Developmental dyslexia, characterized by unexplained difficulty in reading, is associated with behavioral deficits in phonological processing. Functional neuroimaging studies have shown a deficit in the neural mechanisms underlying phonological processing in children and adults with dyslexia. The present study examined whether behavioral remediation ameliorates these dysfunctional neural mechanisms in children with dyslexia. Functional MRI was performed on 20 children with dyslexia (8 -12 years old) during phonological processing before and after a remediation program focused on auditory processing and oral language training. Behaviorally, training improved oral language and reading performance. Physiologically, children with dyslexia showed increased activity in multiple brain areas. Increases occurred in left temporo-parietal cortex and left inferior frontal gyrus, bringing brain activation in these regions closer to that seen in normal-reading children. Increased activity was observed also in right-hemisphere frontal and temporal regions and in the anterior cingulate gyrus. Children with dyslexia showed a correlation between the magnitude of increased activation in left temporo-parietal cortex and improvement in oral language ability. These results suggest that a partial remediation of language-processing deficits, resulting in improved reading, ameliorates disrupted function in brain regions associated with phonological processing and produces additional compensatory activation in other brain regions.

In functional neuroimaging studies, individuals with dyslexia frequently exhibit both hypoactivation, often in the left parietotemporal cortex, and hyperactivation, often in the left inferior frontal cortex, but there has been no evidence to suggest how to interpret the differential relations of hypoactivation and hyperactivation to dyslexia. To address this question, we measured brain activation by functional MRI during visual word rhyme judgment compared with visual cross-hair fixation rest, and we measured gray matter morphology by voxel-based morphometry in dyslexic adolescents in comparison with (i) an age-matched group, and (ii) a readingmatched group younger than the dyslexic group but equal to the dyslexic group in reading performance. Relative to the agematched group (n ‫؍‬ 19; mean 14.4 years), the dyslexic group (n ‫؍‬ 19; mean 14.4 years) exhibited hypoactivation in left parietal and bilateral fusiform cortices and hyperactivation in left inferior and middle frontal gyri, caudate, and thalamus. Relative to the readingmatched group (n ‫؍‬ 12; mean 9.8 years), the dyslexic group (n ‫؍‬ 12; mean 14.5 years) also exhibited hypoactivation in left parietal and fusiform regions but equal activation in all four areas that had exhibited hyperactivation relative to age-matched controls as well. In regions that exhibited atypical activation in the dyslexic group, only the left parietal region exhibited reduced gray matter volume relative to both control groups. Thus, areas of hyperactivation in dyslexia reflected processes related to the level of current reading ability independent of dyslexia. In contrast, areas of hypoactivation in dyslexia reflected functional atypicalities related to dyslexia itself, independent of current reading ability, and related to atypical brain morphology in dyslexia.inferior frontal region ͉ inferior parietal lobule ͉ voxel-based morphometry ͉ functional MRI ͉ compensation D yslexia is a developmental condition characterized by low reading achievement in people who otherwise have cognitive abilities, motivation, and education necessary for accurate and fluent reading (1). Dyslexia, estimated to affect 5-17% of children and 80% of all individuals with a learning disability (2, 3), is characterized by inaccurate and/or slow, effortful reading that typically originates with weakness in the phonological processing of language (4-8).The brain basis of dyslexia has been examined by functional and structural neuroimaging. Functional imaging studies regularly report hypoactivation in dyslexia, especially in the left parietotemporal region, which may support the mapping of phonology onto orthography, and in the left fusiform region, which may support skilled orthographic decoding (9-12). Hyperactivation in dyslexia has also been observed, most frequently in left inferior frontal gyrus (IFG) (13)(14)(15)(16)(17)(18)(19). Hyperactivation in left IFG, a region associated with articulation and naming (20), may reflect compensatory processes engaged by dyslexic individuals attempting to overcome...