Learning Disabilities
LEARNING DISABILITIES
An individual is said to have a learning disability if he or she has difficulty using or understanding written or spoken language (including academic subjects such as reading, writing, and mathematics) in a way that is inconsistent with overall intelligence quotient (IQ). Individuals with low IQ in all areas (for example, in cases of mental retardation) are excluded from the diagnosis. Environmental factors such as deprivation are also excluded (because learning disabilities are defined as congenital rather than acquired problems), as are physical disabilities that might cause secondary learning problems (for example, hearing and vision deficits, epilepsy, or attention deficit and hyperactivity disorder [ADHD]). Although learning disabilities can be concurrent with other physical disabilities (i.e., blind or deaf children can also be learning disabled), it is generally established that the physical disability is not inherently the cause of the learning disability. ADHD has a high concurrence with learning disabilities, but clinicians usually try to establish that attention deficits (not typically considered under the scope of learning disabilities) are not the direct cause of the learning problems. A child who exhibits difficulties with language may be diagnosed with a learning disability (for example, with specific language impairment, or SLI), even before entering school, but typically a diagnosis emerges in the context of an academic setting, for example when a child has unexpected difficulties with reading (called specific reading impairment, or dyslexia). There is significant overlap between preschool SLI and school-age dyslexic populations (Stark and Tallal, 1988).
Learning Disabilities from a Behavioral Perspective
The long-standing assumption that learning disabilities reflect subtle anomalies in the brain is reflected in early terms such as minimal brain damage and minimal brain dysfunction. Although an emergent body of research has shown that learning-disabled populations exhibit neural anomalies, the field remains at a point where behavioral data are used to make an evaluation or clinical diagnosis, and neural features of these behaviorally identified populations are then studied to discern differences from normal controls. A diagnosis of specific reading impairment (or dyslexia) may someday be confirmed or even routinely screened (like vision testing) via neuroimaging. Moreover, neurological diagnosis of learning disorders may alter their very definitions (e.g., it may become possible to diagnose neural anomalies associated with dyslexia prior to behavioral expression of the disorder, possibly even in infancy; see Leppänen and Lyytinen, 1997; Leppänen, Pihko, Eklund, and Lyytinen, 1999; Molfese and Molfese, 1997; Pihko et al., 1999). This dependence on behavioral criteria is reflected in debate over whether traditional health insurance should cover treatment for learning disorders (Tallal, 1988).
Diagnostic dependence on behavioral criteria is associated with other intrinsic pitfalls, including those inherent to the definition of abnormal behavior. This pivotal issue forms the focus of controversy surrounding learning disabilities (e.g., assertions of gender and ethnic bias in school curricula, and over-referral of boys for special education due to boys' more "active" behavior). One objective way that behavior can be quantified is by comparison to a norm derived from sample population data, allowing clinicians to use a standard curve to set cutoff criteria to define when an individual is "significantly impaired" relative to their peers for a specific function. Academic performance in a school setting may also be compared to age-appropriate norms in a more general way by schoolteachers who refer potentially learning disabled children for further testing. Learning disabilities are also defined by comparison of a child's own scores or performance in a specific area relative to their overall intelligence, entailing use of a "discrepancy criteria."
Even with the use of such criteria, clinicians and educators may disagree over the definition of what constitutes "disabled"—for example, whether a child is simply part of the lower tail of a normal curve (e.g., is a poor reader) or whether that child functions distinctly differently from the norm and thus has a clinically defined disorder (e.g., specific reading impairment or dyslexia; see Shaywitz et al., 1992). Moreover, individual cases are sometimes difficult to capture within the parameters of standard behavioral definitions. For example, if a child demonstrates generally superior academic performance but performs only at an average level in one specific area such as reading, is he or she reading impaired? Such a child is unlikely to be referred, at any rate, for special education services. Similarly, if a child demonstrates general intelligence well below the mean, but performs even worse in one specific area (e.g., reading) than would be predicted by nonverbal IQ, is this child mentally retarded, or reading impaired, or both? Confusion surrounding such unresolved issues is fueled by educational dictates that define the aid and curricula a child may receive depending on clinical diagnosis, and also fueled by social controversies surrounding the labeling of children. (These issues are not addressed in this entry, but see Wong, 1986, or Woody, 1989, for review.) Finally, the definition of learning disabilities is weighted to some degree by a standard academic curricula that does not tend to focus on deficiencies in art, music, or sports but, rather, only in reading, writing, and math.
The populations of children who receive special education services at school are distinct but overlapping: Some children are in SE due to lagging academic performance, whereas others in SE classes have been clinically diagnosed as learning disabled. SE encompasses a heterogeneous population of students exhibiting general cognitive delays and deficits, social-environmental deprivation, psychological problems, and concurrent disabilities such as ADHD. This entry focuses on children identified as learning disabled through relatively rigorous clinical diagnosis—that is, language, reading, or mathematically impaired children performing below levels predicted by their overall intelligence in one of these specific academic areas.
Neurobiological Correlates of Learning Disabilities
Advances in neuroimaging and gene linkage technology have expanded research possibilities for noninvasive study of clinical populations, but characteristics of various learning disabilities have yet to be isolated and defined. Reasons for these limitations include:
- Heterogeneity of subject criteria. If the population under study is not homogeneous, biological data from this sample will be difficult to interpret. Also, when different researchers use different behavioral criteria, cross-study comparisons will show inconsistencies.
- Heterogeneity of disorders. Even where careful attention to consistent behavioral criteria is applied, diverse underlying etiologies can produce the same behavioral profile. Conversely, behavioral profiles (even within a relatively specific sub-type of a disorder) can show large individual differences.
- Difficulties inherent to the study of children. Although modern magnetic resonance imaging (MRI) techniques are considered noninvasive, they are stressful and time consuming, and parents will not always consent to participation of their affected children. Although studies can be conducted using adults affected since childhood, the data obtained from such studies may not accurately reflect anomalies that characterize early disruption of brain development. Moreover, retrospective diagnosis of childhood disorders frequently relies on memory (e.g., a patient is asked, "Did you have difficulty reading as a young child?") and hence can be unreliable.
Despite these hindrances, research has uncovered important neurological and genetic features that seem to be associated with specific developmental learning disorders. Such studies have shown that learning disabled children do not exhibit focal damage to specific regions of the brain, with all other systems and functions spared intact. Although localized damage can indeed occur via localized hemorrhage, trauma, or tumor (and can lead to subsequent learning disabilities) these types of injuries comprise acquired rather than congenital disabilities. For example, language deficits caused by an acquired lesion of the left hemisphere are classified as acquired aphasia, rather than developmental language impairment (Tallal, 1987), which is considered congenital. This distinction relies on the notion of "inherent" versus "imposed" neural damage (although most diagnoses accept brain damage of prematurity within the scope of congenital disabilities). Research suggests that some learning disabled children may, in fact, exhibit evidence of relatively focal (i.e., narrowly circumscribed) brain damage of unknown cause from very early (i.e., prenatal) periods of neurodevelopment (e.g., see Galaburda, 1992; Galaburda et al., 1985). This early focal injury—particularly if it occurs during critical neural events such as neuromigration (cortical neurons migrating to cortical layer locations)—may disrupt neurodevelopment, with deleterious behavioral consequences. Unlike damage to a relatively static adult brain, focal damage that occurs during the formation of neural circuitry exerts widely distributed effects on brain organization (see Aicardi, 1994; Galaburda, 1992; Kolb and Fantie, 1989). Some children with learning disabilities appear to have experienced such subtle injuries to the brain or interference with development of the brain during critical periods of growth, resulting in pervasive reorganization of brain systems.
Specific Language Impairment (SLI) and Dyslexia
SLI and dyslexia are the two most frequently studied forms of learning disability. Longitudinal studies suggest that a large majority of children with SLI overcome the most noticeable aspects of language delays of early childhood (e.g., they do eventually learn to talk) but that underlying components of their disorder appear to be expressed more visibly in other areas, for example as the child attempts to use phonological systems to learn to read (see Leonard, 1998, for review). Consequently, studies on the neurophysiology of SLI (which typically comprises a childhood population) are difficult to separate from studies of dyslexia (which frequently is studied in adults).
Some functional deficits in children with SLI may arise from basic sensory integration deficits, reflecting in turn dysfunctional neural processing of rapidly changing sensory information. For example, research has shown that language-impaired children exhibit severe deficits in the ability to perform auditory discriminations of information that changes rapidly in time. Although this deficit is profoundly evident when children with SLI are asked to discriminate speech stimuli characterized by brief and rapidly changing acoustic spectra (e.g., consonant-vowel syllables), deficits are also observed on nonlingual tasks such as tone-sequence discrimination (Tallal and Piercy, 1973). Such rapid auditory processing deficits may disrupt phonological processing and speech perception, leading to developmental impairment of language skills acquisition (Tallal, Miller, and Fitch, 1993). Although a neurophysiological basis for sensory processing deficits in language-impaired children has not been identified, evidence has shown cellular anomalies in the visual and auditory divisions of the thalamus (lateral geniculate and medial geniculate nucleus; LGN and MGN) of dyslexic brains.
Specifically, Livingstone, Rosen, Drislane, and Galaburda (1991) found that the magnocellular component of the visual system, which is responsible for processing fast, low-contrast information, appears to be impaired in dyslexics. Using evoked potential measurements taken from the scalp, the electrophysiologic response to visual stimuli designed to activate the magnocellular subsystem was found to be significantly slower in dyslexic as compared to control subjects. Consistent with this functional data, postmortem studies of several dyslexic brains demonstrated that the magnocellular neurons of the lateral geniculate nucleus (the visual thalamic nucleus, which relays visual information to the cortex) were smaller in dyslexic than in control brains. The authors speculate that electrophysiological and anatomical evidence of a visual processing disturbance could reflect interference with normal reading (see also Lovegrove, Garzia, and Nicholson, 1990; Slaghuis, Lovegrove, and Freestun, 1992). A subsequent postmortem study of the same dyslexic brains studied by Livingstone, Galaburda, Menard, and Rosen (1994) found that there were more small neurons and fewer large neurons in the left medial geniculate nucleus (MGN) of dyslexics as compared to controls. This finding may relate to the behavioral and electrophysiological evidence of disrupted auditory processing in both SLI and dyslexic individuals, which may in turn give rise to the phonological processing deficits observed in these patients (see Tallal, Miller, and Fitch,, 1993, for review).
These findings may further relate to evidence of neuropathologic lesions in dyslexic brains (Benton, 1964; Cohen, Campbell, and Yaghamai, 1989; Galaburda and Kemper, 1979; Galaburda et al., 1985; Humphreys et al., 1991; reviewed in Galaburda, 1992). Specifically, researchers have used postmortem analysis to show evidence of cerebrocortical microdysgenesis consisting of neuronal ectopias in neocortical layer I, subjacent laminar dysplasia, focal microgyria, and microvascular anomalies. These abnormalities tend to be located in prefrontal and perisylvian regions, and they usually involve the left more than the right hemisphere. Evidence from animal models suggests that focal cortical damage during the period of cortical neuromigration induces the formation of cortical cellular anomalies, as well as structural anomalies at the thalamic level, much like those seen in dyslexic brains. Moreover, these anomalies are associated with auditory processing deficits strikingly similar those seen in language-impaired children (Clark, Rosen, Tallal, and Fitch, 2000a, 2000b; Fitch et al., 1994; Fitch, Brown, Tallal, and Rosen, 1997; Herman et al., 1997).
On a more global level, studies of both language impairment and dyslexia have focused heavily on regions of the brain known to be involved in language processing, particularly left-hemisphere regions of temporal, parietal, and frontal cortex such as Wernicke's area and Broca's area. In most normal subjects, the planum temporale (which lies on the superior surface of the temporal lobe and encompasses a portion of Wernicke's area) is larger on the left as compared to the right side of the brain (Geschwind and Levitsky, 1968; Kulynch, Vladar, Jones, and Weinberger, 1994; Teszner, Tzavaras, Gruner, and Hécaen, 1972; Wada, Clarke, and Hamm, 1975; Witelson and Pallie, 1973). Such findings are consistent with left-hemisphere specialization for language processing found in behavioral studies, neuroimaging studies, and studies of the behavioral effects of lateralized lesions. In one of the few studies of neuropathology underlying specific language impairment, Jernigan, Hesselink, Sowell, and Tallal (1991) used MRI techniques to examine a sample of SLI children and showed that the volume of the posterior perisylvian region (which includes the planum temporale) was reduced bilaterally in language-impaired children (markedly so in the left hemisphere; see also Plante, Swisher, Vance, and Rapcsak, 1991). Asymmetries in the inferoanterior and superoposterior cerebral regions showed significant differences between control and impaired children. Neurological studies of dyslexia have also consistently reported anomalous asymmetry of the planum temporale (Dalby, Elbro, and Stodkilde-Jorgensen, 1998; Galaburda et al., 1985; Haslam, Dalby, Johns, and Rademaker, 1981; Hier, LeMay, Rosenberger, and Perlo, 1978; Humphreys et al., 1991; Hynd and Semrud-Clikeman, 1989; Hynd et al., 1990; Hynde, Marshall, and Semrud-Clikeman, 1991; Jancke, Schlaug, Huang, and Steinmetz, 1994; Kushch et al., 1993; Larsen, Hoien, Lundberg, and Odegaard, 1990; Leonard et al., 1993; Rosenberger and Hier, 1980; Rumsey et al., 1986; Schultz et al., 1994). These anatomical anomalies are consistent with evidence of activational differences in the cortex of dyslexics during the performance of reading-related tasks (e.g., Demb, Boynton, and Heeger, 1998; Shaywitz et al., 1998). Atypical asymmetries (along with language difficulties) also occur in the parents and siblings of children with language disabilities (Plante, 1991).
Evidence of structural left hemisphere anomalies in dyslexics is further consistent with data showing anomalous EEG recording from left-hemisphere language regions of dyslexics, as well as anomalous recordings from anterior frontal regions (Duffy and McAnulty, 1990), anomalies in regional cerebral activity in frontal and occipital areas of dyslexics as measured during reading tasks (Gross-Glenn et al., 1991; Shaywitz et al., 1998), and electrophysiological anomalies of cerebral lateralization in learning-disabled children (Mattson, Sheer, and Fletcher, 1992). Significant differences in electrophysiological responses to acoustic stimuli (including tones and speech) have also been reported in studies of both dyslexic and language-impaired individuals (e.g., Brunswick and Rippon, 1994; Byring and Järvilehto, 1985; Dawson, Finley, Phillips, and Lewy, 1989; Jirsa and Clontz, 1990; Kraus et al., 1996; Lincoln, Courchesne, Harms, and Allen, 1995; Neville, Coffey, Holcomb, and Talall, 1993; Pinkerton, Watson, and McClelland, 1989; Tonnquist-Uhlen, Borg, Persson, and Spens, 1996; Wood, Flowers, Buchsbaum, and Tallal, 1991), supporting the existence of an auditory processing deficit in these groups as discussed above.
Conclusion
Learning disabilities are characterized by unexpected difficulties with language, reading, or math that are inconsistent with IQ, or ability in other areas, or both. These problems remain after other known causes for learning problems have been excluded. The neurobiological basis for these disorders remains elusive but appears to involve very early neurodevelopmental disruption leading to distributed processing deficits in the brain. These disruptions appear to leave some higher processing systems intact while causing severe deficits in other systems (e.g., rapid sensory processing). Nevertheless, learning disabilities encompass a wide range of subtypes of disorders, with large individual variability in behavioral expression, and they appear to reflect a heterogeneity of neural anomalies of varied origin, ranging from genetic factors to early focal injury. Improved neuroimaging technology should allow scientists to create more precise neurobehavioral templates of disruption characterizing various subtypes of learning disability, providing in turn more reliable and consistent diagnostic tools for the assessment and remediation of learning disabilities.
Bibliography
Aicardi, J. (1994). The place of neuronal migration abnormalities in child neurology. Canadian Journal of Neurological Sciences 21, 185-193.
Benton, A. L. (1964). Developmental aphasia and brain damage. Cortex 1, 40-52.
Brunswick, N., and Rippon, G. (1994). Auditory event-related potentials, dichotic listening performance, and handedness as indices of lateralisation in dyslexic and normal readers. International Journal of Psychophysiology 18 (3), 265-275.
Byring, R., and Järvilehto, T. (1985). Auditory and visual evoked potentials of schoolboys with spelling disabilities. Developmental Medicine and Child Neurology 27, 141-148.
Clark, M., Rosen, G., Tallal, P., and Fitch, R. H. (2000a). Impaired processing of complex auditory stimuli in rats with induced cerebrocortical microgyria. Journal of Cognitive Neuroscience 12 (5), 828-839.
—— (2000b). Impaired two-tone processing at rapid rates in male rats with induced microgyria. Brain Research 871, 94-97.
Cohen, M., Campbell, R., and Yaghamai, F. (1989). Neuropathological anomalies in developmental dysphasia. Annals of Neurology 25, 567-570.
Dalby, M. A., Elbro, C., and Stodkilde-Jorgensen, H. (1998). Temporal lobe asymmetry and dyslexia: An in vivo study using MRI. Brain and Language 62, 51-69.
Dawson, G., Finley, C., Phillips, S., and Lewy, A. (1989). A comparison of hemispheric asymmetries in speech-related brain potentials of autistic and dysphasic children. Brain and Language 37 (1), 26-41.
Demb, J. B., Boynton, G. M., and Heeger, D. J. (1998). Functional magnetic resonance imaging of early visual pathways in dyslexia. Journal of Neuroscience 18, 6,939-6,951.
Duffy, F. H., and McAnulty, G. (1990). Neuropsychological heterogeneity and the definition of dyslexia: Preliminary evidence for plasticity. Neuropsychologica 28, 555-571.
Fitch, R. H., Brown, C., Tallal, P., and Rosen, G. (1997). Effects of sex and MK-801 on auditory processing deficits associated with developmental microgyric lesions in rats. Behavioral Neuroscience 111, 404-412.
Fitch, R. H., Tallal, P., Brown, C., Galaburda, A., and Rosen, G. (1994). Induced microgyria and auditory temporal processing in rats: A model for language impairment? Cerebral Cortex 4, 260-270.
Galaburda, A. M. (1992). Neurology of developmental dyslexia. Current Opinion in Neurology and Neurosurgery 5 (1), 71-76.
Galaburda, A. M., and Kemper, T. L. (1979). Cytoarchitectonic abnormalities in developmental dyslexia: A case study. Annals of Neurology 6, 94-100.
Galaburda, A. M., Menard, M. T., and Rosen, G. D. (1994). Evidence for aberrant auditory anatomy in developmental dyslexia. Proceedings of the National Academy of Sciences of the United States of America 91, 8,010-8,013.
Galaburda, A. M., Sherman, G. F., Rosen, G. D., Aboitiz, F., and Geschwind, N. (1985). Developmental dyslexia: Four consecutive cases with cortical anomalies. Annals of Neurology 18, 222-233.
Geschwind, N., and Levitsky, W. (1968). Human brain: Left-right asymmetries in temporal speech region. Science 161, 186-187.
Gross-Glenn, K, Duara, R, Barker, W. W., Lowenstein, D, Chang, J. Y., Yoshii, F., Apicella, A. M., Pascal, S., Boothe, T., Sevush, S., Jallad, B. J., Novoa, L., and Lubs, H. A. (1991). Positron emission tomographic studies during serial word reading by normal and dyslexic adults. Journal of Clinical and Experimental Neuropsychology 13, 531-544.
Haslam, R. H. A., Dalby, J. T., Johns, R. D., and Rademaker, A. W. (1981). Cerebral asymmetry in developmental dyslexia. Archives of Neurology 38, 679-682.
Herman, A., Galaburda, A., Fitch, R. H., Carter, A. R., and Rosen, G. (1997). Cerebral microgyria, thalamic cell size, and auditory temporal processing in male and female rats. Cerebral Cortex 7, 453-464.
Hier, D. B., LeMay, M., Rosenberger, P. B., and Perlo, V. P. (1978). Developmental dyslexia. Archives of Neurology 35, 90-92.
Humphreys, P., Rosen, G. D., Press, D. M., Sherman, G. F., and Galaburda, A. M. (1991). Freezing lesions of the newborn rat brain: A model for cerebrocortical microgyria. Journal of Neuropathology and Experimental Neuroloy 50, 145-160.
Hynd, G. W., Marshall, R. M., and Semrud-Clikeman, M. (1991). Developmental dyslexia, neurolinguistic theory, and deviations in brain morphology. Reading and Writing 3, 345-362.
Hynd, G. W., and Semrud-Clikeman, M. (1989). Dyslexia and brain morphology. Psychological Bulletin 106, 447-482.
Hynd, G. W., Semrud-Clikeman, M., Lorys, A. R., Novey, E. S., and Eliopulos, D. (1990). Brain morphology in developmental dyslexia and attention deficit disorder/hyperactivity. Archives of Neurology 47, 919-926.
Jancke, L., Schlaug, G., Huang, Y., and Steinmetz, H. (1994). Asymmetry of the planum temporale. NeuroReport 5, 1,161-1,163.
Jernigan, T. L., Hesselink, J. R., Sowell, E., and Tallal, P. (1991). Cerebral structure on magnetic resonance imaging in language- and learning-impaired children. Archives of Neurology 48, 539-545.
Jirsa, R. E., and Clontz, K. B. (1990). Long latency auditory event-related potentials from children with auditory processing disorders. Ear and Hearing 11 (3), 222-232.
Kolb, B., and Fantie, B. (1989). Development of children's brain and behavior. In C. R. Reynolds and J. Fletcher-Janzen, eds., Handbook of child clinical neuropsychology, pp. 17-40. New York: Plenum Press.
Kraus, N., McGee, T. J., Carrell, T. D., Zecker, S. G., Nicol, T. G., and Koch, D. B. (1996). Auditory neurophysiologic responses and discrimination deficits in children with learning problems. Science 273, 971-973.
Kulynych, J. J., Vladar, K., Jones, D. W., and Weinberger, D. R. (1994). Gender differences in the normal lateralization of the supratemporal cortex: MRI surface-rendering morphometry of Heschl's gyrus and the planum temporale. Cerebral Cortex 4, 107-118.
Kushch, A., Gross-Glenn, K., Jallad, B., Lubs, H., Rabin, M., Feldman, E., and Duara, R. (1993). Temporal lobe surface area measurements on MRI in normal and dyslexic readers. Neuropsychologia 31, 811-821.
Larsen, J., Hoien, T., Lundberg, I., and Odegaard, H. (1990). MRI evaluation of the size and symmetry of the planum temporale in adolescents with developmental dyslexia. Brain and Language 39, 289-301.
Leonard, C., Voeller, K. K. S., Lombardino, L. J., Morris, M. K., Hynd, G. W., Alexander, A. W., Andersen, H. G., Garofalakis, M., Honeyman, J. C., Mao, J., Agee, O. F., and Staab, E. V. (1993). Anomalous cerebral structure in dyslexia revealed with magnetic resonance imaging. Archives of Neurology 50, 461-469.
Leonard, L. B. (1998). Children with specific language impairment. Cambridge, MA: MIT Press.
Leppänen, P. H. T., and Lyytinen, H. (1997). Auditory event-related potentials in the study of developmental language-related disorders. Audiology and Neuro-Otology 2, 308-340.
Leppänen, P. H. T., Pihko, E., Eklund, K. M., and Lyytinen, H. (1999). Cortical responses of infants with and without a genetic risk for dyslexia, Part 2: Group effects. NeuroReport 10, 969-973.
Lincoln, A. J., Courchesne, E., Harms, L., and Allen, M. (1995). Sensory modulation of auditory stimuli in children with autism and receptive developmental language disorder: Event-related brain potential evidence. Journal of Autism and Developmental Disorders 25 (5), 521-539.
Livingstone, M. S., Rosen, G. D., Drislane, F. W., and Galaburda, A. M. (1991). Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia. Proceedings of the National Academy of Sciences of the United States of America 88, 7,943-7,947.
Lovegrove, W., Garzia, R., and Nicholson, S. (1990). Experimental evidence for a transient system deficit in specific reading disability. Journal of the American Optometric Association 2, 137-146.
Mattson, A. J., Sheer, D. E., and Fletcher, J. M. (1992). Electrophysiological evidence of lateralized disturbances in children with learning disabilities. Journal of Clinical and Experimental Neuropsychology 14, 707-716.
Molfese, D. L., and Molfese, V. J. (1997). Discrimination of language skills at five years of age using event-related potentials recorded at birth. Developmental Neuropsychology 13, 135-156.
Neville, H., Coffey, S., Holcomb, P., and Tallal, P. (1993). The neurobiology of sensory and language processing in language impaired children. Journal of Cognitive Neuroscience 5, 235-253.
Pihko, E., Leppänen, P. H. T., Eklund, K. M., Cheour, M., Guttorm, T. K., and Lyytinen, H. (1999). Cortical responses of infants with and without a genetic risk for dyslexia, Part 1: Age effects. NeuroReport 10, 901-905.
Pinkerton, F., Watson, D. R., and McClelland, R. J. (1989). A neurophysiological study of children with reading, writing, and spelling difficulties. Developmental Medicine and Child Neurology 31, 569-581.
Plante, E. (1991). MRI findings in the parents and siblings of specifically language-impaired boys. Brain and Language 41, 67-80.
Plante, E., Swisher, L., Vance, R., and Rapcsak, S. (1991). MRI findings in boys with specific language impairment. Brain and Language 41, 52-66.
Rosenberger, P. B., and Hier, D. B. (1980). Cerebral asymmetry and verbal intellectual deficits. Annals of Neurology 8, 300-304.
Rumsey, J. M., Dorwart, R., Vermess, M., Denckla, M. B., Kruesi, M. J. P., and Rapoport, J. L. (1986). Magnetic resonance imaging of brain asymmetry in severe developmental dyslexia. Archives of Neurology 43, 1,045-1,046.
Schultz, R. T., Cho, N. K., Staib, L. H., Kier, L. E., Fletcher, J. M., Shaywitz, S. E., Shankweiler, D. P., Katz, L., Gore, J. C., Duncan, J. S., and Shaywitz, B. A. (1994). Brain morphology in normal and dyslexic children: The influence of sex and age. Annals of Neurology 35, 732-742.
Shaywitz, S. E., Escobar, M. D., Shaywitz, B. A., Fletcher, J. M., and Makuch, R. (1992). Evidence that dyslexia may represent the lower tail of a normal distribution of reading ability. New England Journal of Medicine 326, 145-150.
Shaywitz, S. E., Shaywitz, B. A., Pugh, K., Fulbright, R., Constable, R., Mencl, W., Shankweiler, D., Liberman, A., Skudlarski, P., Fletcher, J., Katz, L., Marchione, K., Lacadie, C., Gatenby, C., and Gore, J. (1998). Functional disruption in the organization of the brain for reading in dyslexia. Proceedings of the National Academy of Sciences of the United States of America 95, 2,636-2,641.
Slaghuis, W. L., Lovegrove, W. J., and Freestun, J. (1992). Letter recognition in peripheral vision and metacontrast masking in dyslexic and normal readers. Clinical Vision Sciences 7, 53-65.
Stark, R. E., and Tallal, P. (1988). The children with specific language impairment. In R. J. McCauley, ed., Children: Neuropsychological Studies. Boston: College Hill Press.
Tallal, P. (1987). Dysphasia, developmental. In G. Adelman, ed., Encyclopedia of Neuroscience, Vol. 1, 351-353. Boston: Birkhauser Press.
—— (1988). Speech before the US Congress on clinical definitions of developmental disability.
Tallal, P., Miller, S., and Fitch, R. H. (1993). Neurobiological basis of speech: A case for the preeminence of temporal processing. In P. Tallal, A. M. Galaburda, R. Llinas, and C. von Euler, eds., Temporal information processing in the nervous system, with special reference to dyslexia and dysphasia, pp. 27-47. New York: New York Academy of Sciences.
Tallal, P., and Piercy, M. (1973). Defects of non-verbal auditory perception in children with developmental aphasia. Nature 241, 468-469.
Teszner, D., Tzavaras, A., Gruner, J., and Hécaen, H. (1972). L'asymmétrie droite-gauche du planum temporale: A propos de l'étude anatomique de 100 cervaeux. Revue Neurologique 126, 444-449.
Tonnquist-Uhlen, I., Borg, E., Persson, H. E., and Spens, K. E. (1996). Topography of auditory evoked cortical potentials in children with severe language impairment: The N1 component. Electroencephalography and Clinical Neurophysiology 100, 250-260.
Wada, J. A., Clarke, R., and Hamm, A. (1975). Cerebral hemispheric asymmetry in humans. Archives of Neurology 32, 239-246.
Witelson, S. F., and Pallie, W. (1973). Left hemisphere specialization for language in the newborn: Neuroanatomical evidence of asymmetry. Brain 96, 641-646.
Wong, B. Y. L. (1986). Problems and issues in the definition of learning disabilities. In J. R. Torgesen and B. Y. L. Wong, eds., Psychological and educational perpectives on learning disabilities, 3-26. Orlando, FL: Academic Press.
Wood, F., Flowers, L., Buchsbaum, M., and Tallal, P. (1991). Investigation of abnormal left temporal functioning in dyslexia through rCBF, auditory evoked potentials, and positron emission tomography. Reading and Writing 3 (3-4), 379-393.
Woody, R. H. (1989). Public policy and legal issues for clinical child psychology. In C. R. Reynolds and J. Fletcher-Janzen, eds., Handbook of child clinical neuropsychology, 573-584. New York: Plenum Press.
ChrisChase
Paula A.Tallal
ElenaPlante
Revised byR. HollyFitch
Learning Disabilities
Learning Disabilities
Learning disabilities applies to difficulties in reading, mathematics, and written language. Although children with learning disabilities can have difficulty with spoken language and language comprehension, most of the research revolves around the ability to read and understand written information. For further information about oral communication one should look at material in speech and language, which is beyond the scope of this entry.
Learning difficulties can be present in reading (phonics, comprehension), mathematics (calculation, reasoning), language (receptive, expressive), and written expression. Learning disabilities are assumed to be due to central nervous system dys-function (National Joint Committee for Learning Disabilities [NJCLD] 1991) and reflect a discrepancy between ability and achievement.
Diagnosis of Learning Disabilities
The diagnosis of learning disabilities varies depending on where one resides, with different states having different requirements for a learning disability diagnosis. Differences among states vary between psychometric measurement practices, which are called discrepancy models. However, most definitions share the requirement that a significant discrepancy exist between ability and achievement. The Intelligence Quotient (IQ) test becomes an important part of the diagnosis in these definitions. Such a discrepancy model leads to differing numbers of children identified as learning disabled (Sofie and Riccio 2002). Children and adolescents who are in the low average range of intelligence have a more difficult time qualifying for services as they must score very low on an achievement test in order to qualify (Semrud-Clikeman et al. 1992).
Children who have language difficulties frequently score poorly on the verbal portion of the IQ test, thus lowering their scores (Aaron 1997; Morris et al. 1998; Siegel 1992). These children and those from backgrounds other than the middle and upper class may be penalized by standardized tests that are far from culture-free (Greenfield 1997; Siegel 1990; Stanovich 1986). The highest concentration of poor readers has been found in certain ethnic groups and in poor urban neighborhoods (Snow, Burns, and Griffin 1998). Children from impoverished backgrounds or those from a different culture may not have acquired sufficient knowledge in order to answer the IQ test questions correctly. In fact, research has found that many of these children are not classified as learning disabled but rather as slow learners and often not considered bright enough to profit from remediation (Siegel 1990). The current methods of diagnosing children with learning disabilities assume that intelligence is a prerequisite for reading attainment. Research has indicated that IQ scores account for only 25 percent of the variance in reading scores and, as such, is not an important variable in predicting how a child will read (Aaron 1997; Swanson, Hoskyn, and Lee 1999). R. Valencia (1995) found that major achievement tests may underestimate the learning of minority children, particularly those whose primary language is not English. A study found that IQ explained only 6 percent of the variance of a Hispanic child's variance and only 10 percent of an African-American child's grades (Figueroa and Sassenrath, 1989).
Some authors suggest that children reading below grade level should be provided with reading support no matter what ability level they possess. Sally Shaywitz and her colleagues (1992) found that reading disabilities occur along a continuum with no clear difference between children with reading problems and those usually classified as slow learners. Further research has found more similarities than differences between slow learners and those with learning disabilities with few differences present between these two groups on measures of reading, spelling, and phonics knowledge (Siegel 1990). Linda Siegel concluded that the more the task is related to reading the less important intelligence is to reading achievement.
Assessment Issues
Given the above concerns, it is important to provide a comprehensive evaluation of a child with a possible learning disability. Reading is a multidimensional skill involving the ability to read words from sight, sound out words (phonological coding), read fluently and with good speed, and to understand what is read. In any part of this reading process problems can arise and disrupt the reading process. For example, a child who reads haltingly and needs to sound out almost every word will often experience difficulty with comprehension because it takes so long to read a passage and the child is concentrating on the words rather than the information. Evaluation of this child's reading rate and sight-word vocabulary are important aspects. Reading a passage to him/her and checking the comprehension of the passage assists one in understanding whether difficulties in comprehension are due to true comprehension problems or to the difficulty with the reading process. Similarly a child who has difficulty sounding out words may well have an intact sight-word vocabulary. In this case the child will benefit from using this strength with remediation in phonics.
Comorbidity Issues
Learning disabilities often occur in conjunction with other disorders or conditions. Comorbidity refers to multiple disorders within one individual. Learning disabilities occur concurrently with other conditions (for example, sensory impairment or serious emotional disturbance), but is not a result of the comorbid disorder (NJCLD 1991). For example, a child who is hearing-impaired would not qualify for LD services due solely to the hearing impairment.
Attention deficit hyperactivity disorders (ADHD) and learning disabilities are frequently comorbid. However, the inattention and impulsivity characteristic of ADHD make it difficult to determine if academic difficulty is due to the presence of learning disabilities or is a consequence of attention deficits (Semrud-Clikeman et al. 1992). Language disorders, depression, and anxiety are often experienced by those diagnosed with learning disabilities (American Psychiatric Association 1994). Social skills deficits are also frequently found in children diagnosed with learning disability (San Miguel et al. 1996).
Neuropsychology of Learning Disabilities
Learning disabilities is a heterogeneous disorder. The most common type of learning disability is language-based and due to difficulties with the sounding out of words—also called phonological coding deficits (Teeter and Semrud-Clikeman 1997). In this type of learning disability the child has difficulty hearing and/or understanding the differences in the sounds of a word (Mann 1991). For example, the word cat may not be heard as three different sounds—c a t. Reading requires that a child learn the relationship between the written letters and the sound segments—also called sound-symbol learning (Torgesen 1993). This is the most common type of learning disability.
Another type of learning disability involves difficulty with the visual or orthographic features of a word (Stanovich 1992). For example the outward configuration of words such as left and felt are relatively similar—high letter, low letter, two high letters—and may be confused by a child with this type of learning disability. These types of learning disabilities are less common. Visual memory is important in reading and children with this type of learning disability seem to have difficulty recalling what they see (Terepocki, Kruk, and Willows 2002). Children are evaluated in their ability to discriminate phonetically similar words like main from mane and homonyms (e.g., see and sea).
The majority of learning disabilities are reading based and most of the research involves children with reading disabilities (or dyslexia). However, it is important to realize that learning disabilities can also be identified in mathematics and written language. These types of learning problems are not as commonly evaluated or reported as a reading disability. Written language disabilities can have profound effects on a child's ability to generate and organize ideas in written form (Nodine, Barenbaum, and Newcomer 1985). Less is known about written language disabilities than reading disabilities but a study that evaluated children with brain injuries found that these children had intact reading skills but deficits in mathematics and written language, particularly if the damage was in the right hemisphere.
The incidence of math-based learning disabilities suggests that approximately 6 percent of children show a learning disability in this area (Miles and Forcht 1995). Difficulties can be found in mathematics calculations that are often related to difficulties with visual-spatial skills. Children with this type of disability may also show difficulties with social understanding. When mathematics problems and visual-spatial delays occur together, the child may have a nonverbal learning disability. These difficulties involve the child's inability to understand the context of the social situation, to interpret facial and body gestures, and to act accordingly. The relationship between the mathematics difficulties and these social deficits is not fully understood and further research is needed in this area (Semrud-Clikeman and Hynd 1990).
Neuro-Imaging and Learning Disabilities
Differences in brain anatomy have been consistently found in the area where sound-symbol relationships are believed to take place. Neuroimaging has now allowed further evaluation of the brain in living children. Studies found differences in the area of the brain responsible for sound-symbol interpretation (Hynd et al. 1990) as well as in the left hemisphere and frontal areas of the brain believed to be responsible for speaking ( Jernigan et al. 1991; Semrud-Clikeman et al. 1991). Neurons were found to be out of place, additional neurons in places where they should not be were found, and smaller volumes of the planatemporale were found. This area is responsible for auditory processing (Hynd and Semrud-Clikeman 1989). Such regional differences imply a neurodevelopmental process that went awry during gestation rather than brain damage or environmental influences. It is important to note that this asymmetry/symmetry may not be solely responsible for learning disabilities, although it is likely a major contributor to such difficulties (Morgan and Hynd 1998; Steinmetz and Galaburda 1991).
Electrophysiology and Learning Disabilities
Electrophysiological techniques have also been used in the study of learning disabilities to examine the neurobiological mechanisms that underlie these disabilities. The brain has ongoing electrical activity whose waveform can be measured and recorded. Large populations of neurons are measured by electrodes placed on the scalp with changes in the ongoing waveform occurring in response to a cognitive event, such as attention or stimulus discrimination.
Several decades of research have demonstrated different patterns of activation in the brains of children with learning disabilities and those of control groups. Abnormal electrical responses have been found in populations with learning disabilities when they are asked to process phonological information. Studies of components not involving conscious processing have demonstrated that adults and children with reading disabilities process auditory information differently than do normal readers. These components occur later in subjects with learning disabilities, indicating low-level auditory processing deficits. (McAnally and Stein 1996; Baldeweg et al. 1999). This physiological abnormality has also found to be correlated with phonological deficits.
Genetics of Learning Disabilities
The genetics of learning disabilities became of an area of significant interest beginning in the 1990s. Reading disabilities run in families and this familiarity may be due in part to genetic influences and in part to environment. These genetic influences are likely to have a direct impact on the development of the brain or a specific region of the brain that is probably involved in language.
Genetic influences appear to be more prominent in children with phonological coding deficits than in those with visual coding deficits (Pennington 1991). These studies have been generally involved identical and fraternal twins. Deficits in specific processes have been found in phonological coding (the ability to discriminate sounds in words) and phonemic analysis (the ability to sound out words) compared to in visual-spatial deficits (DeFries et al. 1991). The concordance of phonetically based learning problems was 71 percent for identical twins but only 49 percent for fraternal twins. Bruce Pennington and his colleagues (1991) found evidence of a major gene transmission in a large sample of families with reading disabilities linking a small set of genes that indirectly affect reading. Although chromosomes 6 and 15 have been linked to reading problems, it is likely that the difficulty is due to several genes that have not been fully evaluated (Smith, Kimberling, and Pennington 1991). Genetic analysis of children with mathematics or written expression disabilities is another area that requires study.
Environmental influences also impact the brain and culture may change the development of neurons in a specific manner (e.g., reading left to right rather than right to left). Arabic and Hebrew readers have been found to show differences in hemispheric activation on reading tasks—particularly tasks that involve orthographic processing (Eviatar 2000). In addition, preliminary studies have indicated that those readers that read right to left do not show the same right hemispheric preference for the processing of faces and emotion as do those who read left to right (Eviatar 1997; Vaid and Singh 1989). Genetics and neuro-imaging studies may provide more information about these differences.
Familial risk for learning disabilities is clearly significant and substantial in many of the research findings (Gilger, Pennington, and DeFries 1991). Environment may play a role in the development of reading disabilities but no difference has been found between preschool literacy rate in children with reading problems and those without reading problems (Scarborough 1991). What has been found that within the family, the child with a predisposition for a reading problem is less interested in reading and reading-like activities than those without such a predilection (Scarborough, Dobrich, and Hager 1991). Moreover, differences in amount of time being read to, looking at books, and listening to stories were found between siblings with and without later reading difficulties.
Family Aspects of Learning Disabilities
The discussion of the genetics of learning disabilities leads into family aspects as many parents also have a learning disability. It is important to recognize this possibility, particularly when developing interventions and recommendations for these families. It may be unrealistic to ask a parent who also has a learning disability to read to their child, as the action may be fraught with anxiety and difficulty for the parent. It is also important to realize that parents who experienced difficulty in learning themselves may find coming to a school for a parent-teacher conference to be frightening and intimidating (Semrud-Clikeman 1994).
There are few studies in this area but prenatal and postnatal factors have been found to be important in the development of learning problems in the first two years of life (Werner and Smith 1981). Families that were characterized as chaotic or in poverty showed a higher probability of children experiencing learning problems than those without—these variables become more significant as the child becomes older (Teeter and Semrud-Clikeman 1997). Socioeconomic status, home conditions, and educational level of family members appear to act either as complicating factors or as compensatory factors for children with reading problems (Badian 1988; Keogh and Sears 1991).
Robert Jay Green (1992) draws from biological, sociological, and familial sources in evaluating the impact of families on achievement and learning. He suggests that each of these factors interact with one another and either improve learning or impede skill development. These factors work less strongly on biologically based difficulties (e.g., genetically based type of learning disability) than on those environmentally based. However, difficulties in learning and attention are due to the influences of many genes and may well respond to environmental changes that can assist the child in over-coming learning difficulties in an environment that is helpful and exacerbate the difficulties in a less than optimal environment. Green's (1992) model assumes that achievement difficulties can be partially caused or maintained by family factors as well as those present in the school system and social environments. Given these concerns it is important to link school-based interventions with family support.
Interventions
Children with phonological coding deficits appear to respond well to interventions that stress direct training of phonics and place the training within a context (Cunningham 1990). Such a context—metacognitive training—allows the child to learn when to use a particular tactic and how to decide if it is effective (Cunningham 1989). The Reading Recovery Program (Clay 1993) has shown good promise in assisting children with their learning. The program emphasizes understanding the reading process in addition to emphasizing decoding skills. Teaching word families within this context has also been found to be helpful (i.e., an, in, fan, tan, or man).
Early identification of children at risk for learning difficulties is also recommended with specific training in phonemic awareness, rhyming skills, and word families provided in preschool and kindergarten (Felton and Pepper 1995; Wise and Olson 1991). Such early intervention has been found to be most appropriate for children with a family history of learning disabilities (Scarborough 1991). These children demonstrate early on difficulties in language, both in understanding and expressing their thoughts, that later translates into problems in reading readiness (Wise and Olson 1991). Programs, such as FastForword, LindamoodAuditory System, and the Slingerland or Orton-Gillingham method, are helpful to some children with learning disabilities. Websites can be readily found for each of these interventions.
Conclusion
Learning disabilities is a field that is constantly changing. With the advent of techniques that allow scholars to study the brain in action, we may understand not only the normal process of reading but also what happens when the system is not working. The hope is that we will be able to prevent learning disabilities or, at the least, to develop innovative and successful interventions. It is also hoped that we will become more adept at identifying children at earlier ages to prevent some of the emotional and social difficulties that can be associated with a learning disability. Neuroscience is now promising new avenues in our study of learning disabilities as is genetics. Families who have a history of learning disability need further study to provide appropriate support for them as well as to assist with early interventions. Schools are becoming more adept at working with children with differing types of learning disability and it is hoped that our ability to assess minority children appropriately will also improve.
See also:Academic Achievement; Chronic Illness; Development: Cognitive; School
Bibliography
aaron, p. g. (1997). "the impending demise of the discrepancy formula." review of educational research 67:461–502.
american psychiatric association. (1994). diagnostic andstatistical manual of mental disorders, 4th edition. washington, dc: author.
badian, n. (1988). "the prediction of good and poor reading before kindergarten entry: a nine-year follow-up." journal of learning disabilities 21: 98–103.
baldeweg, t.; richardson, a.; watkins, s.; foale, c.; and gruzelier, j. (1999). "impaired auditory frequency discrimination in dyslexia detected with mismatch evoked potentials." annals of neurology 45:495–503.
clay, m. m. (1993). reading recovery: a guidebook forteachers in training. portsmouth, nh: heinemann.
cunningham, a. (1989). "phonemic awareness: the development of early reading competency." reading research quarterly 24:471–472.
cunningham, a. (1990). "explicit versus implicit instruction in phonemic awareness." journal of experimental child psychology 50:429–444.
defries, j. c.; stevenson, j.; gillis, j. j.; and wadsworth, s. j. (1991). "genetic etiology of spelling deficits in the colorado and london twin studies of reading disability." in reading disabilities: genetic and neurological influences, ed. b. f. pennington. boston: kluwer academic.
eviatar, z. (1997). "language experience and right hemisphere tasks: the effects of scanning habits and multilingualism." brain and language 58:157–173
eviatar, z. (2000). "culture and brain organization." brain and cognition 42:50–52.
felton, r. h., and pepper, p. p. (1995). "neuropsychological prediction of reading disabilities." in neuropsychological foundations of learning disabilities: a handbook of issues, methods, and practice, ed. j. e. obrzut and g. w. hynd. san diego, ca: harcourt.
figueroa, r. a., and sassenrath, j. m. (1989). "a longitudinal study of the predictive validity of the system of multicultural pluralistic assessment (sompa)." psychology in the schools 26:5–19.
gilger, j. w.; pennington, b. f.; and defries, j. c. (1991). "risk for reading disability as a function of parental history in three family studies." in reading disabilities: genetic and neurological influences, ed. b. pennington. boston: kluwer academic.
green, r. j. (1992). "learning to learn and the family system: new perspectives on underachievement and learning disorders." in the handbook of family-school intervention, ed. m. j. fine and c. carlson. boston: allyn and bacon.
greenfield, p. m. (1997). "you can't take it with you: why ability assessments don't cross cultures." american psychologist 52:1115–1124.
hynd, g. w., and semrud-clikeman, m. (1989). "dyslexia and brain morphology." psychological bulletin 106: 447–482.
hynd, g. w.; semrud-clikeman, m.; lorys, a. r.; and novey, e. s. (1990). "brain morphology in developmental dyslexia and attention deficit disorder/hyperactivity." archives of neurology 47(8):919–926.
individuals with disabilities education act. (pub. l. no. 101–476) 20 u.s.c. chapter 33. amended by pub. l. no. 105–17 in june 1997. regulations appear at 34 c.f.r. part 300.
jernigan, t. l.; hesselink, j. r.; sowell, e.; and tallal, p. a. (1991). "cerebral structure on magnetic resonanceimaging in language-and learning-impaired children." archives of neurology 48:539–545.
keogh, b. k., and sears, s. (1991). "learning disabilities from a developmental perspective: early identification and prediction." in learning about learning disabilities, ed. b. y. l. wong. orlando, fl: academic press.
mann, v. (1991). "why some children encounter reading problems." in psychology and educational perspectives on learning disabilities, ed. j. torgesen and b. y. l. wong. orlando, fl: academic press.
mcanally, k. i., and stein, j. f. (1996). "auditory temporal coding in dyslexia." proceedings of the royal society of london 263:961–965.
miles, d. d., and forcht, j. p. (1995). "mathematics strategies for secondary students with learning disabilities or mathematical deficiencies: a cognitive approach." intervention in school and clinics 31:91–96.
morgan, a. e., and hynd, g. w. (1998). "dyslexia, neurolinguistic ability, and anatomical variation of the planum temporale." neuropsychology review 8(2): 79–93.
morris, r. d.; stuebing, k. k.; fletcher, j. m.; shaywitz, s. e.; lyon, g. r.; shankweiler, d. p.; katz, l.; francis, d. j.; and shaywitz, b. a. (1998). "subtypes of reading disability: variability around a phonological core." journal of educational psychology 90:347–373.
national joint committee on learning disabilities. (1991). "learning disabilities: issues on definition." asha 33(suppl. 5):18–20.
nodine, b. f.; barenbaum, e.; and newcomer, p. (1985). "story composition by learning disabled, reading disabled, and normal children." learning disability quarterly 8:167–179.
pennington, b. (1991). reading disabilities: genetic andneurological influences. boston: kluwer academic.
pennington, b. f.; gilger, j.; pauls, d.; smith, s. a.; smith, s. d.; and defries, j. (1991). "evidence for major gene transmission of developmental dyslexia." journal of the american medical association 266: 1527–1535.
san miguel, s. k.; forness, s. r.; and kavale, k. a. (1996). "social skills deficits in learning disabilities: the psychiatric comorbidity hypothesis." learning disability quarterly 19(4):252–261.
scarborough, h. s. (1991). "antecedents to reading disability: preschool language development and literacy experiences of children from dyslexic families." in reading disabilities: genetic and neurological influences, ed. b. f. pennington. boston: kluwer academic.
scarborough, h. s.; dobrich, w.; and hager, m. (1991). "preschool literacy experience and later reading achievement." journal of learning disabilities 24(8): 508–511.
semrud-clikeman, m. (1994). child and adolescent therapy. boston: allyn and bacon.
semrud-clikeman, m.; biederman, j.; sprich-buckminster, s.; lehman, b. k.; faraone, s. v.; and norman, d. (1992). "comorbidity between addh and learning disability: a review and report in a clinically referred sample." journal of american academy of child and adolescent psychiatry 31(3):439–448.
semrud-clikeman, m., and hynd, g. w. (1990). "right hemispheric dysfunction in nonverbal learning disabilities: social, academic, and adaptive function in adults and children." psychological bulletin 107: 196–207.
semrud-clikeman, m.; hynd, g. w.; novey, e. s.; and eliopulos, d. (1991). "relationships between neurolinguistic measures and brain morphometry in dyslexic, adhd, and normal children." learning and individual differences 3:225–242.
shaywitz, s. e.; escobar, m. d.; shaywitz, b. a.; fletcher, j. m.; and makuch, r. (1992). "evidence that dyslexia may represent the lower tail of a normal distribution of reading ability." new england journal of medicine 326:145–150.
siegel, l. s. (1990). "iq and learning disabilities: r.i.p." in learning disabilities: theoretical and research issues, ed. h. l. swanson and b. keogh. hillsdale, nj: erlbaum.
siegel, l. s. (1992). "an evaluation of the discrepancy definition of dyslexia." journal of learning disabilities 25:618–629.
smith, s. d.; kimberling, w. j.; and pennington, b. f. (1991). "screening for multiple genes influencing dyslexia." in reading disabilities: genetic and neurological influences, ed. b. f. pennington. boston: kluwer academic.
snow, c. e.; burns, m. s.; and griffin, p. (1998). preventing reading difficulties in young children. washington, dc: national academy press.
sofie, c. a., and riccio, c. a. (2002). "a comparison of multiple methods for the identification of childrenwith reading disabilities." journal of learning disabilities 35:234–244.
stanovich, k. e. (1986). "matthew effects in reading: some consequences of individual differences in the acquisition of literacy." reading research quarterly 21:360–407.
stanovich, k. e. (1992). "developmental reading disorder." in developmental disorders: diagnostic criteria and clinical assessment, ed. s. r. hooper and g. hynd. hillsdale, nj: erlbaum.
steinmetz, h., and galaburda, a. m. (1991). "planum temporale asymmetry: in-vivo morphometry affords a new perspective for neuro-behavioral research." reading and writing 3(3):331–343.
swanson, h. l.; hoskyn, m.; and lee, c. (1999). interventions for students with learning disabilities: a meta-analysis of treatment outcomes. new york: guilford press.
teeter, p. a., and semrud-clikeman, m. (1997). child neuropsychology: assessment and intervention. boston: allyn and bacon.
terepocki, m.; kruk, r. s.; and willows, d. m. (2002). "the incidence and nature of letter orientation errors in reading disability." journal of learning disabilities 35:214–233.
torgesen, j. k. (1993). "variations on theory in learning disabilities." in better understanding learning disabilities: new views from research and their implications for education and public policies, ed. g. r. lyon, d. gray, j. kavanagh, and n. krasnegor. baltimore, md: paul h. brookes.
vaid, j., and singh, m. (1989). "asymmetries in the perception of facial affect: is there an influence of reading habits?" neuropsychologia 27:1277–1287.
valencia, r. r. (1995). "k-abc content bias: comparisons between mexican american and white children." psychology in the schools 32:153–158.
werner, e. e., and smith, r. s. (1981). vulnerable but invincible: a study of resilient children. new york: mcgraw-hill.
wise, b. w., and olson, r. k. (1991). "remediating reading disabilities." in neuropsychological foundations of learning disabilities: a handbook of issues, methods, and practice, ed. j. e. obrzut and g. w. hynd. orlando, fl: academic press.
MARGARET SEMRUD-CLIKEMAN
KELLIE HIGGINS
Learning Disabilities
Learning Disabilities
What Are Learning Disabilities?
How Do People Know They Have a Learning Disability?
Why Do People Have Learning Disabilities?
Living with a Learning Disability
Learning disabilities are disorders that affect people’s ability to interpret information that they see or hear or to link information processed in different parts of the brain. A person with a learning disability may have specific difficulties with language, visual information, or coordination, which in turn can make it very hard to read, spell, write, or do math.
KEYWORDS
for searching the Internet and other reference sources
Dysgraphia
Dyslexia
Learning disorders
What Are Learning Disabilities?
Learning disabilities differ from learning problems (which are less severe) and from mental retardation (which refers to more global learning difficulties). Not every learning problem is a true disorder or disability. Some children are just naturally slower than others in developing certain skills, but most children usually catch up and achieve within the normal range for their age and abilities. Children who are mentally retarded, on the other hand, will never be able to learn and function socially like other children their age. Their general intellectual capacity is much lower than average. Children with mental retardation have learning problems but do not truly have learning disabilities.
Children with learning disabilities typically have average or even above-average intelligence, so they have a marked difference between their intellectual capabilities and what they are actually achieving. In a sense, a person with a learning disability is like a radio that is not tuned exactly to a station. There is nothing wrong with the radio itself or with the signal coming from the station, but the music still sounds garbled. Similarly, people with learning disabilities can see and hear as well as others and have normal general learning capacity, but there is a problem with the way their brains process information.
Learning disabilities are generally classified into two main categories: verbal (having to do with the uses of spoken and written words) and nonverbal (having to do with interpreting visual or spatial information).
Verbal learning disabilities
Developmental speech disorders are usually diagnosed in very young children who have persistent trouble making certain speech sounds; for example, they may say “wabbit” instead of “rabbit” or “thwim” instead of “swim.” Often these speech disabilities improve with age or with the help of a speech therapist.
Developmental language disorders involve the way that children express themselves or how they understand others’ speech. Children with this type of disorder may speak in short phrases instead of full sentences, call objects by the wrong names, have disorganized speech, misunderstand words, or have difficulties following directions.
Reading is a very complex task in which a person has to focus attention on the printed marks, control eye movements across the page, recognize sounds associated with letters, understand words and grammar, build images and ideas, compare new ideas to what is already known, and then store the ideas in memory. This process requires a rich, intact network of nerve cells that connect the brain’s centers of vision, language, and memory. A problem in any of these areas or the connections among them can lead to difficulties with reading. Dyslexia (dis-LEKSee-uh) is the most common and best-known of the reading disorders. It affects 2 to 8 percent of school-age children. Because children with dyslexia have trouble processing the smallest units of language that make up words, they may have trouble with rhyming games or with sounding out individual letters or syllables to form words.
There are other types of reading disorders that affect comprehension (kom-pre-HEN-shun), which is the ability to fully understand and interpret
Understanding Dyslexia
In the mid-1900s, a doctor named Samuel Orton found that several children he was working with had similar problems with reading. In addition to confusing the letter “b” with “d” and the letter “p” with “q,” some could read more easily if they held pages up to a mirror. Orton named this condition strephosymbolia (STREF-oh-sim-BOL-eeuh), which means “twisted symbols.” Now strephosymbolia is called dyslexia, which is derived from the Greek words “dys” (meaning poor or inadequate) and “lexis” (meaning words or language).
Further research has shown that dyslexia involves much more than just seeing letters backwards or reversed. Children with this disorder describe how printed letters and words seem to jump around on the page or that sounds and letters get mixed up or jumbled together. Researchers originally thought that visual and motor problems were at the heart of dyslexia, but they later found that reading disabilities stem from a difficulty with processing the smallest units of language, which are called phonemes (FO-neemz). For example, the “p” of pat and the “f” of fat are two different phonemes, and the word fat has three phonemes linked together. Someone with dyslexia might have trouble telling the difference between these sounds when reading them.
what one reads. A person with this type of disability can read each word but may find it hard to understand the text, form images, or relate new ideas in the text to those in memory. These reading disabilities usually are discovered at a later age than is dyslexia.
Learning involves a complex series of events. The brain receives new information from the outside world all the time, but in order to learn new information, the brain must recognize the information’s importance, interpret it, analyze its meaning, and store it in memory for later use in processing new information. If the brain does not recognize new information as meaningful and important, it will discard it. Learning disorders affect different aspects of this complex process of recognizing, interpreting, understanding, and remembering new information.
A writing disability can result from problems with any area of the brain that controls grammar, hand movement, vocabulary, and memory. Children who have trouble mastering the motor skill of writing are said to have dysgraphia (dis-GRAF-ee-uh).
Nonverbal learning disorder
Nonverbal learning disorder (also called nonverbal learning disabilities), or NVLD, is not as well understood as verbal learning disabilities. People with NVLD often have problems with visual perception, with recalling visual details, and with spatial relationships. Their eyesight is fine, but they may have trouble processing what they see; for example, a student might find it hard to follow a set of instructions demonstrated by a teacher.
Students with NVLD often find it hard to focus on nonverbal academic material as well, which can make it hard to learn math (a disorder called dyscalculia (dis-KAL-kyoo-lee-uh)) and science. They may have trouble recognizing numbers and symbols, memorizing facts such as the multiplication tables, aligning numbers, and understanding abstract concepts like place value and fractions. In both math and science class, students may have difficulty solving problems, forming complex concepts, and making educated guesses and then testing them out. Reading comprehension may be affected as well. Even though students with NVLD may read words and sentences with ease, they might not understand the underlying organization of the story. Dealing with brand-new material is likely to overwhelm children with NVLD.
Some children with NVLD have trouble in other areas as well. They may have poor motor skills and problems with coordination; for example, learning to ride a bike can be very difficult for a child with NVLD. They also may have trouble socializing with other children because they do not pick up on nonverbal social cues, such as tone of voice and body language, or they tend to say the wrong thing at the wrong time. Children with NVLD tend to be easily frustrated and upset. Any new situation can make them anxious because they may have more difficulty adjusting to it.
Other types of learning disabilities
There are many other subtypes of learning disabilities, but verbal and nonverbal learning disabilities are the two main categories. Because many aspects of speaking, listening, reading, writing, and arithmetic overlap and build on the same brain capabilities, it is not unusual for someone to have more than one disorder. For example, most disorders that hinder the ability to understand language will also interfere with learning to read, spell, and write.
Attention Deficit Hyperactivity Disorder*, or ADHD, can also interfere with learning. Children with ADHD often have difficulty focusing on any one task for a period of time. Children with attention problems may have learning problems but attention deficits are not classified as specific learning disabilities. However, more than half of children with ADHD also have learning disabilities.
- * Attention Deficit Hyperactivity Disorder
- , or ADHD, is a condition that makes it hard for a person to pay attention, sit still, or think before acting.
How Do People Know They Have a Learning Disability?
Parents and teachers are usually the first to notice signs of a possible learning disability. A very young child might not speak or listen as well as other children their age or might have trouble with a game’s directions or other activities that other children complete with ease. The classroom teacher may notice persistent difficulties in reading, writing, or math.
The first step in diagnosing a learning disability is to rule out any other possible causes, such as vision or hearing problems or some other medical condition. Once a doctor makes sure that other problems are not to blame, the child might be evaluated by a psychologist* who specializes in learning disabilities. Diagnosing a learning disorder often takes time. The psychologist usually takes a careful history of symptoms, interviews the child, and gives certain tests that compare the child’s level of ability to what is considered appropriate for a person of that age and intelligence.
- * psychologist
- (sy-KOL-uh-jist) is a mental health professional who can do psychological testing and provide mental health counseling.
Dyslexia: Separating Myth from Reality
In a 1996 article published in Scientific American magazine, one of the country’s leading experts on dyslexia tried to correct some of the persistent myths about the disorder, including the following:
MYTH: Mirror writing is a symptom of dyslexia.
REALITY: In fact, backwards writing and reversal of letters are common in the early stages of writing development among children with and without dyslexia. Children with dyslexia have problems in naming letters but not in copying letters.
MYTH: Eye training is an effective treatment for dyslexia.
REALITY: More than two decades of research have shown that dyslexia reflects a linguistic (lin-GWIS-tik; language-related) deficit. There is no evidence that eye training alleviates the disorder.
MYTH: Dyslexia can be outgrown.
REALITY: Yearly monitoring of language processing skills from first through twelfth grade shows that the disability persists into adulthood. Even though most people with dyslexia learn to read accurately, they continue to read slowly and do not read automatically.
MYTH: Smart people cannot be dyslexic.
REALITY: Intelligence is in no way related to language processing skills, and there have been many brilliant and accomplished people with dyslexia, including writers William Butler Yeats and John Irving, scientist Albert Einstein, military leader George Patton, and financial industry leader Charles Schwab.
Why Do People Have Learning Disabilities?
Why certain children develop learning disabilities and others do not remains a mystery. However, researchers believe that learning disabilities can be traced to differences in early brain development that happen before or after birth. During brain development, a few all-purpose cells must grow into a complex organ made of billions of specialized interconnected nerve cells called neurons [NOR-ons]. Researchers are investigating possible causes for differences or disruptions in brain development that include:
- alcohol, tobacco, or drug use by the mother during pregnancy
- problems during pregnancy or delivery that may cause a decrease in the amount of oxygen that reaches the baby’s developing brain
- head injuries
- being exposed to poisonous substances in the environment, such as lead
Also, because some learning disabilities tend to run in families, researchers are looking into how learning differences may be inherited.
Living with a Learning Disability
Because children with learning disabilities typically have normal or abovenormal intelligence, they often can find ways to learn in spite of the disorder. They may need special school programs for the learning disabled or to work with a learning specialist several hours each week while attending regular classes.
Special education teachers can help plan out what is called an Individualized Education Program, or IEP, for a learning-disabled child. This plan outlines the specific skills the child needs to develop as well as appropriate learning activities that build on the child’s strengths and work around his or her difficulties. For example, a student with dyslexia might be encouraged to listen to a book on tape for English class, while another with a writing disorder might take notes or complete an assignment using a laptop computer.
Children with learning disabilities often need emotional support because they may see themselves as dumb or stupid. They may withdraw from their classmates at school or even get into trouble because they are frustrated when learning is difficult for them. Children and their families can often benefit by working with a trained counselor or support group.
Teens with learning disabilities often find a particular way of learning that works for them. Their methods, along with a regained sense of self-confidence, continue to affect their lives outside the classroom, such as in relationships with others and in their careers. Photodisc
See also
Attention
Attention Deficit Hyperactivity Disorder
Intelligence
Memory
Mental Retardation
Self-Esteem
Testing and Evaluation
Resources
Books
Cummings, Rhoda, and Gary Fisher. The Survival Guide for Teenagers with LD. Minneapolis: Free Spirit Publishing, 1993.
Lauren, Jill. Succeeding with LD: 20 True Stories About Real People with LD. Minneapolis: Free Spirit Publishing, 1997. For ages 11 and up.
Levine, Melvin. Keeping a Head in School: A Student’s Book About Learning Disabilities and Learning Disorders. Cambridge, MA: Educators Publishing Services, 1996.
Stern, Judith, and Uzi Ben-Ami. Many Ways to Learn: Young People’s Guide to Learning Disabilities. New York: Magination Press, 1996.
Organizations
The International Dyslexia Association, 8600 LaSalle Road, Chester Building, Suite 382, Baltimore, MD 21286-2044. Telephone 800-ABCD123 http://www.interdys.org
LD Online is an interactive guide to learning disabilities for parents, teachers, and children. The website includes in-depth information about learning disorders, an interactive chat room and bulletin boards, the latest news and resources, and a KidZone that features artwork and stories by young people. http://www.ldonline.org
The Learning Disabilities Association of America (LDA), 4156 Library Road, Pittsburgh, PA 15234-1349. LDA is a national non-profit organization that provides education and support for people with learning disabilities and their families. http://www.ldanatl.org
National Institute of Mental Health (NIMH), National Institutes of Health, 6001 Executive Blvd., Rm. 8184, MSC 9663, Bethesda, MD 20892-9663. The NIMH posts information about learning disabilities at its website. Telephone 301-443-4513 http://www.nimh.nih.gov/publicat/learndis.htm
NLD on the Web! is a website that provides information about nonverbal learning disabilities. http://www.nldontheweb.org.
Learning Disabilities
LEARNING DISABILITIES
It is estimated that 5 percent to 10 percent of school-age children and adolescents have learning disabilities (LDs), with some estimates approaching 17 percent. LDs fall on a continuum and range in severity from subtle to marked impairment. A substantial number of learning-disabled students receive special education services. In 1975 the U.S. Congress enacted the Education for All Handicapped Children Act (PL 94-142), which was an educational bill of rights assuring children with disabilities a free and appropriate education in the least restrictive environment. Disabilities that qualified for services under this law included mental retardation, hearing deficiencies, speech and language impairments, visual impairments, emotional disturbances, orthopedic impairments, a variety of medical conditions (categorized as "other health-impaired"), and specific learning disabilities. This law was reauthorized under the Education of the Handicapped Act amendments and, subsequently, the Individuals with Disabilities Education Act (IDEA). Children with learning disabilities also may receive services under Section 504 of the Rehabilitation Act of 1973 (a civil rights law that protects individuals with disabilities from discrimination by recipients of federal financial assistance). The latter law is designed to provide modifications and accommodations to minimize the negative effect on "major life activities"; all IDEA children qualify under Section 504, but the reverse is not true. As many as 50 percent of children with LDs have concomitant disorders such as attention deficit hyperactivity disorder, anxiety problems, school refusal, depression, Tourette's syndrome, or behavior problems. It is estimated that 35 percent to 50 percent of students seen in mental health clinics have language and/or learning disorders.
Definition of Learning Disabilities
Despite federal regulations, the definition of learning disabilities is controversial. The U.S. government defines a specific learning disability as a disorder in one or more of the basic psychological processes involved in understanding or use of spoken or written language, which may be manifest as an inability to listen, think, speak, read, write, spell, or do mathematic calculations. While the definition could include the conditions of perceptual handicaps, brain injury, minimal brain dysfunction, dyslexia, and developmental aphasia, it is not applicable to students whose learning problems are the result of visual, hearing, or motor handicaps, mental retardation, emotional disturbance, or environmental/cultural disadvantage. The major premise is that a significant discrepancy exists between the child's potential and her actual level of academic or language skills.
Each state, however, may determine cutoffs for discrepancies or definitions of processing disorders, leading to variability among states and even differences among districts within a given state. The definition and diagnosis of an LD vary, depending on whether the purpose is to qualify for services or to clinically identify the reason for a child's poor academic performance. In the former, measurement of intelligence and levels of achievement is employed; in the latter, administration of IQ and achievement is extended to include evaluation of attention, memory, and neuropsychological function. Moreover, the age of identification varies, depending on the type of LD; some may not be apparent early because academic skills in areas affected by the LD have not yet been challenged.
The psychiatric definition of LDs (as found in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders: DSM-IV) differs considerably from both federal and state classification systems, adding further to the ambiguity. Learning disabilities are presumed to be due to central nervous system dysfunction, and occur across the lifespan. They reportedly occur more in males, although research in the late 1990s by Sally Shaywitz has disputed this contention.
The Discrepancy Issue
The "discrepancy issue" has been established as the primary criterion for identifying children with LDs. Unfortunately, discrepancy formulae are controversial, potentially inaccurate, and inappropriate for detecting cognitive deficits. There are three types of discrepancy formulae.
With an aptitude-achievement discrepancy, a disparity exists between a child's intellectual ability (as measured by an intelligence test) and his actual level of academic achievement (measured by an achievement test). Certain LDs (e.g., a short-term memory problem or central processing dysfunction), however, may also affect a child's performance on IQ tests, thereby reducing the discrepancy between aptitude and achievement. This discrepancy model is useful from third grade onward, and certain disabilities (such as fine motor dyspraxia, retrieval memory dys-function, and organization problems) often are not detected. Children with the most severe LDs frequently have the smallest discrepancy.
An intracognitive discrepancy (a disturbance in basic psychologic processes) occurs in children who have a specific type of cognitive dysfunction such as a deficit in auditory processing, short-term memory, or visual processing. This type of LD is difficult to operationalize, but is useful in identifying preschool and primary-age children who have learning problems.
An intra-achievement discrepancy reflects divergence or inconsistency in educational achievement performances. This could occur between academic areas (such as reading versus mathematics) or within an academic area (such as a marked difference between reading decoding and reading comprehension).
Regression models, which attempt to correct the problems inherent in discrepancy comparisons, are used in many states. Here a statistical relationship between IQ and achievement is considered, allowing for equal probability of identification of an LD across IQ levels, thereby potentially enhancing identification rates. Research in the 1990s, however, failed to demonstrate valid differences on school-related measures between poorly achieving groups of students with an IQ/achievement discrepancy and those with poor school performance and no discrepancy.
Learning Disability Subtypes
There are many different subtypes of learning disabilities. Byron Rourke, writing in 1993, reported three major groupings: (1) reading/spelling, (2) arithmetic, and (3) reading/spelling/arithmetic. Larry Silver, also writing in 1993, suggested a model that includes input disabilities (visual/perceptual, auditory/perceptual, and sensory integrative), integrative disabilities (sequencing, abstraction, and organization), memory disabilities, and output disabilities (language and motor). Reading/spelling disabilities are by far the most prevalent form, with such disabilities estimated to comprise from 5 percent up to 17 percent of the child and adolescent population. Estimates for the occurrence of disorders of written expression range from 2 percent to 8 percent. Although the prevalence of arithmetic LDs ranges from 1 percent to 6 percent, it is not clear whether weak mathematics performance is due to the quality of instruction or an actual LD.
Nonverbal LDs are often overlooked, occur less frequently than reading disorders, and are characterized by problems in arithmetic computation, graphomotor skills, reading comprehension, math reasoning, science, complex concept formation, visual memory, and social-behavioral skills; these are often found in children with white-matter disorders, and are assumed to be more right-hemisphere-based. As of the late 1990s, a classification schema (based on reading disability/dyslexia research) was applied to all achievement domains included in federal and state definitions of LD. Three major types of LDs were identified: specific language impairment, specific reading disability/dyslexia, and specific math disability.
The area of greatest knowledge is reading disorders. These fall into two main groupings: phonological (dysphonetic) and orthographic (dyseidetic). The former is more prevalent and is characterized by deficits in decoding and word analysis, with guesses made based on the initial letter of the word and misspellings being phonetically inaccurate. Shaywitz wrote in 1998 that a deficit in basic phonemic awareness (inability to segment phonemes [the smallest unit of sound] into phonological units) is the underlying cause in virtually all cases of dyslexia. The orthographic reading disability subtype involves an inability to develop a memory for the whole word (gestalt), with visuospatial reversals occurring (e.g., "was" read as "saw") and misspellings being phonetically accurate. There also is a mixed reading disorder, which consists of characteristics found in both types of deficit. The major new finding is that reading disabilities are more strongly associated with auditory rather than visual deficits.
Causes and Diagnosis
With regard to causes, research extends to family, genetic, and neuroanatomic bases, with most work being done in language and reading disabilities. There appears to be heritability in language and reading LDs, with similar LDs being found in 35 percent to 45 percent of first-degree relatives. Also, identical twins are more likely to have similar LDs than fraternal twins. Chromosomes 6 and 15 have been implicated frequently as possible genetic causes of LDs. Neuroimaging techniques, such as functional magnetic resonance imaging, have documented differences among dyslexic and nonreading-disabled individuals. Studies have found that in individuals with dyslexia, certain areas of the brain are different than in individuals without dyslexia. Nonetheless, there are no neuroanatomic or neuroelectric diagnostic tests that identify LDs in the brain. Although LDs are found more frequently in children subject to brain insult (such as premature birth and asphyxia), many children display LDs without any identifiable cause.
Outcomes
Learning disabilities do not disappear; rather, students compensate and learn bypass strategies, allowing for academic progress. The long-term outcome is variable, depending on the type of LD, degree of impairment, intelligence, environment, type of interventions provided, and presence of other disorders. For example, in the case of dyslexia, students often show improvement, but the underlying deficits in phonemic awareness skills prevent the individual from reading in an "automatic," appropriately speeded fashion.
Conclusions
To adequately understand an LD, the following areas must be considered: educational achievement, educational opportunity, cognitive functioning, potential emotional issues, peripheral sensory and neurological function (e.g., vision, hearing), family history, academic history, and age of onset of the LD. More specific tests need to be employed as necessary. Only in this way can a proper diagnosis and effective intervention plan be made.
See also:DEVELOPMENTAL DISABILITIES
Bibliography
American Academy of Child and Adolescent Psychiatry. "Practice Parameters for the Assessment and Treatment of Children and Adolescents with Language and Learning Disorders." Journal of the Academy of Child and Adolescent Psychiatry 37 (1998 supplement):46S-62S.
American Psychiatric Association. The Diagnostic and Statistical Manual of Mental Disorders: DSM-IV. Washington, DC: American Psychiatric Association, 1994.
Aylward, Glen. Practitioner's Guide to Developmental and Psychological Testing. New York: Plenum Medical, 1994.
Kavale, K. A., and S. R. Forness. The Nature of Learning Disabilities: Critical Elements of Diagnosis and Classification. Mahwah, NJ: Erlbaum, 1995.
Mather, Nancy, and William Healy. "Deposing Aptitude-Achievement Discrepancy as the Imperial Criterion for Learning Disabilities." Learning Disabilities 1 (1989):40-48.
Morris, Robin, Karla Stuebing, Jack Fletcher, Sally Shawitz, G. Reid Lyon, Donald Shankweiler, Leonard Katz, David Francis, and Bennett Shaywitz. "Subtypes of Reading Disability Variability around a Phonological Core." Journal of Educational Psychology 90 (1998):347-373.
Padget, S. Y. "Lessons from Research on Dyslexia: Implications for a Classification System for Learning Disabilities." Learning Disability Quarterly 21 (1998):167-178.
Pennington, Bruce. "Genetics of Learning Disabilities." Journal of Child Neurology 10 (1995 supplement):S69-S77.
Rourke, Byron. "Arithmetic Disabilities, Specific and Otherwise." Journal of Learning Disabilities 26 (1993):214-226.
Rourke, Byron. Syndrome of Nonverbal Learning Disabilities. New York: Guilford Press, 1995.
Shaywitz, Sally. "Dyslexia." Scientific American 275 (1996):98-104.
Shaywitz, Sally. "Dyslexia." New England Journal of Medicine 338(1998):307-312.
Silver, Larry. "Introduction and Overview to the Clinical Concepts of Learning Disabilities." Child and Adolescent Psychiatric Clinics of North America 2 (1993):181-192.
Tomblin, J. B., and P. R. Buckwalter. "Studies of the Genetics ofSpecific Language Impairment." In R. Watkins and M. Rice eds., Specific Language Impairments in Children. Baltimore: Paul H. Brookes, 1994.
Glen P.Aylward
Learning Disability
Learning disability
A disorder that causes problems in speaking, listening, reading, writing, or mathematical ability.
A learning disability , or specific developmental disorder, is a disorder that inhibits or interferes with the skills of learning, including speaking, listening, reading, writing, or mathematical ability . Legally, a learning disabled child is one whose level of academic achievement is two or more years below the standard for his age and IQ level. It is estimated that 5-20% of school-age children in the United States, mostly boys, suffer from learning disabilities (currently, most sources place this figure at 20%). Often, learning disabilities appear together with other disorders, such as attention deficit/hyperactivity disorder (ADHD). They are thought to be caused by irregularities in the functioning of certain parts of the brain . Evidence suggests that these irregularities are often inherited (a person is more likely to develop a learning disability if other family members have them). However, learning disabilities are also associated with certain conditions occurring during fetal development or birth , including maternal use of alcohol, drugs, and tobacco, exposure to infection, injury during birth, low birth weight, and sensory deprivation .
Aside from underachievement, other warning signs that a person may have a learning disability include overall lack of organization, forgetfulness, and taking unusually long amounts of time to complete assignments. In the classroom, the child's teacher may observe one or more of the following characteristics: difficulty paying attention, unusual sloppiness and disorganization, social withdrawal, difficulty working independently, and trouble switching from one activity to another. In addition to the preceding signs, which relate directly to school and schoolwork, certain general behavioral and emotional features often accompany learning disabilities. These include impulsiveness, restlessness, distractibility, poor physical coordination, low tolerance for frustration, low self-esteem , daydreaming , inattentiveness, and anger or sadness.
Types of learning disabilities
Learning disabilities are associated with brain dysfunctions that affect a number of basic skills. Perhaps the most fundamental is sensory-perceptual ability—the capacity to take in and process information through the senses. Difficulties involving vision , hearing , and touch will have an adverse effect on learning. Although learning is usually considered a mental rather than a physical pursuit, it involves motor skills, and it can also be impaired by problems with motor development. Other basic skills fundamental to learning include memory , attention, and language abilities.
The three most common academic skill areas affected by learning disabilities are reading, writing, and arithmetic. Some sources estimate that between 60-80% of children diagnosed with learning disabilities have reading as their only or main problem area. Learning disabilities involving reading have traditionally been known as dyslexia ; currently the preferred term is developmental reading disorder . A wide array of problems is associated with reading disorders, including difficulty identifying groups of letters, problems relating letters to sounds, reversals and other errors involving letter position, chaotic spelling, trouble with syllabication, failure to recognize words, hesitant oral reading, and word-by-word rather than contextual reading. Writing disabilities, known as dysgraphia, include problems with letter formation and writing layout on the page, repetitions and omissions, punctuation and capitalization errors, "mirror writing," and a variety of spelling problems. Children with dysgraphia typically labor at written work much longer than their classmates, only to produce large, uneven writing that would be appropriate for a much younger child. Learning abilities involving math skills, generally referred to as dyscalcula (or dyscalculia), usually become apparent later than reading and writing problems—often at about the age of eight. Children with dyscalcula may have trouble counting, reading and writing numbers, understanding basic math concepts, mastering calculations, and measuring. This type of disability may also involve problems with nonverbal learning, including spatial organization.
Treatment
The principal forms of treatment for learning disabilities are remedial education and psychotherapy . Either may be provided alone, the two may be provided simultaneously, or one may follow the other. Schools are required by law to provide specialized instruction for
children with learning disabilities. Remediation may take place privately with a tutor or in a school resource center. A remediator works with the child individually, often devising strategies to circumvent the barriers caused by the disability. A child with dyscalcula, for example, may be shown a "shortcut" or "trick" that involves memorizing a spatial pattern or design and then superimposing it on calculations of a specific type, such as double-digit multiplication problems. The most important aspect of remediation is finding new ways to solve old problems. In this respect, remediation diverges from ordinary tutoring methods that use drill and repetition, which are ineffective in dealing with learning disabilities. The earlier remediation is begun, the more effective it will be. At the same time that they are receiving remedial help, children with learning disabilities spend as much time as possible in the regular classroom.
While remediation addresses the obstacles created by the learning disability itself, psychotherapy deals with the emotional and behavioral problems associated with the condition. The difficulties caused by learning disabilities are bound to affect a child's emotional state and behavior. The inability to succeed at tasks that pose no unusual problems for one's peers creates a variety of unpleasant feelings, including shame, doubt, embarrassment, frustration, anger, confusion, fear , and sadness. These feelings pose several dangers if they are allowed to persist over time. First, they may aggravate the disability: excessive stress can interfere with the performance of many tasks, especially those that are difficult to begin with. In addition, other, previously developed abilities may suffer as well, further eroding the child's self-confidence. Finally, destructive emotional and behavioral patterns that begin in response to a learning disability may become entrenched and extend to other areas of a child's life. Both psychoanalytic and behaviorally oriented methods are used in therapy for children with learning disabilities.
The sensitivity developed over the past two decades to the needs of students with learning disabilities has extended to adults as well in some sectors. Some learning disabled adults have been accommodated by special measures such as extra time on projects at work. They may also be assigned tasks that does not require a lot of written communication. For example, a learning disabled person might take customer service phone calls, rather than reading and processing customer comment cards.
Because there is no "cure" for learning disability, it will continue to affect the lives of learning-disabled people, and the strategies they may have learned to succeed in school must also be applied in their vocation.
Further Reading
Tuttle, Cheryl Gerson, and Gerald A. Tuttle, eds. Challenging Voices: Writings By, For, and About People with Learning Disabilities. Los Angeles: Lowell House, 1995.
Wong, Y.L., ed. Learning About Learning Disabilities. San Diego: Academic Press, 1991.
Further Information
Association for Children and Adults with Learning Disabilities. 4900 Girard Rd., Pittsburgh, PA 15227–1444, (412) 881–2253.
National Center for Learning Disabilities. 99 Park Ave., New York, NY 10016, (212) 687–7211.
learning disabilities
According to Galen, the supreme medical authority before modern times, human reason was activated by ‘animal spirits’ which moved around the brain and, if sluggish, caused amentia (mindlessness); however, any normal individual could experience this condition temporarily. Sometimes a landowner's heir might suffer from congenital incompetence, but this was a problem for lawyers, not doctors; it was not distinguished from the assumed incompetence of the entire labouring population, and where people did not own property there was no problem. Nor was congenital incompetence necessarily permanent: God might cure it providentially. People whom we might now call ‘learning disabled’ were depicted by artists; but neither their behavioural gestures and bodily features, nor their social role, were clearly distinct from those of jesters and professional fools whose minds were perfectly sound. Medical writers did not research the causes of mental (or physical) monstrosity, since these were God's responsibility; rather, monstrosity demonstrated His marvellous creative powers. Only mavericks among them, such as astrologers or followers of the derided Paracelsus, had a specifically medical interest in connections between the body and permanent lack of reason. Even for them, reason tended to mean divine illumination rather than the personal mental equipment described by modern psychology.
In the seventeenth-century roots of that psychology we begin to find a learning disabled type recognizable to ourselves, defined by the purely mental characteristics of an individual. The influential philosopher John Locke summarized these as a lack of ability to think ‘abstractly’, and psychology has refined this picture very little since then. However, the approach to physiological phenomena associated with ‘idiocy’ (as it was then technically known) has changed frequently. These changes have social and political connections. Locke was also a leading Whig theoretician, and saw idiots as people who lacked the mental equipment needed to exercise their individual autonomy, the basis of the new Whig political philosophy of government by consent. As a medical practitioner himself, he thought this lack might be caused by their having different bodily mechanisms. He did not investigate further, possibly because the discipline of anatomy was controlled by his political opponents. His Tory contemporary, Thomas Willis, believed there was an anatomical distinction between the brains of ‘stupid’ and ‘mad’ people, although he also continued to believe Galen's hypothesis of slow-moving ‘animal spirits’. Descartes's discussion of the mind (one of the sources for modern accounts of a distinctly human psychology) located the reasoning soul in the pineal gland, which previously had been merely a valve controlling the flow of animal spirits. Anatomists under Descartes's influence, dissecting the corpses of mad people and idiots, claimed that the former possessed excessively flexible pineal glands, the latter excessively rigid ones.
Eighteenth-century medical theorists opened up an empire of the mind, developing psychological classifications in terms similar to those of bodily disease. At the same time their interest in the physiology of idiots largely reverted to external characteristics, particularly facial features (physiognomics) and skull shape (phrenology). In the mid nineteenth century, with the rise of colonialism and anthropology, theories of idiocy and race were united. The mental characteristics of idiots were identified with the alleged psychological inabilities and corresponding external physical characteristics of non-whites. Fetal development was thought to retrace the primitive stages of human history which the non-white races still exhibited; sometimes development was arrested, a notion embodied in the ‘mongol’, whose facial features apparently betrayed a low level of psychological competence comparable with that of the mongoloid races. Segregated institutions and then sterilization programmes arose from this culture, with the aim of improving the health of the race. Administered largely by practitioners of physical medicine, they appeared first in the Anglo-Saxon countries; in Germany the same culture led to mass exterminations of learning disabled people at the end of the 1930s.
Since then a rapid refinement in the diagnostic technology of chromosomes and genes has renewed our interest in internal bodily causes. There has been a correspondingly rapid increase in the number of psychological labels attached to syndromes (e.g. ‘fragile X’); the human genome project now promises to locate DNA markers for the lower band of a socially determined ‘normal IQ’. This profusion of learning disabled conditions has interacted with rapid changes in their social status and acceptance. Pathology advances in some directions while retreating in others. At the time of writing, for example, genetically-related autism has fanned out into an autistic ‘spectrum’, annexing and reinventing ‘Asperger's syndrome’ as a mild variant which may affect the apparently normal population. Its socially segregating effects are inseparable from the diagnosis itself, by which autistic people are said to belong mentally in a separate world from others; this notion reinforces a separate professional specialization, creating more research and labelling. In a simultaneous but contrary tendency, numbers of prospective parents reject termination after a positive test for Down's syndrome, partly because children and young adults with this condition have become increasingly integrated in the community.
People began by wanting a physical diagnosis of learning disability, for various religious and political reasons, in the seventeenth century when biochemistry was inconceivable. But whatever the precision of today's diagnostic techniques in this respect, it has not been matched, either in psychology or in cognitive and behavioural genetics, by a corresponding precision in the diagnosis and description of the ‘mental’ aspects; these remain as fluid and subject to social context as ever.
Christopher Goodey
Bibliography
Wright, D. and and Digby, A. (1996). From idiocy to mental deficiency: historical perspectives on people with learning disabilities. London.
Trent, J. (1994). Inventing the feeble mind: a history of mental retardation in the United States. Berkeley.
See also intelligence.
learning disability
learn·ing dis·a·bil·i·ty • n. a condition giving rise to difficulties in acquiring knowledge and skills to the level expected of those of the same age, esp. when not associated with a physical handicap.DERIVATIVES: learn·ing-dis·a·bled adj.
learning disability
learning disability
www.bild.org.uk Website of the British Institute for Learning Disabilities