Developmental dyslexia is a specific learning disability characterized by difficulties with accurate and fluent word recognition and poor spelling and decoding abilities, despite adequate intelligence, instruction, and motivation. Affecting 5-10% of the population, dyslexia is the most common learning disability and has been extensively studied from cognitive, neurological, and genetic perspectives.
The Phonological Deficit Hypothesis
The most widely supported explanation is the phonological deficit hypothesis: dyslexia stems from a core difficulty in processing the sound structure of language. This impairs phonological awareness (detecting and manipulating speech sounds), phonological memory (verbal short-term memory), and rapid automatized naming (quickly naming familiar visual items). The phonological deficit disrupts the mapping between written letters and speech sounds that is essential for learning to read alphabetically.
Neural and Genetic Basis
Neuroimaging reveals underactivation in left-hemisphere posterior reading regions (temporoparietal and occipitotemporal cortex) and sometimes compensatory overactivation in right-hemisphere and frontal regions. Structural differences in white matter tracts connecting language areas have been identified. Dyslexia is highly heritable (40-60% of variance is genetic), with several susceptibility genes identified that are involved in neuronal migration and axon guidance during brain development.
The most effective interventions focus on explicit, systematic instruction in phonological awareness and phonics — teaching the relationships between letters and sounds through structured, multisensory approaches. Early intervention (before or during first grade) is more effective than later intervention, but improvements can be achieved at any age. Accommodations (extra time, audiobooks, text-to-speech technology) help manage the condition, while intervention targets the underlying phonological deficit.