Auditory event-related potentials differ in dyslexics even when auditory psychophysical performance is normal

Stoodley, Catherine J.; Hill, Penelope R.; Stein, John; Bishop, Dorothy V. M.

doi:10.1016/j.brainres.2006.08.095

Cited by 51 publications

(44 citation statements)

References 46 publications

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“…Such discrepant findings are not uncommon in the literature, e.g. Stoodley et al (2006) reported that auditory event-related potentials differ in dyslexics even when auditory psychophysical performance is normal. These authors argued that dyslexics' successful coping strategies may positively influence their performance on auditory behavioural measures.…”

Section: Discussionmentioning

confidence: 88%

Auditory sensory deficits in developmental dyslexia: A longitudinal ERP study

et al. 2011

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Section: Discussionmentioning

confidence: 88%

Auditory sensory deficits in developmental dyslexia: A longitudinal ERP study

et al. 2011

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“…For example, a comparison between children with RD, and typical readers with and without hearing loss found that FM discrimination differed significantly only in the hearing loss group [84]. Another study found no behavioral difference in 5-Hz FM discrimination between adults with and without RD, but found reduced mismatch negativity amplitudes in adults with RD [83], suggesting that there are subtle auditory processing impairments in RD, even when these are not behaviorally evident.…”

Section: Sensory Processingmentioning

confidence: 99%

“…A review [59] found a moderate effect size (d = 0.6) for impaired discrimination of frequency-modulated (FM) stimuli at slow (2 Hz) modulation rates in RD in both children and adults. Although FM discrimination has been found to be a predictor of reading ability [82], some studies have failed to find FM discrimination differences between RD and typical readers [83]. For example, a comparison between children with RD, and typical readers with and without hearing loss found that FM discrimination differed significantly only in the hearing loss group [84].…”

mentioning

confidence: 99%

Neural Noise Hypothesis of Developmental Dyslexia

Hancock¹,

Pugh²,

Hoeft³

2017

Trends in Cognitive Sciences

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Developmental dyslexia (decoding-based reading disorder; RD) is a complex trait with multifactorial origins at the genetic, neural, and cognitive levels. There is evidence that low-level sensory-processing deficits precede and underlie phonological problems, which are one of the best-documented aspects of RD. RD is also associated with impairments in integrating visual symbols with their corresponding speech sounds. Although causal relationships between sensory processing, print-speech integration, and fluent reading, and their neural bases are debated, these processes all require precise timing mechanisms across distributed brain networks. Neural excitability and neural noise are fundamental to these timing mechanisms. Here, we propose that neural noise stemming from increased neural excitability in cortical networks implicated in reading is one key distal contributor to RD. Premise of the Neural Noise HypothesisDevelopmental dyslexia (specific reading disabilities/disorders, or decoding-based RD) is a neurodevelopmental disorder contributed to by multiple genetic, neural, and cognitive factors [1], yet neurobiological models that account for the diversity of RD phenotypes remain elusive. An increasing number of studies have investigated the function of RD risk genes in animal models [2][3][4][5][6][7][8][9][10][11][12][13], and the neurobiological and behavioral consequences of genetic RD risk variants in humans [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31], motivating the need for a synthesis of these findings, especially because they relate to emerging avenues of human research on the role of neurochemistry [32] and neural oscillations [33][34][35][36] in RD. Here, we present a timely integration of diverse lines of current research linking some of the key neural and behavioral deficits associated with RD to basic neural processes.A variety of neurobiological contributors to RD have been proposed, ranging from disrupted structural and functional connectivity [37,38] to atypical neural migration [39]. Recent work has investigated the neural dynamics that support language and sensory processing [40][41][42] and how these dynamics may be altered in RD [36,43]. We integrate these emerging lines of research to propose that excess neural noise (Box 1) within cortical regions implicated in reading may be a distal contributor to RD. We suggest that multifactorial sources of neural noise, for example arising from neural hyperexcitability related to RD risk genes, disrupt two key processes important for reading [phonological awareness [44] (see Glossary) and multisensory integration of visual symbols with their corresponding speech sounds [45,46]] through the impact of excess noise on neural synchrony and sensory representations (Figure 1). The neural noise hypothesis of RD synthesizes a range of neurobiological findings, providing a mechanistic framework for understanding the deficits observed in RD and identifying targets for systems-level intervention. While the potential for noisy proce...

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“…4,8,11,24 In children at risk for dyslexia, a bilateral topography of the late speech MMN was found suggesting lateralization differences of this component in dyslexic children 24 and a predictor for word reading in fifth grade children. 8 This late MMN component was suggested as a correlate for reduced auditory memory span 25 and a more specific correlate for linguistic processing. 21 Speech processing depends on the rapid integration of a complex set of acoustic features such as amplitude, frequency, duration, and rapid changes of speech signals.…”

Section: Introductionmentioning

confidence: 99%

“…17,18 This fronto-centrally predominant scalp distribution of the MMN is mainly explained by the sum of generator activity in supratemporal cortices of both hemispheres. 19,20 Experiments using complex stimuli such as speech sounds, as opposed to simpler sounds such as sinus tones, detect a later MMN component, with a latency from 300 to 600 ms [8][9][10][21][22][23][24][25] and a left lateralized topography of the speech MMN in young children, adolescents, and adults. 4,8,11,24 In children at risk for dyslexia, a bilateral topography of the late speech MMN was found suggesting lateralization differences of this component in dyslexic children 24 and a predictor for word reading in fifth grade children.…”

Section: Introductionmentioning

confidence: 99%

First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children

et al. 2009

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Dyslexia is one of the most common learning disorders affecting about 5% of all school-aged children. It has been shown that event-related potential measurements reveal differences between dyslexic children and age-matched controls. This holds particularly true for mismatch negativity (MMN), which reflects automatic speech deviance processing and is altered in dyslexic children. We performed a whole-genome association analysis in 200 dyslexic children, focusing on MMN measurements. We identified rs4234898, a marker located on chromosome 4q32.1, to be significantly associated with the late MMN component. This association could be replicated in an independent second sample of 186 dyslexic children, reaching genome-wide significance in the combined sample (P = 5.14eÀ08). We also found an association between the late MMN component and a two-marker haplotype of rs4234898 and rs11100040, one of its neighboring single nucleotide polymorphisms (SNPs). In the combined sample, this marker combination withstands correction for multiple testing (P = 6.71eÀ08). Both SNPs lie in a region devoid of any protein-coding genes; however, they both show significant association with mRNA-expression levels of SLC2A3 on chromosome 12, the predominant facilitative glucose transporter in neurons. Our results suggest a possible transregulation effect on SLC2A3, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks.

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Auditory event-related potentials differ in dyslexics even when auditory psychophysical performance is normal

Cited by 51 publications

References 46 publications

Auditory sensory deficits in developmental dyslexia: A longitudinal ERP study

Auditory sensory deficits in developmental dyslexia: A longitudinal ERP study

Neural Noise Hypothesis of Developmental Dyslexia

First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children

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