Journal of Neuroscience. Abnormal Cortical Processing of the Syllable Rate of Speech in Poor Readers. Introduction Reading proficiency relies on the confluence of rudimentary perceptual abilities and higher-order linguistic function (Schlaggar and McCandliss, 2007).
While normal reading is thought to rely on an array of abilities, it is widely thought that reading-impaired individuals suffer from a specific deficit in representing or recalling the precise phonological structure of words (Ramus, 2001). A Computational Model of Implicit Memory Captures Dyslexics' Perceptual Deficits. Introduction The controversy surrounding the deficits underlying dyslexics' difficulties is still unresolved.
The prevailing theory claims that dyslexics' phonological representations, whose adequacy is crucial for efficient usage of the alphabetical code, are impaired (Snowling, 2000). However, dyslexics perform well on some tasks that rely on adequate phonological representations (for review, see: Ramus and Ahissar, 2012). During Visual Word Recognition, Phonology Is Accessed within 100 ms and May Be Mediated by a Speech Production Code: Evidence from Magnetoencephalography. Participants.
Twenty native English-speaking, strongly right-handed adults (mean age 23.2 years, SD 5.97 months; 12 female) gave informed consent to participate in the study. None had been diagnosed reading disabled and all read normally based on WRAT-III performance. Handedness was defined by the Annett Hand Preference Questionnaire (Annett, 1967). The study conformed with The Code of Ethics of the World Medical Association (Declaration of Helsinki). Stimuli. Genetic Variants of FOXP2 and KIAA0319/TTRAP/THEM2 Locus Are Associated with Altered Brain Activation in Distinct Language-Related Regions. Introduction Human language is under strong genetic influence, as indicated by familial studies of clinical populations affected by language impairment (LI) or by reading disability (dyslexia) (Pennington et al., 1991; DeFries, 1996; Stromswold, 2001).
A candidate gene for LI was first evidenced in members of the KE family affected by a missense mutation in FOXP2 gene (chromosome 7q31) that disrupts the DNA-binding site of the protein (Lai et al., 2001). They exhibited severe speech and language deficits as well as orofacial dyspraxia (Vargha-Khadem et al., 1995). Towards a New Neurobiology of Language. Until ∼25 years ago, our knowledge of the brain basis of language processing, the mental faculty considered to be at the very core of human nature, derived largely from rather coarse measures (neurobiologically speaking): deficit-lesion correlations in stroke patients, electrophysiological data from electroencephalographic as well as occasional intracranial recordings (associated with surgical interventions), and relatively crude measures such as the Wada test for language lateralization.
The “classical model” of brain and language, developed in the 19th century by the insightful neurologists Broca (1861), Wernicke (1874), Lichtheim (1885), and others, dominated discourse in the field for more than one hundred years. To this day the Wernicke-Lichtheim model of a left inferior frontal region and a posterior temporal brain area, connected by the arcuate fasciculus fiber bundle, is familiar to every student of the neurosciences, linguistics, and psychology. Figure 1. Figure 2. Unstable Representation of Sound: A Biological Marker of Dyslexia. Jane Hornickel1 and Nina Kraus1,2,3 +Show Affiliations Author contributions: J.H. and N.K. designed research; J.H. performed research; J.H. contributed unpublished reagents/analytic tools; J.H. analyzed data; J.H. and N.K. wrote the paper.