Causes of Learning Disabilities (page 2)
In most cases, the cause (etiology) of a child’s learning disability is unknown. Many causes have been proposed, a situation that probably reflects the highly diverse nature of students with learning disabilities. Just as there are different types of learning disabilities (e.g., dyslexia, language disabilities, math disabilities), there are likely to be different causes. Four suspected causal factors are brain damage, heredity, biochemical imbalance, and environmental causes.
Brain Damage or Dysfunction
Some professionals believe that all children with learning disabilities suffer from some type of brain injury or dysfunction of the central nervous system. Indeed, this belief is inherent in the NJCLD definition of learning disabilities, which states that learning disorders are “presumed to be due to central nervous system dysfunction.” In cases in which actual evidence of brain damage cannot be shown (and this is the situation with the majority of children with learning disabilities), the term minimal brain dysfunction is sometimes used, especially by physicians. This wording implies brain damage by asserting that the child’s brain does not function properly.
Recent advances in magnetic resonance imaging (MRI) technology have enabled researchers to discover that specific regions of the brains of some individuals with reading and language disabilities show activation patterns during phonological processing tasks that are different from the patterns found in the brains of nondisabled individuals (Miller, Sanchez, & Hynd, 2003; Richards, 2001; Simos, Breier, Fletcher, Bergman, & Papanicolaou, 2000). The actual structure of the brain of some children with reading disabilities is slightly different from that of children without disabilities (Leonard, 2001).
This research holds great promise for understanding the biological bases of dyslexia and other specific learning disabilities. However, as Leonard (2001) points out, we do not yet know how and to what extent the brain’s neural networks are affected by the child’s experiences (i.e., learning) and vice versa. Thus, we do not know whether neurobiological factors associated with learning disabilities contribute to the learning problems of children, are the product of an unstimulating environment, or a combination. However, there is growing evidence that differences in the ways in which reading-disabled and normal children’s brains are activated weakens with intensive remedial reading instruction (Richards, 2001). Shaywitz et al. (2004) reported that an average of 105 hours of individual tutoring that focused on teaching the alphabetic principle (how letters and combinations of letters represent the small segments of speech called phonemes) and oral reading fluency practice not only improved children’s reading fluency but “facilitated the development of the neural systems that underline skilled reading”.
Special educators must be aware of placing too much emphasis on theories linking learning disabilities to brain damage or brain dysfunction, for three major reasons. First, not all children with learning disabilities display clinical (medical) evidence of brain damage, and not all children with brain damage have learning disabilities. The second problem is that assuming a child’s learning problems are caused by a dysfunctioning brain can serve as a built-in excuse for ineffective instruction. When a student with suspected brain damage fails to learn, his teachers may be quick to presume that the brain injury prevents him from learning and be slow to analyze and change instructional variables. Third, whether “learning disabilities in an individual case are symptoms that result from brain injury or developmental delay will not essentially alter the methods of teaching the student” (Myers & Hammill, 1990, p. 22).
Current interpretations of the role of constitutional factors show reciprocal relations with the environment, such that environmental factors (e.g., instruction) must be in place to develop the neural networks that support academic skills. Even genetic studies of reading disability show that only about 50 percent of the variability in reading skills can be explained by genetic factors—the remainder is environmental. Learning disabilities represent interplays of constitutional and environmental factors that are not yet well understood. (Fletcher et al., 2001, p. 7)
Siblings and children of persons with reading disabilities have a slightly greater than normal likelihood of having reading problems. There is growing evidence that genetics may account for at least some family links with dyslexia (Pennington, 1995; Raskind, 2001). Research has located possible chromosomal loci for the genetic transmission of phonological deficits that may predispose a child for reading problems later (Cardon et al., 1994; Kaplan et al., 2002).
It was once theorized that biochemical disturbances within a child’s body caused learning disabilities. For example, Feingold (1975, 1976) claimed that artificial colorings and flavorings in many of the foods children eat can cause learning disabilities and hyperactivity. He recommended a treatment for learning disabilities that consisted of a diet with no foods containing synthetic colors or flavors. In a comprehensive review of research studies that tested the special diet, Spring and Sandoval (1976) concluded that there was very little scientific evidence to support Feingold’s theory. In response to the controversy over diet treatments, the American Council on Science and Health (1979) issued the following statement:
Hyperactivity will continue to be a frustrating problem until research resolves the questions of its cause, or causes, and develops an effective treatment. The reality is that we still have a great deal to learn about this condition. We do know now, however, that diet is not the answer. It is clear that the symptoms of the vast majority of the children labeled “hyperactive” are not related to salicylates, artificial food colors, or artificial flavors. The Feingold diet creates extra work for homemakers and changes the family lifestyle . . . but it doesn’t cure hyperactivity.
It was also suggested that learning disabilities can be caused by the inability of a child’s bloodstream to synthesize a normal amount of vitamins (Cott, 1972). Some physicians began megavitamin therapy with children with learning disabilities, which consisted of massive daily doses of vitamins in an effort to overcome the suspected vitamin deficiencies. Two studies designed to test the effects of megavitamin treatment with learning disabled and hyperkinetic children found that huge doses of vitamins did not improve the children’s performance (Arnold, Christopher, Huestis, & Smeltzer, 1978; Kershner, Hawks, & Grekin, 1977). Today, most professionals in learning disabilities give little credence to biochemical imbalance as a significant cause of children’s learning problems.
Although very difficult to document as primary causes of learning disabilities, environmental factors—particularly impoverished living conditions early in a child’s life and poor instruction—probably contribute to the achievement deficits experienced by many children in this special education category. The tendency for learning disabilities to run in families suggests a correlation between environmental influences on children’s early development and subsequent achievement in school. Evidence for this relationship can be found in longitudinal research such as that conducted by Hart and Risley (1995), who found that infants and toddlers who received infrequent communication exchanges with their parents were more likely to show deficits in vocabulary, language use, and intellectual development before entering school.
Another environmental variable that is likely to contribute to children’s learning problems is the quality of instruction they receive. Many special educators today believe that Engelmann (1977) was correct when he claimed more than 25 years ago that the vast majority of “children who are labeled ‘learning disabled’ exhibit a disability not because of anything wrong with their perception, synapses, or memory, but because they have been seriously mistaught”.
Although the relationship between poor instruction and learning disabilities is not clear, there is a great deal of evidence showing that many students’ learning problems can be remediated by direct, intensive, and systematic instruction. It would be naive to think, however, that the achievement problems of all children with learning disabilities are caused entirely by inadequate instruction. Nevertheless, from an educational perspective, intensive, systematic instruction should be the treatment of first choice for all students with learning disabilities.
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