The Right to Read, Chapter 2: Birth of a Syndrome

the-right-to-readWe must take all history seriously — the history of what we did right and the history of what we did wrong. People learn from both their successes and their failures.1— Blatt



On Saturday, April 6, 1963, a new disease was invented in Chicago, Illinois, that over the next twenty years would slowly begin to infect millions of schoolchildren nationwide. This was no simple virus or common bacteria. Hidden deep within the neurological system, it resisted detection by medical personnel, evaded clear diagnosis through testing, and had no discernible cure. The federal government would spend billions of dollars on this affliction over the next twenty years, and yet between 1977 and 1983 the number of sufferers would double...

It was on that Saturday in April that Samuel Kirk, then a professor of special education at the University of Illinois, told a group of concerned parents about learning disabilities. He suggested that they use the term to describe “children who have disorders in development of language, speech, reading, and associated communication skills.” They enthusiastically agreed and shortly thereafter established the Association for Children with Learning Disabilities.

Since that time, the learning disability (LD) movement has mushroomed, with the founding of many more organizations, the writing of hundreds of books and tens of thousands of articles. The popular media have made it a suitable subject for dramatic television shows and full-length feature films. More importantly, and devastatingly, millions of children have been labeled learning disabled, dyslexic, hyperactive, and a host of related terms, then sent to special programs to be treated for their “condition.”2

Problems with learning and behavior in children are certainly not a new phenomenon. Long before 1963 teachers and parents were complaining that some children are difficult to teach and control, that they underachieve academically or that they can’t sit still. As early as 1867, Heinrich Stotzner, a German teacher of the deaf, founded a school for slow learning children. These children did not have mental retardation but, according to Stotzner, their memories were too weak to retain letters, and due to the poor motor coordination of their fingers, they had difficulty learning to write. Stotzner understood that the learning problems of these children called for remedial teaching efforts.3

Even earlier, in 1845, the physician Heinrich Hoffman had written and illustrated the story Zappelphilipp (“Fidget Philipp”) for his own son. Philipp was a hyperactive boy, rocking in his chair at the dinner table until everything fell to the ground with the tablecloth. Zappelphilipp at the time was probably the most popular book for the young, at least in Germany.4 Half a century later, in 1907, the neurologist Hermann Oppenheim reported his clinical experience with children who could not sit still, could not keep their extremities calm and caused significant trouble for parents and teachers with their fidgeting and their uninhibited translation of psychic processes into motoric acts.5

Problems with learning and behavior have therefore always been around, although they may perhaps never before have existed in the alarming numbers that they occur now. What also did not exist until 6 April 1963, was the increasingly fashionable attribution of these problems to neurological abnormalities and to describe “these affected children” as victims of a clearly defined medical syndrome.6 According to this medical explanation, learning disabilities has a biological cause. To be more exact, there is something wrong with the child’s brain. In accordance with this view, learning is a neurological “process” which takes place inside the brain. On these grounds it is supposed that the child who struggles to learn must have a neurological “dysfunction.”

The idea of a neurological dysfunction soon became more and more popular, giving rise to an armada of theories. According to one such a theory, dyslexia is the result when the link between the language, hearing and comprehension centers of the brain is somehow misconfigured during fetal development.7 Other theories state that dyslexia is caused by “faulty wiring in the brain,”8 or a subtle impairment of vision.Dr. Harold N. Levinson blames it on a cerebellar-vestibular dysfunction,10 while in an article in The Economist it was stated, “natural selection has equipped mankind with impressive spoken-language skills. But it never had a chance to prepare people for reading. The first known language in which written letters corresponded to particular sounds was developed by the Canaanites around 1700 B.C. By then the human brain had already been chiseled into its current form.”11 The list of proposed causes for reading and learning failure is endless.

It is impossible to trace any of these supposed neurological abnormalities through any form of medical examination or test. The abnormality is nevertheless inferred from observing the child’s behavior. Bob Algozzine, once professor of special education at the University of Florida and contributing editor to The Journal of Learning Disabilities, wrote: “No…one has been able to demonstrate to me that a specific, distinctly unique group of behaviors differentiate LD children from many of their classmates. To build an empire on such a foundation is very dishonest.”12

Professor Coles concurs. After decades of research, he says, it has still not been demonstrated that disabling neurological dysfunctions exist in more than a minuscule number of children. The few research studies that have made such claims, have serious methodological flaws. Through repeating these ideas and beliefs over and over, however, the theory of a neurological dysfunction has taken on the authority of proven fact.13 And indeed, this “fact” has become the point of departure in the science of learning disabilities.

To have a better understanding of this medical fabrication it is necessary to go back in history to the time when the ideas on learning disabilities originated. The present can only be fully understood if one examines its roots in the past. In this case the key to comprehension resides in the work of James Hinshelwood, a Glasgow eye surgeon, who today is cited as the first major figure in what became the field of learning disabilities, and in the research done by two German refugees, the psychiatrist Alfred Strauss and the psychologist Heinz Werner. These two scholars were employed during the late 1930s at the Wayne County Training School in Northville, Michigan, a school for educable mentally retarded children.

In 1907, a schoolmaster in Glasgow, Scotland, mentioned to a county Medical Officer of Health that he was “greatly puzzled” about four of his students. They were the youngest brothers in a family of eleven children and, unlike their seven siblings, had “experienced the greatest difficulties in learning to read.” The medical officer, a former student of James Hinshelwood, “at once recognized” the “true nature of the difficulty.” He referred the boys to his former mentor to confirm the diagnosis and provide the schoolmaster with expert help.

Hinshelwood confirmed the medical officer’s preliminary conclusions: the boys indeed had congenital word-blindness, a condition that “frequently assumes a family type,” that probably was hereditary and that was caused by a defective language-related area of the brain. He reasoned that, because the reading problems were clustered in one family, and because the four boys had normal general intelligence, lacked visual problems, had good visual memory except for letters and words, had a family life which had not impeded their siblings’ learning, but had failed to read with school instruction that had been successful with their siblings, it was “evident that their cerebral defect was a purely local one,…that it was strictly confined to the cerebral area for the visual memory of words and letters, the left angular gyrus, and did not extend at all beyond that.”14

Hinshelwood concluded that the root of congenital word-blindness lay in children’s brains because he had observed that dysfunctional reading symptoms found in adults with brain lesions were analogous to those of certain children with reading problems. If an inability to recognize and remember letters and words, or to unite recognizable letters into syllables or into words, was acquired word-blindness, a symptom of localized brain damage in adults; and if it was clear that sensory functioning, intellectual functioning and environmental conditions could be excluded as causes of the reading disability, and if the reading symptoms were similar to those of acquired word-blindness, it was “evident” — Hinshelwood’s exact word — that the problem was caused by localized brain damage that was probably hereditary.15

This line of reasoning, however, comprises an invalid argument: If A then B; B; therefore A.

Hinshelwood’s argument can be summarized as follows:

If an individual has brain damage, he exhibits reading problems.
This individual exhibits reading problems.
Therefore, this individual is brain damaged.
There may perhaps be some readers who are unable to see that the above argument is invalid. For their benefit, another argument, showing the same form as the above one is offered below. The invalidity of this argument, however, cannot be doubted.

If I am Superman, then I am a man.
I am a man.
Therefore, I am Superman.
Goodman used another analogy to point out the logical flaw inherent in Hinshelwood’s reasoning: A drought can kill vegetation. If, however, we find dead vegetation, we cannot assume that drought was the cause. The vegetation could have been destroyed, not by drought but by any number of causes including nonbiological ones such as lumbering.16 Consider also that, when a person is being chased by a ferocious bull, he will run. However, when we see a person running, we cannot jump to the conclusion that he is being chased by a bull. Similarly, if a brain-damaged person exhibits certain characteristics, we cannot simply jump to the conclusion that a person is brain damaged when we see him exhibiting the same characteristics. There may be many other reasons for his behavior.

In his diagnosis of the four boys, Hinshelwood rejected or ignored the role that school, family, and other environmental conditions may have played. As Coles points out, there were other plausible explanations for the boys’ reading difficulties. Perhaps by the time the eighth child arrived, the parents of this large mining family were too busy and too tired to provide the nurturing they had given the others. Perhaps a large family dependent upon a small salary had become increasingly poor as the family grew, and the diminishing financial means relative to family needs had adversely affected the younger children.17 Hinshelwood also ignored the role motivation might have played. Upon leaving school, the oldest of the four boys, motivated by his enthusiasm for football (soccer), managed to master on his own the vocabulary of football terms, and could read, “fairly well,” the football reports of a sports newspaper that he religiously bought. Yet, the young man had great difficulty reading a child’s first primer or an “ordinary book.”18

At the beginning of the twentieth century the number of children that were diagnosed as cases of congenital word-blindness was still small. However, following research that was done during the 1930s and 1940s by Strauss and Werner, this situation was to change dramatically during and after the 1960s.

While Strauss and Werner were employed at the Wayne County Training School, they came to believe that their educable mentally retarded students were of two basic types. The first group, which they referred to as the endogenous type, consisted of children who had a family history of mental deficiency. The second group, which they referred to as the exogenous type, had, on the other hand, no family history of mental deficiency. According to Strauss and Werner, their retardation was caused by brain injury — before, during or after birth. In comparing endogenous and exogenous children on perceptual and cognitive tasks, they found the endogenous group to be more successful than the brain-injured children regarding these abilities. The endogenous children had no behavioral problems, while the brain-injured children engaged in — what they described as — disturbed, unrestrained and volatile behavior. Furthermore, the endogenous children exhibited a small increase in their IQ scores during their stay at the Wayne County Training School, while the exogenous children displayed a small decrease. Strauss and Werner concluded that the IQ changes indicated that the curriculum for the mentally retarded was ineffective for the brain-damaged children.19

A few years later Strauss and another coworker, Newell Kephart, expanded the study of brain injury to include children of normal intelligence. They argued that the kind of perceptual-motor and cognitive problems and behavior problems, that Strauss and Werner had found among the exogenous group, were not only to be found in mentally defective children. These problems were also found in children of normal intelligence. On these grounds they concluded that children of normal intelligence, who exhibited these learning and behavior problems, were also brain damaged.20 In this way, they committed the same logical error that Hinshelwood had committed earlier: If A then B; B; therefore A.

The research of Strauss and Werner has been criticized by many. Kenneth Kavale of the University of Iowa and Steven Forness of the University of California, for example, reanalyzed Strauss and Werner’s original studies on brain-injured children. They concluded that the performance differences reported between the two groups of children — the endogenous and exogenous — were in fact too small to justify the distinction which Strauss and Werner had made.21

There was, furthermore, a critical problem involved in their research. Neither Strauss and Werner in their initial research with mentally defective children nor Strauss and Kephart in their studies of children with normal intelligence provided evidence of brain damage or other neurological dysfunctions. The brain damage was inferred only from the children’s behavior.22

The Learning Disabilities Scapegoat

Despite these obvious problems and the criticism, the work of Strauss and Kephart has been continued by many. Although these followers of Strauss and Kephart could also provide no proof of brain damage or neurological abnormalities in otherwise normal children, the idea became more and more popular. The term “brain damage” was, however, mitigated to a less deleterious one, namely “minimal brain dysfunction.” A few years later this term also fell into disfavor in educational circles, and was replaced with the term “learning disabilities.”

In spite of the inability of experts to prove any neurological dysfunction, middle-class parents, especially, accepted this idea with great relief. Before the 1960s their children were often described as “dumb,” “mixed up” and “lazy,” even though they were smart in some ways, were not crazy, often tried very hard, and “would learn if only they could.”23 Children were frequently misdiagnosed as mentally retarded and had to live with this stigma for the rest of their lives. One cannot but sympathize with the parents and the children of that time. “You felt like you were all alone,” one parent said, “and no one could help. The educators made you feel like your child was a freak, and most of the medical people just didn’t understand.”24

Many middle-class parents thought that special-education classifications such as “mentally retarded” and “emotionally disturbed” and prevailing social science categories for explaining academic failure such as “culturally deprived” seemed appropriate for children from minority and poor communities, but not for children from the middle class:

The variety of problems afflicting minority groups and the poor were said to affect the emotions and intellect of children in ways that explained their difficulties in school. An applicable but different explanation was needed for children who had grown up in the suburbs, with the advantages of middle-class life, and who, despite their academic problems, often appeared to be good learners outside of school. The learning-disabilities explanation — that the problem was caused not by retardation or other exclusionary factors, but by a minor neurological “glitch” — made sense to many. The explanation also offered different advantages to different interests: it was less pejorative than other special-education categories and it did not consider or criticize any role schools, families, or other social influences might have had in creating the learning disabilities.25

Within a few years after the idea of a minimal brain dysfunction and learning disability had taken root, it was not only the cause of poor school achievement, but of nearly any physical or psychological problem, and simply any form of behavior that adults found troublesome. William Cruickshank is worth quoting at length:

Parents attending a lecture on learning disabilities have…seen fit in a public forum to question me about their child who stuttered, who teased the family cat, who could not deal with geometry in the tenth grade but who otherwise was getting along well in school, who had night terrors, who was diagnosed by the family psychiatrist as depressed — all of these under the label of learning disabilities. I have had parents question me on the failure of the child of nine years of age to be able to swim, another who could type but could not write legibly, another who masturbated, and still another who did not like to go with girls. Parents in their concept of learning disability have talked with me about nail biting, poor eating habits, failure of the child to keep his room neat, unwillingness to take a bath, failure to brush teeth…. One parent asked me if the fact that his college-student son wore long hair and, he “suspected,” lived with a girl outside his dormitory was the result of a learning disability.26

Even parents’ problems were considered to be the result of a dysfunction inside the child’s brain. Nancy Ramos, once president of the California Association for Neurologically Handicapped Children, echoes the message: “A good many LD children come from single-parent homes, but it’s not the broken marriages that cause LD, it’s that the learning-disabled child broke up the marriage in the first place.”27

Keeping the Syndrome Alive

The LD enterprise soon became an enormous machine — indeed a factory — with attending cottage industries, fueled by legal, sociopolitical, educational, and entrepreneurial energy.28 By the end of the 1960s children began to be classified as “learning disabled” and an “antidote” for the syndrome had to be found. State funds were appropriated for LD curricula. An array of tests and remedial materials were devised and published. Schools catering specifically for learning-disabled children started rising up like anthills. The number of journal articles and books on the subject multiplied. A profusion of LD research projects commenced and pharmaceutical companies promoted and profited from drugs for the learning disabled.29

Advocacy groups, in the rush to generate public awareness of the condition of dyslexia, with the cooperation of a compliant media, have perpetuated the belief that a host of famous individuals such as Albert Einstein, Auguste Rodin, George Patton, and Woodrow Wilson were dyslexic. The folk myth — the “affliction of the geniuses” — continues to be spread despite the fact that knowledge of the definition of dyslexia and the reading of any standard biographies would immediately reveal the inaccuracy of many such claims.30 For example, as Coles points out, Einstein’s reading of Kant and Darwin at age thirteen is hardly representative of individuals who are currently labeled dyslexic.31 According to Moats and Lyon, parental advocacy groups have remained the strongest force in keeping alive the concept of learning disabilities. “Science has taken a back seat (and more accurately, the rumble seat.)”32

In spite of the obviously illogical roots of this idea, it nevertheless spread like wildfire throughout nearly the whole world. In South Africa, for example, it was taken so seriously that in 1968 a commission of enquiry was appointed by the then Minister of Education to investigate the prevalence of minimal brain dysfunction among South African schoolchildren. Following the report by this commission in 1969, a network of school psychologists was established all over the country. Remedial education for the children with supposed minimal brain dysfunction was undertaken with great fervor and a course in minimal brain dysfunction was offered to teachers at the College of Education for Further Training.33 The large number of teachers who followed this course shows how much easier it is to swim downstream. Once a sizeable number of people have started moving in a certain direction, it seems that, like with the lemmings in the Arctic regions, it is always easy for them to entice others to join them.

Professionals from different spheres of scientific endeavor started going along with the stream. Using modern techniques, screens and tests to diagnose and treat the LD child, they built a mystical aura around the field, remarked Peter Schrag and Diane Divoky in their classic book The Myth of the Hyperactive Child. The professionals can “see” things in the child that the layman can never see. But, upon investigating the results they achieve, we find that LD children continue to fail miserably in the classroom.34

“Treatment” is seldom, if ever, directed at the environment. The possibility that there may be other problems relating to the home, school or other social conditions is ignored. The teacher may be fickle, brutal and stupid, but when a child fails or cannot adjust, only the child is tested and treated. Does this perhaps imply that every teacher, school, and the schooling system are perfect? Does this further imply that all teachers are equally capable, that “if I cannot teach him, nobody can teach him?”

An interesting research study in this regard was done in a school where the children were from poor socio-economic backgrounds. The study compared the success of children of similar backgrounds, who had been randomly placed in three first-grade classrooms. Their teachers had taught in this school for many years.

The researchers found that although family status and conditions were related to academic success, the effect of teacher influence was quite strong. Using reading achievement as the primary measure of educational achievement, they found that 64 percent of the children in the class of one teacher (Miss A) were high achievers, compared to 28 percent of the other first-grade classes. Conversely, Miss A had 7 percent low achievers, while the other teachers had 28 percent low achievers. Furthermore, the average academic achievement of children from Miss A’s class remained consistently higher throughout their elementary school years.

How did Miss A enable so many of her pupils to do well academically? A reporter who did an in-depth story on Miss A and her pupils found that her attitude was, “It did not matter what background or abilities the beginning pupil had; there was no way the pupil was not going to read at the end of first grade.” Miss A imbued her pupils with self-confidence and an appreciation of the importance of schooling. Hard work was one of the keys to her success with students: for children who were slow learners, Miss A devoted extra hours.35

This study, however, reveals more than just the effect of successful teaching, but also an implicit school policy of indifference. Although the school administrators had a standard in Miss A’s teaching by which they could judge teaching success, they did not intervene or take corrective measures to change less effective instruction and less favorable academic outcomes in the other classrooms. Because schools simply accept that a proportion of their pupils would fail, Miss A’s colleagues appeared to have been doing an acceptable and normal job. Miss A’s success remained hers alone. Had she been much less successful, less would have been just as acceptable.36

Teachers often underestimate the importance of their role in determining a child’s future success. The story is told about a woman who attended her twenty-year high school reunion. There she encountered her freshman year art teacher. She told him that she decided to go to college as a result of his inspiration and that she was now an art professor at a large state university.

At the end of the evening’s festivities, the teacher searched out his former student, shook her hand and said, “Thank you for saying those nice things about my teaching. You’ve really made my day.”

“You’re welcome,” said the woman as she hugged him, “But let me thank you — you’ve made my life.”

In 1974 Bateman recommended that the term “learning disabilities” be replaced by the term teaching disabilities. The focus should be on the inadequacies of teachers’ skills and the teaching environment, instead of always blaming the student’s inadequacies.37 In 1987 Dr. Thomas Armstrong coined the word dysteachia to refer to the children suffering from “pedagogical illness” or inappropriate teaching strategies. He wrote, “if we taught children to speak the way we teach them to read, we’d have a nation of stutterers. This is just another way of saying that our schools are selling millions of kids short by putting them into remedial groups or writing them off as underachievers, when in reality they are disabled only by poor teaching methods.”38

But let us not be too hard on teachers. Even if one considers just the two illustrations given below, it should be clear that poor pedagogical preparation must be recognized as a major reason for poor teaching. In fact, if elementary school teachers succeed in teaching at least some of the children in their classes to read, they deserve to be patted on the back. In 1961, in her book The Torch Lighters, Mary C. Austin made the shocking revelation that only seven states in the U.S.A. required a course in the teaching of reading for certification of elementary teachers. As a result, instruction in reading methods was most often imbedded in a block course, or in one in the language arts. In 60 percent of these broad courses, the actual time devoted to reading methods ranged from 4½ to 11¼ clock hours; 30 percent of these courses gave reading even less time.39 Three decades later, writing in the Journal of Teacher Education, Nolen et al. raised the same concerns. They reported that only twenty-nine states required elementary teachers in training to have course-work specific to reading instruction, and even in those states only about twelve hours of graduate training is mandated.40

The role that the parents might have played in creating the learning problem is also never considered — as if parents were infallible. A tragic defect of our society is the fact that we are not allowed to take upon ourselves the responsibility of doing the work of a policeman, or of a teacher, or of an attorney, or of any other work without having undergone prior training. No training, however, is provided on how to bring up children. Many parents believe that they are doing everything that can be expected from them if they provide for their children’s physical needs, and then send them to nursery school or school, supposedly there to be educated.

The school has grown from the modest institution it was in the nineteenth century, with limited functions, to one that is now blamed for all the ills of society and is also seen as potentially capable of curing them. It has extended — some would overextended — its reach and therefore is exceedingly vulnerable to criticism.41 It is very important to note, however, that the whole of education does not take place in the school and that not only teachers are educators. Parents, in fact, are children’s primary educators and among many other duties and responsibilities they have, it is also their task to make sure that their children are suitably equipped that they may profit from the subject instruction offered to them at school. The important role of the parents in a child’s school achievement is confirmed by the famous Coleman report in the U.S.A., which stated that achievement differences in schoolchildren were accounted for mostly by what the children brought with them to school.42

The objective of this book, however, is not to fling about accusations and to create feelings of guilt. Parents need feel no more guilty about their LD child than did Dr. Samuel Johnson, the author of the first English dictionary, who was once twitted about a silly error he had made in defining a term. When asked by a lady why he had made the mistake, he looked at her and thundered, “Ignorance, Madam! Sheer ignorance!”43 In the camera obscura that has been built by the notion of learning disabilities, the intention of this book is not to blame but to shine a ray of light. The intention is to show parents that they, like teachers, can make a difference, and this book will tell them how. The myth of learning disabilities has for long enough maintained its position at the top of the educational pecking order. The time has come to depose it and expose it for what it really is: a mere fabrication. The time has come that we should all take the words of Dr. Thomas Armstrong, which he wrote in the preface of his book In Their Own Way, to heart:

Six years ago I quit my job as a learning disabilities specialist. I had to. I no longer believed in learning disabilities. After teaching for several years in public and parochial special education classes in the United States and Canada, I realized I was going nowhere with a concept that labeled children from the outset as handicapped learners. I also began to see how this notion of learning disabilities was handicapping all of our children by placing the blame for a child’s learning failure on mysterious neurological deficiencies in the brain…44


  1. Blatt, B., “Bandwagons also go to funerals,” Journal of Learning Disabilities, 1979, vol. 12(4), 222-224.
  2. Armstrong, T., In Their Own Way: Discovering and Encouraging Your Child’s Personal Learning Style (Los Angeles: Jeremy P. Tarcher, Inc., 1987), 6-7.
  3. Stotzner, H. E., Schulen für schwachbefähigte Kinder (Berlin, Germany: Marhold, 1864), cited in G. Opp, “Historical roots of the field of learning disabilities,” Journal of Learning Disabilities, January 1994, vol. 27, 10.
  4. Opp, “Historical roots of the field of learning disabilities.”
  5. Oppenheim, H., Nervenleiden und Erziehung (Berlin: Karger, 1907), cited Opp, “Historical roots of the field of learning disabilities.”
  6. Schrag, P., & Divoky, D., The Myth of the Hyperactive Child and Other Means of Child Control (Middlesex: Penguin Books, 1975).
  7. Turner, R. D., “Beating dyslexia: The reading and language disorder is often misdiagnosed,” Emerge, 31 March 1994.
  8. Kantrowitz, B., Underwood, A., & Wingert, P., “Dyslexia and the new science of reading,” Newsweek, 22 November 1999, 72.
  9. Yee, K., “Dyslexia may be caused by visual impairment,” University Wire, 15 January 1998.
  10. Coles, G. S., The Learning Mystique (New York: Pantheon Books, 1987).
  11. “The cat sat on the tam,” The Economist, 6 December 1997, vol. 345.
  12. Tucker, J., Stevens, L. J., & Ysseldyke, J. E., “Learning disabilities: The experts speak out,” Journal of Learning Disabilities, January 1983, vol. 27, 9, cited in Armstrong, In Their Own Way, 7.
  13. Coles, The Learning Mystique, xii.
  14. Hinshelwood, J., “Four cases of congenital word-blindness occurring in the same family,” British Medical Journal, 1907, vol. 2, 1229-1232, cited in Coles, The Learning Mystique, 3-5.
  15. Coles, The Learning Mystique, 5-6.
  16. Goodman, J. F., “Organicity as a construct in psychological diagnosis,” in T. R. Kratochwill (ed.), Advances in School Psychology (Hillsdale: Lawrence Erlbaum, 1983), 101-139.
  17. Coles, The Learning Mystique, 4.
  18. Hinshelwood, “Four cases of congenital word-blindness,” cited in Coles, The Learning Mystique, 4.
  19. Franklin, B. M., “From brain injury to learning disability: Alfred Strauss, Heinz Werner and the historical development of the learning disabilities field,” in B. M. Franklin (ed.), Learning Disability: Dissenting Essays (Philadelphia: The Falmer Press, 1987), 29-46.
  20. Ibid.
  21. Kavale, K. A., & Forness, S. R., “The historical foundation of learning disabilities: A quantitative synthesis assessing the validity of Strauss and Werner’s exogenous versus endogenous distinction of mental retardation,” Remedial and Special Education, 1985, vol. 65, 18-24; Kavale, K. A., & Forness, S. R., The Science of Learning Disabilities (San Diego: College Hill Press, 1985).
  22. Franklin, “From brain injury to learning disability.”
  23. Smith, C. R., Learning Disabilities. The Interaction of Learner, Task, and Setting(Boston: Allyn and Bacon, 1991), 8.
  24. Schrag & Divoky, The Myth of the Hyperactive Child.
  25. Coles, The Learning Mystique, xiii.
  26. Cruickshank, W., “Some issues facing the field of learning disability,” Journal of Learning Disabilities, vol. 5, 1972, 380-388, cited in J. G. Carrier, Learning Disability: Social Class and the Construction of Inequality in American Education (New York: Greenwood Press, 1986), 100.
  27. Schrag & Divoky, The Myth of the Hyperactive Child.
  28. Moats, L. C., & Lyon, G. R., “Learning disabilities in the United States: Advocacy, science, and the future of the field,” Journal of Learning Disabilities, May 1993, vol. 26, 282-294.
  29. Coles, The Learning Mystique, 23-24.
  30. Stanovich, K. E., “Learning disabilities in broader context,” Journal of Learning Disabilities, May 1989, vol. 22(5), 287-297.
  31. Coles, The Learning Mystique, 124.
  32. Moats & Lyon, “Learning disabilities in the United States.”
  33. Verslag van die Komitee van Ondersoek na die Opvoeding van Kinders met Minimale Breindisfunksie (Department of Higher Education, South Africa, 1969).
  34. Schrag & Divoky, The Myth of the Hyperactive Child.
  35. Pederson, E., Faucher, T. A., & Eaton, W. W., “A new perspective on the effects of first-grade teachers on children’s subsequent adult status,” Harvard Business Review, 1978, vol. 48, 1-31, cited in Coles, The Learning Mystique, 156-157.
  36. Coles, The Learning Mystique, 157.
  37. Bateman, B., “Educational implications of minimal brain dysfunction,” Reading Teacher, 1974, vol. 27, 662-668.
  38. Armstrong, T., In Their Own Way, 40.
  39. Austin, M. C., The Torch Lighters (Cambridge, Mass.: Harvard University Press, 1961).
  40. Nolen, P. A., McCutchen, D., & Berninger, V., “Ensuring tomorrow’s literacy: A shared responsibility,” Journal of Teacher Education, 1990, vol. 41, 63-72.
  41. Schmidt, W. H. O., Child Development: The Human, Cultural, and Educational Context(New York: Harper & Row, 1973), 12.
  42. Kerlinger, F. N., Foundations of Behavioral Research (New York: CBS Publishing Ltd., 1986).
  43. Van Riper, C., Teaching Your Child to Talk (New York: Harper & Row Publishers, 1950), 75.
  44. Armstrong, In Their Own Way, ix.
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