Functional disruption in the organization of the brain for reading in dyslexia

Abstract

Learning to read requires an awareness that spoken words can be decomposed into the phonologic constituents that the alphabetic characters represent. Such phonologic awareness is characteristically lacking in dyslexic readers who, therefore, have difficulty mapping the alphabetic characters onto the spoken word. To find the location and extent of the functional disruption in neural systems that underlies this impairment, we used functional magnetic resonance imaging to compare brain activation patterns in dyslexic and nonimpaired subjects as they performed tasks that made progressively greater demands on phonologic analysis. Brain activation patterns differed significantly between the groups with dyslexic readers showing relative underactivation in posterior regions (Wernicke's area, the angular gyrus, and striate cortex) and relative overactivation in an anterior region (inferior frontal gyrus). These results support a conclusion that the impairment in dyslexia is phonologic in nature and that these brain activation patterns may provide a neural signature for this impairment.Speech enables its users to create an indefinitely large number of words by combining and permuting a small number of phonologic segments, the consonants and vowels that serve as the natural constituents of the biologic specialization for language. An alphabetic transcription brings this same ability to readers but only as they connect its arbitrary characters (letters) to the phonologic segments they represent. Making that connection requires an awareness that all words, in fact, can be decomposed into phonologic segments. Thus, it is this awareness that allows the reader to connect the letter strings (the orthography) to the corresponding units of speech (phonologic constituents) that they represent. As numerous studies have shown, however, such awareness is largely missing in dyslexic children and adults (1-4). Not surprisingly, then, perhaps the most sensitive measure of the reading problem in dyslexia is inability to read phonologically legal nonsense words (5-7). As for why dyslexic readers should have exceptional difficulty developing phonologic awareness, there is support for the notion that the difficulty resides in the phonologic component of the larger specialization for language (8)(9)(10). If that component is imperfect, its representations will be less than ideally distinct and, therefore, harder to bring to conscious awareness.Previous efforts using functional imaging methods to examine brain organization in dyslexia have been inconclusive (11-17) largely, we think, because the experimental tasks tapped the several aspects of the reading process in somewhat unsystematic ways. Our aim therefore was to develop a set of hierarchically structured tasks that control the kind of language-relevant coding required, including especially the demand on phonologic analysis, and then to compare the performance and brain activation patterns (as measured by functional MRI) of dyslexic (DYS) and nonimpaired (NI) readers. Thus, procee...

The visual word form area: expertise for reading in the fusiform gyrus

“…Over the course of years of extensive experience in extracting invariant information from visual word stimuli, perceptual processes are progressively reorganized, but only in those who become skilled readers. Research with dyslexic adults indicates that, among other areas, the VWFA fails to increase its activity in response to word forms [44,45] (Box 3). A basic functional anatomical model of the typical development of this specialization might provide a framework for the investigation and treatment of atypical development, as in the case of developmental dyslexia.…”

“…Adults with a history of developmental dyslexia demonstrate a reduced tendency to activate VWFA (see Fig. I), among other regions, in response to visual words and pseudowords as measured by fMRI [44,45] and MEG responses within the first 200 ms [14]. Such differences have not yet been associated with neuropathology in this region, but may instead reflect the absence of a specialization that accrues over the course of years of successful reading experience [55].…”

Early emergence of deviant frontal fMRI activity for phonological processes in poor beginning readers

“…In the frontal cortex, phonological processing most often has been attributed to the activity in the posterior and dorsal part of the inferior frontal gyrus and along the precentral gyrus (Jobard et al, 2003;Poldrack et al, 1999;Vigneau et al, 2006), and this frontal activity differed between normal and poor readers. Some studies on reading and rhyming in adults found more left inferior frontal activation for those with dyslexia than for controls (Brunswick et al, 1999;Rumsey et al, 1997;Shaywitz et al, 1998), but others reported more activation for controls (GrossGlenn et al, 1991;Paulesu et al, 1996). Also for children the results are rather inconsistent with dyslexia leading to either more (Georgiewa et al, 2002;Temple et al, 2001) or less activation in the inferior frontal gyrus (Bolger et al, 2008b;Booth et al, 2007;Booth et al, 2008;Cao et al, 2006;Georgiewa et al, 1999;Shaywitz et al, 2002).…”

“…To examine phonological processing, auditory (Booth et al, 2007), visual word (Bolger et al, 2008b;Cao et al, 2006;Hoeft et al, 2006) or letter rhyming tasks (Paulesu et al, 1996;Shaywitz et al, 1998;Temple et al, 2003) have typically been used. In German visual rhyming tasks, rhyming word pairs usually have an increased visual similarity compared to nonrhyming pairs, with the consequence that pure visual matching strategies allow to solve rhyming tasks, without phonological processing.…”

ATP2C2andDYX1C1are putative modulators of dyslexia‐related MMR

“…The heritability was estimated at 50%–70% (de Kovel et al., 2004; Harlaar, Spinath, Dale, & Plomin, 2005; Shaywitz et al., 1998), but only a small proportion of the genetic basis of dyslexia has been uncovered. Linkage studies pointed at nine chromosomal regions (termed DYX1 to 9) and subsequent association studies identified several dyslexia‐related genes within these regions, for example, DYX1C1 , DCDC2 , KIAA0319 , and ROBO1 .…”