Deficits in perceptual noise exclusion in developmental dyslexia

Sperling, Anne J.; Lü, Zhong-Lin; Manis, Franklin R.; Seidenberg, Mark S.

doi:10.1038/nn1474

Cited by 255 publications

(262 citation statements)

References 12 publications

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“…Thus, the present results raise the possibility that children with language learning disabilities have very serious problems with noise exclusion, which will certainly have tremendous consequences for normal phonological development. A similar proposal has recently been made with regard to visual (magnocellular) deficits that seem frequently associated with dyslexia (45). The authors showed that dyslexic children do not have visual (magnocellular) processing problems per se but rather problems of noise exclusion that become apparent in visual tasks using noisy displays.…”

Section: Discussionmentioning

confidence: 52%

Deficits in speech perception predict language learning impairment

Ziegler

Pech-Georgel

George

et al. 2005

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

178

146

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Specific language impairment (SLI) is one of the most common childhood disorders, affecting 7% of children. These children experience difficulties in understanding and producing spoken language despite normal intelligence, normal hearing, and normal opportunities to learn language. The causes of SLI are still hotly debated, ranging from nonlinguistic deficits in auditory perception to high-level deficits in grammar. Here, we show that children with SLI have poorer-than-normal consonant identification when measured in ecologically valid conditions of stationary or fluctuating masking noise. The deficits persisted even in comparison with a younger group of normally developing children who were matched for language skills. This finding points to a fundamental deficit. Information transmission of all phonetic features (voicing, place, and manner) was impaired, although the deficits were strongest for voicing (e.g., difference between͞b͞and͞p͞). Children with SLI experienced perfectly normal ''release from masking'' (better identification in fluctuating than in stationary noise), which indicates a central deficit in feature extraction rather than deficits in low-level, temporal, and spectral auditory capacities. We further showed that speech identification in noise predicted language impairment to a great extent within the group of children with SLI and across all participants. Previous research might have underestimated this important link, possibly because speech perception has typically been investigated in optimal listening conditions using non-speech material. The present study suggests that children with SLI learn language deviantly because they inefficiently extract and manipulate speech features, in particular, voicing. This result offers new directions for the fast diagnosis and remediation of SLI.phonetic deficit ͉ auditory deficit ͉ speech intelligibility ͉ masking noise ͉ specific language impairment M any children experience unexpected difficulties in understanding and producing spoken language despite normal intelligence, normal hearing, normal opportunities to learn language, and in the absence of any obvious neurological problems (for review, see ref. 1). This disorder is typically called specific language impairment (SLI). In the past years, research on SLI has experienced a growth of interest partially because it has become clear that more children than initially thought show language learning difficulties. Indeed, recent epidemiological studies estimate the incidence of SLI to be Ϸ7.4% in a population of monolingual English-speaking kindergarten children (2). Children with SLI exhibit deficits in several aspects of language, including phonology, morphology, and syntax (1, 3). One of the hallmarks of SLI is a deficit in the use of function morphemes (e.g., the, a, and is) and other grammatical morphology (e.g., plural -s, past tense -ed). Children with SLI also are at high risk for subsequent literacy problems (4).The causes of SLI are still hotly debated. Current theories of SLI fall into two categ...

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Section: Discussionmentioning

confidence: 52%

Deficits in speech perception predict language learning impairment

Ziegler

Pech-Georgel

George

et al. 2005

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

178

146

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“…The fact that patterns of impairment are dissociable from cortical-dorsal stream function (Figure 7) shows that the discovery of a novel mechanism of disease can also bring new insights into brain function. Indeed, our findings seem to seriously challenge theories that explain global coherence deficits based on magnocellular impairment (e.g., dyslexia) (25)(26)(27)(28)(29).…”

Section: Figurementioning

confidence: 57%

Visual phenotype in Williams-Beuren syndrome challenges magnocellular theories explaining human neurodevelopmental visual cortical disorders

Mendes¹,

Sebastião²,

Reis³

et al. 2007

J. Clin. Invest.

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Williams-Beuren syndrome (WBS), a neurodevelopmental genetic disorder whose manifestations include visuospatial impairment, provides a unique model to link genetically determined loss of neural cell populations at different levels of the nervous system with neural circuits and visual behavior. Given that several of the genes deleted in WBS are also involved in eye development and the differentiation of retinal layers, we examined the retinal phenotype in WBS patients and its functional relation to global motion perception. We discovered a low-level visual phenotype characterized by decreased retinal thickness, abnormal optic disk concavity, and impaired visual responses in WBS patients compared with age-matched controls by using electrophysiology, confocal and coherence in vivo imaging with cellular resolution, and psychophysics. These mechanisms of impairment are related to the magnocellular pathway, which is involved in the detection of temporal changes in the visual scene. Low-level magnocellular performance did not predict high-level deficits in the integration of motion and 3D information at higher levels, thereby demonstrating independent mechanisms of dysfunction in WBS that will require remediation strategies different from those used in other visuospatial disorders. These findings challenge neurodevelopmental theories that explain cortical deficits based on low-level magnocellular impairment, such as regarding dyslexia.

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“…However, the causal relation between sensory deficits and dyslexia is highly controversial because several studies have found that (i) not all dyslexic persons have sensory deficits and (ii) dyslexics' sensory impairments are not confined to tasks that require rapid sensory processing (31)(32)(33). The lack of a consistent sensory deficit associated with dyslexia has been taken to support the phonological deficit hypothesis, i.e., the view that dyslexia is caused by a deficit that is specific to phoneme processing (1,5,6).…”

Section: Discussionmentioning

confidence: 99%

Dysfunction of the auditory thalamus in developmental dyslexia

Díaz¹,

Hintz²,

Kiebel

et al. 2012

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

153

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Developmental dyslexia, a severe and persistent reading and spelling impairment, is characterized by difficulties in processing speech sounds (i.e., phonemes). Here, we test the hypothesis that these phonological difficulties are associated with a dysfunction of the auditory sensory thalamus, the medial geniculate body (MGB). By using functional MRI, we found that, in dyslexic adults, the MGB responded abnormally when the task required attending to phonemes compared with other speech features. No other structure in the auditory pathway showed distinct functional neural patterns between the two tasks for dyslexic and control participants. Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task modulation of the MGB is critical for performance in dyslexics. These results suggest that deficits in dyslexia are associated with a failure of the neural mechanism that dynamically tunes MGB according to predictions from cortical areas to optimize speech processing. This view on task-related MGB dysfunction in dyslexics has the potential to reconcile influential theories of dyslexia within a predictive coding framework of brain function.functional MRI | speech recognition | auditory processing | magnocellular

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Deficits in perceptual noise exclusion in developmental dyslexia

Cited by 255 publications

References 12 publications

Deficits in speech perception predict language learning impairment

Deficits in speech perception predict language learning impairment

Visual phenotype in Williams-Beuren syndrome challenges magnocellular theories explaining human neurodevelopmental visual cortical disorders

Dysfunction of the auditory thalamus in developmental dyslexia

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