在多发性硬化症相关的疲劳中,整受体和皮层-皮下区域的功能连接性发生变化
Carla Silva-Batista1, Ishu Arpan1, Mariana Penteado Nucci2
1Department of Neurology, Oregon Health & Science University, Portland, OR, United States.
Neuroscience
|December 21, 2024
概括
多发性硬化症的疲劳可能源于大脑连接的改变. 疲劳的个体表现出增加的整感受性大脑活动和减少的运动网络连接,这表明这种致残症状的核心原因.
科学领域:
- 神经科学是一个神经科学.
- 医疗成像医学成像
- 神经学 神经学
背景情况:
- 疲劳是多发性硬化症 (PwMS) 患者的一种复杂和致残的症状.
- 与MS相关的疲劳的潜在神经机制尚不清楚.
- 现有研究表明,与疲劳感知相关的大脑网络的潜在变化.
研究的目的:
- 调查疲劳和非疲劳PwMS之间的静止状态功能连接 (rsFC) 的差异.
- 探索rsFC与PwMS中疲劳感知之间的关系.
- 为了确定与MS相关的疲劳的潜在核心原因.
主要方法:
- 招募了23个复发性缓解性PwMS和21个年龄匹配的健康对照.
- 将PwMS分为疲劳 (修改疲劳影响量表得分≥38) 和非疲劳的组.
- 使用休息状态功能磁共振成像 (rs-fMRI) 来评估大脑连接.
主要成果:
- 与非疲劳的PwMS相比,疲劳的PwMS在皮层-基底状腺网络中表现出减少的rsFC.
- 疲劳的PwMS显示在脑内全感受区域 (杏仁体,ACC,insula) 的rsFC增加.
- 增加的整受体rsFC与更高的疲劳得分相关,并且特定于疲劳的PwMS.
结论:
- 与MS相关的疲劳可能源于脑内感知活动增加,特别是对身体状态的感知增加.
- 皮质 - 基底质网络的连接性发生变化与疲劳时的运动性能感知有关.
- 这些发现表明MS疲劳的核心神经基础,强调了针对大脑电路重组的干预措施的必要性.
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