Publications (2)17.9 Total impact
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Article: A developmental fMRI study of self-regulatory control.
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ABSTRACT: We used functional magnetic resonance imaging (fMRI) to investigate the neural correlates of self-regulatory control across development in healthy individuals performing the Stroop interference task. Proper performance of the task requires the engagement of self-regulatory control to inhibit an automatized response (reading) in favor of another, less automatic response (color naming). Functional MRI scans were acquired from a sample of 70 healthy individuals ranging in age from 7 to 57 years. We measured task-related regional signal changes across the entire cerebrum and conducted correlation analyses to assess the associations of signal activation with age and with behavioral performance. The magnitude of fMRI signal change increased with age in the right inferolateral prefrontal cortex (Brodmann area [BA] 44/45) and right lenticular nucleus. Greater activation of the right inferolateral prefrontal cortex also accompanied better performance. Activity in the right frontostriatal systems increased with age and with better response inhibition, consistent with the known functions of frontostriatal circuits in self-regulatory control. Age-related deactivations in the mesial prefrontal cortex (BA 10), subgenual anterior cingulate cortex (BA 24), and posterior cingulate cortex (BA 31) likely represented the greater engagement of adults in self-monitoring and free associative thought processes during the easier baseline task, consistent with the improved performance on this task in adults compared with children. Although we cannot exclude the possibility that age-related changes in reading ability or in the strategies used to optimize task performance were responsible for our findings, the correlations of brain activation with performance suggest that changes in frontostriatal activity with age underlie the improvement in self-regulatory control that characterizes normal human development.Human Brain Mapping 12/2006; 27(11):848-63. · 5.88 Impact Factor -
Article: Habit learning in Tourette syndrome: a translational neuroscience approach to a developmental psychopathology.
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ABSTRACT: The etiology of Tourette syndrome (TS) involves disturbances in the structure and function of the basal ganglia. The basal ganglia mediate habit learning. To study habit learning in persons with TS. Patients with TS were compared with normal controls in performance on a probabilistic classification, or habit-learning task (weather prediction). University research institute. One hundred twenty-three children and adults, 56 with a diagnosis of TS and 67 healthy control subjects. Habit learning was assessed by the extent of improvement in accuracy of predictions and reaction times over trial blocks during performance of the weather prediction task. Declarative learning was assessed by performance on 3 tasks that required intact declarative memory functioning. Children with TS were impaired at habit learning relative to normal controls (P = .01). This finding was replicated in the independent sample of adults with TS (P = .01). The rate of learning correlated inversely with the severity of tic symptoms across both samples (r = -0.34; P = .01). Thus, impaired learning accompanied more severe symptoms. Measures of declarative memory functioning, in contrast, were normal in the TS groups. Striatal learning systems are uniquely dysfunctional in both children and adults with TS. The correlation of habit learning with symptom severity suggests that the number and severity of tics are a function of the degree to which the system for habit learning is dysfunctional. Thus, both the deficits in habit learning and the tic symptoms of TS are likely to be consequences of the previously reported anatomical and functional disturbances of the striatum in children and adults who have TS. The existence of a well-developed animal model for this learning system, which permits study of the neural and molecular bases of habit learning, has important implications for the neurobiological study of TS and for the development of new or improved therapeutics for this condition.Archives of General Psychiatry 01/2005; 61(12):1259-68. · 12.02 Impact Factor
