Large-fiber neuropathy in Parkinson's disease: a narrative review.

Q2 Medicine
Eun Hae Kwon, Julia Steininger, Raphael Scherbaum, Ralf Gold, Kalliopi Pitarokoili, Lars Tönges
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Abstract

Background: Numerous studies reported a higher prevalence of polyneuropathy (PNP) in patients with Parkinson's disease (PD) compared to the general population. Importantly, PNP symptoms can aggravate both motor and sensory disturbances in PD patients and negatively impact the disease course. Recent analyses indicate distinct PNP patterns in PD.

Main text: This review aims to provide an overview of the current insights into etiological factors, diagnostic methods, and management strategies of large fiber neuropathy in PD. Despite the higher prevalence, the causes of PNP in PD are still not fully understood. A genetic predisposition can underlie PNP onset in PD. Main research attention is focused on long-term levodopa exposure which is suggested to increase PNP risk by depletion of methylation cofactors such as vitamin B12 and accumulation of homocysteine that altogether can alter peripheral nerve homeostasis. Beyond a potential "iatrogenic" cause, alpha-synuclein deposition has been detected in sural nerve fibers that could contribute to peripheral neuronal degeneration as part of the systemic manifestation of PD. Whereas mild axonal sensory PNP predominates in PD, a considerable proportion of patients also show motor and upper limb nerve involvement. Intriguingly, a correlation between PNP severity and PD severity has been demonstrated. Therefore, PNP screening involving clinical and instrument-based assessments should be implemented in the clinical routine for early detection and monitoring. Given the etiological uncertainty, therapeutic or preventive options remain limited. Vitamin supplementation and use of catechol-O-methyltransferase-inhibitors can be taken into consideration.

Conclusion: PNP is increasingly recognized as a complicating comorbidity of PD patients. Long-term, large-scale prospective studies are required to elucidate the causative factors for the development and progression of PD-associated PNP to optimize treatment approaches. The overall systemic role of "idiopathic" PNP in PD and a putative association with the progression of neurodegeneration should also be investigated further.

帕金森病的大纤维神经病变:叙述性综述。
背景:许多研究报告显示,帕金森病(PD)患者的多发性神经病(PNP)发病率高于普通人群。重要的是,多发性神经病症状会加重帕金森病患者的运动和感觉障碍,并对病程产生负面影响。最近的分析表明,帕金森病患者的 PNP 模式各不相同:本综述旨在概述目前对帕金森病大纤维神经病变的病因、诊断方法和管理策略的认识。尽管帕金森病的发病率较高,但其病因仍未完全明了。遗传易感性可能是帕金森病大纤维神经病发病的基础。研究的主要关注点集中在长期左旋多巴暴露上,这被认为会增加 PNP 风险,因为甲基化辅助因子(如维生素 B12)的消耗和同型半胱氨酸的积累会共同改变周围神经的稳态。除了潜在的 "先天性 "原因外,α-突触核蛋白沉积已在硬神经纤维中检测到,这可能会导致外周神经元变性,成为脊髓灰质炎全身表现的一部分。虽然轻度轴索感觉型帕金森病在帕金森病中占主导地位,但也有相当一部分患者表现为运动神经和上肢神经受累。耐人寻味的是,PNP 的严重程度与帕金森病的严重程度之间存在相关性。因此,应在临床常规中实施包括临床和仪器评估在内的 PNP 筛查,以便及早发现和监测。鉴于病因的不确定性,治疗或预防方案仍然有限。可以考虑补充维生素和使用儿茶酚-O-甲基转移酶抑制剂:PNP越来越多地被认为是帕金森病患者的并发症之一。需要进行长期、大规模的前瞻性研究,以阐明与帕金森病相关的 PNP 发生和发展的致病因素,从而优化治疗方法。此外,还应进一步研究 "特发性 "PNP 在帕金森病中的整体系统性作用以及与神经退行性病变进展之间的假定关联。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.40
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