The Right to Read, Chapter 3: Brains, Genes and Education

the-right-to-readWe are educators — we need NOT know what goes on in the brain.1— Poplin.



One could probably fill a vast library if one would put together all the research studies that attempted to prove that a learning disability is caused by either a neurological dysfunction, or that it is a genetically transferred disorder. The problem faced by researchers, who try to prove that it is a brain dysfunction, is that it is impossible to directly examine the living brain of a learning-disabled person in order to discover whether there is an abnormality in the brain. They have therefore been forced to study the brain indirectly. Although many methods and measuring instruments have so far been employed — including autopsies on the brains of deceased learning-disabled people and advanced technological developments — proof of a neurological dysfunction still eludes the researchers.

It is not the intention — and it will also be impossible — to discuss all of these studies in this book. The intention is rather first, to demonstrate that a brain difference — the heart of the LD notion — is not necessarily the equivalent of a brain dysfuntion, and second, that a human being is more than the sum of his genes.


Up to the late 1970s, authoritative publications listed the EEG among the ten most frequently recommended diagnostic tests for LD.2 An EEG, or electroencephalogram, uses electrodes to measure electrical activity at various points near the outer surface of the brain. The electrical signals are amplified and graphed on a continuously moving paper. It had been assumed that because the EEG could detect tumors, malformations, convulsive disorders, sleep states and coma, it might also shed light on the brain functioning of the learning disabled.3 For quite a while it appeared as though the EEG might have won the day. These hopes were, however, dashed towards the end of the 1970s.

A paper in 1949 reported an ample 75 percent of EEG abnormalities in a group of dyslexic children. Research the following year reported a dip to 59 percent, but the percentage picked up in the next decade, soaring to 88 percent in the early 1960s and peaking in the mid-1960s at an astronomical 95 percent.4 However, the 1960s ended with a decline to 50 percent and the 1970s opened with 37 percent. By 1973, reported EEG abnormalities in the learning disabled had fallen to only 32 percent. Toward the end of the 1970s there was strong doubt that any significant EEG abnormalities could be found in the learning disabled.5

This decline in percentages was caused by more stringent research methods being used. One of these more stringent research methods, which seemingly caused the faith in the EEG to take a nose-dive, was the use of replication studies done “blindly.” In the studies that reported a high percentage of EEG abnormalities in learning-disabled children, the researchers knew beforehand that the children were learning disabled. Their foreknowledge encouraged them to “find” what they were looking for in an “abnormal” group, and caused them to interpret the EEG results as abnormal much too easily.6 In replication studies done blindly, EEGs of learning-disabled children were mixed with EEGs of normal or typical learners, and the researchers had to analyze whether a child is learning disabled or not according to his EEG result. Now, that was a different matter! The EEGs of the two groups proved to be indistinguishable from one another.

The following research studies compared the EEGs of typical and disabled learners, and found that there are no differences in the number of typical and disabled learners who show abnormal EEGs. In the left-hand column are the percentages of poor learners who show abnormal EEGs, and in the right-hand column the percentages of typical learners who show abnormal EEGs:

Poor learners:Typical learners:
41%30%Myklebust and Boshes 19697
10%10%Meier 19718
14%22%Owen et al. 19719
23%32%Harris 198310

Even when children are known to have suffered brain injury, their EEGs often are normal.11

A 1967 review by Freeman concluded that for detecting LD brain dysfunctions the EEG is not the outstanding diagnostic tool that people had once thought. His conclusions remain valid today:

The EEG appears to be regarded with more awe than it deserves. It is not very reliable, and there are many technical problems in its use with children, yet our electronic age, with its admiration for gadgets and the paucity of knowledge in the behavior sciences, lends to this instrument a certain mystique…. The influence of the EEG among educators may possibly be due to the inundation of the literature with poorly done papers describing children with supposed minimal brain damage.12

Neurological Signs

One often finds that “soft neurological signs” are mentioned in clinical reports of learning-disabled children. The term “hard neurological signs” points to behavioral signs that always reflect brain injury, for example seizures, cerebral palsy, cranial nerve abnormalities leading to blindness and deafness and microcephaly.13

Soft neurological signs, on the other hand, point to a lag in children’s gross- and fine-motor development, such as poor balance and coordination difficulties.14 Studies trying to prove that the learning disabled have more neurological signs than typical learners, fared no better than EEG-studies. In one study, in fact, children with the most neurological signs actually had the fewest learning problems.15 In the most comprehensive study of this type in the U.S.A., the so-called National Collaborative Perinatal Project, the relationship between neurological signs and learning disabilities in 7-year-olds could account for only one percent of the learning problems.16

Structural Brain Assymetry

Because it can create visual projections of the brain in layers and from various angles, the LD field has considered computerized axial tomography, known as the CAT scan, an excellent method of comparing the size and shape of the brains of disabled and normal readers.17

The brain consists of three sections, the forebrain, the midbrain and the hindbrain. The forebrain is the largest of the three sections and takes up the complete top section of the skull. The most important area of the forebrain is the cerebral cortex, which among other things is responsible for learning, memory, speech and thought, and is usually looked upon as the damaged portion of the learning-disabled person’s brain. The cerebral cortex is divided into two halves — the left and the right hemispheres. Each hemisphere performs its own functions. In 90 percent of all people the left hemisphere of the cerebral cortex is responsible for language and structured thought, while the right hemisphere is responsible for visual perception, music, emotions and associated with instinctive and nonverbal responses. Damage to the left hemisphere will therefore have different effects than damage caused to the right hemisphere. For example, a person who loses his ability to talk and read after a stroke, will have damage to the left hemisphere of the cerebral cortex, while damage to the right hemisphere will result in depression or improper emotional reactions.

Some evidence of structural brain asymmetry in dyslexics has been reported. In the general population, CAT scans have found that the rear portion of the left hemisphere tends to be slightly wider than the right. In normal people there is a high percentage of asymmetry in the planum temporale, the upper surface of the posterior temporal lobe, a lobe involved in language processing, such as analyzing and synthesizing speech sounds, naming objects, and recalling words. For example, in approximately 65 percent of autopsied adults, the surface area of the planum temporale was found to be larger on the left; for 11 percent it is larger on the right; and the two areas are approximately equal in 24 percent.18 These differences were not found in dyslexics, for whom a CAT-scan study reported a larger right-surface area in 42 percent of the dyslexics examined. Along with the reverse asymmetry, these 42 percent — or ten of twenty-four subjects — had lower verbal IQs and a greater incidence of delayed speech than the remaining fourteen dyslexics. From these findings the researchers hypothesized that brain structure differences preventing normal development of brain functioning in language-related areas might cause dyslexia.19 Another paper two years later by two members of this study group described similar findings.20 This research was soon cited in texts and articles as “convincing” evidence “that cerebral asymmetries may be related to functional problems in reading and learning.”21

A year after the second paper was published, a replication study appeared. Using identical measurement procedures this study failed to find “an increased frequency of reversed occipital asymmetry with reading disability reported by others.” Reversed asymmetry was found in only 12 percent of the dyslexics, a percentage similar to that found in normal readers in the first studies. Furthermore, no relationship was found between the “posterior width of the hemispheres” and either verbal IQ scores, delayed acquisition of speech, or reading problems.22

Many other studies followed, involving magnetic resonance (MR) imaging, functional magnetic resonance imaging (fMRI), positron emission tomography (PET), and single photon emission computerized tomography (SPECT). Yet, they also failed to demonstrate specific diagnostic abnormalities. “To date, no diagnostic conclusions have been drawn utilizing these methods in the assessment of the [supposedly] neurobiologic basis to LD,” Bigler et al. summarized the results in an article published by the Journal of Learning Disabilities, thirty-five years after Samuel Kirk had established the term “learning disabilities.23

Known for conducting autopsies on the brains of deceased dyslexics, neurologist Albert Galaburda and his team of researchers seemed to have found a difference between dyslexic persons and nondyslexics in the size of nerve cells in the part of the brain that helps process sounds — the left MGN, or left medial geniculate nucleus. However, as neurobiologist Margaret Livingstone at Harvard Medical School points out, Galaburda’s results are not conclusive because of the small numbers studied.24

Brain Differences: An Alternative Interpretation

At the time of writing it was still not conclusive that the function or structure of the dyslexic’s brain is different from the brain of the normal reader. Of course the inability to find such differences can be interpreted as the absence of any such abnormalities. But, on the other hand, they may well exist. Should this be the case, then obviously such a premise would have to be interpreted, especially in relation to the question of cause and effect. Which of the two, the different brain structure or the learning disability, is the cause and which one is the effect? This, of course, can easily be misinterpreted.

Let us, for a moment, accept the hypothesis that there are differences between the brains of dyslexics and normal readers. Because of the biological determinists’ reluctance to recognize that the environment can affect brain function and structure, they will immediately and uncritically assume that these differences must be the cause and the learning disability the result. On the other hand, in order to establish their position, the antideterminists often undermine themselves by thinking they must deny any brain differences between disabled and nondisabled groups.25 Instead of denying this, we would like to present arguments that may lead to a reversal of the cause-effect problem. In other words, we hypothesize that dyslexia may cause differences in brain function and structure.

A logical point of departure for such an argument would be to first establish if brain function and structure could be altered. There is ample confirmation in the literature that indeed it can. In 1979, in an article in the Journal of Learning Disabilities, Doctors Marianne Frostig and Phyllis Maslow stated, “Neuropsychological research has demonstrated that environmental conditions, including education, affect brain structure and functioning.”26 In their book Brain, Mind, and Behavior Floyd E. Bloom, a neuropharmacologist, and Arlyne Lazerson, a professional writer specializing in psychology, state, “Experience [learning] can cause physical modifications in the brain.”27 This is confirmed by Michael Merzenich of the University of San Francisco. His work on brain plasticity shows that, while areas of the brain are designated for specific purposes, brain cells and cortical maps do change in response to experience (learning).28 It seems that, while stimulation causes brain growth on the one hand, the lack of stimulation, on the other hand, causes a lack of brain growth.

A good example of brain growth, caused by stimulation, can be found in Glenn Doman’s research on severely brain-damaged children. At the beginning of the twentieth century brain-damaged children were still regarded as “monsters,” and the “disgrace” that this brought on parents had to be hidden at all cost. Only towards the 1930s and early 1940s did research in this field begin to make the public aware of the needs of these children. Glenn Doman of Philadelphia was one of the pioneers in this field. Thanks to the work of Doman and his colleagues, the quality of life of many severely brain-damaged children has improved — some quite drastically. We have met several of these children ourselves.

Apparently Doman later broadened his audience to include learning-disabled children of normal intelligence. In the mid-1960s, he and Carl Delacato opened several treatment centers to which parents flocked with their children. However, their technique did not achieve sufficient results in remediating the supposedly “minimal” brain damaged, and as a result they fell into disfavor among LD practitioners: “The extravagant and rather bizarre claims made for this technique prompted a number of researchers to study it more closely, and they concluded that the program was worthless.”29 Moreover, a number of professional and parents’ associations took the unusual step of denouncing the Doman and Delacato method publicly.30

Doman’s failures seemingly caused researchers to reject his work altogether. This is unfortunate, because his successes — his work with severely brain-damaged children — certainly throws important light on brain development.

The heads of truly brain-damaged children usually grow at a slower rate than those of normal children. In one research analysis done by Doman, on 278 case histories of consecutively admitted brain-damaged children, 82.2 percent were below normal in head size at the start of treatment. All but thirty-seven of the children moved to an above-average rate of growth in head size over the fourteen-month period covered by the survey. In fact, the average rate of growth during treatment was 254 percent — between two to three times faster — of the normal for that age. As a result of the therapy, the brain started growing.31

An example of a lack of stimulation, causing a lack of brain growth, can be found in the work of Doctors Bruce D. Perry and Ronnie Pollard, two researchers at Baylor College of Medicine. They found that children raised in severely isolated conditions, where they had minimal exposure to language, touch and social interactions, developed brains 20 to 30 percent smaller than normal for their age.32

In order to find out what really happens to the brain in such cases, one would have to remove the brain from the skull. Experiments in this regard have been done on animals. Of course, no conclusions on human learning or functioning can be drawn from experiments on animals, but it is nevertheless interesting to take note of such experiments, because they seem to confirm that stimulation does indeed change brain structure.

Professor Klosovskii, a neurosurgeon in Moscow, took newborn litters of kittens and puppies and divided them into two exactly equal groups, one as the experimental group and the other as the control group. The kittens and puppies in the control group were permitted to grow in the usual way in which kittens and puppies normally grow. The experimental animals, however, were placed on a slowly revolving turntable and lived there throughout the experiment. The only difference in what happened to each of the groups was that the experimental group experienced a moving world while the control group experienced only as much as newborn kittens and puppies normally do. When the animals were ten days old, Klosovskii began to sacrifice matched pairs of the puppies and kittens to take their brains. The last of them were sacrificed by the nineteenth day of life. The animals on the turntable had from 22.8 percent to 35 percent (one third) more growth in the vestibular areas of their brains than did the control group animals. Just what does more growth mean? Did Klosovskii see one-third larger number of brain cells in his microscope? Not at all; he saw the same number of brain cells but one third larger and one third more mature.33

Mark Rosenzweig and his associates have shown that the brains of rats raised in an “enriched” laboratory environment — in a large cage containing many fellow rats and playthings that could be explored and manipulated — differed markedly in a number of respects from rats raised in small, isolated cages. The rats in the enriched environment had a greater weight and thickness of cerebral cortex than the ones raised in isolation. The researchers found more spines — which often serve as receivers in synaptic contacts — on the dendrites of cortical neurons in rats from enriched environments.34 Synaptic junctions in rats from enriched environments averaged about 50 percent larger than those in rats raised in isolation,35 and synaptic contacts were more frequent in the rats from enriched environments.36

The researchers wondered which of the many stimuli in the enriched environment had the most effect on the development of the rats’ brains. Further experiments brought surprising findings to light. Exercising and physical activity had no effect in terms of enriching their brains; visual stimulation wasn’t necessary to create enriched brains, as demonstrated by blind rats; handling and petting had no effect; whether the rats were together or isolated didn’t matter; and teaching the rats to press a lever helped only a little. The experimenters found only one aspect that helped to enrich the rats’ brains — the freedom to roam a large, object-filled space. Rats appear to be able to develop a good “space-brain” (one that helps them locate points in space and objects to climb over or through) rather than a “reasoning brain.” Or, as David Krech, one of the experimenters put it, “For each species there exists a set of species-specific experiences that are maximally enriching and maximally efficient in developing its brain.”37

Let us now theorize on the findings of Doman, Perry and Pollard, Klosovskii and Rosenzweig, and even compare the development of the brain with the development of the body.

The structure of a person’s body, as we all know, is to a great extent determined by the type and amount of physical exercise it receives. By lifting weights in the gymnasium Arnold Schwarzenegger’s muscles became big and strong — the structure changed. A person, whose physical activity centers on typing, or who exercises only once in a while, will certainly not have muscles like Schwarzenegger. In the same way, the type and amount of mental exercise a person receives, may determine the structure of the person’s brain. As Dworetzky states, citing Rosenzweig’s experiments, “it may well be that only a very few specific stimuli are necessary for a full neural, sensory, and perceptual development to occur. Although it remains to be demonstrated, the opportunity to engage in language, problem-solving, and thinking may be for the human child what the freedom to roam an object-filled environment is for the rat.”38 Of course, there may well be other even more important stimuli than language, problem-solving and thinking. The point is, that the dyslexic may not have received a sufficient amount of these stimuli and therefore his brain may be structurally different from that of a person who did. The structural difference is therefore not necessarily the cause of learning problems, but may be an effect.

At this point the argument of LD specialists would probably be that little Johnny would never look like Arnold Schwarzenegger, even if he spent twice as much time in the gymnasium. This, of course, is true. The basic blueprint of Johnny’s body structure may to a large extent already have been determined at conception. But nobody would deny that, if Johnny spent the same amount of time in the gymnasium as Schwarzenegger, his body would look completely different after two years.

We are all born with bodies that look different. In the same way, we are all born with neurological differences. We all have different talents, aptitudes and capabilities, but it is doubtful whether a difference represents a dysfunction or a disability. Naturally, it will be harder for some children to learn to read and there will always be those who can read better, just as we cannot all be tennis champions. In fact, some people may even find it very hard to learn to play tennis. But by following the correct method of instruction and with sustained practice according to this method, any person will at least learn to play acceptable tennis. In the same way any child can learn to read at least acceptably if the correct method of instruction is followed and if enough practice is provided. The correct method of instruction to the LD person, however, can only be found once the cause of a learning disability has been determined.

Researchers in the field of LD often underestimate the wonderful potential and capacity of the human brain. Compare the idea of a “learning disability” with Chafetz’s view that “the human mind can learn anything.”39 His optimism is shared by Litvak when he says that “the human brain has extensive capacities beyond those normally tapped,”40 and by Minninger and Dugan who say, “the simplest mind today controls dazzling skills, the very same skills that put the universe itself within our grasp.”41 Such conflicting views cannot exist together — either all the supporters of the “learning disabilities” idea are wrong, or Chafetz, Litvak, Minninger and Dugan and a host of others are.

Their optimism is confirmed by cases on record in which one of the hemispheres of the brain of a person was removed surgically and then the remaining hemisphere was afterwards able to take over the functions of the removed one. Consider the case of 13-year-old Brandi Binder, who developed such severe epilepsy that surgeons at UCLA had to remove the entire right side of her brain when she was six. Binder lost virtually all the control she had established over muscles on the left side of her body, the side controlled by the right side of her brain. Yet today, after years of therapy ranging from leg lifts to math and music drills, Binder is an A student at the Holmes Middle School in Colorado Springs, Colorado. She loves music, math and art — skills usually associated with the right half of the brain. And while Binder’s recuperation is not 100 percent — for example, she never regained the use of her left arm — it comes close.42

Even more astonishing than the Binder case is the story of John Lorber, a British pediatrician, who studied an individual who, due to neurological illness, had virtually no brain. Instead of the normal 4.5-centimeter thickness of cerebral cortex, this young student had just a thin layer measuring a millimeter or so. In spite of this obvious shortcoming, he was measured as having an IQ of 126, was socially competent, and gained first-class honors in mathematics.43

If it is possible to learn to function normally — or close to normal — with half a brain or with virtually no brain, then there must certainly be hope for the supposedly learning disabled, and even for the minuscule number of children who may truly suffer from a minimal brain dysfunction.

Genetics in Learning Disabilities

Some researchers blame a supposed neurological dysfunction on brain damage before, during, or after birth. Others hold that the neurological dysfunction is genetically determined and inherited from generation to generation. They support this view by referring to many studies that have indicated that there is often a family history of learning disabilities. Hornsby, for example, state that 88 percent of dyslexics had a near relative who had similar problems with reading and spelling.44 According to an American study the risk that a child will have a reading problem is increased from four to thirteen times if one of the parents has a similar problem.45 This tendency for dyslexia to “run in families” have been confirmed by numerous studies.

Many possible explanations have been offered for this tendency. While Dr. Toril Fagerheim of Norway has apparently identified the involvement of chromosome 2,46 others maintain that the quantitative trait locus on the short arm of chromosome 6 is involved, and Lubs et al. say that chromosome 15 is involved too.47

It would be foolish to deny that genes may play a role in human capabilities and talents or even difficulties. However, to determine the relative importance of the role of genes and the role of the environment will forever be impossible. How much does the genetic make-up of a person contribute to his talents or difficulties, and how much the fact that the family members share the same unique environment? Take Mozart as an example. He was one of the most brilliant musicians of all time. All the members of his family were musicians and from the moment of his birth he was continually exposed to music. Suppose he had been adopted immediately after birth by other parents who played no music. Would we then have known about Mozart? It is possible, but highly unlikely.

The brilliant work done by the late Shinichi Suzuki of Japan also shows how musical talent may be developed by exposure. Suzuki trained thousands of violinists, who from a very young age took part in concerts lasting more than two hours, playing works by Mozart, Beethoven and Liszt. He started stimulating these future violinists from before birth. As a result of his research he concluded that what a child becomes, is totally dependent on how he is educated.48 “Talent is not an accident of birth,” he said.49

Research on the role of the environment in children’s intellectual development has also shown that a stimulating environment can dramatically increase IQ, whereas a deprived environment can lead to a decrease in IQ. A particularly interesting project on early intellectual stimulation involved twenty-five children in an orphanage. These children were seriously environmentally deprived because the orphanage was crowded and understaffed. Thirteen babies of the average age of nineteen months were transferred to the Glenwood State School for retarded adult women and each baby was put in the personal care of a woman. Skeels, who conducted the experiment, deliberately chose the most deficient of the orphans to be placed in the Glenwood School. Their average IQ was 64, while the average IQ of the twelve who stayed behind in the orphanage was 87.50

In the Glenwood State School the children were placed in open, active wards with the older and relatively bright women. Their substitute mothers overwhelmed them with love and cuddling. Toys were available, they were taken on outings and they were talked to a lot. The women were taught how to stimulate the babies intellectually and how to elicit language from them.

After eighteen months, the dramatic findings were that the children who were placed with substitute mothers, and therefore received additional stimulation, on average showed an increase of 29 IQ points! A follow-up study was conducted two and a half years later. Eleven of the thirteen children originally transferred to the Glenwood home had been adopted and their average IQ was now 101. The two children who had not been adopted were reinstitutionalized and lost their initial gain. The control group, the twelve children who had not been transferred to Glenwood, had remained in institution wards and now had an average IQ of 66 (an average decrease of 21 points).51 Although the value of IQ tests is grossly exaggerated today (see chapter four), this astounding difference between these two groups is hard to ignore.

More telling than the increase or decrease in IQ, however, is the difference in the quality of life these two groups enjoyed. When these children reached young adulthood, another follow-up study brought the following to light: “The experimental group had become productive, functioning adults, while the control group, for the most part, had been institutionalized as mentally retarded.”52

From the examples above, a few more in further chapters in this book (see especially chapter seven), and many other cases in the literature, we contend that, even if it were possible to inherit a learning disability, a human being is not merely a slave to his genes, but can learn to overcome this problem. Human life can be compared to a game of cards. At birth, every person is dealt a hand of cards — his genetic make-up. Some receive a good hand, others a less good one. Success in any game, however, is almost always a matter of erudition. It is undeniably so that there are often certain innate qualities that will give one person an advantage over another in a specific game. However, without having learned the game and without regular and rigorous practice, nobody will ever become a champion at any game. In the same way the outcome of the game of life is not solely determined by the quality of a person’s initial hand of cards, but also by the way in which he takes part in the game of life. His ability to take part in the game of life satisfactorily, perhaps even successfully, will be determined to a very large extent by the quality and quantity of education that he has enjoyed.

Perhaps it is appropriate to elaborate on Poplin’s well-known dictum that we are educators and need NOT know what goes on in the brain. Perhaps we should add that we are educators of children — not of brains, and also not of genes.


  1. Poplin, M. “Learning disabilities at the crossroads,” 46th Yearbook of the Claremont Reading Conference, 1982, 41-52.
  2. Coles, “The learning-disabilities test battery: Empirical and social issues,” Harvard Educational Review, 1978, vol. 48, 313-340.
  3. Smith, C. R., Learning Disabilities. The Interaction of Learner, Task, and Setting (Boston: Allyn and Bacon, 1991), 78.
  4. Ayers, F. W., & Torres, F., “The incidence of EEG abnormalities in a dyslexic and a control group,” Journal of Clinical Psychology, 1967, vol. 23, 334-336, cited in G. S. Coles, The Learning Mystique (New York: Pantheon Books, 1987), 76; Hughes, J. R., “Electroencephalographic and neurophysiological studies in dyslexia,” in A. L. Benton & D. Pearl (eds.), Dyslexia: An Appraisal of Current Knowledge (N. Y.: Oxford, 1978).
  5. Hughes, “Electroencephalographic and neurophysiological studies.”
  6. Coles, The Learning Mystique, 76, 84.
  7. Myklebust, H. R., & Boshes, B., Minimal Brain Damage in Children (Washington, DC: Neurological and Sensory Disease Program, Department of Health, Education and Welfare, 1969), cited in Smith, Learning Disabilities, 78.
  8. Meier, J. H., “Prevalence and characteristics of learning disabilities found in second grade children,” Journal of Learning Disabilities, 1971, vol. 4, 1-16, cited in Smith, Learning Disabilities, 78.
  9. Owen, F. W., et al., “Learning disorders in children: Sibling studies,” Monographs of the Society for Research in Child Development, 1971, vol. 36(4), cited in Smith, Learning Disabilities, 78.
  10. Harris, R., “Clinical neurophysiology in pediatric neurology,” in E. M. Brett (ed.), Paediatric Neurology, (Edinburgh: Churchill Livingstone, 1983), cited in Smith, Learning Disabilities, 78.
  11. Freeman, R. D., “Special education and the electroencephalogram: Marriage of convenience,” Journal of Special Education, 1967, vol. 2, 61-73; Black, F. W., “Neurological dysfunction and reading disorders,” Journal of Learning Disabilities, 1973, vol. 6, 313-316.
  12. Freeman, “Special education and the electroencephalogram.”
  13. Smith, Learning Disabilities, 78.
  14. Ibid.
  15. Ingram, T. T. S., Mason, A. W., & Blackburn, I., “A retrospective study of 82 children with reading disability,” Developmental Medicine and Child Neurology, 1970, vol. 12, 271-279.
  16. Nichols, P., & Chen, T., Minimal Brain Dysfunction: A Prospective Study (Hillsdale, NJ: Lawrence Earlbaum, 1981).
  17. Coles, The Learning Mystique, 83.
  18. Hier, D. B., et al., “Developmental dyslexia: Evidence for a subgroup with a reversal of cerebral asymmetry,” Archives of Neurology, 1978, vol. 35, 90-92, cited in Coles, The Learning Mystique, 83.
  19. Ibid.
  20. Rosenberger, P. B., & Hier, D. B., “Cerebral asymmetry and verbal intellectual deficits,” Annals of Neurology, 1980, vol. 8, 300-304, cited in Coles, The Learning Mystique, 83-84.
  21. Coles, The Learning Mystique, 84.
  22. Haslam, R. H., et al., “Cerebral asymmetry in developmental dyslexia,” Archives of Neurology, 1981, vol. 38, 679-682, cited in Coles, The Learning Mystique, 84.
  23. Bigler, E. D., Lajiness-O’Neill, R., & Howes, N-L., “Technology in the assessment of learning disability,” Journal of Learning Disabilities, January 1998, vol. 31.
  24. Cooke, R., “Dyslexia linked to hearing defect. Size of nerve cells may be key,” Newsday, 16 August 1994, A15.
  25. Stanovich, K. E., “Learning disabilities in broader context,” Journal of Learning Disabilities, 1989, vol. 22(5), 287-291.
  26. Frostig, M., & Maslow, P., “Neuropsychological contributions to education.” Journal of Learning Disabilities, October 1979, vol. 12(8).
  27. Bloom, F. E., & Lazerson, A., Brain, Mind, and Behavior (2nd ed.), (New York: W. H. Freeman and Company, 1985).
  28. Merzenich, M., et al., “Temporal processing deficits of language,” “Learning impaired children ameliorated by training” and “Giving language skills a boost,” Science, 5 January 1996, vol. 272.
  29. Carrier, J. G., “The politics of early learning disability theory,” in B. M. Franklin (ed.), Learning Disability: Dissenting Essays (Philadelphia: The Falmer Press, 1987), 58.
  30. Carrier, J. G, Learning Disability: Social Class and the Construction of Inequality in American Education (New York: Greenwood Press, 1986), 111.
  31. Doman, G., What to Do About Your Brain-Injured Child (New York: Doubleday & Company, Inc., 1982), 188.
  32. Perry, B. D., & Pollard, R., “Altered brain development following global neglect in early childhood,” Society for Neuroscience: Proceedings from Annual Meeting, New Orleans, 1997.
  33. Doman, G., What to Do About Your Brain-Injured Child, 189-190.
  34. Globus, A., et al., “Effects of differential experience on dendritic spine counts in rat cerebral cortex.” Journal of Comparative Physiology and Psychology, 1973, vol. 82, 175-181, cited in Bloom & Lazerson, Brain, Mind, and Behavior, 265.
  35. MØllgaard, K., et al., “Quantitative synaptic changes with differential experience in rat brain,” International Journal of Neuroscience, 1971, vol. 2, 356-368, cited in Bloom & Lazerson, Brain, Mind, and Behavior, 265.
  36. Greenough, W. T., West, R. W., & DeVoodg, T. J., “Subsynaptic plate perforations: Changes with age and experience in the rat,” Science, 1978, vol. 202, 1096-1098, cited in Bloom & Lazerson, Brain, Mind, and Behavior, 265.
  37. Krech, D., “Don’t use the kitchen-sink approach to enrichment,” Today’s Education, 1970, vol. 59(7), 30-32, cited in J. P. Dworetzky, Introduction to Child Development (St. Paul: West Publishing Company, 1981), 193-194.
  38. Dworetzky, Introduction to Child Development, 194.
  39. Chafetz, M. D., Smart for Life. How to Improve Your Brain Power at Any Age (New York: Penguin Books, 1992).
  40. Litvak, S. B., Use Your Head. How to Develop the Other 80% of Your Brain (Englewood Cliffs: Prentice-Hall, Inc., 1982).
  41. Minninger, J., & Dugan, E., Make Your Mind Work for You (New York: Pocket Books, 1988).
  42. Nash, J. M., “Special report: Fertile minds from birth, a baby’s brain cells proliferate wildly, making connections that may shape a lifetime of experience. The first three years are crucial,” Time, 3 February 1997.
  43. Lewin, R. “Is your brain really necessary?” Science, 12 December 1980, vol. 210, 1232-1234, cited in T. Armstrong, In Their Own Way: Discovering and Encouraging Your Child’s Personal Learning Style (Los Angeles: Jeremy P. Tarcher, Inc., 1987), 12.
  44. Hornsby, B., Overcoming Dyslexia (Johannesburg: Juta and Company Ltd., 1984), 16.
  45. Vogler, G. P., DeFries, J. C., & Decker, S., “Family history as an indicator of risk for reading disability,” Journal of Learning Disabilities, 1985, vol. 7, 419-421.
  46. “New gene for dyslexia located,” Journal of Medical Genetics, 7 September 1999.
  47. Brooks, L., Revised version of a paper presented at the DI Guild Symposium, November 1996.
  48. Suzuki, S., Nurtured by Love: A New Approach to Education (New York: Exposition Press, 1969).
  49. Price, B., “Dr. Shinichi Suzuki (1898-1997),” Issue of Women Newsmagazine, Autumn 1998.
  50. Skeels, H. M., et al., “A study of environmental stimulation: An orphanage preschool project,” University of Iowa Studies in Child Welfare, 1938, vol. 15(4), cited in Dworetzky, Introduction to Child Development, 211-212.
  51. Ibid.
  52. Clark, B., Growing Up Gifted (3rd ed.), (Columbus: Merrill, 1988), cited in P. Engelbrecht, S. Kriegler & M. Booysen (eds.), Perspectives on Learning Difficulties (Pretoria: J. L. van Schaik, 1996), 176.
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