Voxel-based morphometry (VBM) has demonstrated structural brain changes between patients with Major Depressive Disorder (MDD) and healthy individuals. The initial response to antidepressants is crucial to predict prognosis in the treatment of MDD. The aim of the present study was to investigate gray matter abnormalities predicting antidepressant responsiveness and the relationships between volumetric differences and clinical/cognitive traits in MDD patients.
Tourette syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics. Tics are repetitive and uncontrolled behaviours that have been associated with basal ganglia dysfunction. We investigated saccadic eye movements in a group of young people with TS but without co-morbid ADHD. Participants performed two tasks. One required them to perform only pro-saccade responses (pure pro-saccade task). The other involved shifting, unpredictably, between executing pro- and anti-saccades (mixed saccade task). We show that in the mixing saccade task, the TS group makes significantly fewer errors than an age-matched control group, while responding equally fast. By contrast, on the pure pro-saccade task, the TS group were shown to be significantly slower to initiate and to complete the saccades (longer movement duration and decreased peak velocity) than controls, while movement amplitude and direction accuracy were not different. These findings demonstrate enhanced shifting ability despite slower reflexive responding in TS and are discussed with respect to a disorder-related adaptation for increased cognitive regulation of behaviour.
The uncertainty over the true morphological changes in brains with major depressive disorder (MDD) underlines the necessity of comprehensive studies with multimodal structural brain imaging analyses. This study aimed to evaluate the differences in cortical thickness, cortical and subcortical volume, and white matter integrity between first episode, medication-naïve MDD patients and healthy controls.
Children with neurological disorders may follow unique developmental trajectories whereby they undergo compensatory neuroplastic changes in brain structure and function that help them gain control over their symptoms. We used behavioral and brain imaging techniques to investigate this conjecture in children with Tourette syndrome (TS). Using a behavioral task that induces high levels of intermanual conflict, we show that individuals with TS exhibit enhanced control of motor output. Then, using structural (diffusion-weighted imaging) brain imaging techniques, we demonstrate widespread differences in the white matter (WM) microstructure of the TS brain that include alterations in the corpus callosum and forceps minor (FM) WM that significantly predict tic severity in TS. Most importantly, we show that task performance for the TS group (but not for controls) is strongly predicted by the WM microstructure of the FM pathways that lead to the prefrontal cortex and by the functional magnetic resonance imaging blood oxygen level-dependent response in prefrontal areas connected by these tracts. These results provide evidence for compensatory brain reorganization that may underlie the increased self-regulation mechanisms that have been hypothesized to bring about the control of tics during adolescence.
Tourette syndrome [TS] is a neurodevelopmental disorder characterised by chronic vocal and motor tics. TS has been associated with dysfunctional cognitive (inhibitory) control of behaviour, however the evidence for this, beyond the occurrence of tics, is scant. Furthermore, in recent studies of uncomplicated TS, it has been shown that adolescents with TS exhibit paradoxically enhanced cognitive control of motor output, consistent with the typical developmental profile of increasing control of tics during adolescence. Here we present arguments, together with new data, that run counter to the widely held view that prefrontal cortex (PFC) is the source of inhibitory task-control signals. Instead, we argue that PFC should be viewed as a source of facilitatory signals that bias competition in brain areas more directly involved in motor execution. Importantly, we argue that in TS, over-activation of PFC may contribute to the hyper-excitability of motor regions and the occurrence of tics; and that compensatory changes, leading to enhanced cognitive control in TS, may primarily be implemented by distributed changes in local cortical excitability.
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