The Neurobiological Strands of Developmental Dyslexia: What We Know and What We Don’t Know

Abstract

This chapter focuses on the definition of dyslexia as “neurobiological in origin” as prescribed by the International Dyslexia Association and National Institute of Child Health and Human Development. The chapter examines the notion of dyslexia as a specific learning disability and challenges the presumption that impairments are specific or limited to reading behavior based on behavioral and neurobiological evidence. The authors argue that the convergence of evidence from neuroimaging studies leading up to the adoption of the definition of dyslexia in 2003 is belied by a larger set of more divergent findings suggesting a variety of etiologies of the disorder. Moreover, the argument for a central phonological deficit behaviorally with neurobiological impairments in regions associated with receptive language processing (roughly surrounding Wernicke’s area) may be just as much an outcome determined by multiple sources of lower-level impairments as it is a cause of dyslexia. Familial risk factors of the disorder are reflected in brain development, and behavior and evidence of genetic markers suggest a certain degree of heritability. However, clear evidence for environmental mediators and successful interventions yields a complex dynamic of how nature and nurture interact in the emergence of the disorder. Thus, this likely equifinality of the disorder requires that large datasets of neurobiological and behavioral data be culled to uncover endophenotypic subtypes or biotypes of dyslexia that may reflect differential responses to intervention.