Individuals with developmental dyslexia vary in their ability to improve reading skills, but the brain basis for improvement remains largely unknown. We performed a prospective, longitudinal study over 2.5 y in children with dyslexia (n = 25) or without dyslexia (n = 20) to discover whether initial behavioral or brain measures, including functional MRI (fMRI) and diffusion tensor imaging (DTI), can predict future long-term reading gains in dyslexia. No behavioral measure, including widely used and standardized reading and language tests, reliably predicted future reading gains in dyslexia. Greater right prefrontal activation during a reading task that demanded phonological awareness and right superior longitudinal fasciculus (including arcuate fasciculus) white-matter organization significantly predicted future reading gains in dyslexia. Multivariate pattern analysis (MVPA) of these two brain measures, using linear support vector machine (SVM) and cross-validation, predicted significantly above chance (72% accuracy) which particular child would or would not improve reading skills (behavioral measures were at chance). MVPA of whole-brain activation pattern during phonological processing predicted which children with dyslexia would improve reading skills 2.5 y later with >90% accuracy. These findings identify right prefrontal brain mechanisms that may be critical for reading improvement in dyslexia and that may differ from typical reading development. Brain measures that predict future behavioral outcomes (neuroprognosis) may be more accurate, in some cases, than available behavioral measures.inferior frontal gyrus | prediction | compensation | fractional anisotropy | rhyming D evelopmental dyslexia, which occurs in 5-17% of children, is a persistent difficulty in learning to read that is not explained by sensory deficits, cognitive deficits, lack of motivation, or lack of adequate reading instruction (1). Approximately one-fifth of individuals with developmental dyslexia manage to compensate for their underlying learning difficulties and develop adequate reading skills by the time they reach adulthood (2), but the mechanisms by which this compensation occurs remain largely unknown. Improved reading observed in developmental dyslexia is rarely complete, but instead refers to a level of reading superior to clinical cutoff scores that closes the gap between poor reader and typical readers, and that allows children to read adequately for purposes of learning. Many factors likely influence whether dyslexic children make substantial progress in reading, including access to educational resources and interventions, and neuropsychological and behavioral characteristics (reviewed in refs. 3 and 4), such as whether children have multiple deficits (e.g., in both rapid naming and phonological processing; ref. 5). A number of studies have examined neuropsychological, behavioral, and demographic predictors of developing dyslexia (e.g., refs. 6-8) and short-term response to intervention (RTI) (3, 4), but there is little evidence...

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...

Humour is a vital component of human socio-affective and cognitive functioning. Recent advances in neuroscience have enabled researchers to explore this human attribute in children and adults. Humour seems to engage a core network of cortical and subcortical structures, including temporo-occipito-parietal areas involved in detecting and resolving incongruity (mismatch between expected and presented stimuli); and the mesocorticolimbic dopaminergic system and the amygdala, key structures for reward and salience processing. Examining personality effects and sex differences in the neural correlates of humour may aid in understanding typical human behaviour and the neural mechanisms underlying neuropsychiatric disorders, which can have dramatic effects on the capacity to experience social reward.