脑震荡后症状持续存在者步态过程中的前额叶皮层活动。

Neurorehabilitation and neural repair Pub Date : 2024-05-01 Epub Date: 2024-03-20 DOI:10.1177/15459683241240423
Douglas N Martini, Martina Mancini, Prokopios Antonellis, Paul McDonnell, Rodrigo Vitorio, Samuel Stuart, Laurie A King
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引用次数: 0

摘要

背景:脑震荡导致的短暂症状源于大脑皮层的新陈代谢能量危机。虽然这种代谢能量危机通常会在一个月内缓解,但症状可能会持续数年。症状持续期与步态功能障碍有关,而大脑皮层对步态功能障碍的基础知之甚少。对步态过程中的前额叶皮质(PFC)活动进行定量分析可能有助于了解脑震荡后的步态功能障碍。本研究旨在探讨持续性脑震荡症状对步态过程中前额叶皮质活动的影响。我们假设,与对照组相比,有持续性脑震荡症状的成年人在步态过程中会有更大的 PFC 活动。在脑震荡组中,我们假设更严重的症状将与步态中PFC活动的增加有关,而PFC活动的增加将与更严重的步态特征有关:神经行为症状量表(NSI)描述了脑震荡症状。功能性近红外光谱法量化了14名脑震荡患者和25名对照组患者的PFC活动(氧合血红蛋白[HbO2]的相对浓度变化)。使用六个惯性传感器对脑震荡组的步态进行了评估:结果:NSI 总分平均为 26.4(13.2)分。与对照组(-0.016 [0.057])相比,脑震荡组的 HbO2(0.058 [0.108])明显更高(P = .007)。在脑震荡组中,HbO2 与 NSI 症状总分(ρ = .62;P = .02)、矢状运动范围(r = .79;P = .001)和步幅时间变异性(r = -.54;P = .046)相关:这些数据表明,PFC 活动与持续性脑震荡症状患者的症状严重程度和某些步态特征有关。确定脑震荡后步态障碍的神经生理学基础扩展了我们对持续性脑震荡症状患者运动行为障碍的认识。
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Prefrontal Cortex Activity During Gait in People With Persistent Symptoms After Concussion.

Background: Concussions result in transient symptoms stemming from a cortical metabolic energy crisis. Though this metabolic energy crisis typically resolves in a month, symptoms can persist for years. The symptomatic period is associated with gait dysfunction, the cortical underpinnings of which are poorly understood. Quantifying prefrontal cortex (PFC) activity during gait may provide insight into post-concussion gait dysfunction. The purpose of this study was to explore the effects of persisting concussion symptoms on PFC activity during gait. We hypothesized that adults with persisting concussion symptoms would have greater PFC activity during gait than controls. Within the concussed group, we hypothesized that worse symptoms would relate to increased PFC activity during gait, and that increased PFC activity would relate to worse gait characteristics.

Methods: The Neurobehavior Symptom Inventory (NSI) characterized concussion symptoms. Functional near-infrared spectroscopy quantified PFC activity (relative concentration changes of oxygenated hemoglobin [HbO2]) in 14 people with a concussion and 25 controls. Gait was assessed using six inertial sensors in the concussion group.

Results: Average NSI total score was 26.4 (13.2). HbO2 was significantly higher (P = .007) for the concussed group (0.058 [0.108]) compared to the control group (-0.016 [0.057]). Within the concussion group, HbO2 correlated with NSI total symptom score (ρ = .62; P = .02), sagittal range of motion (r = .79; P = .001), and stride time variability (r = -.54; P = .046).

Conclusion: These data suggest PFC activity relates to symptom severity and some gait characteristics in people with persistent concussion symptoms. Identifying the neurophysiological underpinnings to gait deficits post-concussion expands our knowledge of motor behavior deficits in people with persistent concussion symptoms.

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