
tinguished through study of the learning curve of
the individual. The author describes a sensori
motor learning test used to measure the learning
curve, and a ”Regulari.ty Learning Index” calcula
ted from scores on tests, which is found to be
more sensitive than the I. Q. in distinguishing
true and false mental deficiency.'5
Retardation due to social or educational
disadvantages is most commonly falsely identified
as feeblemindedness.4
2 William G. Hardy, ”The Relations Between Im
paired Hearing and Pseudo-feeblemindedness”, Hervous Child.
7:452-445, 1949
^ Jose Allable Prinado, ”The Role of Psychometry
in the Differential Diagnosis of Some Forms of ’Pseudo-
Feeblemindedness.1” Hervous Child. 7:407-415, 1949
4 Debra Safran, and Ernest Harms, ”Social and
Education Impairments Wrongly Diagnosed as Feeblemindedness”,
Hervous Child. 7:497-415
l f . 8
The I. Q. is meaningless unless related to
the total child, speech, vision, hearing, reading
ability, disease, the effects of drugs, hunger,
physical discomfort are all factors which may lead
to an erroneous judgment of mental retardation.®
Three groups®
1. Absolutely feebleminded
A. Requiring custodial management
2. Relatively feebelminded
A. Requiring special educational and voca
tional facilities.
3. Pseudo-feebleminded
A. Requiring adequate diagnosis and treatment
of their handicaps.
® Charlotte A. Washowitz, "The Psychologists
Contribution to the Recognition of Pseudo-Feeblemindedness”
Rervous Child, 7:398-406, 1949
6 Leo Kanner, "Feeblemindedness: Absolute Rela
tive and Apparent" Kervous Child, 7:365, 1949
BIBLIOGRAPHY
A. BOOKS
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New York: Houghton Mifflin Company., 1924 pp
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\
Harrow, B., Textbook of Biochemistry. Philadelphia:
B. Saunders Co., 1947
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Albert, Kathryn., Hoch, Paul., and Waelsch, Heinrich, ”Pre-
liminary Reports on the Effect of^ Glutamic Acid Admin
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Albert, Kathryn., and Warden C. J., ”The Level of Perform
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Arthur, Grace, ’ ’State Public School”, American Journal of
Mental Deficiency. 52:137-142, 1947
Atwell, J. C., ’ ’ Encephalis as Sequela of Measles”, Pennsyl
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Bernhardt, K. S., ’ ’The Effect of Yitamin B Deficiency During
Nursing on the Subsequent Learning in the Rat,” Journal
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Brinton, D., ”Nervous Diseases-Benzedrine Sulfate,” The
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Clifford, Stewart, H., ”The Effects of Asphyxia on the New
born Infant”, J ournal of Ped., 18:567-578, 1941
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Cook, R., ’ ’ The Rh Gene as a Cause of Mental Deficiency,”
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$1
De Mare, Feliee., "A Case of Encephalitis after Measles”,
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Davidoff, E., "A Clinical Study of the Effect of Benzedrine
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Faber, Harold K. "Cerebral Damage in Infants and in Child
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Finkelman, I., and Shapiro, L. B., "Benzedrine and Atrophine
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Fox, M. J., and Bortin, M. M., "Rubella in Pregnancy,
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Fritz, M. F., "Maze Performance of White Rats in Relation to
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J ournal of Comparative Psychology. 13:365-390 (1932)
Guttman, E., "The Effect of Benzedrine on Depressive States”
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Hardy, William G., "The Relations Between Impaired Hearing
and Pseudo-feeblemindedness”, Nervous Child. 7:432-445,
1949
Harrell, Ruth P, "Mental Response to Added Thiamine," Journal
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52
Heath, Parker, "Measles Encephalitis” American J ournal of
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Heckel, George D., "Chemotherapy During Pregnancy; Danger
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October 18, 1941
Kanner, Leo, "Feeblemindedness: Absolute Relative, and
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Kugelmeas, Isaac N., Poull, L. E., and Samuel, E. E.,
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Suggestions as to Prevention." American J ournal of
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1941
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Abstract (if available)
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Krutoff, Edwin D.
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Core Title
Causative factors of mental retardation.
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Master of Science
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Education,Special Education
Publisher
University of Southern California
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education, special,OAI-PMH Harvest
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