Developmental dyslexia and dysgraphia and the neural bases of written language processing

1. Developmental dyslexia and dysgraphia and the neural bases of written language processing

2. Developmental dyslexia • Individuals who fail to develop written language skills in a normal fashion; defined by exclusion: difficulties cannot be attributed to sensory deficits, emotional problems, low intelligence or lack of educational opportunity • First published reports 1896 • Originally compared to acquired reading deficits • Referred to as “word blindness” -Hinshelwood

3. Genetic Bases Pennington (1989) • Unexpected difficulty in the acquisition of reading and spelling • Prevalence: 5-10% • Male/female: 3/5-4.0/1 • Familiality: does the disorder run in families? • Compare rates in relatives of an affected person to baseline in the general population • Heritability: Is there a genetic contribution? • Compare twins reared apart vs. together; monozygotic/dizogotic twins

4. Familial riskVogler et al. (1985) • Dyslexic son: • Father dyslexic: 40% • Mother dyslexic: 35% • (5-7 x normal rate) • Dyslexic daughter: • Father dyslexic: 17-18% • Mother dyslexic: 17-18% • (10-12 x normal rate)

5. Range of proposed underlying causes • Crossed laterality • Visual perception deficit • Eye-movement deficit • Attentional deficit • Eye focusing deficit • Short term memory limitations • Sequencing (temporal and/or spatial) deficit • Maturational lag • Deficiency in metalinguistic abilities • Incompatibility of teaching and learning styles • Perceptual-motor deficit

6. Why has it been so difficult to understand the underlying deficits? • Poor understanding of the normal process of reading acquisition • Differences in teaching approaches • Different experiences at home and school • Difficulties in separating development of general cognitive skills from reading-specific skills • The underlying assumption of virtually all research in the field: a homogenous disorder with one underlying cause (or at most two) • If the assumption is erroneous, groups in different studies will be heterogenous (a mixture of deficits) and studies will contradict each other

7. Phonological/auditory/language differences in developomental dyslexia (1) Bradley & Bryant • Phonological awareness (2) Galaburda et al. • Planum temporale • Ectopias • Tallal et al. Processing of brief, transient auditory/phonological information

8. A quick neuroanatomical overview

13. CORTEX: Grey matter: CELL BODIES White matter: AXONS 2.5 SQ. FEET(UNFOLDED) 10-15 BILLION NEURONS 6 LAYERS, 1.5-4 MM THICK NEOCORTEX

14. WHITE MATTER: AXONS FIBERS COMMISSURES (CORPUS CALLOSUM) GYRI, SULCI, FISSURES CENTRAL (ROLANDIC) FISSURE LATERAL (SYLVIAN FISSURE) 4 LOBES: FRONTAL TEMPORAL PARIETAL OCCIPITAL NEOCORTEX

16. coronal sagittal Horizontal/axial

17. sagittal

19. coronal

21. axial

23. Neuroanatomical Asymmetries

24. Galaburda et al. • Planum temporale in unselected brains-anatomical asymmetry: • L>R 65% • L<R 11% • L=R 24% • Developmental dyslexia: • 7 consecutive brains: L= R

26. Galaburda, et al. • Ectopias: • Found occasionally in routine autopsies (3-15% of the time; typically in the frontal lobes, RH> LH) • 5 male dyslexic brains: • All showed mircrodysgenesis • Bilateral, LH> RH • Perisylvian • Experimental animal work indicates they can develop late in corticogenesis (when the last waves of neurons are migrating to the cortex) • Potentially related to immune based injury (testosterone)

28. Tallal, et al. • “the basic deficit in processing brief, transient sensory information initially leads to a failure by the infant to set up distinctive phonological representations for the sounds of its native language…” • “…children who cannot process the acoustic cues that are required to discriminate individual phonemeswithin words cannot become aware that words are made up of smaller units (phonemes): that is these children have phonological awareness deficits…”

29. Deficit in processing brief transients Tasks: • Two tones presented sequentially: • Repetition: subjects trained to match tone to button, in the test indicate the order of the tones by pressing respective buttons (1-1, 1-2, 2-1, 2-2) • Discrimination: indicate if the two tones are the same or different

30. Consonants: brief transitions

33. Tallal et al.: Intervention study • 22 children with LLI (language Learning impairment) • Severe auditory rate processing deficits (assessed with Tallal Repetition Test) • Experiencing severe difficulty learning to read • Divided into two matched groups Treatment: • Experimental group: computer games that adaptively trained temporal processing + language exercises recorded with acoustically modified speech (prolonged speech signal by 50% and made the fast transitional elements (3-30 Hz) louder • Control group: same tasks but the computer games were not temporally adaptive and the language exercises did not involve modified speech

35. Tallal’s temporal order hypothesis: Outstanding issues • Difficulties in replication • Concern that groups were not controlled for ADHD • The results are representative of a small subset of dyslexics—namely those that have a primary spoken language deficit

36. Visual system differences in developmental dyslexia • Galaburda et al. • Magno/parvo cell size in the LGN • Eden et al. • Behavior and brain in motion detection

37. Visual pathway

38. CENTRAL RELAY FOR SENSORY AND MOTOR INFORMATION TO CORTEX LATERAL GENICULATE: VISUAL INFO MEDIAL GENICULATE: AUDITORY INFO THALAMUS

42. Protons are exposed to a steady magnetic field spin axes align in the field direction A brief pulse  spin axes tip away from their orientation with the external magnetic field Pulse is turned off  protons return to alignment with external field, releasing energy: the MR signal MRI (magnetic resonance imaging)

43. Paramagentic agents produce local magnetic fields disrupting the realignment  reducing MR signal Deoxygenated hemoglobin acts as a paramagentic agent, reducing MR signal As neural activity increases, blood flow increases  increasing ratio of oxy to deoxy hemoglobin Track neural activity by tracking changes in the ratio of oxy/deoxy hemoglobin fMRI: Measuring changing brain events

44. Sample Experimental Conditions Goal: identify areas of the brain sensitive to visual motion Conditions: 40 sec repeating epochs of: 1- blank screen 2-randomly positioned white dots on a black background, moving 3-randomly positioned white dots on a black background, stationary

45. What would happen if you compared activation for movement vs. stationary conditions in: -primary visual cortex? -area MT?

47. Data analysis (cont) Output of the analysis: • NOT pictures! • Numerical values (statistical significance) for each voxel • Numerical values are typically superimposed on a structural image (different value ranges are assigned different colors)

48. Eden et al. (1996) Subjects: 8 male controls 6 male dyslexics (adults) Tasks: • behavioral: stimulus velocity judgment task • fMRI: compare activation for: • Stationary, high contrast patterned stimulus (ideal Parvo activator): patterned dot field • Moving, low-contrast random-dot stimulus (ideal Magno activator): black dots on grey background • Fixation cross on a uniformly illuminated field