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Contribution of therapeutic strategies for understanding the Tourette syndrome
- L. Mallet, E. Burguière, Y. Worbe, A. Hartmann
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- Journal:
- European Psychiatry / Volume 30 / Issue S2 / November 2015
- Published online by Cambridge University Press:
- 15 April 2020, pp. S19-S20
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Motion is a behavior involving a motor act programmed and executed in a particular cognitive and emotional context. Deep structures of the brain, including the basal ganglia, appear to play a crucial role in the integration of these three kinds of cortex information (motion, cognition, emotion). Through its organization, the basal ganglia system enables learning and memorization of behavioral sequences, which can then be executed as routines. Their dysfunctions seem to be associated with many psychopathological situations. Thus, tics in Tourette's syndrome (TS) can be seen as a control routines defect that may result from wiring anomaly between the cortex and the basal ganglia. By precisely targeting deep brain circuits implicated in psychiatric disorders, deep brain stimulation (DBS) offers hope for the alleviation of severe illnesses resistant to drug therapies and provides a novel tool to investigate the neuroanatomic and physiological bases of certain disorders, including Obsessive-Compulsive Disorder (OCD) and TS, for which early results indicate positive therapeutic outcomes, even during the long-term follow-up. The pathophysiologies of OCD and of TS share dysfunctions of the associative and limbic circuits running between cortical and sub-cortical structures. Recent pathophysiological hypotheses suggest that TS symptoms result from a dysfunction of the basal ganglia circuitry, notably of the ventral striatum. These data are consistent with the supposed function of cortico-basal ganglia circuits in habit learning and routine performance of habits. Based on early reports indicating that high-frequency stimulation of structures along the cortico-basal ganglia axis might be effective in alleviating TS symptoms, DBS is being tested across the world at several nodes of this circuit, including the pallidum, and thalamus. Increasing our knowledge of the functional organization of the cortico-basal ganglia circuits and of their dysfunction in pathological repetitive behaviors would certainly contribute to better define the surgical therapeutic targets, thereby improving available treatments.
Impulsivity in disorders of food and drug misuse
- T. B. Mole, M. A. Irvine, Y. Worbe, P. Collins, S. P. Mitchell, S. Bolton, N. A. Harrison, T. W. Robbins, V. Voon
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- Journal:
- Psychological Medicine / Volume 45 / Issue 4 / March 2015
- Published online by Cambridge University Press:
- 14 August 2014, pp. 771-782
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Background.
Evidence suggests some overlap between the pathological use of food and drugs, yet how impulsivity compares across these different clinical disorders remains unclear. Substance use disorders are commonly characterized by elevated impulsivity, and impulsivity subtypes may show commonalities and differences in various conditions. We hypothesized that obese subjects with binge-eating disorder (BED) and abstinent alcohol-dependent cohorts would have relatively more impulsive profiles compared to obese subjects without BED. We also predicted decision impulsivity impairment in obesity with and without BED.
Method.Thirty obese subjects with BED, 30 without BED and 30 abstinent alcohol-dependent subjects and age- and gender-matched controls were tested on delay discounting (preference for a smaller immediate reward over a larger delayed reward), reflection impulsivity (rapid decision making prior to evidence accumulation) and motor response inhibition (action cancellation of a prepotent response).
Results.All three groups had greater delay discounting relative to healthy volunteers. Both obese subjects without BED and alcohol-dependent subjects had impaired motor response inhibition. Only obese subjects without BED had impaired integration of available information to optimize outcomes over later trials with a cost condition.
Conclusions.Delay discounting appears to be a common core impairment across disorders of food and drug intake. Unexpectedly, obese subjects without BED showed greater impulsivity than obese subjects with BED. We highlight the dissociability and heterogeneity of impulsivity subtypes and add to the understanding of neurocognitive profiles across disorders involving food and drugs. Our results have therapeutic implications suggesting that disorder-specific patterns of impulsivity could be targeted.