Walton Courtney C, O'Callaghan Claire, Hall Julie M, Gilat Moran, Mowszowski Loren, Naismith Sharon L, Burrell James R, Shine James M, Lewis Simon J G
Parkinson's Disease Research Clinic, Brain and Mind Centre, University of Sydney, 94 Mallett Street, Camperdown, NSW, Australia.
Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.
J Neurol. 2015 Dec;262(12):2745-54. doi: 10.1007/s00415-015-7910-5. Epub 2015 Oct 13.
Freezing of gait is a poorly understood symptom of Parkinson's disease (PD) that is commonly accompanied by executive dysfunction. This study employed an antisaccade task to measure deficits in inhibitory control in patients with freezing, and to determine if these are associated with a specific pattern of grey matter loss using voxel-based morphometry. PD patients with (n = 15) and without (n = 11) freezing along with 10 age-matched controls were included. A simple prosaccade task was administered, followed by a second antisaccade task that required subjects to either look towards or away from a peripheral target. Behavioral results from the antisaccade task were entered as covariates in the voxel-based morphometry analysis. Patient and control groups performed equally well on the first task. However, patients with freezing were significantly worse on the second, which was driven by a specific impairment in suppressing their responses toward the target on the antisaccade trials. Impaired antisaccade performance was associated with grey matter loss across bilateral visual and fronto-parietal regions. These results suggest that patients with freezing have a significant deficit of inhibitory control that is associated with volume reductions in regions crucial for orchestrating both complex motor behaviors and cognitive control. These findings highlight the inter-relationship between freezing of gait and cognition and confirm that dysfunction along common neural pathways is likely to mediate the widespread cognitive dysfunction that emerges with this symptom.
冻结步态是帕金森病(PD)中一种尚未被充分理解的症状,通常伴有执行功能障碍。本研究采用反扫视任务来测量冻结患者的抑制控制缺陷,并使用基于体素的形态测量法确定这些缺陷是否与特定的灰质丢失模式相关。纳入了有冻结症状的PD患者(n = 15)和无冻结症状的PD患者(n = 11)以及10名年龄匹配的对照者。先进行一个简单的顺向扫视任务,然后进行第二个反扫视任务,要求受试者看向或远离一个外周目标。反扫视任务的行为结果作为协变量纳入基于体素的形态测量分析。患者组和对照组在第一个任务上表现相当。然而,有冻结症状的患者在第二个任务上明显更差,这是由反扫视试验中抑制对目标反应的特定损伤所驱动的。反扫视表现受损与双侧视觉和额顶叶区域的灰质丢失有关。这些结果表明,有冻结症状的患者存在显著的抑制控制缺陷,这与对协调复杂运动行为和认知控制至关重要的区域的体积减少有关。这些发现突出了冻结步态与认知之间的相互关系,并证实共同神经通路的功能障碍可能介导了伴随该症状出现的广泛认知功能障碍。