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...

Adults and children with developmental dyslexia exhibit reduced parietotemporal activation in functional neuroimaging studies of phonological processing. These studies used age-matched and/or intelligence quotient-matched control groups whose reading ability and scanner task performance were often superior to that of the dyslexic group. It is unknown, therefore, whether differences in activation reflect simply poorer performance in the scanner, the underlying level of reading ability, or more specific neural correlates of dyslexia. To resolve this uncertainty, we conducted a functional magnetic resonance imaging study, with a rhyme judgment task, in which we compared dyslexic children with two control groups: age-matched children and reading-matched children (younger normal readers equated for reading ability or scanner-performance to the dyslexic children). Dyslexic children exhibited reduced activation relative to both age-matched and reading-matched children in the left parietotemporal cortex and five other regions, including the right parietotemporal cortex. The dyslexic children also exhibited reduced activation bilaterally in the parietotemporal cortex when compared with children equated for task performance during scanning. Nine of the 10 dyslexic children exhibited reduced left parietotemporal activation compared with their individually selected age-matched or reading-matched control children. Additionally, normal reading fifth graders showed more activation in the same bilateral parietotemporal regions than normal-reading third graders. These findings indicate that the activation differences seen in the dyslexic children cannot be accounted for by either current reading level or scanner task performance, but instead represent a distinct developmental atypicality in the neural systems that support learning to read.