Dyslexia: A Cognitive Neuroscience Approach Rod Nicolson

1. 1 Dyslexia: A Cognitive Neuroscience ApproachRod Nicolson Dyslexia: Definition & Theories Phonological Deficit Hypothesis Double Deficit Hypothesis 2. Key Questions for Dyslexia research 3. The Magnocellular Deficit Hypothesis 4. Nicolson/Fawcett Research Programme Automaticity Deficit Hypothesis Cerebellar Deficit Hypothesis 5. Initial Answers 6. The way forward Acknowledgements Angela Fawcett, Paul Dean

2. 2 Definitions � Reading performance that is markedly below what is expected, based on a person's intelligence.� � �a disorder in children who, despite conventional classroom experience, fail to attain the language skills of reading, writing and spelling commensurate with their intellectual abilities�. World Federation of Neurology (1968) � an �enigma� � a mess fail for two years before diagnosis possible... �You taught him to read Jean, so he can�t be dyslexic�� Symptom not cause

3. 3 Reasons for high interest in dyslexia high incidence in Western populations (~5% is a typical estimate, Badian, 1984; Jorm et al, 86) high financial stakes (statutory requirement in many Western countries to provide educational support for children with dyslexia). Challenging paradox to a wide variety of researchers � why do these articulate, intelligent people show such a problem in one of our most routine skills? �> Continuing high international public profile e.g. US NICHD (National Institute of Child Health and Human Development) dyslexia funding now ~ $15m p.a.

4. 4 1. The Phonological Deficit Hypothesis The reading difficulties are attributable to problems in phonological processing, that is breaking a word down into its constituent sounds. These difficulties cause problems in sound segmentation and also in word blending, both of which are critical for development of reading and spelling. Lundberg, Olofsson & Wall (1980); Bradley and Bryant (1983), Lundberg & H�ien (1989) Kindergarten children with poor phonological awareness later develop reading difficulties Support [specifically] with phonological awareness at kindergarten reduces the subsequent reading difficulties

5. 5 The phonological core deficit Stanovich (1988). �Phonological core, variable difference� model one key to fluent reading is the development of an autonomously functioning module at the word recognition level � failure to develop such a module may derive from impairments in phonological processing

6. 6 Unresolved issues for P.D.H Diagnosis Phonological skills are learned, or, failing that, they may be taught following appropriate support, a dyslexic child should be able to overcome his/her phonological and reading difficulties to the extent that he/she is no longer diagnosable as dyslexic. Theory Slow learners show equal or greater phonological difficulties. This finding has led some researchers (Shaywitz, Stanovich) to argue that distinction between the two groups is counter-productive. What causes the phonological deficits!?

7. 7 2. The Double Deficit Hypothesis (eg. Wolf & Bowers, 1997) Wolf and Bowers argue that dyslexic children suffer from two crucial deficits: (i) Phonological processing problems (ii) Rapid processing problems and provide strong evidence that if a child suffers from both problems (as indicated by difficulties say on segmentation [phonology] and rapid naming [speed], his/her educational outlook is significantly worse than a child suffering from only one deficit [though they will also have a worse outlook than a child suffering from neither].

8. 8 Reading with brief presentationYap & van der Leij (1993) U: stimulus present until responded S: stimulus shown for only 200 ms Even when matched for reading age, dyslexic children have particular difficulty with nonwords presented for a brief period.

9. 9 3. Magnocellular Deficit Hypotheses (i) there are difficulties in processing rapidly changing visual stimuli (Lovegrove) or auditory stimuli (Tallal) (ii) Galaburda & colleagues have demonstrated that analysis of brains in the Orton dyslexia �brain bank� indicates significantly fewer magnocells in the visual and auditory pathways (iii) Eden (96) demonstrated that dyslexic children had reduced activation in area V5 (MT) [magnocellular area] in response to slowly moving targets. Other researchers (Cornelissen, Talcott) have also demonstrated abnormal visual processing. Hence, Tallal and Stein argue, independently, that dyslexic children have abnormal magnocellular pathways, and that this causes the reading problems.

10. 10 4. The Automatisation Deficit Hypothesis Nicolson and Fawcett (1990) argue that the concept of an �automatisation deficit� provides a coherent framework for the explanation of the range of problems shown by dyslexic children. Dyslexic children will have difficulties on any task that requires automatisation of skill. Even on task where they appear to be performing normally they have to try harder to achieve the same results.

11. 11 5. The Cerebellar Deficit Hypothesis Early research (Denckla and Rudel) suggested that dyslexic children showed a range of �soft neurological signs�. These are consistent with cerebellar abnormality, but these researchers repudiated this theory as proposed by Levinson (1973). Recent research by Nicolson, Fawcett and Dean on cerebellar function in dyslexia suggested that, after all, the cerebellum may be an underlying causal factor.

12. 12 Questions How different are these theories? Is this like the four men and the elephant? How do we characterise a theory and an explanation? Answer: (i) Different theories are at different levels of explanation (ii) The type of explanation that is most valuable depends upon the question you are asking! (iii) It may be that different dyslexic children suffer from different underlying causes.

13. 13 Key Questions for Dyslexia Research Q1. What is the underlying cause? Q2. Why does it appear specific to reading? Q3. Why are some dyslexic people high achievers? Q4. How can we identify dyslexia before a child fails to learn to read? Q5. Do we need different methods to teach dyslexic children? If so, what? Q6. What are the policy implications? Q7. Why is it all so controversial? Q8. What should we do next?

14. 14 Stages in Scientific Explanation 1. Description - Read, Observe, Listen, Analyse - Avoid premature commitment 2. Quantification - Measurement, Comparison 3. Theory Creation - level, completeness, scope 4. Theory testing - data, fruitfulness, testability 5. Theory refinement 6. Control

15. 15 Levels of Analysis

16. 16 The Target Causal Analysis � a true causal theory of dyslexia should explain not only the symptoms but also the underlying cause of the symptoms.

17. 17 Levels of the theories Phonological Cognitive Magnocellular Brain Double Deficit Cognitive Automatisation Cognitive Cerebellum Brain But: the same brain mechanism can cause a range of cognitive difficulties And: the same cognitive difficulties may arise from different brain mechanisms

18. 18 Stage 1: Description 1. Read Language-based theories (phonology). NICHD. Vision-based theories Sensory processing theories 2. Observe Not noticeably different in any skills, but subtle difficulties in many 3. Listen Dexterity, working memory, developmental delay Trauma

19. 19 The Magnocellular deficit hypothesis Early work by Tallal & Piercy. The SLI children�s performance broke down when the interval between stimuli was reduced to 350 ms, whereas the controls performed well at only 30 ms ISI

20. 20 Dyslexia similar mechanism to SLI? Tallal ? temporal processing speed deficit could underlie established phonological difficulties such as distinguishing /da/ from /ga/ since this requires discrimination of differences of the order of 30 ms in the speech train. Almost all SLI children go on to show characteristic dyslexic difficulties ? the phonological difficulties (and hence the reading-related difficulties) shown by dyslexic children may be attributable to the underlying difficulty in rapid auditory processing, & hence temporal processing is a causal explanation

21. 21 Training Study: Tallal and Merzenich (1996) SLI children trained on computer program designed to improve their temporal processing skills. (i) Circus sequence: perceptual identification - which sound (of 2) was first? (ii) Phonetic element recognition which one of two phonetic elements was first (eg. /be/ out of /be/ .. /de/) Started easy and made the onsets faster and faster. 5-10 hours� practice in 20 min sessions ? significant improvements in ability on the games and on the Tallal test. NB. Range of criticisms from many dyslexia researchers. (i) Need for control group who receive some alternative training to control for Hawthorne effects etc. (ii) Need to show that this helps the reading or phoneme identification etc. (iii) Most researchers would expect that substantial training on a particular task would lead to improvements at it! To outrage in the dyslexia community, Tallal, Miller, Merzenich & Fitch have now founded a commercial company to market these products, Scientific Learning Corporation, and it is available under the name Fast ForWord.

22. 22 Conclusions (Tallal, Miller and Fitch, 1993) A basic rapid temporal processing impairment in language-impaired children underlies their ability to integrate sensory information that converges in rapid succession in the CNS. the deficit is pansensory � it affects processing in multiple sensory modalities, and also affects motor output within the millisecond time frame temporal integration deficits are linked to specific patterns of speech perception and speech production deficits in SLI children the basic temporal deficits cause a cascade of effects starting with the disruption of the normal development of an efficient phonological system these phonological processing effects result in subsequent failure to learn to speak and read normally. Tallal et al. suggest these difficulties may also apply to dyslexic children, citing the range of difficulties in speeded processing.

23. 23 Rapid temporal processing as a causal explanation Limitations It appears to conflate a whole range of reasons for problems in rapid processing. Why should difficulties in perceptual processing via the magnocellular pathways lead to the problems of motor output for articulation? There are other theories [see Cerebellum!] that provide a natural explanation of speed problems. It does not give a convincing explanation of the range of difficulties in dyslexia, with the primary limitation being an inability to explain why dyslexic children have particular difficulties with rhymes (slow processing) and with spelling.

24. 24 Dyslexia: Armchair Task Analysis Deficits in reading, writing and spelling: They are all related to language They all have a visual component They all involve some form of rapid processing Common Sense None is innate They are all important school attainments They are all take thousands of hours to master They are all complex, learned skills

25. 25 Dyslexia as a Learning Disability The �correct� description of dyslexia is �Specific Learning Difficulties� or �Learning Disability� Dyslexia is [some] general deficit in learning For some reason it is difficult for dyslexic children to become �expert� in a task ������...whether it is a cognitive task or a motor task. The Automatisation Deficit hypothesis (N & F 1990) Dyslexic children have problems making skills automatic and need therefore to �consciously compensate� even for simple skills

26. 26 N&F Theory : Phase 1 Logic Reading-related tests do not discriminate between the theories What is needed is a test in a domain where the theories predict no deficit - this is Popper�s falsification approach. We tested their motor skills. They were worse than normal!

27. 27 Balance and Dyslexia Under optimal conditions dyslexic children can balance as well as controls. The controls balanced automatically. The dyslexic children did not. There seem to be automatisation problems even for balance!

28. 28 Phase 2: Primitive Skills and Dyslexia Complete Cross-Section of Skills Programmatic series of controlled studies generating solid data �across the board�. Compare the severity of deficits across tasks the pattern of severity may indicate the underlying cause(s) Groups of dyslexic and control children at different ages

29. 29 Results across the board

30. 30 Summary of the Primitive Skills Analysis In one sense all the research teams were right! There are severe deficits in Phonological skill, Speed of processing and Motor skill Fundamentally, no single theory was supported. Deficits were not limited to a specific domain like phonological skill, speed of information processing, or motor skill. Most of the children were impaired on most of the tasks! Theoretically, it was rather a puzzle. What cause(s) could underlie such a range of diverse difficulties?

31. 31 Stage 3: Theory � The Cerebellum In humans, 10-15% of brain weight, 40% of brain surface area, 50% of the brain�s neurons. The �hind brain�. Dexterity, automaticity. �� the 2-way connections linking the cerebellum to Broca�s area make it possible for it to improve language dexterity, which combines motor and mental skills.�

32. 32 The Cerebellum & Skill (Leiner, Leiner & Dow, 1989/93) (1) motor skill � �a rapid information-processing mechanism to generate rapid responses to the input received via automatisation�. (2) Human cerebellum has 2-way neural connections to/from: cognitive areas of the superior prefrontal cortex language areas of the inferior prefrontal cortex. �� the 2-way connections linking the cerebellum to Broca�s area make it possible for it to improve language dexterity, which combines motor and mental skills.�

33. 33 The expanding role of the cerebellumDesmond & Fiez 98

34. 34 The role of the cerebellum in dyslexia ? near-perfect fit between primitive skills analysis and the neuroscience findings on cerebellar role! But: if dyslexic children do have some problem with the cerebellum, why has no-one noticed this? �Classic� Cerebellar Signs Inco-ordination (severe cases walk as though drunk) Balance, Sway, Difficulties with complex movements Dystonia (loss of muscle tone) Floppiness, Difficulty in arresting movement,Tremor

35. 35 Comparison of Cerebellar deficits with other deficits

36. 36 Dyslexia: A PET studyNicolson, Fawcett, Berry, Jenkins, Dean & Brooks (1997) Task developed by Jenkins, a sequence learning task. Four fingers, had to learn a simple sequence of 8 presses, cued by Right/Wrong tone Their work indicates that the cerebellum (and other brain areas) activated both in executing a previously learned sequence, and when learning a new sequence �the cerebellum is involved in the process by which skills become automatic� Six dyslexic and 6 matched control adults (i) Prelearned a sequence of 8 presses until completely automatic on the morning of the test (ii) Tested in scanner on both the Prelearned sequence and when learning a New sequence

37. 37 PET Study Results:Pre vs Rest Regions of significantly greater rCBF p<.01 corrected for multiple comparison (p<.05). 12mm smooth Controls Dyslexics Controls vs Dyslexics

38. 38 Results: Controls vs DyslexicsNew vs Rest (8 mm smooth) PET SPM96 data superimposed on standard MR image centred on point of maximum activation (p<.01 corrected for multiple comparisons). Note here on this finer analysis the cerebellar vermis is also showing significant differences in activation. It is particularly striking that the only region of significant difference (at this high level of significance) is cerebellar cortex plus vermis.

39. 39 Stage 4: Causal ExplanationConverging on the Cerebellum

40. 40 The Target Causal Analysis � a true causal theory of dyslexia should explain not only the symptoms but also the underlying cause of the symptoms.

41. 41 Dyslexia: an ontogenetic Causal Chain

42. 42 Key Questions for Dyslexia Research Q1. What is the underlying cause? Q2. Why does it appear specific to reading? Q3. Why are some dyslexic people high achievers? Q4. How can we identify dyslexia before a child fails to learn to read? Q5. Do we need different methods to teach dyslexic children? If so, what? Q6. What are the policy implications? Q7. Why is it all so controversial? Q8. What should we do next?

43. 43 Dyslexia: New Answers to Old Questions Q1. What is the underlying cause? Cerebellar impairment normally dating back to gestation. Maybe also in other parts of the cerebellar/cortical loop Q2. Why does it appear specific to reading? Very severe problems arise for reading and spelling, because they require both good phonological skills and good automatisation - double whammy!

44. 44 Are Dyslexic Children Clever?! Q3. Given this wide range of difficulties, why are there so many high achieving dyslexic people? The cerebellum is needed primarily for unconscious development of skill fluency. Skills can be acquired without the cerebellum � they are just less fluent and more attention-demanding. The traditional seat of intellectual behaviour, the frontal lobes of the cortex, may well be completely spared, or even over-achieving. IQ, metacognition, strategy use, knowledge etc. are all fine.

45. 45 Theoretical Conclusions Impaired cerebellar functioning gives a good account of dyslexia, its symptoms, and how they arise. It integrates data on both phonological deficits and speed deficits and suggests a complete route from birth to school, from brain to cognition. The analysis provides fruitful suggestions for the search for early precursors. But: the cerebellum is a large structure � And there may be other causes - 5% of population...

46. 46 To the Future : Questions Theory: sub-types link to diagnosis and treatment Diagnosis: Brain-based vs symptom-based Links to other learning disabilities Support: Cost-effectiveness How can we teach them the way they learn? Can we �accelerate� them to learn the way we teach?

47. 47 Bibliography Demonet, J. F., Taylor, M. J., & Chaix, Y. (2004). Developmental dyslexia. Lancet, 363(9419), 1451-1460. Nicolson, R. I., & Fawcett, A. J. (1990). Automaticity: A new framework for dyslexia research? Cognition, 35(2), 159-182. Nicolson, R. I., Fawcett, A. J., & Dean, P. (2001). Developmental dyslexia: The cerebellar deficit hypothesis. Trends in Neurosciences, 24(9), 508-511 Shaywitz, S. (1996). Dyslexia. Scientific American(November), 78-84. Stein, J. F., & Walsh, V. (1997). To see but not to read; the magnocellular theory of dyslexia. Trends in Neurosciences, 20, 147-152. Tallal, P., Miller, S., & Fitch, R. H. (1993). Neurobiological basis of speech - a case for the pre-eminence of temporal processing. Annals of the New York Academy of Sciences, 682, 27-47. Vellutino, F. R., Fletcher, J. M., Snowling, M., & Scanlon, D. M. (2004). Specific reading disability (dyslexia): What have we learned in the past four decades? Journal of Child Psychology and Psychiatry, 45(1) Wolf, M., & Bowers, P. G. (1999). The double-deficit hypothesis for the developmental dyslexias. Journal of Educational Psychology, 91, 415-438.