Abstract
Current research suggests that the neurobiological substrate of dyslexia involves the dysfunctional orchestration of a multi-dimensional and hierarchical circuitry of at least three neuronal networks. This circuitry principally involves the posterior corpus callosum, left arcuate fasciculous, and the right frontostriatal attentional control network. The key to understanding the disability and in forging a comprehensive theory of dyslexia may be found in investigations aimed at interactions among all three networking territories.
Highlights
Current research suggests that the neurobiological substrate of dyslexia involves the dysfunctional orchestration of a multi-dimensional and hierarchical circuitry of at least three neuronal networks
Studies have produced strong support in some individuals with dyslexia for deficits in spatial and auditory attention [11,12], visual magnocellulardorsal pathway deficits [13], deficits in cerebellar functions [14], and deficits in interhemispheric processing [15]. While each of these behavioral and neurological factors may be clinically important when considering intervention and counselling, each has been linked with phonological deficits, suggesting a deficiency in phonological processing may constitute a common final pathway of the disability
The review will present the broad outlines of a theory of dyslexia that attempts to integrate the variety of subtypes and putative etiological factors into a unified circuitry of interconnected neuronal networks: a tripartite widely distributed, attentionally-controlled, cortical-subcortical
Summary
The most common finding revealed by functional magnetic resonance imaging (fMRI) studies is that poor readers underactivate attentionally-controlled left hemisphere posterior areas, principally including dorsal temporoparietal and ventral occipitotemporal cortex [1]. Studies have shown that reading instruction with illiterate adults, and intensive remedial training with children who are poor readers can produce structural improvements of the left arcuate concomitant with gains in reading [28,29]. Studies have found that the initial coherence of the direct segment of the left arcuate was (1) already anomalous in prereaders at familial risk for dyslexia [31] and (2) predictive in normal children of their reading ability over a three year period [32]. The structural integrity of the left arcuate fasciculus appears to be receptive to reading instruction, and a significant cause of reading failure in children and adults
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