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Fatigue, depression, and pain in multiple sclerosis: How neuroinflammation translates into dysfunctional reward processing and anhedonic symptoms
Multiple Sclerosis Journal ( IF 5.8 ) Pub Date : 2020-11-12 , DOI: 10.1177/1352458520972279
Henrik Heitmann 1 , Till F M Andlauer 2 , Thomas Korn 3 , Mark Mühlau 4 , Peter Henningsen 5 , Bernhard Hemmer 6 , Markus Ploner 4
Affiliation  

Fatigue, depression, and pain affect the majority of multiple sclerosis (MS) patients, which causes a substantial burden to patients and society. The pathophysiology of these symptoms is not entirely clear, and current treatments are only partially effective. Clinically, these symptoms share signs of anhedonia, such as reduced motivation and a lack of positive affect. In the brain, they are associated with overlapping structural and functional alterations in areas involved in reward processing. Moreover, neuroinflammation has been shown to directly impede monoaminergic neurotransmission that plays a key role in reward processing. Here, we review recent neuroimaging and neuroimmunological findings, which indicate that dysfunctional reward processing might represent a shared functional mechanism fostering the symptom cluster of fatigue, depression, and pain in MS. We propose a framework that integrates these findings with a focus on monoaminergic neurotransmission and discuss its therapeutic implications, limitations, and perspectives.

中文翻译:

多发性硬化症的疲劳、抑郁和疼痛:神经炎症如何转化为功能失调的奖赏处理和快感缺失症状

疲劳、抑郁和疼痛影响了大多数多发性硬化症 (MS) 患者,这给患者和社会带来了沉重的负担。这些症状的病理生理学并不完全清楚,目前的治疗方法只是部分有效。在临床上,这些症状都有快感缺乏的迹象,例如动力降低和缺乏积极影响。在大脑中,它们与参与奖励处理的区域中重叠的结构和功能改变有关。此外,神经炎症已被证明直接阻碍在奖励处理中起关键作用的单胺能神经传递。在这里,我们回顾了最近的神经影像学和神经免疫学发现,这些发现表明功能失调的奖赏处理可能代表了一种共同的功能机制,促进了疲劳、抑郁、和 MS 的疼痛。我们提出了一个框架,将这些发现与单胺能神经传递相结合,并讨论其治疗意义、局限性和前景。
更新日期:2020-11-12
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