Functional compensation or pathology in cortico-subcortical interactions in preclinical Huntington's disease?

被引:47
作者
Beste, Christian
Saft, Carsten
Yordanova, Juliana
Andrich, Juergen
Gold, Ralf
Falkenstein, Michael
Kolev, Vasil
机构
[1] WHO Collaborating Ctr Occupat Hlth & Human Factor, Leibniz Res Ctr Working Environm & Human Factors, D-44139 Dortmund, Germany
[2] Ruhr Univ Bochum, St Josef Hosp, Huntingdon Ctr NRW, Dept Neurol, Bochum, Germany
[3] Bulgarian Acad Sci, Inst Physiol, BU-1113 Sofia, Bulgaria
关键词
event-related potential (ERP); error negativity (Ne/ERN); time-frequency decomposition; performance monitoring; Huntington's disease; flanker task; ADENOSINE A(2A) RECEPTORS; ERROR-RELATED NEGATIVITY; DOPAMINE-RECEPTORS; ERP COMPONENTS; MOUSE MODEL; ONSET; BRAIN; DYSFUNCTION; MARKERS; CORTEX;
D O I
10.1016/j.neuropsychologia.2007.06.004
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Huntington's disease (HD) is an autosomal dominant neurological disorder, with degeneration amongst others affecting the basal ganglia dopaminergic system. Recent findings suggest compensatory as well as pathogenetic mechanisms mediated via the adenosine receptor system in the presymptomatic stage (pHD) of HD. The adenosine receptor system is functionally related to the dopaminergic system. In this study, we assessed error processing, a dopamine-dependent cognitive function, using an event-related potential the error negativity (Ne/ERN) in pHD and controls. This was done by means of a flanker task. The Ne consists of a cognitive and a motor component, expressed via different frequency bands. Time-frequency decomposition of the Ne into delta and theta sub-components was applied to assess if degeneration or compensation predominantly involve cognitive or motor processes. No parameter of the behavioral data (reaction times, error frequency, corrections, post-error slowing) differed between the groups. A selective increase in the power of the cognitive delta-Ne component was found in pHD relative to controls inversely related to the estimated age of onset (eAO). Thus, the increase in the power of the cognitive delta-Ne component was stronger in pHD with an earlier eAO. An earlier eAO implies stronger pathogenetic mechanisms. Due to the behavioral data our results speak for a solely cognitive compensating-mechanism controlling performance monitoring in pHD. In contrast, correlations with eAO suggest that the increase in delta-Ne activity is also related to pathogenesis. It is proposed that compensation is a transient effect of the whole pathogenetic dynamics of HD, with these two processes not foreclosing each other. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:2922 / 2930
页数:9
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