Teixeira Micael, Mancini Christian, Wicht Corentin Aurèle, Maestretti Gianluca, Kuntzer Thierry, Cazzoli Dario, Mouthon Michael, Annoni Jean-Marie, Chabwine Joelle Nsimire
Neurology Unit, Medicine Section, Laboratory for Cognitive and Neurological Science, Department of Neuroscience and Movement Science, Faculty of Science and Medicine, University of Fribourg, Fribourg, Switzerland.
Faculty of Medicine, University of Bern, Bern, Switzerland.
Front Neurosci. 2021 Feb 26;15:594536. doi: 10.3389/fnins.2021.594536. eCollection 2021.
This preliminary investigation aimed to assess beta (β) oscillation, a marker of the brain GABAergic signaling, as a potential objective pain marker, hence contributing at the same time to the mechanistic approach of pain management. This case-control observational study measured β electroencephalographic (EEG) oscillation in 12 right-handed adult male with chronic neuropathic pain and 10 matched controls (∼55 years). Participants were submitted to clinical evaluation (pain visual analog scale, Hospital Anxiety, and Depression scale) and a 24-min high-density EEG recording (BIOSEMI). Data were analyzed using the EEGlab toolbox (MATLAB), SPSS, and R. The global power spectrum computed within the low (Lβ, 13-20 Hz) and the high (Hβ, 20-30 Hz) β frequency sub-bands was significantly lower in patients than in controls, and accordingly, Lβ was negatively correlated to the pain visual analog scale ( = -0.931, = 0.007), whereas Hβ correlation was at the edge of significance ( = -0.805; = 0.053). Patients' anxiety was correlated to pain intensity ( = 0.755; = 0.003). Normalization of the low and high β global power spectrum (GPS) to the GPS of the full frequency range, while confirming the significant Lβ power decrease in chronic neuropathic pain patients, vanished the significance of the Hβ decrease, as well as the correlation between Lβ power and pain intensity. Our results suggest that the GABAergic Lβ EEG oscillation is affected by chronic neuropathic pain. Confirming the Lβ GPS decrease and the correlation with pain intensity in larger studies would open new opportunities for the clinical application of gamma-aminobutyric acid-modifying therapies.
本初步研究旨在评估作为大脑GABA能信号标志物的β振荡，将其作为一种潜在的客观疼痛标志物，从而同时为疼痛管理的机制性方法做出贡献。这项病例对照观察性研究测量了12名患有慢性神经性疼痛的右利手成年男性和10名匹配对照（约55岁）的β脑电图（EEG）振荡。参与者接受了临床评估（疼痛视觉模拟量表、医院焦虑和抑郁量表）以及24分钟的高密度EEG记录（BIOSEMI）。使用EEGlab工具箱（MATLAB）、SPSS和R对数据进行分析。在低β频率子带（Lβ，13 - 20 Hz）和高β频率子带（Hβ，20 - 30 Hz）内计算的全局功率谱在患者中显著低于对照组，相应地，Lβ与疼痛视觉模拟量表呈负相关（r = -0.931，p = 0.007），而Hβ的相关性处于显著边缘（r = -0.805；p = 0.053）。患者的焦虑与疼痛强度相关（r = 0.755；p = 0.003）。将低β和高β全局功率谱（GPS）归一化为全频率范围的GPS，在确认慢性神经性疼痛患者中Lβ功率显著降低的同时，消除了Hβ降低的显著性以及Lβ功率与疼痛强度之间的相关性。我们的结果表明，GABA能的Lβ EEG振荡受慢性神经性疼痛影响。在更大规模的研究中证实Lβ GPS降低以及与疼痛强度的相关性将为γ-氨基丁酸调节疗法的临床应用开辟新机会。
