Evoked mid-frontal activity predicts cognitive dysfunction in Parkinson's disease.
Evoked mid-frontal activity predicts cognitive dysfunction in Parkinson's disease.
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DOI：
10.1136/jnnp-2022-330154
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发表时间：
2023-11
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--
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认知功能障碍是帕金森病（PD）的主要特征，但其病理生理机制尚不清楚。一个潜在的机制是异常的低频皮质节律，其参与认知功能并且在PD中缺乏。我们检验了额叶中部δ/θ节律预测PD认知功能障碍的假设。我们招募了100名PD患者和49名人口统计学相似的对照参与者，他们完成了一系列认知控制任务，包括Simon，oddball和间隔计时任务。我们关注的是认知正常、轻度认知障碍（PDMCI）或痴呆（PDD）的PD患者中单个中额EEG电极（Cz）的提示诱发δ（1-4 Hz）和θ（4-7 Hz）节律。我们发现，PD相关的认知功能障碍与所有任务中反应潜伏期增加和中额叶三角洲功率降低相关。在PD患者中，来自单个电极（Cz）的诱发EEG特征的第一主成分与蒙特利尔认知评估（莫卡; rho=0.34）和NIH工具箱执行功能评分（rho=0.46）等临床指标密切相关。这些数据表明，线索诱发的额叶中部三角洲/θ节律直接涉及到PD的认知。我们的研究结果提供了深入了解低频额叶节律的性质，并表明PD相关的认知功能障碍的结果从减少三角洲/θ活动。这些发现可能有助于开发新的生物标志物和PD认知症状的靶向治疗。
Cognitive dysfunction is a major feature of Parkinson’s disease (PD), but the pathophysiology remains unknown. One potential mechanism is abnormal low-frequency cortical rhythms which engage cognitive functions and are deficient in PD. We tested the hypothesis that midfrontal delta/theta rhythms predict cognitive dysfunction in PD. We recruited 100 PD patients and 49 demographically-similar control participants who completed a series of cognitive control tasks, including the Simon, oddball, and interval timing tasks. We focused on cue-evoked delta (1-4 Hz) and theta (4-7 Hz) rhythms from a single midfrontal EEG electrode (Cz) in PD patients who were either cognitively normal, with mild-cognitive impairments (PDMCI), or had dementia (PDD). We found that PD-related cognitive dysfunction was associated with increased response latencies and decreased midfrontal delta power across all tasks. Within PD patients, the first principal component of evoked EEG features from a single electrode (Cz) strongly correlated with clinical metrics such as the Montreal Cognitive Assessment (MOCA; rho=0.34) and with NIH-toolbox Executive Function scores (rho=0.46). These data demonstrate that cue-evoked midfrontal delta/theta rhythms directly relate to cognition in PD. Our results provide insight into the nature of low-frequency frontal rhythms and suggest that PD-related cognitive dysfunction results from decreased delta/theta activity. These findings could facilitate the development of new biomarkers and targeted therapies for cognitive symptoms of PD.
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