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- W2105659672 abstract "Diverses pathologies neuropsychiatriques, dont le syndrome de Gilles de la Tourette ou la chorée d’Huntington, comportent l’expression de mouvements anormaux et de troubles du comportement. La clinique suggère la possibilité d’une relation avec des dysfonctionnements intéressant les ganglions de la base. L’organisation anatomique de ces structures sous-corticales est décrite en soulignant l’importance de leurs relations avec des aires du cortex cérébral ayant des compétences motrices mais aussi cognitives ou motivationnelles–émotionnelles, avec formation de circuits corticocorticaux distincts via les ganglions de la base et le thalamus. Effectivement, des perturbations cognitives ou motivationelles sont présentes dans plusieurs pathologies lésionnelles exemplaires de ces structures. Ces données cliniques ont été reproduites sur le primate non-humain avec emploi de diverses méthodologies : comportementales, anatomiques et imagerie cérébrale. Ainsi, des activations locales et réversibles, obtenues par micro-injection de bicuculline, entraînent l’expression de réponses parfaitement reproductibles en fonction de la localisation des sites d’injections : expression de mouvements anormaux après atteinte du territoire moteur du segment externe du globus pallidus, d’hyperactivité avec trouble attentionnel pour celle des territoires associatifs, de stéréotypies pour celle du territoire limbique. Au niveau du striatum, on retrouve une partition analogue avec production de mouvements anormaux comme l’expression de tics moteurs ou de troubles de comportement, comme d’hyperactivité, ou au contraire d’apathie, de stéréotypies ou encore d’activités sexuelles. Les analyses anatomiques confirment une organisation en circuits distincts pour chaque type de comportement évoqué. Ainsi, ces résultats valident l’hypothèse d’une participation des ganglions de la base à des troubles de la vie mentale. Abnormal movements and behavioral disorders are characteristic manifestations observed in certain neuropsychiatric diseases such as Tourette's syndrome or Huntington Disease. Together with brain imaging findings, the clinical data could suggest a relationship with basal ganglia dysfunction. In the first part of this review, we recall the anatomic relationships existing, via segregated cortico-cortical circuits, between these structures and the cortical areas having motor and cognitive or motivational–emotional attributes. This structure suggests that in pathologies like Parkinson's or Huntington disease cognitive and motivational–emotional disorders as well motor disturbances could be related to lesions or dysfunctions involving individual or combined zones of the basal ganglia. The second part of the paper focuses on a description of the various methodologies used to explore these relationships: behavioral, anatomic and brain imaging methods are used in non-human primate models in order to reproduce motor and behavioral disturbances and to determine the neuronal circuits involved. Microinjection of bicucullin into the external globus pallidus has been found to induce localized and reversible neuronal activation. Abnormal movements can be obtained from the motor territory of the external globus pallidus whereas hyperactivity with attentional deficit or stereotypies have been obtained from the associative or limbic territory of the same structure. In the striatum, the same pharmacological activation can induce either abnormal movements from motor and associative functional territories or behavioural changes with hyperactivity or, on the contrary, hypoactivity from associative functional territory with stereotyped behavior and sexual manifestations when the microinjections were done in the limbic striatum. Anatomic studies as well as brain imaging using PET confirm the involvement of segregated anatomic pathways through the basal ganglia in behavioral as well as motor disorders." @default.
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- W2105659672 date "2009-09-01" @default.
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- W2105659672 title "Troubles psychiatriques et ganglions de la base : une validation expérimentale" @default.
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- W2105659672 doi "https://doi.org/10.1016/j.pharma.2009.06.003" @default.
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