- AutorIn
- Christian Beste
- Mark Humphries
- Carsten Saft
- Titel
- Striatal disorders dissociate mechanisms of enhanced and impaired response selection — Evidence from cognitive neurophysiology and computational modelling
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:14-qucosa-147586
- Quellenangabe
- NeuroImage: Clinical, 2014, Volume 4, pp. 623-634, ISSN: 2213-1582
- Erstveröffentlichung
- 2014
- Abstract (EN)
- Paradoxically enhanced cognitive processes in neurological disorders provide vital clues to understanding neural function. However, what determines whether the neurological damage is impairing or enhancing is unclear. Here we use the performance of patients with two disorders of the striatum to dissociate mechanisms underlying cognitive enhancement and impairment resulting from damage to the same system. In a two-choice decision task, Huntington\'s disease patients were faster and less error prone than controls, yet a patient with the rare condition of benign hereditary chorea (BHC) was both slower and more error prone. EEG recordings confirmed significant differences in neural processing between the groups. Analysis of a computational model revealed that the common loss of connectivity between striatal neurons in BHC and Huntington\'s disease impairs response selection, but the increased sensitivity of NMDA receptors in Huntington\'s disease potentially enhances response selection. Crucially the model shows that there is a critical threshold for increased sensitivity: below that threshold, impaired response selection results. Our data and model thus predict that specific striatal malfunctions can contribute to either impaired or enhanced selection, and provide clues to solving the paradox of how Huntington\'s disease can lead to both impaired and enhanced cognitive processes.
- Andere Ausgabe
- DOI: 10.1016/j.nicl.2014.04.003
- Link zur Originalpublikation in der Zeitschrift NeuroImage: Clinical.
Link: http://dx.doi.org/10.1016/j.nicl.2014.04.003 - Freie Schlagwörter (DE)
- Computersimulation, Basalganglien, Exekutive Funktionen, Benigne hereditäre Chorea, Chorea Huntington, EEG, TU Dresden, Publikationsfonds
- Freie Schlagwörter (EN)
- Computational modelling, Basal ganglia, Executive control, Benign hereditary chorea, Huntington's disease, EEG, Technical University Dresden, Publication funds
- Klassifikation (DDC)
- 610
- Klassifikation (RVK)
- XA 10000
- Verlag
- Elsevier, Amsterdam
- URN Qucosa
- urn:nbn:de:bsz:14-qucosa-147586
- Veröffentlichungsdatum Qucosa
- 15.07.2014
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
- CC BY-NC-ND 3.0