Understanding the Dyslexia Field - Research Paper Example

Dyslexia Introduction In recent years progress has been made understanding the psychological processes related to dyslexia, leading to a more sophisticated definition of the phenotype for reading failure (Stanovich, 2003; Klein & McMullen, 1999). Many critical advancements in understanding were precipitated by a fundamental shift in dyslexic research that, beginning in the 1960's, moved steadily away from the clinical description of behavior, and toward questions of etiology and pathogenesis (Snowling, 2000). The explicit goal of most research since this shift has been to understand the cognitive basis of dyslexia, which was thought to offer a more scientific and parsimonious account of the behavioral symptoms associated with reading failure (Frith, 1986; Klein & McMullen, 1999). Grounded in the broader field of cognitive neuropsychology, the modern study of dyslexia is notable for a reliance on theory-driven research, the search for causal cognitive explanations, and the view that such cognitive deficits have unique neurological underpinnings (Lyon, Shaywitz, & Shaywitz, 2003). This approach has proven remarkably successful at delineating the cognitive underpinnings of dyslexia, and has motivated a body of research that spans several domains. As such, any attempt to understand the interdisciplinary study of dyslexia necessarily begins with a consideration of the cognitive-neuropsychological view of reading failure. This paper provides a brief overview of the cognitive-neuropsychological approach to dyslexia, which represents the prevailing paradigm for both research and practice. The aim is to offer a sense of the genuine strengths of this approach, and also the inherent weaknesses. Next section opens with a discussion of the assumptions of cognitive neuropsychology. This is followed with an overview of the key advancements that have been made working within this framework, focusing on the success of prominent single-cause cognitive models of dyslexia, and the brain imaging research it has motivated. While acknowledging the importance of this approach for advancing the science of reading failure, this paper concludes with a critique of the cognitive-neuropsychological view, centering on three issues: (1) the heterogeneity of symptoms present in dyslexia, (2) the comorbidity of dyslexia and AD /HD, and (3) the lack of consideration for developmental factors. Taken together, these issues call into question the usefulness of any single-cause model of dyslexia, and suggest the need for a more flexible view of reading failure. Assumptions of Cognitive Neuropsychology The dominant research paradigm in dyslexia today is anchored in the relatively new field of cognitive neuropsychology, and it is worth briefly considering the key assumptions of this approach. Cognitive neuropsychology aims to understand the cognitive architecture of the mind (Caramazza & Coltheart, 2006), although recent efforts (influenced by cognitive neuroscience) have also focused on localizing such mechanisms in the brain (Lyon, Shaywitz, & Shaywitz, 2003). This reciprocal view of the mind and brain-where cognitive research can inform us about how the brain must work, and brain research helps refine our understanding of the characteristics of cognition (Caramazza, 1992)-is widely shared in dyslexic research (Bishop, 1997). To appreciate the ramifications of this approach for education, it must be recognize that this view carries assumptions about the nature of dyslexia, which may or may not reflect reality. Specifically, this approach holds at least three axioms: (1) the modularity of mind, (2) the universality principle, and (3) the specificity of deficits. (1) Modularity of mind. This assumption holds that the architecture of the mind is largely compartmentalized, and that highly specialized cognitive systems (e.g., language) consist of multiple component processes, each dedicated to one aspect of the job (i.e., phonological versus semantic systems) (Fodor, 1983). There are published articles that provide a thorough treatment of both modularity as a concept, and the long-standing arguments for and against such a view of the mind (e.g., Barrett & Kurzban, 2006). It is sufficient to point out that when researchers speak of a 'modular' system, they typically mean that the system possesses at least two characteristics: (a) domain-specificity, in that it only responds to a certain class of stimuli (i.e., an module driven by auditory stimuli would not respond to light); and (b) information-encapsulation, in that the system is largely invariant to outside information or processes (i.e., a visual module would not be modulated by auditory stimuli) (Morton & Munakata, 2005). While researchers disagree about the nature and extent of the modularity of mind, the concept continues to have a profound influence on the scope and direction of research and practice in dyslexia. (2) The universality principle. This is perhaps the fundamental assumption on which the cognitive-neuropsychological enterprise rests-without it there is question as to whether the methods and tools of this approach are valid at all (Caramazza & Coltheart, 2006). Basically, the principle is that there is no qualitative variation in cognitive systems across individuals, without specific brain damage (Caramazza, 1986). For dyslexia this means that, absent brain damage, the cognitive systems involved in reading are relatively invariant in the population (Klein & McMullen, 1999). (3) Specificity of deficits. Driven by the assumptions of both modularity and universality, cognitive-neuropsychological research has historically eschewed a focus on the clustering of symptoms (i.e., the clinical 'syndrome') in favor of an emphasis on the study of individual symptoms (Barrett & Kurzban, 2006). At a theoretical level, this perspective reflects the view that the heterogeneous symptoms present in dyslexia at the behavioral level can be reduced to a relatively circumscribed dysfunction in the cognitive architecture of the mind (Morton & Munakata, 2005). Translated to learning disabilities, this has fueled the notion that there can be specific deficits-where all other cognitive systems are 'intact', with the exception of the one mechanism in question (Shaywitz & Shaywitz, 2005). In dyslexia research this led to a focus on models that seek unitary causal explanations at the cognitive level. The key here is that, as with the cognitive-neuropsychological approach to all learning disorders, the emphasis is overwhelmingly on a problem that is inherent to the individual (Tannock, 1998). Cognitive Foundations, Causal Explanations Perhaps the single most important consequence of the shift toward cognitive-level explanations in the field of dyslexia has been the increased focus on both theory and theory driven research. The development of testable (and falsifiable) theories of dyslexia effectively moved the field beyond the inherent limitations of clinical description, and placed it on the kind of scientific footing that naturally facilitates the growth of sustainable, integrative, and cumulative knowledge (Berninger & Shaywitz, 2006). Over the past twenty years a multitude of models have emerged to explain the underlying mechanisms responsible for dyslexia ­some scientific, others not. Most were dismissed in relatively short-order, either by the force of sheer logic, or in light of emerging findings, While there are a handful of theories that find support in the scientific community today (Ramus, White, & Frith, 2006), following section will focus on one-the phonological core-deficit model-as it has been the dominant paradigm for the study of dyslexia over the past twenty years. Dyslexia, in Theory Building on advancements made in our understanding of human speech (Liberman, Cooper, Shankweiler, & Studdert, 1967; Just & Carpenter, 1992), over the past several years researchers have made substantial progress delineating the critical link between reading failure and more subtle deficits in oral language (Klein & McMullen, 1999). Grounded in cognitive neuropsychology, the model that has come to dominate the field of dyslexia emphasizes the importance of inefficient word recognition, which is thought to stem from a dysfunction in the phonological system of language (Torgesen, Wagner, & Rashotte, 1994). Through this lens, children with dyslexia are viewed as having a specific deficit in phonological processing (Stanovich, 1988) that limits their ability to categorize speech sounds and relate them to orthography (Snowling, 2000). The concept of 'phonological processing' is an umbrella term that is typically indexed by several subcomponent skills, including: (1) Phonological Awareness: explicit awareness of the sound-structure of language (Byrne, Fielding-Barnsley, & Ashley, 1996); (2) Phonological Memory: the ability to retain phonological representations in short-term memory (Baddeley, Gathercole, & Papagno, 1998); and (3) Rapid Lexical Retrieval: the speed and accuracy with which phonological codes are retrieved from memory (Wolf, 1999). Within the current conceptualization of dyslexia, phonological deficits are assumed to lead causally to single-word decoding problems which, in turn, create a cascade of secondary problems that can disrupt overall literacy development (Snowling, 2000). The phonological model of dyslexia has come to dominate research and practice over the past 20 years, and has motivated an unprecedented level of research dedicated to the topic of reading failure (Klein & McMullen, 1999). While disagreements exist, there is a general consensus that the cognitive model is basically correct, in that evidence overwhelmingly supports a role for phonological processing in dyslexia (Vellutino, Fletcher, Snowling, & Scanlon, 2004). An indicator of the success of this model is the fact that most current research is no longer focused on the validity of the phonological hypothesis itself, but on understanding the nature of the phonological construct (Marshall, Snowling, & Bailey, 2001) and its antecedents (Thomson, Fryer, Maltby, & Goswami, 2006). Neurological Correlates of Dyslexia Given the strong influence of cognitive neuropsychology on research and theory in dyslexia, it is perhaps not surprising that the success of the cognitive model has motivated a considerable body of research seeking to delineating the cortical underpinnings of reading failure. While the notion of a brain basis for dyslexia is not new, it has only been in recent years, with the emergence of powerful and non-invasive imaging techniques, that genuine advancements have been made understanding the neural circuitry that mediates the cognitive deficits in dyslexia. While still in its infancy, evidence from the functional imaging literature provides support for the notion of a neurobiological signature for dyslexia (Shaywitz & Shaywitz, 2005). Specifically, several studies of children and adults with dyslexia have found structural and functional abnormalities in predominantly left-hemisphere language areas, suggesting a broad disruption to several linguistically-oriented brain systems that are involved in normal reading (Simos et al., 2000; Lyon, Shaywitz, & Shaywitz, 2003). Despite considerable variability across studies, the imaging research has generally supported the broad claims of the phonological-deficit cognitive model of dyslexia (Lyon, Shaywitz, & Shaywitz, 2003). The Limits of Brain Imaging There is no doubt that brain imaging represents an important domain for future research in dyslexia; however, there are serious limitations with most current studies. Many of the critical issues simply reflect the broader concerns about the utility of the cognitive neuropsychological approach to studying dyslexia. However, special attention is warranted here, due to a near universal lack of appreciation for the limits of modern brain research. While converging evidence does suggest a neurological correlate for dyslexia, extreme caution must be exercised when drawing inferences from this body of research. Too often scientists, clinicians, and educators assume that current evidence supports a neurological cause for dyslexia. While such a view lends itself nicely to current cognitive theories, it is not that simple. No matter how intuitive, biological correlates are not the same as biological causes. The brain is incredibly dynamic, and it is well understood that experience alters both the structure and function of those very cortical areas associated with dyslexia (Rubia, 2002). Research does support a brain-behavior relationship for dyslexia; it does not provide unequivocal evidence regarding the direction of this link. Emerging brain research represents an important source of insight for understanding dyslexia, but we must not endow these studies with an authority that extends beyond their scientific merit. Intervention/Treatment In an attempt to discover a way to enhance reading in dyslexic children, Breznitz (1997a) used reading acceleration and auditory masking. Reading accelera­tion was thought to reduce the reliance on phonologically based decoding by increas­ing the reliance on orthographic and contextual cues. Auditory masking was thought to interfere with phonological deficits by overloading the phonological processing with task-irrelevant information. Breznitz used 104 Hebrew-speaking children, evenly divided into dyslexic and normal readers. The dyslexic children ranged in age from 8 years, 7 months to 9 years, 10 months. The normal children ranged in age from 6 years, 4 months to 7 years, 5 months. Tests in materials word recognition, PA, and comprehension were given to all participants. Raw results were analyzed using two­ way MANOVA and a univariate ANOVA. Results showed improvement using both reading acceleration and auditory masking. Reading acceleration appeared to improve reading comprehension. Auditory masking was done using a familiar children's tune; it appeared to reduce oral reading errors, increase reading speed, and increase the benefits of reading acceleration. Even greater improvement was shown when both variables were used together. There was no attempt to distinguish between prelexical and postlexical phonological interference. This study was done in Israel, so there might be other confounds if it were attempted in other countries. Breznitz (1997b) looked at accelerated reading and memory for text. This study involved 23 Hebrew-speaking dyslexic children with a mean age of 9 years, 3 months. The measures were a variety of verbal and nonverbal short-term memory tests. The students read from a computer three times, first at their normal speed, then at an accelerated speed, and then again at normal speed. Four experiments assessed (a) recognition and recall of semantic content and exact wording of text, (b) memory for wording and word order, (c) memory for wording compared with memory for semantic information, and (d) the effects of reading acceleration on short-term memory func­tioning. Analysis was by within-subjects ANOVA for the first experiment and by repeated measures ANOVA for the other experiments. Results for experiment 1 showed improvement in reading rate, accuracy, and comprehension but no improve­ment in exact wording in accelerated reading. Results for experiment 2 showed improvement in forward order recall and better recall of primacy parts of items. Results for experiment 3 showed greater improvement in identification of word conditions than semantic wording conditions. Results for experiment 4 showed more recall of prior words than subsequent words. The overall indications were that accelerated reading was associated with increased reading rate, accuracy, and compre­hension. The results also indicated that a reliance on context was important; there appeared to be an improvement with short-term memory functioning under those circumstances. Since this study was done in Israel, replication in other languages would be recommended, preferably with a larger participant base. Outstanding Issues Despite the unquestionable success of the current phonological model of dyslexia, it is important to point out that this approach is not without problems. The truth is that the current model is fundamentally limited in several ways, and that many of the most critical questions about dyslexia remain unanswered. Relevant for educational researchers and policy makers, the phonological model has proven incapable of accounting for (a) the heterogeneity of behavioral and cognitive symptoms associated with dyslexia, (b) the considerable overlap of dyslexic and ADHD symptoms, and (c) the changing relationship between word reading deficits and more complex problems with comprehension across developmental time. (a) Heterogeneity of symptoms. At all levels (e.g., behavioral, cognitive, neurological, and genetic) dyslexia has proven to be a heterogeneous syndrome (Ramus, White, & Frith, 2006). The phonological model provides a parsimonious account for many behavioral and cognitive deficits associated with reading failure; however, it cannot adequately account for a host of non-linguistic impairments routinely observed in children with dyslexia, including problems with low-level perceptual processing, motor coordination, attention, and verbal short-term/ working memory (Everatt, Bradshaw, & Hibbard, 1999). Unfortunately, there are few studies that have systematically examined non-linguistic processes concurrently with phonological processing in the same individuals, so it is difficult to know how (or even if) they are related. However, the limited evidence that does exist suggests that a wide variety of symptoms are relevant to dyslexia, and that many of them cannot be explained by phonological processing impairments alone (Eden, VanMeter, Rumsey, & Zefflro, 1996). (b) Comorbidity with ADHD. A second issue that has been difficult to explain in the current cognitive model is the frequent co-occurrence of dyslexic and ADHD symptoms. Despite seemingly disparate behavioral and cognitive phenotypes, dyslexia and ADHD co­occur at a rate far greater than chance, with overlap rates reported anywhere from 25-50% in community-based samples (Willcutt & Pennington, 2000). Recently, prominent researchers working within the cognitive-neuropsychological framework have acknowledged that current models of dyslexia cannot account for this overlap, suggesting a near fatal blow for the utility of single-deficit models of reading failure (pennington, 2006). In short, it is absolutely clear that phonological deficits alone do not provide a sufficient explanation for persistent deficits in inattention, impulsivity, and hyperactivity (the hallmark symptoms of ADHD) that often manifest in children and adolescents with dyslexia. (c) Reading comprehension. Over the past several years there has been growing interest in bridging the gap between single-word deficits in dyslexia-where there is a substantial body of scientific evidence-and more complex issues of connected-text fluency and reading comprehension in adolescence (Katzir et al., 2006). The phonological model assumes that problems in comprehension are a secondary impairment, arising as a product of a deficit in phonological processing (Lyon, Shaywitz, & Shaywitz, 2003). Researchers who support this view point out that a large portion of the variance in reading comprehension in dyslexia is explained by variability in single-word reading (Perfetti, 1993). However, this research has largely been restricted to young children (Holsgrove & Garton, 2006), and there are reasons to question how well the results generalize beyond this restricted age group (Albert, 1999). Notably, in the adolescent literature comprehension deficits are commonly found in dyslexic students, and often persist even when phonological or single ­word deficits are no longer apparent (Ransby & Swanson, 2003). Further, empirical evidence suggests that the relationship between single-word reading and comprehension is nowhere near as strong in adolescence as it is in childhood (Savage et al., 2005). Literature Summary As outlined in this paper, the field of dyslexia has witnessed unparalleled growth over the past thirty years. Research during this time span has been heavily influenced by cognitive neuropsychology, where the emphasis has been on understanding the cognitive underpinnings of reading failure, and more recently on localizing these deficits in the brain. The most notable characteristics of this approach have been the emphasis on questions of etiology and pathogenesis, and the emergence of theory-driven research that seeks causal explanations at the cognitive level. The strength of this framework for studying dyslexia is evident by the overwhelming success of the single-cause cognitive models it has generated. Most prominent is the phonological model, which suggests that the proximal problem in dyslexia is at the level of single-word decoding, arising as a result of a fundamental deficit in phonological processing. This model has been the catalyst for unprecedented levels of research into the nature of reading failure, and has motivated an impressive body of work that now spans multiple disciplines simultaneously. Beyond its influence in research, this approach has become the dominant lens through which educators and policy makers view dyslexia: it specifies the mechanisms by which we determine whether a child is learning disabled (and thus is entitled to individualized remediation) or not. Despite the progress that has been made in understanding dyslexia (and perhaps because of it) the field has reached a point where it is beginning to hit upon some of the weaknesses of the phonological model. Among the most salient limitations that are relevant to education, evidence suggests that the phonological model cannot easily account for the heterogeneity of symptoms evident in children with dyslexia, or the substantial overlap of dyslexic and ADHD symptoms. Researchers are also beginning to question the utility of this approach for addressing the complex issue of reading comprehension failure in adolescents with dyslexia. While the growth of theory-driven research-and in particular the work motivated by the phonological model of dyslexia-has helped advance the science of reading failure, emerging findings provide a strong argument against the utility of any single ­cause explanation for something as complex as dyslexia. That is, while there is little question phonological deficits play an important (and likely proximal) role in the dyslexic phenotype, there is considerable doubt whether such a parsimonious account is sufficient to explain the rich variability evident in dyslexia at all levels of analysis. Annotated Bibliography Klein, Raymond, & McMullen, Patricia A. (1999). Converging Methods for Understanding Reading and Dyslexia (Language, Speech, and Communication). 1 edition, The MIT Press. Raymond Klein and Patricia McMullen illustrate different approaches used by scientists to understand the complex skill of reading and its breakdown” two rather different approaches to understanding developmental dyslexia: remediation effectiveness and behavioral-genetic analysis. Breznitz, Z. (1997). Effects of accelerated reading rate on memory for text among dyslexic readers. Journal of Educational Psychology, 89(2),289-297. Zvia Breznitz ,On the basis of findings that reading performance improves substantially among dyslexic children. Verbal or phonological short term memory (STM) is thought to play a significant part in the acquisition of decoding skills, the mastery of which is critical to learning to read. Data obtained through this research paradigm consistently indicate that reading rate can function as an independent variable that influences the quality of reading performance. References Albert, M. G. (1999). Developmental dyslexia: a multilevel syndrome. Dyslexia, 5(4),183-191. Baddeley, A., Gathercole, S., & Papagno, C. (1998). The phonological loop as a language learning device. Psychological Review, 105(1), 158-173. Barrett, H. c., & Kurzban, R. (2006). Modularity in cognition: Framing the debate. P Psychological Review, 113 (3), 628-647. Berninger, V. W., & Shaywitz, B. A. (2006). Special issue: Brain imaging: Window on reading and its disorders - Introduction to the special issue. Developmental Neuropsychology, 30(1), 527-530. Bishop, D. V. M. (1997). Cognitive neuropsychology and developmental disorders: Uncomfortable bedfellows. Quarterly Journal of Experimental Psychology Section a-Human Experimental Psychology, 50(4), 899-923. Breznitz, Z. (1997a). Enhancing the reading of dyslexic children by reading acceleration and auditory making. Journal of Educational Psychology, 89, 103-113. Breznitz, Z. (1997b). Effects of accelerated reading rate on memory for text among dyslexic readers. Journal of Educational Psychology, 89(2),289-297. Byrne, B., Fielding-Barnsley, R., & Ashley, L. (1996). What does the child bring to the task of learning to read? A summary of the New England reading acquisition projects. Australian Journal of Psychology, 48(3), 119-123. Caramazza, A. (1992). Is cognitive neuropsychology possible? Journal of Cognitive Neuroscience, 4(1),80-95. Caramazza, A., & Coltheart, M. (2006). Cognitive neuropsychology twenty years on. Cognitive Neuropsychology, 23(1),3-12. Eden, G. F., VanMeter, J. W., Rumsey, J. M., & Zeffiro, T. A. (1996). The visual deficit theory of developmental dyslexia. Neuroimage, 4, S108-117. Everatt, J., Bradshaw, M., & Hibbard, P. (1999). Visual processing and dyslexia. Perception, 28(2), 243 - 254. Fodor, J. A. (1983). Modularity of Mind: An Essay on Faculty Psychology. Cambridge, MA.: MIT Press. Frith, U. (1986). A developmental framework for developmental dyslexia. Annals of Dyslexia, 36,69-81. Holsgrove, J. V., & Garton, A. F. (2006). Phonological and syntactic processing and the role of working memory in reading comprehension among secondary school students. Australian Journal of Psychology, 58(2), 111-118. Just, M. A., & Carpenter, P. A. (1992). A capacity theory of comprehension - Individual differences in working memory. Psychological Review, 99(1), 122-149. Katzir, T., Kim, Y., Wolf, M., O'Brien, B., Kennedy, B., Lovett, M., et al. (2006). Reading fluency: The whole is more than the parts. Annals of Dyslexia, 56(1), 51-82. Liberman, A. M., Cooper, F. S., Shankweiler, D., & Studdert, M. (1967). Perception of Speech Code. Psychological Review, 74(6),431-&. Lyon, G. R., Shaywitz, S. E., & Shaywitz, B. A. (2003). A definition of dyslexia. Annals of Dyslexia, 53, 1-14. Marshall, C. M., Snowling, M. J., & Bailey, P. J. (2001). Rapid auditory processing and phonological ability in normal readers and readers with dyslexia. Journal of Speech Language and Hearing Research, 44(4), 925-940. Morton, J. B., & Munakata, Y. (2005). What's the difference? Contrasting modular and neural network approaches to understanding developmental variability. Journal of Developmental and Behavioral Pediatrics, 26(2), 128-139. Pennington, B. F. (2006). From single to multiple deficit models of developmental disorders. Cognition, 101 (2), 385-413. Perfetti, C. A. (1993). Reading and its development: Component skills approaches. Contemporary Psychology, 38(2), 136-137. Ramus, F., White, S., & Frith, U. (2006). Weighing the evidence between competing theories of dyslexia. Developmental Science, 9(3), 265-269. Ransby, M. J., & Swanson, H. L. (2003). Reading comprehension skills of young adults with childhood diagnoses of dyslexia. Journal of Learning Disabilities, 36(6), 538-555. Rubia, K. (2002). The dynamic approach to neuro developmental psychiatric disorders: use of fMRI combined with neuropsychology to elucidate the dynamics of psychiatric disorders, exemplified in AD HD and schizophrenia. Behavioural Brain Research, 130(1­2),47-56. Savage, R. S., Frederickson, N., Goodwin, R., Patni, u., Smith, N., & Tuersley, L. (2005). Relationships among rapid digit naming, phonological processing, motor automaticity, and speech perception in poor, average, and good readers and spellers. Journal of Learning Disabilities, 38(1), 12-28. Shaywitz, S. E., & Shaywitz, B. A. (2005). Dyslexia (specific reading disability). Biological Psychiatry, 57(11), 1301-1309. Simos, P. G., Breier, J. I., Wheless, J. W., Maggio, W. W., Fletcher, J. M., Castillo, E. M., et al. (2000). Brain mechanisms for reading: the role of the superior temporal gyrus in word and pseudoword naming. Neuroreport, 11(11),2443-2447. Snowling, M. J. (2000). Dyslexia: Blackwell. Stanovich, K. E. (1988). The right and wrong places to look for the cognitive locus of reading-disability. Annals of Dyslexia, 38, 154-177. Stanovich, K. E. (2003). Understanding the styles of science in the study of reading. Scientific Studies of Reading, 7(2), 105-126. Tannock, R. (1998). Attention deficit hyperactivity disorder: Advances in cognitive, neurobiological, and genetic research. Journal of Child Psychology and Psychiatry, 39(1), 65-99. Thomson, J. M., Fryer, B., Maltby, J., & Goswami, U. (2006). Auditory and motor rhythm awareness in adults with dyslexia. Journal of Research in Reading, 29(3),334-348. Torgesen, J., Wagner, R., & Rashotte, C. (1994). Longitudinal-studies of phonological processing and reading. Journal of Learning Disabilities, 27(5), 276-286. Vellutino, F. R., Fletcher, J. M., Snowling, M. J., & Scanlon, D. M. (2004). Specific reading disability (dyslexia): what have we learned in the past four decades? Journal of Child Psychology & Psychiatry & Allied Disciplines, 45(1), 2-40. Willcutt, E. G., & Pennington, B. F. (2000). Psychiatric comorbidity in children and adolescents with reading disability. Journal of Child Psychology and Psychiatry, 41 (8), 1039­-1048. Wolf, M. (1999). What time may tell: Towards a-new conceptualization of developmental dyslexia. Annals if Dyslexia, 49, 3-28. Read More