Dyslexia-specific brain activation profile becomes normal following successful remedial training

Simos, Panagiotis G.; Fletcher, Jack Μ.; Bergman, E.; Breier, Joshua I.; Foorman, Barbara R.; Castillo, Eduardo M.; Davis, Robert N.; Fitzgerald, Michele E.; Papanicolaou, Andrew C.

doi:10.1212/wnl.58.8.1203

Cited by 378 publications

(293 citation statements)

References 48 publications

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“…The upper panel shows the typical brain activation map from magnetic source imaging studies of dyslexia, with predominant activity in temporal and parietal areas of the right hemisphere, but little activation in homologous areas of the left hemisphere. In the lower panel there is a significant increase in the activation of these left temporoparietal areas associated with the significant improvement in word reading accuracy that parallels the patterns observed in proficient readers (based on Simos et al, 2002a).…”

Section: Genetic Studiessupporting

confidence: 61%

Specific reading disability (dyslexia): what have we learned in the past four decades?

Vellutino

Fletcher

Snowling

et al. 2004

Child Psychology Psychiatry

2,024

1,591

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We summarize some of the most important findings from research evaluating the hypothesized causes of specific reading disability (ÔdyslexiaÕ) over the past four decades. After outlining components of reading ability, we discuss manifest causes of reading difficulties, in terms of deficiencies in component reading skills that might lead to such difficulties. The evidence suggests that inadequate facility in word identification due, in most cases, to more basic deficits in alphabetic coding is the basic cause of difficulties in learning to read. We next discuss hypothesized deficiencies in readingrelated cognitive abilities as underlying causes of deficiencies in component reading skills. The evidence in these areas suggests that, in most cases, phonological skills deficiencies associated with phonological coding deficits are the probable causes of the disorder rather than visual, semantic, or syntactic deficits, although reading difficulties in some children may be associated with general language deficits. Hypothesized deficits in general learning abilities (e.g., attention, association learning, cross-modal transfer etc.) and low-level sensory deficits have weak validity as causal factors in specific reading disability. These inferences are, by and large, supported by research evaluating the biological foundations of dyslexia. Finally, evidence is presented in support of the idea that many poor readers are impaired because of inadequate instruction or other experiential factors. This does not mean that biological factors are not relevant, because the brain and environment interact to produce the neural networks that support reading acquisition. We conclude with a discussion of the clinical implications of the research findings, focusing on the need for enhanced instruction.

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Section: Genetic Studiessupporting

confidence: 61%

Specific reading disability (dyslexia): what have we learned in the past four decades?

Vellutino

Fletcher

Snowling

et al. 2004

Child Psychology Psychiatry

2,024

1,591

View full text Add to dashboard Cite

show abstract

“…One of the most consistent results in these studies is a finding of reduced or absent activation among poor readers in the left parietotemporal and/or occipito-temporal cortices (e.g. Aylward et al, 2003;Brunswick, McCroy, Price, Frith, & Frith, 1999;Corina et al, 2001;Eden et al, 2004;Georgiewa et al, 1999;Hoeft et al, 2006Paulesu et al, 1996;Rumsey et al, 1992Rumsey et al, , 1997Shaywitz et al, 1998Shaywitz et al, , 2002Shaywitz et al, , 2003Shaywitz et al, , 2004Simos, Breier, Fletcher, Bergman, & Papanicolaou, 2000;Simos et al, 2002;Temple et al, 2003). While only a few studies have examined cortical function among poor readers in higher-level reading tasks, evidence is beginning to emerge indicating that underactivation in the parietotemporal and occipito-temporal regions may likewise characterize poor readers when they are reading sentences for comprehension (e.g.…”

Section: Introductionmentioning

confidence: 67%

“…A consistent result emerging from these studies is that remedial treatment increases not only reading ability in impaired readers (measured behaviorally), but also the activation in the left parieto-temporal cortex, as measured by functional neuroimaging techniques (Aylward et al, 2003;Eden et al, 2004;Shaywitz et al, 2004;Simos et al, 2002;Temple et al, 2003). Thus, this formerly underactivating region becomes more active following effective instruction, essentially resulting in a normalization of function.…”

Section: Introductionmentioning

confidence: 68%

Modifying the brain activation of poor readers during sentence comprehension with extended remedial instruction: A longitudinal study of neuroplasticity

et al. 2008

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a b s t r a c tThis study used fMRI to longitudinally assess the impact of intensive remedial instruction on cortical activation among 5th grade poor readers during a sentence comprehension task. The children were tested at three time points: prior to remediation, after 100 h of intensive instruction, and 1 year after the instruction had ended. Changes in brain activation were also measured among 5th grade good readers at the same time points for comparison. The central finding was that prior to instruction, the poor readers had significantly less activation than good readers bilaterally in the parietal cortex. Immediately after instruction, poor readers made substantial gains in reading ability, and demonstrated significantly increased activation in the left angular gyrus and the left superior parietal lobule. Activation in these regions continued to increase among poor readers 1 year post-remediation, resulting in a normalization of the activation. These results are interpreted as reflecting changes in the processes involved in word-level and sentencelevel assembly. Areas of overactivation were also found among poor readers in the medial frontal cortex, possibly indicating a more effortful and attentionally guided reading strategy.

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“…[40][41][42]. These regions have shown to be hypoactivated in children and adults with a diagnosis of dyslexia (44,(46)(47)(48)(49)(50)(51)79). Therefore, we chose to investigate the following left-hemispheric regions of interest: LG, STG/PG, and MTG.…”

Section: Methodsmentioning

confidence: 99%

Functional characteristics of developmental dyslexia in left-hemispheric posterior brain regions predate reading onset

Raschle

Zuk²,

Gaab³

2012

Proc. Natl. Acad. Sci. U.S.A.

206

190

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Individuals with developmental dyslexia (DD) show a disruption in posterior left-hemispheric neural networks during phonological processing. Additionally, compensatory mechanisms in children and adults with DD have been located within frontal brain areas. However, it remains unclear when and how differences in posterior left-hemispheric networks manifest and whether compensatory mechanisms have already started to develop in the prereading brain. Here we investigate functional networks during phonological processing in 36 prereading children with a familial risk for DD (n = 18, average age = 66.50 mo) compared with age and IQ-matched controls (n = 18; average age = 65.61 mo). Functional neuroimaging results reveal reduced activation in prereading children with a family-history of DD (FHD + ), compared with those without (FHD − ), in bilateral occipitotemporal and left temporoparietal brain regions. This finding corresponds to previously identified hypoactivations in left hemispheric posterior brain regions for school-aged children and adults with a diagnosis of DD. Furthermore, left occipitotemporal and temporoparietal brain activity correlates positively with prereading skills in both groups. Our results suggest that differences in neural correlates of phonological processing in individuals with DD are not a result of reading failure, but are present before literacy acquisition starts. Additionally, no hyperactivation in frontal brain regions was observed, suggesting that compensatory mechanisms for reading failureare not yet present. Future longitudinal studies are needed to determine whether the identified differences may serve as neural premarkers for the early identification of children at risk for DD.is a specific learning disability that affects about 5-17% of all children (1, 2). DD is characterized by difficulties with accurate and fluent word recognition and poor spelling and decoding performance. DD cannot be accounted for by poor vision, hearing, or a lack of motivation. Molecular-genetic, twin, and family studies have shown a marked familial risk for DD, with an increasing prevalence in families with one or more members with a diagnosis of DD or reading difficulties (e.g., refs. 3 and 4). In addition, several DD susceptibility genes crucial for early brain development have been reported (5-8). DD can have severe social and psychological consequences (9-11) and may impact a child's life beyond their academic pursuits. Studies have shown that children with learning disabilities are less likely to complete high school (12) and are more likely to enter the juvenile justice system (13).Most researchers, clinicians, and reading specialists agree that DD typically results from a weakness in the ability to manipulate oral speech sounds of language (2,14). Individuals with DD are often unable to access the underlying sound structures of words, creating a difficulty in mapping sounds to written language (15-18). Phonological processing skills have been found to be a key predictor of later reading ability in pr...

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Dyslexia-specific brain activation profile becomes normal following successful remedial training

Cited by 378 publications

References 48 publications

Specific reading disability (dyslexia): what have we learned in the past four decades?

Specific reading disability (dyslexia): what have we learned in the past four decades?

Modifying the brain activation of poor readers during sentence comprehension with extended remedial instruction: A longitudinal study of neuroplasticity

Functional characteristics of developmental dyslexia in left-hemispheric posterior brain regions predate reading onset

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