Impaired learning of phonetic consistency and generalized neural adaptation deficits in dyslexia

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2012.Cataloged from PDF version of thesis.Includes bibliographical references (p. 81-93).Developmental dyslexia is a neurological condition that specifically impairs the development of expert reading ability. Phonological processing deficits -- impaired representation of, or access to, the abstract units of spoken language -- have been implicated as the principal source of reading difficulties in dyslexia, independent of other cognitive factors. However, the source of these phonological impairments remains unknown: What mechanisms preclude development of the robust phonological representations critical for reading development? Experiments with phonological processing in dyslexia typically employ metalinguistic tasks that require explicit knowledge about phonological structure, failing to distinguish between access to representations and the representations themselves. Here I report a series of experiments that elucidate the nature of phonological impairments in dyslexia by examining the implicit processing of phonetic variability. Phonetic variability affects language processing at the interface between perceiving the physical speech signal and mapping it onto stored linguistic representations. This approach is well-suited to interrogate the integrity of phonological processing in dyslexia and to provide insight into how phonological representations may come to be impaired in this disorder. In Experiment 1, individuals with dyslexia demonstrated profoundly reduced ability to learn to use phonetic consistency in talker identification, thus reifying the status of phonological representations themselves as fundamentally impaired in this disorder. In Experiment 2, functional magnetic resonance imaging (fMRI) adaptation revealed reduced neural sensitivity to phonetic consistency during speech perception in individuals with dyslexia, indicating impaired rapid, implicit learning of phonetic-phonological consistency. The neural mechanisms that support such learning may be a specific instance of general brain mechanisms for adapting to stimulus consistency. In Experiment 3, fMRI adaptation further revealed that such exiguous neural plasticity in dyslexia is not limited to speech phonetics; instead, the core mechanisms of rapid adaptation to stimulus consistency appear to be dysfunctional in dyslexia, such that neural adaptation was reduced to all stimuli measured, whether auditory or visual, linguistic or non-linguistic. Deficits in neural adaptation may represent disruption of a core rapid plasticity mechanism for perceptual learning, dysfunction of which would impair the ability to develop the robust perceptual (phonological) representations critical to reading development.by Tyler K. Perrachione.Ph.D

Shared Neuroanatomical Substrates of Impaired Phonological Working Memory Across Reading Disability and Autism

Background Individuals with reading disability and individuals with autism spectrum disorder (ASD) are characterized, respectively, by their difficulties in reading and social communication, but both groups often have impaired phonological working memory (PWM). It is not known whether the impaired PWM reflects distinct or shared neuroanatomical abnormalities in these two diagnostic groups. Methods White-matter structural connectivity via diffusion weighted imaging was examined in 64 children, age 5 to 17 years, with reading disability, ASD, or typical development, who were matched on age, gender, intelligence, and diffusion data quality. Results Children with reading disability and children with ASD exhibited reduced PWM compared with children with typical development. The two diagnostic groups showed altered white matter microstructure in the temporoparietal portion of the left arcuate fasciculus and in the occipitotemporal portion of the right inferior longitudinal fasciculus (ILF), as indexed by reduced fractional anisotropy and increased radial diffusivity. Moreover, the structural integrity of the right ILF was positively correlated with PWM ability in the two diagnostic groups but not in the typically developing group. Conclusions These findings suggest that impaired PWM is transdiagnostically associated with shared neuroanatomical abnormalities in ASD and reading disability. Microstructural characteristics in left arcuate fasciculus and right ILF may play important roles in the development of PWM. The right ILF may support a compensatory mechanism for children with impaired PWM

Optimized Design and Analysis of Sparse-Sampling fMRI Experiments

Sparse-sampling is an important methodological advance in functional magnetic resonance imaging (fMRI), in which silent delays are introduced between MR volume acquisitions, allowing for the presentation of auditory stimuli without contamination by acoustic scanner noise and for overt vocal responses without motion-induced artifacts in the functional time series. As such, the sparse-sampling technique has become a mainstay of principled fMRI research into the cognitive and systems neuroscience of speech, language, hearing, and music. Despite being in use for over a decade, there has been little systematic investigation of the acquisition parameters, experimental design considerations, and statistical analysis approaches that bear on the results and interpretation of sparse-sampling fMRI experiments. In this report, we examined how design and analysis choices related to the duration of repetition time (TR) delay (an acquisition parameter), stimulation rate (an experimental design parameter), and model basis function (an analysis parameter) act independently and interactively to affect the neural activation profiles observed in fMRI. First, we conducted a series of computational simulations to explore the parameter space of sparse design and analysis with respect to these variables; second, we validated the results of these simulations in a series of sparse-sampling fMRI experiments. Overall, these experiments suggest the employment of three methodological approaches that can, in many situations, substantially improve the detection of neurophysiological response in sparse fMRI: (1) Sparse analyses should utilize a physiologically informed model that incorporates hemodynamic response convolution to reduce model error. (2) The design of sparse fMRI experiments should maintain a high rate of stimulus presentation to maximize effect size. (3) TR delays of short to intermediate length can be used between acquisitions of sparse-sampled functional image volumes to increase the number of samples and improve statistical power.Ellison Medical FoundationNational Science Foundation (U.S.) Graduate Research Fellowship ProgramNational Institutes of Health (U.S.) (Grant R03-EB008673

Electrophysiological correlates of perceptual prediction error are attenuated in dyslexia

A perceptual adaptation deficit often accompanies reading difficulty in dyslexia, manifesting in poor perceptual learning of consistent stimuli and reduced neurophysiological adaptation to stimulus repetition. However, it is not known how adaptation deficits relate to differences in feedforward or feedback processes in the brain. Here we used electroencephalography (EEG) to interrogate the feedforward and feedback contributions to neural adaptation as adults with and without dyslexia viewed pairs of faces and words in a paradigm that manipulated whether there was a high probability of stimulus repetition versus a high probability of stimulus change. We measured three neural dependent variables: expectation (the difference between prestimulus EEG power with and without the expectation of stimulus repetition), feedforward repetition (the difference between event-related potentials (ERPs) evoked by an expected change and an unexpected repetition), and feedback-mediated prediction error (the difference between ERPs evoked by an unexpected change and an expected repetition). Expectation significantly modulated prestimulus theta- and alpha-band EEG in both groups. Unexpected repetitions of words, but not faces, also led to significant feedforward repetition effects in the ERPs of both groups. However, neural prediction error when an unexpected change occurred instead of an expected repetition was significantly weaker in dyslexia than the control group for both faces and words. These results suggest that the neural and perceptual adaptation deficits observed in dyslexia reflect the failure to effectively integrate perceptual predictions with feedforward sensory processing. In addition to reducing perceptual efficiency, the attenuation of neural prediction error signals would also be deleterious to the wide range of perceptual and procedural learning abilities that are critical for developing accurate and fluent reading skills.National Institutes of Health (Grants UL1RR025758, R03HD096098, T32DC000038 and F31HD100101

Dysfunction of Rapid Neural Adaptation in Dyslexia

Identification of specific neurophysiological dysfunctions resulting in selective reading difficulty (dyslexia) has remained elusive. In addition to impaired reading development, individuals with dyslexia frequently exhibit behavioral deficits in perceptual adaptation. Here, we assessed neurophysiological adaptation to stimulus repetition in adults and children with dyslexia for a wide variety of stimuli, spoken words, written words, visual objects, and faces. For every stimulus type, individuals with dyslexia exhibited significantly diminished neural adaptation compared to controls in stimulus-specific cortical areas. Better reading skills in adults and children with dyslexia were associated with greater repetition-induced neural adaptation. These results highlight a dysfunction of rapid neural adaptation as a core neurophysiological difference in dyslexia that may underlie impaired reading development. Reduced neurophysiological adaptation may relate to prior reports of reduced behavioral adaptation in dyslexia and may reveal a difference in brain functions that ultimately results in a specific reading impairment.NIH (Grant UL1RR025758