识别神经炎症:脑电图中纺锤波过度β的诊断潜力。

IF 1.7
Lorrianne M Morrow, Emma A Barr, Enzo Grossi, Vijayan K Pillai, Kristin A Kight, Ethan B Wright, Robert P Turner, Ronald J Swatzyna
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引用次数: 0

摘要

本文探讨了神经炎症在中枢神经系统(CNS)中的关键作用,特别是考虑到COVID-19大流行的影响。神经炎症是一种防御各种损伤的机制,包括毒素、感染和创伤。然而,如果不及时治疗,神经炎症会变成慢性的,导致严重的症状性和结构性脑损伤。值得注意的是,神经炎症可以模仿心理障碍,使诊断和治疗复杂化。目前神经炎症的诊断方法,如腰椎穿刺、核磁共振、脑活检、血液检查和PET扫描,往往受到不准确、侵入性和成本的阻碍。这项研究认为,脑电图(EEG),特别是识别纺锤体过度β (SEB)活动,为检测神经炎症提供了一种有前途的、非侵入性的、经济有效的替代方法。本研究探讨了SEB活性与神经炎症的关系,重点是创伤性脑损伤(TBI)。通过统计分析1233例精神病患者的脑电图数据,我们确定并比较了两组:75例非苯二氮卓类药物使用的无TBI成人和79例非苯二氮卓类药物使用的有SEB活性的TBI成人。我们确定了难治性精神疾病患者中SEB的显著患病率,强调了这种生物标志物对神经炎症的重要性。此外,我们研究了通过胍法辛联合n -乙酰半胱氨酸(NAC)、光生物调节和高压氧治疗等干预措施减少SEB的治疗意义,所有这些干预措施都证明了减轻神经炎症的疗效。这些发现表明,脑电图可能在神经炎症的早期发现和治疗中发挥变革性作用,为更个性化和有效的精神健康障碍治疗铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Identifying Neuroinflammation: The Diagnostic Potential of Spindling Excessive Beta in the EEG.

This manuscript examines the pivotal role of neuroinflammation in the central nervous system (CNS), particularly considering the impact of the COVID-19 pandemic. Neuroinflammation serves as a defense mechanism against various insults, including toxins, infections, and trauma. However, if left untreated, neuroinflammation can become chronic, leading to significant symptomatic and structural brain damage. Notably, neuroinflammation can mimic psychological disorders, complicating diagnosis and treatment. Current diagnostic methods for neuroinflammation-such as lumbar punctures, MRIs, brain biopsies, blood tests, and PET scans-are often hindered by inaccuracy, invasiveness, and cost. This study posits that electroencephalography (EEG), particularly identifying spindling excessive beta (SEB) activity, offers a promising, non-invasive, and cost-effective alternative for detecting neuroinflammation. This study investigates the relationship between SEB activity and neuroinflammation, focusing on traumatic brain injury (TBI). Through statistical analysis of EEG data from 1,233 psychiatric patients, we identified and compared two groups: 75 non-benzodiazepine-using adults without TBI and 79 non-benzodiazepine using adults with TBI exhibiting SEB activity. We identified a significant prevalence of SEB in individuals with refractory psychiatric conditions, underscoring the significance of this biomarker for neuroinflammation. Furthermore, we examine the therapeutic implications of reducing SEB through interventions such as guanfacine combined with N-Acetyl Cysteine (NAC), photobiomodulation, and hyperbaric oxygen therapy, all of which have demonstrated efficacy in mitigating neuroinflammation. These findings suggest that EEG could play a transformative role in the early detection and management of neuroinflammatory conditions, paving the way for more personalized and effective treatments for mental health disorders.

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