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Review Functional disturbances within frontostriatal circuits across multiple childhood psychopathologies. 2009
Marsh R, Maia TV, Peterson BS. · Department of Psychiatry, Division of Child and Adolescent Psychiatry, Columbia College of Physicians and Surgeons, New York State Psychiatric Institute, 1051 Riverside Dr., Unit 74, New York, NY 10032, USA. · Am J Psychiatry. · Pubmed #19448188 No free full text.
Abstract: OBJECTIVE: Neuroimaging studies of healthy individuals inform us about the normative maturation of the frontostriatal circuits that subserve self-regulatory control processes. Findings from these studies can be used as a reference frame against which to compare the aberrant development of these processes in individuals across a wide range of childhood psychopathologies. METHOD: The authors reviewed extensive neuroimaging evidence for the presence of abnormalities in frontostriatal circuits in children and adults with Tourette's syndrome and obsessive-compulsive disorder (OCD) as well as a more limited number of imaging studies of adolescents and adults with anorexia nervosa or bulimia nervosa that, together, implicate dysregulation of frontostriatal control systems in the pathogenesis of these eating disorders. RESULTS: The presence of an impaired capacity for self-regulatory control that derives from abnormal development of frontostriatal circuits likely interacts in similar ways with normally occurring somatic sensations and motor urges, intrusive thoughts, sensations of hunger, and preoccupation with body shape and weight to contribute, respectively, to the development of the tics of Tourette's syndrome, the obsessions of OCD, the binge eating behaviors of bulimia, and the self-starvation of anorexia. CONCLUSIONS: Analogous brain mechanisms in parallel frontostriatal circuits, or even in differing portions of the same frontostriatal circuit, may underlie the differing behavioral disturbances in these multiple disorders, although further research is needed to confirm this hypothesis.
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Article Habit learning in Tourette syndrome: a translational neuroscience approach to a developmental psychopathology. free! 2004
Marsh R, Alexander GM, Packard MG, Zhu H, Wingard JC, Quackenbush G, Peterson BS. · Division of Child and Adolescent Psychiatry in the Department of Psychiatry, New York State Psychiatric Institute and College of Physicians and Surgeons, Columbia University, New York 10032, USA. · Arch Gen Psychiatry. · Pubmed #15583117 links to free full text
Abstract: BACKGROUND: The etiology of Tourette syndrome (TS) involves disturbances in the structure and function of the basal ganglia. The basal ganglia mediate habit learning. OBJECTIVE: To study habit learning in persons with TS. DESIGN: Patients with TS were compared with normal controls in performance on a probabilistic classification, or habit-learning task (weather prediction). SETTING: University research institute. PARTICIPANTS: One hundred twenty-three children and adults, 56 with a diagnosis of TS and 67 healthy control subjects. MAIN OUTCOME MEASURES: 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. RESULTS: 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. CONCLUSIONS: 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.
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