Journal
BRAIN
Volume 131, Issue -, Pages 165-179Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/awm278
Keywords
frontal; striatal; paediatric; brain imaging; disorder
Categories
Funding
- NATIONAL INSTITUTE OF MENTAL HEALTH [K08MH072958] Funding Source: NIH RePORTER
- NIMH NIH HHS [K08 MH072958] Funding Source: Medline
Ask authors/readers for more resources
Tourette syndrome (TS) is a neurodevelopmental disorder characterized by involuntary motor and phonic tics. It is hypothesized that excess dopamine leads to an imbalance in the pathways through the basal ganglia, resulting in unchecked movements via thalamic disinhibition. It has been unclear whether TS is associated with cognitive control deficits as well as pure motor control deficits, or whether cognitive deficits are associated with the presence of comorbid conditions. Furthermore, little is known about the neural underpinnings of TS in childhood, prior to the long-term effects of medication on brain function. Here, children with TS and typically developing children performed a cognitive control task during event-related fMRI data acquisition. The study included 18 native English-speaking 713-year-old children with TS (M = 10.42; 15 males), and 19 healthy, age-matched native English-speaking volunteers (M = 10.33; 11 males). The task involved three separate manipulations of cognitive control. Behaviourally, higher tic severity was correlated with slower task performance on the most demanding task conditions. Neurally, higher tic severity was associated with enhanced activation of dopaminergic nuclei (substantia nigra/ventral tegmental area) and cortical, striatal and thalamic regions in the direct pathway. Heightened tic severity was also associated with greater engagement of the subthalamic nucleus area, suggestive of a compensatory mechanism. Overall, patients engaged left prefrontal cortex more strongly than typicals during task performance. These data suggest that children aged 713 unmedicated for TS exhibit increased activation in the direct pathway through the basal ganglia, as well as increased compensatory activation in prefrontal cortex and the subthalamic nucleus.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available