Injury patterns associated with cognitive motor dissociation.
Injury patterns associated with cognitive motor dissociation.
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DOI：
10.1093/brain/awad197
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发表时间：
2023-08
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通讯作者：
Eva Franzova;Qi-Feng Shen;K. Doyle;Justine M Chen;Jennifer Egbebike;Athina Vrosgou;J. Carmona;Lauren Grobois;Gregory Heinonen;Angela Velazquez;Ian Jerome Gonzales;Satoshi Egawa;Sachin Agarwal;D. Roh;Soojin Park;E. Connolly;J. Claassen
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作者：
Eva Franzova;Qi-Feng Shen;K. Doyle;Justine M Chen;Jennifer Egbebike;Athina Vrosgou;J. Carmona;Lauren Grobois;Gregory Heinonen;Angela Velazquez;Ian Jerome Gonzales;Satoshi Egawa;Sachin Agarwal;D. Roh;Soojin Park;E. Connolly;J. Claassen
在急性脑损伤的无意识出现的患者中，对运动命令的故意大脑激活而没有命令遵循的行为迹象，称为认知运动分离（CMD），与功能恢复相关。CMD可以通过将机器学习应用于在行为无反应患者的运动命令呈现期间记录的EEG来检测。识别患有CMD的患者对患者的互动、与家人的沟通以及治疗决策的指导具有临床意义，但CMD的潜在机制仍然未知。通过分析结构性病变模式和网络水平功能障碍，我们测试的假设，在保留唤醒和命令理解的情况下，未能整合理解的运动命令与运动输出的基础CMD。在接受基于EEG的CMD评估和MRI的连续无反应的急性脑损伤患者（n = 107）中，对T2液体衰减反转恢复和弥散加权成像序列进行手动分割，量化结构损伤。应用病变模式分析来确定CMD患者（n = 21）和非CMD患者（n = 86）中常见的病变模式。分别采用ABCD功率谱密度图分类和加权成对相位一致性（WPPC）对静息EEG评估丘脑皮质和皮质-皮质网络连通性。两个不同的结构性病变的模式，确定了对CMD和非CMD患者的MRI。在非CMD患者中，观察到包括中脑在内的脑干唤醒通路损伤，而CMD患者没有中脑病变。一组非CMD患者被确定为左丘脑损伤，可能涉及语言理解困难。共同的病变模式苍白球和壳核被视为一组CMD患者，这已牵连的一部分，前前脑中回路的可逆性意识障碍的患者。CMD患者中丘脑皮质网络功能障碍较不常见[ABCD指数2.3（四分位数范围，IQR 2.1-3.0）对1.4（IQR 1.0-2.0），P < 0.0001; D的存在36%对3%，P = 0.0006]，但WPPC没有差异。双侧皮质病变见于CMD患者和非CMD患者。CMD患者的丘脑皮质破坏没有差异，但长程WPPC在1-4 Hz频率范围内降低[比值比（OR）0.8; 95%置信区间（CI）0.7-0.9]，在1 - 4 -30 Hz频率范围内增加（OR 1.2; 95% CI 1.0-1.5）。这些结构和功能的数据牵连的运动命令整合在前脑中回路水平与保留丘脑皮质网络功能的CMD患者皮层下病变的失败。在双侧皮质病变患者中，保留的皮质-皮质网络功能与CMD检测相关。这些数据可能允许基于广泛使用的结构MRI和静息EEG来筛查CMD。
In unconscious appearing patients with acute brain injury, wilful brain activation to motor commands without behavioural signs of command following, known as cognitive motor dissociation (CMD), is associated with functional recovery. CMD can be detected by applying machine learning to EEG recorded during motor command presentation in behaviourally unresponsive patients. Identifying patients with CMD carries clinical implications for patient interactions, communication with families, and guidance of therapeutic decisions but underlying mechanisms of CMD remain unknown. By analysing structural lesion patterns and network level dysfunction we tested the hypothesis that, in cases with preserved arousal and command comprehension, a failure to integrate comprehended motor commands with motor outputs underlies CMD. Manual segmentation of T2-fluid attenuated inversion recovery and diffusion weighted imaging sequences quantifying structural injury was performed in consecutive unresponsive patients with acute brain injury (n = 107) who underwent EEG-based CMD assessments and MRI. Lesion pattern analysis was applied to identify lesion patterns common among patients with (n = 21) and without CMD (n = 86). Thalamocortical and cortico-cortical network connectivity were assessed applying ABCD classification of power spectral density plots and weighted pairwise phase consistency (WPPC) to resting EEG, respectively. Two distinct structural lesion patterns were identified on MRI for CMD and three for non-CMD patients. In non-CMD patients, injury to brainstem arousal pathways including the midbrain were seen, while no CMD patients had midbrain lesions. A group of non-CMD patients was identified with injury to the left thalamus, implicating possible language comprehension difficulties. Shared lesion patterns of globus pallidus and putamen were seen for a group of CMD patients, which have been implicated as part of the anterior forebrain mesocircuit in patients with reversible disorders of consciousness. Thalamocortical network dysfunction was less common in CMD patients [ABCD-index 2.3 (interquartile range, IQR 2.1-3.0) versus 1.4 (IQR 1.0-2.0), P < 0.0001; presence of D 36% versus 3%, P = 0.0006], but WPPC was not different. Bilateral cortical lesions were seen in patients with and without CMD. Thalamocortical disruption did not differ for those with CMD, but long-range WPPC was decreased in 1-4 Hz [odds ratio (OR) 0.8; 95% confidence interval (CI) 0.7-0.9] and increased in 14-30 Hz frequency ranges (OR 1.2; 95% CI 1.0-1.5). These structural and functional data implicate a failure of motor command integration at the anterior forebrain mesocircuit level with preserved thalamocortical network function for CMD patients with subcortical lesions. Amongst patients with bilateral cortical lesions preserved cortico-cortical network function is associated with CMD detection. These data may allow screening for CMD based on widely available structural MRI and resting EEG.