Impulsivity and apathy in Parkinson's disease

被引:71
|
作者
Sinha, Nihal [1 ,2 ,3 ,4 ]
Manohar, Sanjay [1 ,2 ,3 ,4 ]
Husain, Masud [1 ,2 ,3 ,4 ]
机构
[1] Univ Oxford, Nuffield Dept Clin Neurosci, Oxford OX3 9DU, England
[2] Univ Oxford, Dept Expt Psychol, Oxford OX3 9DU, England
[3] UCL, Inst Cognit Neurosci, London WC1E 6BT, England
[4] UCL, Inst Neurol, London WC1E 6BT, England
关键词
SUBTHALAMIC NUCLEUS STIMULATION; STRIATAL DOPAMINE RELEASE; DEEP BRAIN-STIMULATION; DECISION-MAKING; CONTROL DISORDERS; STOP-SIGNAL; PREFRONTAL CORTEX; BASAL GANGLIA; NEUROPSYCHIATRIC SYMPTOMS; BEHAVIORAL-INHIBITION;
D O I
10.1111/jnp.12013
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Impulse control disorders (ICDs) and apathy are recognized as two important neuropsychiatric syndromes associated with Parkinson's disease (PD), but as yet we understand very little about the cognitive mechanisms underlying them. Here, we review emerging findings, from both human and animal studies, that suggest that impulsivity and apathy are opposite extremes of a dopamine-dependent spectrum of motivated decision making. We first argue that there is strong support for a hypodopaminergic state in PD patients with apathy, as well as for an association between dopamine therapy and development of ICDs. However, there is little evidence for a clear dose-response relationship, and great heterogeneity of findings. We argue that dopaminergic state on its own is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their surface' manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural and neurobiological evidence leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD.
引用
收藏
页码:255 / 283
页数:29
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