Pediatric Annals

Theories About the Causes of Dyslexia and Their Implications

Drake D Duane, MD

Abstract

There are two basic reasons why the pediatrician who evaluates and treats patients with developmental dyslexia should be familiar with the purported etiologic factors in specific written-language underachievement. First, the causes proposed will influence the manner in which evaluation and therapy are carried out. Second, familiarity with the suggested etiologic concepts and treatments is necessary so that the questions apt to be raised by the patient and the parents can be answered.

The physician should bear in mind that no single etiologic concept has satisfactorily explained the cause of developmental dyslexia or of the more heterogeneous group of disorders referred to as minimal brain dysfunction. (The former may be less heterogeneous than the latter, but it is not likely to be homogeneous.) It is probable, however, that the more precisely the group in question can be characterized behaviorally, the greater is the likelihood that the cause will be well defined. Yet highly speculative and untraditional explanations are being offered for a poorly defined group of children with behaviors assumed to be pertinent to scholastic underachievement. The physician should remain cognizant that although his or her training has emphasized the detection of cause as being important to the natural history of, and the form of remediation for, a disorder, it has generally not been accepted within the educational establishment as being pertinent to the development of remedial techniques.

The major etiologic factors proposed as germane to the clinical expression of developmental dyslexia are listed in Table 1 . Overlapping detailed surveys have been provided by Benton,1 Duane,2 and Silver3 and in the papers emanating from the conference on minimal brain dysfunction held by the New York Academy of Sciences.4 In assessing the various causes that have been proposed, one should bear in mind that more than one factor may play a role in a given case, and one mechanism need not exclude another.

Two broad subcategorizations of these suggested causes may be made. First, there is separation into acquired versus genetic mechanisms. Even here, one must remain cognizant that environmental factors do not operate independently of the genetic substrate. Also, the physician should be reminded that the term "genetic" implies biologic cellular mechanisms that may be hereditary (familial). That genetic factors should be taken into account is based on the frequent clinical observation, particularly with patients who have specific reading retardation, that other members of the family are similarly affected.

Table

Such complications of pregnancy and early childhood illness are known to place the child at risk for the development of clear-cut neurologic syndromes, and some children with reading underachievement may have undergone a potentially significant experience; the possibility that such traumatic insults to the central nervous system are causally related to the school failure has been raised.32 However, with regard to circumscribed academic underachievement, such factors have been shown to be insufficiently frequent to provide an etiologic explanation for most dyslexia.33,34

Brain-stem, oculomotor theories. A variety of theories propose that impaired performance is due to deficits in presumed developmentally and hierarchically essential reflexes and "perceptual" competencies.35"37 These theories imply deficits at the brain-stem level or in the oculomotor system. Each such concept is associated with a remediation technique that is controversial and may be encompassed by the term neurophysiology retraining. Such approaches as patterning, developmental optometry, and sensory integrative therapy lack objective scientific support of their therapeutic worth. Each has been carefully reviewed and discredited by Silver.3 The alleged applicability of such therapies to diverse learning disorders and their lack of an active language component weaken their justification in the therapy of the developmental dyslexic.

Cerebellar theory. Another notion -…

There are two basic reasons why the pediatrician who evaluates and treats patients with developmental dyslexia should be familiar with the purported etiologic factors in specific written-language underachievement. First, the causes proposed will influence the manner in which evaluation and therapy are carried out. Second, familiarity with the suggested etiologic concepts and treatments is necessary so that the questions apt to be raised by the patient and the parents can be answered.

The physician should bear in mind that no single etiologic concept has satisfactorily explained the cause of developmental dyslexia or of the more heterogeneous group of disorders referred to as minimal brain dysfunction. (The former may be less heterogeneous than the latter, but it is not likely to be homogeneous.) It is probable, however, that the more precisely the group in question can be characterized behaviorally, the greater is the likelihood that the cause will be well defined. Yet highly speculative and untraditional explanations are being offered for a poorly defined group of children with behaviors assumed to be pertinent to scholastic underachievement. The physician should remain cognizant that although his or her training has emphasized the detection of cause as being important to the natural history of, and the form of remediation for, a disorder, it has generally not been accepted within the educational establishment as being pertinent to the development of remedial techniques.

The major etiologic factors proposed as germane to the clinical expression of developmental dyslexia are listed in Table 1 . Overlapping detailed surveys have been provided by Benton,1 Duane,2 and Silver3 and in the papers emanating from the conference on minimal brain dysfunction held by the New York Academy of Sciences.4 In assessing the various causes that have been proposed, one should bear in mind that more than one factor may play a role in a given case, and one mechanism need not exclude another.

Two broad subcategorizations of these suggested causes may be made. First, there is separation into acquired versus genetic mechanisms. Even here, one must remain cognizant that environmental factors do not operate independently of the genetic substrate. Also, the physician should be reminded that the term "genetic" implies biologic cellular mechanisms that may be hereditary (familial). That genetic factors should be taken into account is based on the frequent clinical observation, particularly with patients who have specific reading retardation, that other members of the family are similarly affected.

Table

TABLE 1PROPOSED CAUSES OF DEVELOPMENTAL DYSLEXIA

TABLE 1

PROPOSED CAUSES OF DEVELOPMENTAL DYSLEXIA

SUGGESTED GENETIC CAUSES

The outstanding studies of the genetics of specific reading retardation are those of Hallgren5 and Finucci et al.6 In the latter, more recent study, 45 per cent of first-degree relatives were affected by some manifestation of reading disability; the general clinical experience that males are predominantly affected was confirmed, but no single mode of genetic transmission was evident. These findings suggested genetic heterogeneity. Twin studies of reading disability further support a genetic hereditary factor.7 To this date, there remains no simple explanation for the threefold to fivefold higher frequency of occurrence of specific reading retardation in males than in females. The sex disparity cannot be explained on the basis of differential rates of maturation, for the ratio appears to be approximately the same in students of older age and among adults. An excellent review of the literature regarding genetic factors of dyslexia has recently been provided by Finucci.8

SUGGESTED ORGANIC CAUSES

The second major subclassification of proposed causes is divided into those having to do with focal or localized alteration in central nervous system function and those concerned with general brain organization, particularly regarding hemispheric specialization or lack thereof. Some theoretical constructs do not specify the site(s), but they still imply focal, multifocal, or diffuse central nervous system alteration.

One approach to constitutional reading disorders has been to use the analogy of acquired dyslexia in the adult. This has limitations in that the loss of previously acquired functions in the adult is not comparable with the situation of evolving functions within the developing nervous system.9,10 Acquired lesions that produce dyslexia with or without dysgraphia are almost invariably in the left parietal region.

Figure 1 demonstrates a computerized tomography scan of the head with such a lesion due to metastatic carcinoma from the lung in which dyslexia, dysgraphia, and right homonymous hemianopia were manifest. Theoretically, early injury, malformation, or alteration in physiologic function of that region might explain impaired acquisition of reading skill. Figure 2 illustrates a case of an adult dyslexic patient with partial compensation who deteriorated in written-language performance after an infarct in the left parietooccipital region; this suggests that compensation by the individual was in part dependent upon the integrity of the left posterior cerebral structure and its presumed function.

Recent studies of spectral analysis of electroencephalograms,11 and many studies of visual evoked responses of individuals and family members with specific reading retardation, have raised questions regarding intrahemispheric differences in amplitude.12"14 However, visual evoked responses in disabled readers have been shown to be bilaterally reduced in some instances;13 in another study they were found not to be significantly different from those in controls.15 Therefore, these studies provide tantalizing reinforcement of the concept of alteration in central nervous system function in the dyslexic but require further analysis before their true significance can be appreciated.16 Furthermore, should these visual evoked asymmetries in response be verified, the mechanism of their appearance (maturational, due to injury, genetic, or biochemical) will remain to be defined.

The concept that impaired development of cerebral dominance might be a factor in developmental dyslexia was introduced by Orton.17 This theory applies to a general alteration in the organization of cerebral function. Struck by the firequency of directional errors in the reading and writing of dyslexic children, along with the frequency of left-handedness, ambidexterity, and mixed laterality (alone or in combination), Orton suggested that the usual course of language development involved bilaterality of language representation, which becomes lateralized to the left hemisphere, and that such lateralization is defective in the dyslexic. Thus, there is presumed to be inefficient suppression of the right hemisphere by the left; this results in competing mirror images within the central nervous system, explaining the clinical observations he made.

Figure 1. Computerized tomography scan of the head with contrast in a right-handed 62-year-old man, showing left parietal metastatic carcinoma. Patient demonstrated recent dyslexia, dysgraphia, and right homonymous hemianopia.

Figure 1. Computerized tomography scan of the head with contrast in a right-handed 62-year-old man, showing left parietal metastatic carcinoma. Patient demonstrated recent dyslexia, dysgraphia, and right homonymous hemianopia.

Figure 2. Computerized tomography scan of the head in a right-handed 47-year-old man, demonstrating a left parietooccipital infarct. This patient probably suffered from developmental dyslexia before the infarct and before this event had deficient written-language performance, which declined further after the cerebral-vascular occlusion.

Figure 2. Computerized tomography scan of the head in a right-handed 47-year-old man, demonstrating a left parietooccipital infarct. This patient probably suffered from developmental dyslexia before the infarct and before this event had deficient written-language performance, which declined further after the cerebral-vascular occlusion.

Although the incidence of left-handedness is higher in the dyslexic than in the general population, and mixed laterality is not uncommonly observed in dyslexies, this cannot be proved as being causal, for groups of children selected for mixed laterality show no higher incidence of reading retardation.18

One could construe the derived electroencephalographic studies referred to above as supportive of Orton's hypothesis of a physiologic basis; or future anatomic studies of the planum temporale and other regions of the brain could demonstrate patterns of asymmetry at variance from those observed in the general population.19,20 Indeed, recent studies using computerized tomography of the head have suggested a subgroup in which there is a reversal of the usual pattern of cerebral asymmetry as ascertained by that procedure.21 (Figure 3).

Witelson,22 using neuropsychologic techniques in the assessment of hemispheric specialization, has suggested that developmental dyslexies may be characterized as possessing bihemispheric representation of spatial functions and typical left hemispheric representation of linguistic function, resulting in a spatial-holistic cognitive reading strategy. This hemispheric organization is presumed to be inefficient in the acquisition of reading skills for phonetically coded languages, such as English. However, the same author has described similar behaviors in girls with normal reading, and she suggests that dyslexic boys may have a deficient left hemisphere. This would imply that dyslexia in girls is the result of a different and unexplained mechanism. Although this is possible, the observation would seem to weaken the original postulate.

Cortical theories. Since the language behaviors in persons with developmental dyslexia are similar to those observed in supposedly normal children of younger chronologic age, the possibility of a delay in the maturation of specific cortical association areas has been proposed.23,24 Presumably, the neurodevelopmental lag has its basis in the rate of myelination, synaptic growth, or neurohumoral transmitter concentration delay. The concomitance of relative immaturity in spatial functions and in finger localization is regarded as supportive evidence and appears to be of some value in identifying the child who is at risk for reading failure.25 Furthermore, authors who were formerly convinced that this disorder was an acquired, pure syndrome appear to have accepted this concept.26'27

Figure 3. Computerized tomography scans of the head of two dyslexic patients. On the left is the usual pattern, in which the left posterior region of the head is wider than the right. Illustration on right shows that in another dyslexic person the right parieto-occipital region is wider than the left; this is referred to as reversal of asymmetry. This reversal of asymmetry was seen in a higher proportion of dyslexic patients in the study than would be expected by chance. (Reproduced by permission from Hier, D. B., et al.21)

Figure 3. Computerized tomography scans of the head of two dyslexic patients. On the left is the usual pattern, in which the left posterior region of the head is wider than the right. Illustration on right shows that in another dyslexic person the right parieto-occipital region is wider than the left; this is referred to as reversal of asymmetry. This reversal of asymmetry was seen in a higher proportion of dyslexic patients in the study than would be expected by chance. (Reproduced by permission from Hier, D. B., et al.21)

This descriptively sound view should not, however, be carried to the extreme conclusion that the discrepant behavior will correct itself with passage of time alone. Even with remediation, most patients with moderate to severe dyslexia continue to have impaired spelling performance into adulthood. Years of reading failure invariably have an adverse effect on personal adjustment of the disabled reader, with further complications in educational growth.28 Figure 4 illustrates persistent written-language impairment in an adult who has eluded remediation. In contrast to concepts concerning brain damage, the theory of a delay in maturation reinforces the possibility of improved function.29

In an era of expanding knowledge about the biochemical events within the central nervous system and their clinical pertinence to parkinsonism and the affective disorders, one could have expected theories invoking biochemical factors in disorders of academic behavior.30 Such concepts have been applied to the heterogeneous category of minimal brain dysfunction, including hyperkinesis, but less frequently to the more restricted category of developmental dyslexia.27,30,31 When disturbances of behavior and attention respond to pharmacologic treatment, neurochemical postulates are not unreasonable. However, such favorable results appear to be obtained through reduction in the interference with academic achievement imposed by impulsiveness and reduced attention rather than through effects on the mechanisms underlying reading or learning in general.

Figure 4. Writing spontaneously (top line) and to dictation (below) by a 34-year-old left-handed dyslexic man of aboveaverage intelligence and good oral fluency Top line: "is the can good or is the can bad." Second line, as dictated, was: "The phenomenon was alleged to represent the activities of a UFO.''

Figure 4. Writing spontaneously (top line) and to dictation (below) by a 34-year-old left-handed dyslexic man of aboveaverage intelligence and good oral fluency Top line: "is the can good or is the can bad." Second line, as dictated, was: "The phenomenon was alleged to represent the activities of a UFO.''

Such complications of pregnancy and early childhood illness are known to place the child at risk for the development of clear-cut neurologic syndromes, and some children with reading underachievement may have undergone a potentially significant experience; the possibility that such traumatic insults to the central nervous system are causally related to the school failure has been raised.32 However, with regard to circumscribed academic underachievement, such factors have been shown to be insufficiently frequent to provide an etiologic explanation for most dyslexia.33,34

Brain-stem, oculomotor theories. A variety of theories propose that impaired performance is due to deficits in presumed developmentally and hierarchically essential reflexes and "perceptual" competencies.35"37 These theories imply deficits at the brain-stem level or in the oculomotor system. Each such concept is associated with a remediation technique that is controversial and may be encompassed by the term neurophysiology retraining. Such approaches as patterning, developmental optometry, and sensory integrative therapy lack objective scientific support of their therapeutic worth. Each has been carefully reviewed and discredited by Silver.3 The alleged applicability of such therapies to diverse learning disorders and their lack of an active language component weaken their justification in the therapy of the developmental dyslexic.

Cerebellar theory. Another notion - that dyslexia emanates from brain-stem and cerebellar dysfunction - has been put foward.38 I have heard that for such cases, medications used for vestibular dysfunction or in the prevention of seasickness, such as dimenhydrinate (Dramamine), have been suggested. I am not aware of any objective scientific evidence that indicates that either the theory or this form of treatment has any merit.

SUGGESTED ENVIRONMENTAL CAUSES

In an era in which our society is inspecting environmental pollutants carefully, it is perhaps not surprising that such factors as lead,39 fluorescent lighting,40, and food additives41 have been implicated in academic underachievement. However, such proposals, although appealing to the public because of their simplicity, remain unsubstantiated. Also, these theories are directed at a diverse population of school-age children, and this makes it difficult to determine whether they have applicability to any given segment of the population. The most carefully conceived study of the potential relationship of food additives to hyperkinesis showed little favorable effect on this behavior. At best, therefore, this factor should be construed as being peripheral to the basic problem of the retarded reader.42

Finally, it is clear that basic nutritional needs must be met for normal prenatal and postnatal central nervous system development.43 However, this scientifically sound observation has been perverted by the proposition that essential vitamins may be needed in massive doses, that trace elements may be deficient, and that hypoglycemia is a common cause of, and its correction a necessary form of remediation for, an ill-defined population of academic underachieve«.44 Again, scientific verification is lacking for this proposition,3 and the physician would do well for the patient and his family to sound a note of caution regarding such therapies. However, a five-hour glucose-tolerance test can clarify the question when the family seeks specific reassurance regarding hypoglycemia.

CONCLUSION

The refined diagnostic category of developmental dyslexia is best conceived of as a constitutional variance in the development of specific language skills; it represents a delay in development in contrast to the patient's chronologic peers and is often under polygenetic influence. Contemporary neurologic research continues to suggest that there are central nervous system concomitants to the disorder, but the specifics of that relationship remain elusive.

The most appropriate therapy is specific educational remediation. The physician acts as an informational resource for the school and family; stimulates the development of appropriate educational alternatives within his community; provides informal and formal emotional support; and, when poor impulse control and reduced attention act as impediments to effective educational remediation, supervises the use of the necessary medication.

BIBLIOGRAPHY

1. Benton, A. L. Developmental dyslexia: Neurological aspects. Adv. Neurol. 7 (1975), 1-47.

2. Duane, D. D. A neurologic overview of specific language disability for the non- neurologist. BuI/. Orton Soc. 24 (1974), 5-36.

3. Silver, L. B. Acceptable and controversial approaches to treating the child with learning disabilities. Pediatrics 55 (1975), 406-415.

4. De Ia Cruz, F. F., Fox. B. H., and Roberts, R. H. (eds.). Minimal brain dysfunction. Ann. N. Y. Acad. Sci. 205 (1973), 1-396.

5. Hallgren, B. Specific dyslexia ("congenital word-blindness"): A clinical and genetic study. Acta Psychiatr. Neurol. (Suppl. 65, 1950), 1-287.

6. Finucci, J. M., et al. The genetics of specific reading disability. Ann. Hum. Genet. 40 (1976), 1-23.

7. Zerbin-Rudin, E. Kongenitale Wortblindheit oder spezifische Dyslexie (congenital word-blindness) (Vandenberg, S. G., transi.). Bull Orton. Soc. 17 (1967), 47-54.

8. Finucci, ). M. Genetic considerations in dyslexia. In Myklebust, H R. (ed.). Prioress in Learning Disabilities, Volume 4. New York: Grune & Stratton, 1978, pp. 41-63.

9. Hinshelwood, J. Congenital word-blindness. Lancet 1 (1900), 1506-1508.

10. Geschwind, N. Disconnexion syndromes in animals and man. Brain 88 (1965), 237-294, 585-644.

11. Sklar, B., Hartley, }., and Simmons, W. W. An EEG experiment aimed toward identifying dyslexic children (letter to the editor). Nature 240 (1972), 414-416.

12. Conners, C. K. Cortical visual evoked response in children with learning disorders. Psychophysiology 7 (1970), 418-428.

13. Symann-Louett, N., Gascon, G. G., Matsumiya, Y., and Lombroso, C. T. Wave form difference in visual evoked responses between normal and reading-disabled children. Neurology 27 (1977), 156-159.

14. Preston, M. S., Guthrie, J. T., and Childs, B. Visual evoked responses (VERs) in normal and disabled readers. Psychophysiology 11 (1974), 452-457.

15. Weber, B. A., and Omenn, G. S. Auditory and visual evoked responses in children with familial reading disabilities. /. Learn. Disotti. 10 (1977) 153-158.

16. Duane, D. D. Toward the démystification of the clinical electroencephalogram. In Cruickshank, W. M., Lerner, I., Silver, A., and Tash, E. (eds.). Proceedings of the 1979 International Conference of the Association for Children With Learning Disabilities. Syracuse, N. Y.: Syracuse University Press (in press).

17. Orton, S. T. Reading, Writing, and Speech Problems in Children. New York: W. W. Norton & Company, 1937.

18. Belmont, L., and Birch, H. G. Lateral dominance, lateral awareness, and reading disability. CWM. Dev. 36 (1965), 57-71.

19. Geschwind, N., and Levitsky, W. Human brain: left-right asymmetries in temporal speech region. Science 161 (1968), 186-187.

20. Witelson, S. F., and Pallie, W. Left hemisphere specialization for language in the newborn: Neuroanatomical evidence of asymmetry. Brain % (1973), 641-646.

21. Hier, D. B., LeMay, M., Rosenberger, P. B.. and Perlo, V. P. Developmental dyslexia: Evidence for a subgroup with a reversal of cerebral asymmetry. Ardi. Neurol. 35 (1978), 90-92.

22. Witelson, S. F. Developmental dyslexia: Two right hemispheres and none left. Science 195 (1977), 309-311.

23. Kinsbourne, M., and Warrington, E. K. Developmental factors in reading and writing backwardness. Br. /. Psychol. 54 (1963), 145156.

24. Satz, P., and Sparrow, S. Dyslexia, laterality and neuropsychological development. In Bakker, D. I., and Satz, P. (eds.). Specific Reading Disability: Advances in Theory and Method. Rotterdam: Rotterdam University Press, 1970, pp. 69-80.

25. Satz, P., Friel, J., and Goebel, R. A. Some predictive antecedents of specific reading disability: A three-year follow-up. Bull. Orton Soc. 25 (1975). 91-110.

26. Thompson, L. J. Learning disabilities: An overview. Am. J. Psychiatry 130 (1973), 393-399.

27. Critchley, M. Developmental dyslexia: Its history, nature and prospects. In Duane, D. D., and Rawson, M. B. (eds.). Reading, Perception and Language. Baltimore: York Press, 1975, pp. 9-14.

28. Eisenberg, L. Psychiatric aspects of language disability. In Duane, D. D., and Rawson, M. B. (eds). Reading, Perception and Language. Baltimore: York Press, 1975, pp. 215-229.

29. Kinsbourne, M. Models of learning disability: Their relevance to remediation. Can Med. Assoc. J. 113 (1975),1066-1067, 1069.

30. Wender, P. H. The minimal brain dysfunction syndrome in children. 1: The syndrome and its relevance for psychiatry. ?: A psychological and biochemical model for the syndrome. J. Nerv. Ment. Dis. 155 (1972), 55-71.

31. Silver, L. B. A proposed view on the etiology of the neurological learning disability syndrome. J. Learn. Disabil. 4 (1971), 123-133.

32. Kawi, A. A., and Pasamanick, B. Association of factors of pregnancy with reading disorders in childhood. J.A.M.A. 166 (1958), 1420-1423.

33. Ingram, T. T. S., Mason, A. W., and Blackburn, I. A retrospective study of 82 children with reading disability. Dev. Med. CWM Neurol. 12 (1970), 271-281.

34. Rutter, M., Tizard, J., and Whitmore. K. Education, Health and Behaviour: Psychological and Medical Study of Childhood Development. New York: John Wiley & Sons, 1970.

35. Doman, C, and Delacato, C. Learning and human achievement Philosophy and concepts. Hum. Potential 1 (1968), 113-120.

36. Flax, N. The eye and learning disabilities. /. Learn. Disabil. 6 (1973), 328-333.

37. Ayres, A. J. Deficits in sensory integration in educationally handicapped children. /. Learn. Disabil. 2 (1969), 160-168.

38. Frank, }., and Levinson, H. Dysmetric dyslexia and dyspraxia: Hypothesis and study. /. Am. Acad. Child Psychiatry 12 (1973), 690701.

39. David, O., dark, ]., and Voeller, K. Lead and hyperactivity. Lancet 2 (1972), 900-903.

40. Ott, ]. N. Influence of fluorescent lights on hyperactivity and learning disabilities. J. Learn. Disabil. 9 (1976), 417-422.

41. Feingold, B. F. Why Your Child Is Hyperactive. New York: Random House, 1975.

42. Harley, ). P. Diet and behavior in hyperactive children: Testing the Feingold hypothesis. Read at the meeting of the American Psychological Association, Washington, D.C., September 3-7, 1976.

43. Winick, M., and Rosso, P. The effect of severe early malnutrition on cellular growth of human brain. Pediatr. Res. 3 (1969), 181.

44. Cott, A. The orthornoiecular approach to behavioral disorders and learning disabilities. Acad. Ther. 7 (1972), 245-258.

TABLE 1

PROPOSED CAUSES OF DEVELOPMENTAL DYSLEXIA

10.3928/0090-4481-19791101-06

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