Biology:Neurological research into dyslexia

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Dyslexia is defined by the difficulty in an individual's ability to read given adequate intelligence and normal opportunities. While such a distinction provides a useful advantage to clinicians and diagnosticians alike, it does not carry implications that are of practical significance to scientist and researchers so as to facilitate further development of interventions that would allow dyslexics to learn as normal individuals. Current neurological research has uncovered clear evidence of biophysical and structural anomalies in individuals who are affected by the disorder. FMRI and behavioral experiments have generated significant results so as to suggest the disorder be viewed as having neurological causes.

History

During the twentieth century, dyslexia was primarily seen as a phonological deficit (specifically phonological awareness) that resulted in a reading deficit.[1][2][3] Dyslexia was seen as an issue with reading achievement specifically, caused by deficits in discrimination of written word sounds as opposed to a broader disorder of brain function. However, much research from the 1990s onward has focused on the potential biological bases of dyslexia and understanding dyslexia as a disorder of brain function. One of the first weaknesses of the strictly phonological deficit hypothesis for dyslexia was its inability to account for the genetic link of dyslexia.[4] Specifically, it's been shown that "Relatively high heritabilities were observed for both reading ability and dyslexia indicating substantial genetic influences."[5] In a large twin study (sample 1031 twins), Gayan and Olson established that dyslexia was highly heritable, while a family study by Pennington (sample 1698 individuals) showed familial risk rates of 35-45%.[6][7] Without a biological explanation for dyslexia, this heritability went unexplained. Not only must the heritability be explained, but also the environmental factors that protected at-risk children from developing dyslexia. Research began to focus on potential biological causes and to center the study of dyslexia in a developmental framework. A second major weakness of the strictly phonological deficit hypothesis was its strict definition of dyslexia as a reading disorder. Consequently, the various secondary symptoms were unable to be explained, including automatization deficits of both skill and knowledge acquisition, balance impairments, motor skill/writing deficits, and muscle tone underdevelopment.[3] New theories of dyslexia began to be a focus of research, with the most well established being the magnocellular deficit theory the automatization deficit theory, and the double-deficit hypothesis.[5][page needed] Each of these theories tried to account for a subset of the variety of common secondary symptoms.

Overview

Modern neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have produced clear evidence of structural differences in the brains of children with reading difficulties. It has been found that people with dyslexia have a deficit in parts of the left hemisphere of the brain involved in reading, which includes the inferior frontal gyrus, inferior parietal lobule, and middle and ventral temporal cortex.[8]

That dyslexia is neurobiological in origin is supported by what Lyon et al. proclaimed as "overwhelming and converging data from functional brain imaging investigations" (2003, p. 3). The results of these studies suggest that there are observable differences in how the dyslexic brain functions when compared to the brain of a typical reader. Using fMRI, Shaywitz found that good readers show a consistent pattern of strong activation in the back of the brain with weaker activation in the front of the brain during reading tasks. In contrast, the brain activation pattern in dyslexics is the opposite during reading tasks—the frontal part of the brain becomes overactive with weaker activation in the back. Shaywitz points out "It is as if these struggling readers are using the systems in the front of the brain to try to compensate for the disruption in the back of the brain."[9]

Fluent word identification in reading is related to the amount of activity in the Left hemisphere posterior system.[10] In dyslexia the posterior system is often disrupted.[10] As mentioned above, in order to compensate for lower activity in the posterior system people with dyslexia rely more on the inferior frontal and right hemisphere regions.[10]

Brain activation studies using PET to study language have produced a breakthrough in understanding of the neural basis of language over the past decade. A neural basis for the visual lexicon and for auditory verbal short term memory components have been proposed,[11] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural).[12]

White matter organization and right prefrontal activity can predict future gain in reading ability.[13] Greater right prefrontal activity during reading tasks has been associated with reading improvement later in life.[13] Language training has been shown to improve neural mechanisms of selective auditory attention of children with learning disabilities.[14]

Neuroimaging Techniques

Brain scanning or neuroimaging as we know it today began to be developed in the 1980s and 1990s. The present day Brain Imaging Techniques are:

The neuroimaging techniques mainly used in dyslexia research have been functional Magnetic Resonance Imaging (fMRI) and positron emission tomography (PET), both of which have produced clear evidence of structural differences in the brains of children with reading difficulties.

Past Research

Visio-Neurological Research

Visual processes constitute an important part of higher cortical functioning.[15] The encoding and interpretation of retinal stimulation occur at the neurological level upon reception of afferent input from the eyes. Reading, for example, requires the possession of both adequate vision and the neurological ability to process what is seen. In the past, many researchers have associated anomalies in the visual system as the main cause of dyslexia. While acknowledging that most such theories are untenable, visual system deficits have been shown to contribute to symptoms of dyslexia, such as word reversal and skipping words.[15]

A small subset of dyslexic individuals have been demonstrated to have deficits in the magnocellular visual system.[16] A compromised magnocellular system, responsible for the processing of images with high temporal frequencies and high degree of movement, might be the main contributing factor to the reported "masking" of words reported amongst dyslexic individuals.[16] Researchers posit that such a "masking" effect is due to the abnormal longevity of the visual trace produced in the magnocellular system, resulting in a lapse in acuity as effected individuals attempt to process connected text.[15] While the idea of visual trace persistence being a cause of dyslexia seems appealing, there is lack of understanding both in depth and generalizability to form a basis for the treatment of dyslexia.

Anomalies in saccadic movement, which are instantaneous, fast, oscillating eye movements essential for unimpaired reading have been observed in dyslexic patients. When corrected for reading ability, dyslexic individuals demonstrate below normal saccadic eye movements, suggesting that the severity reading disorders may be due to oculo-motor deficits.[17] However, further examination of the phenomenon shows that saccadic patterns in dyslexics seem to be a result and not the cause of the disorder, as decoding and comprehension failure were isolated as the antecedent for impairments in both the speed and accuracy with which dyslexics read. Also, there is no evidence that children with oculomotor impariments are at risk of developing dyslexia,[18] suggesting that the two disorders are likely unrelated.

Also suspected are convergence insufficiency and poor accommodation, both of which are uncommon in children, can interfere with the physical act of reading but not with decoding.[19] Thus, treatment of these disorders can make reading more comfortable and may allow reading for longer periods of time but does not directly improve decoding or comprehension. In addition. many children with reading disabilities enjoy playing video games, including handheld games, for prolonged periods. Playing video games requires concentration, visual perception, visual processing, eye movements, and eye-hand coordination. Convergence and accommodation are also required for handheld games. Thus, if visual deficits were a major cause of reading disabilities, children with such disabilities would reject this vision-intensive activity.

Language Orthography and Neuroimaging Research

Brain activation studies using PET to study language have produced a breakthrough in our understanding of the neural basis of language over the past decade. For example, It has been found that people with dyslexia have a deficit in parts of the left hemisphere of the brain involved in reading, which includes the inferior frontal gyrus, inferior parietal lobule, and middle and ventral temporal cortex.[20][21] A neural basis for the visual lexicon and for auditory verbal short term memory components have been proposed. Wernicke's and Broca's areas are being recast in terms of localized components of phonological input and output. Some classical regions, such as the arcuate fasciculus, are having their "classical" roles questioned, while other regions, such as the basal temporal language zone, are growing progressively in terms of their recognized importance.[22][23] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i. e., functional rather than structural)[24]

A University of Hong Kong study argues that dyslexia affects different structural parts of children's brains depending the language in which the children read.[25] The study focused on comparing children that were raised reading English and children raised reading Chinese. Using fMRI technology researchers found that the children reading English used a different part of the brain than those reading Chinese. Researchers were surprised by this discovery and hope that the findings will help lead them to any neurobiological cause for dyslexia.[25][26]

A University of Maastricht (Netherlands) study revealed that adult dyslexic readers have under-activated superior temporal cortices, a brain region responsible for the integration of letters and speech sounds. This reduced audiovisual integration is directly associated with a more fundamental deficit in auditory processing of speech sounds, which in turn predicts performance on phonological tasks. The data also provides a neurofunctional account of developmental dyslexia, in which phonological processing deficits are linked to reading failure through a deficit in neural integration of letters and speech sounds.[27]

Dyslexia and Working Memory

Dyslexia patients have been commonly associated with working memory deficits, along with reduced activity in the pre-frontal and parietal cortex. Beneventi, Tonessen, Ersland & Hughdahl conducted a series of experiment bridging the gap between known neurological abnormalities in dyslexic patients and their behavioral consequences.[28] Beneventi et al. provides supporting evidence that reading impairment observed in dyslexic subjects can be associated with general deficits in working memory.In an experiment done using BOLD fMRI to compare neurological activity before and during a reading task is administered to subjects, it was found that patients with dyslexia demonstrate categorically different neural patterns from normal individuals.

Observed differences in the neural pattern of dyslexic patients, namely decreased activation in the left [29] and posterior [30] midfrontal gyrus (LMG, PMG) and superior parietial regions of the brain further supports the view that deficits in working memory contribute to dyslexia. LMG and PMG are commonly associated with working memory processes such as memory updating and temporal order memory.[29] It is also noteworthy that behavioral experiments in dyslexia have largely been supportive of the mediating role assumed by working memory between neurological abnormalities and dyslexic behavior.[31]

Multi-disciplinary approaches

In support of a working memory model of reading disability, Berninger et al.[32] (2008) provided experimental evidence in the form of genetics, neural imaging comparisons, categorical differences across forms of dyslexia (different working memory deficits),[33] and developmental linguistics.[34] The summation of such results adds to the overall validity of Berninger et al. 's construct of dyslexia as a manifestation of working memory deficit.

Berninger's article provides a multiple- disciplinary basis for comparison on the back of various scientific evidence that uniquely describe dyslexia as a neuro-developmental condition.[32] The results of their attempt supported the claim that working memory indeed plays a role in facilitating reading behavior and the lack of such components would result in language impairment. They explored different phonological, orthographical and morphological conditions and manifestations on the ability of dyslexic patients to read.

Cerebellar theory

Originally advanced by Fawcett and Nicholson in the 1990s, the cerebellar deficit hypothesis argues that biological differences in the cerebellum, most likely prenatal, cause a different development trajectory that can include motor skill deficits (including speech), automatization deficits, balance impairment, and phonological awareness. This collection of problems, in all or in any individual part, can lead to the reading deficits of dyslexia.[35]:84.[36][page needed]

Implications

A better neurological understanding of dyslexia would provide a more accurate, distinct definition of the disorder and thereby facilitate more effective treatment protocols. A study by researchers at the University of Texas Health Science Center, Houston utilized behavioral techniques to isolated speech-processing sites from uninvolved ones associated with other facets of language processing, namely memory and semantics .[37] Their results indicated at the presence of a potential central marker of reading impairment that renders it difficult for dyslexic individuals to process words whilst reading. The results reiterated results claims made with prior evidence that young dyslexic subjects demonstrated a lesser involvement of auditory association centers located in the left temporal hemisphere than their control counterparts.

In an effort to utilize neuroimaging as a tool for diagnosing and treating dyslexia, a longitudinal study was conducted by Fumiko Hoeft and colleagues to match the different neural states of dyslexic individual to varying future gains in reading ability.[38] With the help of sophisticated functional MRI and diffusion tensor imaging technology, Hoeaft et al. were able to tease out predictive relationships between the activation right pre-frontal brain mechanisms and patients' progress in reading skills 2.5 years after testing with more than 90% accuracy.

Limitations

In explaining increased pre-frontal cortical activations in language-related areas such as left and right posterior, Beneventi et al. included the possibility that it is the result of a nonverbal compensatory process (and not a direct manifestation of dyslexic behavior itself). Also, in accounting for the observed differences in cerebral activation between the experimental conditions, the possibility of articulatory sub-vocal rehearsal ~ another confounding factor[39] was not discounted, and could be consistent with the cerebellar deficit hypothesis as proposed by Nicolson, Fawcett, & Dean in 2001.[31]

Berninger et al. (2008) acknowledged several methodological limitations faced when trying to isolated multiple facets of working memory deficits in influencing the manifestation of dyslexic behavior. For example, the response to instruction by children performing the related tests is itself confounded by a subject's preexisting profile of working memory components, such as "executive functions, loops, and word-forms, and oral language metalinguistic awareness of phonology, morphology, and syntax, " that are in turn products of one's environments, genetics and socio-economic status.

References

  1. ↑ Christo, Catherine; John M. Davis; Stephen E. Brock (2009). Identifying, Assessing, and Treating Dyslexia at School.. New York: Springer. 
  2. ↑ Ott, Philomena (2006). Teaching Children with Dyslexia: A Practical Guide.. Routledge. ISBN 978-0415324540. 
  3. ↑ 3.0 3.1 Reid, Gavin (2012). The Routledge Companion to Dyslexia. Taylor & Francis. ISBN 978-0415430784. 
  4. ↑ McGill-Franzen, Anne; Allington, Richard L. (2012). Handbook of Reading Disability Research.. New York: Routledge. ISBN 978-0805853346. 
  5. ↑ 5.0 5.1 Reid, Gavin, (2016). Dyslexia: A Practitioner's Handbook.. Chichester : Wiley Blackwell. ISBN 978-0470760406. 
  6. ↑ "Reading Disability: Evidence for a Genetic Etiology". European Child & Adolescent Psychiatry 8: 52–55. 1999. 
  7. ↑ "Evidence for Major Gene Transmission of Developmental Dyslexia". JAMA: The Journal of the American Medical Association 266 (11): 1527–1534. 1991. doi:10.1001/jama.1991.03470110073036. PMID 1880884. 
  8. ↑ "Deficient orthographic and phonological representations in children with dyslexia revealed by brain activation patterns". Journal of Child Psychology and Psychiatry, and Allied Disciplines 47 (10): 1041–50. October 2006. doi:10.1111/j.1469-7610.2006.01684.x. PMID 17073983. 
  9. ↑ Shaywitz, Sally (2003). Overcoming dyslexia: a new and complete science-based program for reading problems at any level. Vintage Books. p. 81. ISBN 0-679-78159-5. 
  10. ↑ 10.0 10.1 10.2 "Functional neuroimaging studies of reading and reading disability (developmental dyslexia)". Ment. Retard. Dev. Disabil. Res. Rev. 6 (3): 207–13. 2000. doi:10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P. PMID 10982498. 
  11. ↑ "PET activation and language". Clinical Neuroscience 4 (2): 78–86. 1997. PMID 9059757. https://www.nlm.nih.gov/medlineplus/nuclearscans.html. 
  12. ↑ "Abnormal functional activation during a simple word repetition task: A PET study of adult dyslexics". Journal of Cognitive Neuroscience 12 (5): 753–62. September 2000. doi:10.1162/089892900562570. PMID 11054918. 
  13. ↑ 13.0 13.1 "Neural systems predicting long-term outcome in dyslexia". Proc. Natl. Acad. Sci. U.S.A. 108 (1): 361–6. January 2011. doi:10.1073/pnas.1008950108. PMID 21173250. 
  14. ↑ "Neural mechanisms of selective auditory attention are enhanced by computerized training: electrophysiological evidence from language-impaired and typically developing children". Brain Research 1205: 55–69. April 2008. doi:10.1016/j.brainres.2007.10.108. PMID 18353284. PMC 2426951. http://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)00297-7. 
  15. ↑ 15.0 15.1 15.2 Vellutino, Frank R.; Fletcher, Jack M.; Snowling, Margaret J.; Scanlon, Donna M. (1 January 2004). "Specific reading disability (dyslexia): what have we learned in the past four decades?". Journal of Child Psychology and Psychiatry 45 (1): 2–40. doi:10.1046/j.0021-9630.2003.00305.x. PMID 14959801. 
  16. ↑ 16.0 16.1 Stein, John (1 January 2001). "The magnocellular theory of developmental dyslexia". Dyslexia 7 (1): 12–36. doi:10.1002/dys.186. PMID 11305228. 
  17. ↑ Olitsky, SE; Nelson, LB (February 2003). "Reading disorders in children.". Pediatric Clinics of North America 50 (1): 213–24. doi:10.1016/s0031-3955(02)00104-9. PMID 12713114. 
  18. ↑ Hodgetts, DJ; Simon, JW; Sibila, TA; Scanlon, DM; Vellutino, FR (June 1998). "Normal reading despite limited eye movements.". Journal of AAPOS 2 (3): 182–3. doi:10.1016/S1091-8531(98)90011-8. PMID 10532756. 
  19. ↑ Granet, D. B.; Castro, E. F.; Gomi, C. F. (1 January 2006). "Reading: Do the Eyes Have It?". American Orthoptic Journal 56 (1): 44–49. doi:10.3368/aoj.56.1.44. 
  20. ↑ Cao, F; Bitan, T; Chou, TL; Burman, DD; Booth, JR (2006). "Deficient orthographic and phonological representations in children with dyslexia revealed by brain activation patterns". Journal of Child Psychology and Psychiatry, and Allied Disciplines 47 (10): 1041–50. doi:10.1111/j.1469-7610.2006.01684.x. PMID 17073983. 
  21. ↑ Shaywitz, BA; Lyon, GR; Shaywitz, SE (2006). "The role of functional magnetic resonance imaging in understanding reading and dyslexia". Developmental Neuropsychology 30 (1): 613–32. doi:10.1207/s15326942dn3001_5. PMID 16925477. 
  22. ↑ Chertkow, H; Murtha, S (1997). "PET activation and language". Clinical Neuroscience 4 (2): 78–86. PMID 9059757. 
  23. ↑ Paulesu, E; Frith, U; Snowling, M; Gallagher, A; Morton, J; Frackowiak, RS; Frith, CD (1996). "Is developmental dyslexia a disconnection syndrome? Evidence from PET scanning". Brain 119 (1): 143–57. doi:10.1093/brain/119.1.143. PMID 8624677. 
  24. ↑ Mccrory, E; Frith, U; Brunswick, N; Price, C (2000). "Abnormal functional activation during a simple word repetition task: A PET study of adult dyslexics". Journal of Cognitive Neuroscience 12 (5): 753–62. doi:10.1162/089892900562570. PMID 11054918. 
  25. ↑ 25.0 25.1 Siok, WT; Niu, Z; Jin, Z; Perfetti, CA; Tan, LH (2008). "A structural-functional basis for dyslexia in the cortex of Chinese readers". Proceedings of the National Academy of Sciences of the United States of America 105 (14): 5561–6. doi:10.1073/pnas.0801750105. PMID 18391194. 
  26. ↑ Eden, GF; Jones, KM; Cappell, K; Gareau, L; Wood, FB; Zeffiro, TA; Dietz, NA; Agnew, JA et al. (2004). "Neural changes following remediation in adult developmental dyslexia". Neuron 44 (3): 411–22. doi:10.1016/j.neuron.2004.10.019. PMID 15504323. 
  27. ↑ Lando, HA; Bluhm, J; Forster, J (1991). "The ban on cigarette vending machines in Bloomington, Minnesota". American Journal of Public Health 81 (10): 1339–40. doi:10.2105/AJPH.81.10.1339. PMID 1928540. 
  28. ↑ BENEVENTI, HARALD; TØNNESSEN, FINN EGIL; ERSLAND, LARS; HUGDAHL, KENNETH (15 March 2010). "Executive working memory processes in dyslexia: Behavioral and fMRI evidence". Scandinavian Journal of Psychology 51 (3): 192–202. doi:10.1111/j.1467-9450.2010.00808.x. PMID 20338015. 
  29. ↑ 29.0 29.1 Wager, TD; Smith, EE (December 2003). "Neuroimaging studies of working memory: a meta-analysis.". Cognitive, Affective & Behavioral Neuroscience 3 (4): 255–74. doi:10.3758/cabn.3.4.255. PMID 15040547. 
  30. ↑ Vasic, N; Lohr, C; Steinbrink, C; Martin, C; Wolf, RC (2008-01-31). "Neural correlates of working memory performance in adolescents and young adults with dyslexia.". Neuropsychologia 46 (2): 640–8. doi:10.1016/j.neuropsychologia.2007.09.002. PMID 17950764. 
  31. ↑ 31.0 31.1 Nicolson, RI; Fawcett, AJ; Dean, P (September 2001). "Developmental dyslexia: the cerebellar deficit hypothesis.". Trends in Neurosciences 24 (9): 508–11. doi:10.1016/S0166-2236(00)01896-8. PMID 11506881. 
  32. ↑ 32.0 32.1 Berninger, Virginia W.; Raskind, Wendy; Richards, Todd; Abbott, Robert; Stock, Pat (5 November 2008). "A Multidisciplinary Approach to Understanding Developmental Dyslexia Within Working-Memory Architecture: Genotypes, Phenotypes, Brain, and Instruction". Developmental Neuropsychology 33 (6): 707–744. doi:10.1080/87565640802418662. PMID 19005912. 
  33. ↑ CATTS, HUGH W. (1 January 2003). "LANGUAGE BASIS OF READING DISABILITIES AND IMPLICATIONS FOR EARLY IDENTIFICATION AND REMEDIATION". Reading Psychology 24 (3–4): 223–246. doi:10.1080/02702710390227314. 
  34. ↑ Catts, H. W.; Adlof, S. M.; Weismer, S. E. (28 April 2006). "Language Deficits in Poor Comprehenders: A Case for the Simple View of Reading". Journal of Speech, Language, and Hearing Research 49 (2): 278–293. doi:10.1044/1092-4388(2006/023). PMID 16671844. 
  35. ↑ Fawcett, Angela J.; Nicolson, Roderick I. (2013). "Chapter 4:Dyslexia and the Cerebellum". The SAGE Handbook of Dyslexia. ISBN 9781412945134. 
  36. ↑ Nicolson R; Fawcett A (2010). Dyslexia, Learning, and the Brain.. MIT Press. ISBN 9780262515092. https://books.google.com/books/about/Dyslexia_Learning_and_the_Brain.html?id=4xOOcpshF5sC. 
  37. ↑ Breier, Joshua I.; Simos, Panagiotis G.; Fletcher, Jack M.; Castillo, Eduardo M.; Zhang, Wenbo; Papanicolaou, Andrew C. (1 January 2003). "Abnormal Activation of Temporoparietal Language Areas During Phonetic Analysis in Children With Dyslexia". Neuropsychology 17 (4): 610–621. doi:10.1037/0894-4105.17.4.610. PMID 14599274. 
  38. ↑ Hoeft, F.; McCandliss, B. D.; Black, J. M.; Gantman, A.; Zakerani, N.; Hulme, C.; Lyytinen, H.; Whitfield-Gabrieli, S. et al. (20 December 2010). "Neural systems predicting long-term outcome in dyslexia". Proceedings of the National Academy of Sciences 108 (1): 361–366. doi:10.1073/pnas.1008950108. PMID 21173250. 
  39. ↑ Müller, NG; Knight, RT (2006-04-28). "The functional neuroanatomy of working memory: contributions of human brain lesion studies.". Neuroscience 139 (1): 51–8. doi:10.1016/j.neuroscience.2005.09.018. PMID 16352402. 




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