Neurological research into dyslexia

Main articles: Dyslexia and Dyslexia research

Neuroimaging in Dyslexia: Definition and Implications

Dyslexia is a behavioral condition characterized by 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. fMRI and behavioral experiments have generated significant results so as to suggest the disorder be viewed as having neurological causes.

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:

• Computed tomography (CT) or computed axial tomography (CAT)
• Diffuse optical imaging (DOI) or Diffuse Optical Tomography (DOT)
• Event-related optical signal (EROS)
• Magnetic resonance imaging (MRI),
• Functional magnetic resonance imaging (fMRI)
• Magnetoencephalography (MEG) which also uses superconducting quantum interference devices (SQUIDs)
• Positron emission tomography (PET)
• Single photon emission computed tomography (SPECT).

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

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.^[1][2] 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.^[3][4] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural)^[5]

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.^[6] 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.^[6][7]

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.^[8]

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.^[9] 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 ^[10]and posterior ^[11] midfrontal gyrus and superior parietial regions of the brain, are brain regions that were previously associated with working memory processes such as memory updating and temporal order memory. ^[12]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.^[13]

Multi-disciplinary approaches

In support of a working memory model of reading disability, Berninger et al.^[14] (2008) provided experimental evidence in the form of genetics, neural imaging comparisons,categorical differences across forms of dyslexia (different working memory deficits)^[15], and developmental linguistics ^[16]. 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.^[17] 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.

Implications

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.^[18] 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.

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 .^[19] 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 auditroy association centers located in the left temporal hemisphere than their control counterparts.

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^[20] was not discounted, and could be consistent with the cerebellar deficit hypothesis as proposed by Nicolson, Fawcett, & Dean in 2001.^[21]

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. ^ 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. PMC 2617739. PMID 17073983. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2617739. 
2. ^ 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. 
3. ^ Chertkow, H; Murtha, S (1997). "PET activation and language". Clinical neuroscience 4 (2): 78–86. PMID 9059757. 
4. ^ 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 : a journal of neurology 119 ( Pt 1): 143–57. PMID 8624677. 
5. ^ 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. 
6. ^ ^{a b} 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. PMC 2291101. PMID 18391194. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2291101. 
7. ^ 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. 
8. ^ 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. PMC 1405340. PMID 1928540. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1405340. 
9. ^ 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. 
10. ^ Wager, TD; Smith, EE (2003 Dec). "Neuroimaging studies of working memory: a meta-analysis.". Cognitive, affective & behavioral neuroscience 3 (4): 255–74. PMID 15040547. 
11. ^ Vasic, N; Lohr, C, Steinbrink, C, Martin, C, Wolf, RC (2008 Jan 31). "Neural correlates of working memory performance in adolescents and young adults with dyslexia.". Neuropsychologia 46 (2): 640–8. PMID 17950764. 
12. ^ Wager, TD; Smith, EE (2003 Dec). "Neuroimaging studies of working memory: a meta-analysis.". Cognitive, affective & behavioral neuroscience 3 (4): 255–74. PMID 15040547. 
13. ^ Nicolson, RI; Fawcett, AJ, Dean, P (2001 Sep). "Developmental dyslexia: the cerebellar deficit hypothesis.". Trends in neurosciences 24 (9): 508–11. PMID 11506881. 
14. ^ 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. 
15. ^ 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. 
16. ^ 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). 
17. ^ 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. 
18. ^ Hoeft, F.; McCandliss, B. D., Black, J. M., Gantman, A., Zakerani, N., Hulme, C., Lyytinen, H., Whitfield-Gabrieli, S., Glover, G. H., Reiss, A. L., Gabrieli, J. D. E. (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. 
19. ^ 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. 
20. ^ Müller, NG; Knight, RT (2006 Apr 28). "The functional neuroanatomy of working memory: contributions of human brain lesion studies.". Neuroscience 139 (1): 51–8. PMID 16352402. 
21. ^ Nicolson, RI; Fawcett, AJ, Dean, P (2001 Sep). "Developmental dyslexia: the cerebellar deficit hypothesis.". Trends in neurosciences 24 (9): 508–11. PMID 11506881.