Reading requires the interaction between multiple cognitive processes situated in distant brain areas. This makes the study of functional brain connectivity highly relevant for understanding developmental dyslexia. We used seed-voxel correlation mapping to analyse connectivity in a left-hemispheric network for task-based and resting-state fMRI data. Our main finding was reduced connectivity in dyslexic readers between left posterior temporal areas (fusiform, inferior temporal, middle temporal, superior temporal) and the left inferior frontal gyrus. Reduced connectivity in these networks was consistently present for 2 reading-related tasks and for the resting state, showing a permanent disruption which is also present in the absence of explicit task demands and potential group differences in performance. Furthermore, we found that connectivity between multiple reading-related areas and areas of the default mode network, in particular the precuneus, was stronger in dyslexic compared with nonimpaired readers.
Language difficulties after stroke are commonly thought to stabilise within a year. Hope et al. report surprising evidence to the contrary, showing that the language skills of patients with post-stroke aphasia continue to change even years after stroke. The changes are associated with structural adaptation in the intact right hemisphere.
Time-stable personality traits, such as impulsivity and its relationship with functional and structural brain alterations, have gained much attention in the recent literature. Evidence from functional neuroimaging data implies an association between impulsivity and cortical as well as subcortical areas of the reward system. Discounting future rewards during impulsive decisions can be related to activation in the orbitofrontal cortex and striatum. Cortical structural changes in prefrontal regions have been found for introspective impulsivity measures. The present study focuses on brain regions associated with delay discounting to investigate structural manifestations of trait impulsivity. To test this, seventy subjects underwent structural magnetic resonance imaging (MRI) followed by a behavioral delay discounting task outside of the scanner to measure impulsivity with questions like: “Would you like to have 3€ immediately or 10€ in 5 days?”. The amount of smaller-but-sooner decisions was calculated and used as a measure of behavioral impulsivity. Furthermore, we estimated subject’s individual delay discounting parameter K reflecting the tendency to discount future rewards. Behaviorally, we found strong evidence in favor of a discounting utility model compared to a standard hyperbolic model of choice valuation. Neuronally, we focused on cortical and subcortical brain structure and investigated the association of behavioral impulsivity with delay discounting tendencies and gray matter volume. Voxel-based morphometric analyses showed positive correlations between delay discounting and gray matter volume in the striatum. Additional analyses using Freesurfer provided evidence for a positive correlation between delay discounting and gray matter volume of the caudate. Taken together, our study provides strong evidence for a structural manifestation of time-stable trait impulsivity in the human brain.
This study investigated how sample size affects the reproducibility of findings from univariate voxel-based lesion-deficit analyses (e.g., voxel-based lesion-symptom mapping and voxel-based morphometry). Our effect of interest was the strength of the mapping between brain damage and speech articulation difficulties, as measured in terms of the proportion of variance explained. First, we identified a region of interest by searching on a voxel-by-voxel basis for brain areas where greater lesion load was associated with poorer speech articulation using a large sample of 360 right-handed English-speaking stroke survivors. We then randomly drew thousands of bootstrap samples from this data set that included either 30, 60, 90, 120, 180, or 360 patients. For each resample, we recorded effect size estimates and p values after conducting exactly the same lesion-deficit analysis within the previously identified region of interest and holding all procedures constant. The results show (1) how often small effect sizes in a heterogeneous population fail to be detected; (2) how effect size and its statistical significance varies with sample size; (3) how low-powered studies (due to small sample sizes) can greatly over-estimate as well as under-estimate effect sizes; and (4) how large sample sizes (N ≥ 90) can yield highly significant p values even when effect sizes are so small that they become trivial in practical terms. The implications of these findings for interpreting the results from univariate voxel-based lesion-deficit analyses are discussed.
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