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[平衡系统中的内置紧急制动装置。动物实验研究表明,在急性外周前庭功能衰退后,一系列机制会进行代偿]

[Built-in emergency brake in the balance system. Animal experiment research shows that a hierarchy of mechanisms compensate after acute peripheral vestibular decline].

作者信息

Magnusson Anna K, Tham Richard

机构信息

Abteilung Neurobiologie, Ludwig-Maximilians Universität, München.

出版信息

Lakartidningen. 2005;102(20):1524-6, 1529.

Abstract

A sudden unilateral loss of peripheral vestibular input results in the onset of acute dizziness and imbalance associated with spontaneous nystagmus, postural instability and nausea. Fortunately, these symptoms ameliorate rapidly, even without treatment, due to central nervous plastic changes which are collectively termed "vestibular compensation". This concept has become a widely accepted research model for studying lesion-induced plasticity. Recent research has dealt in particular with the plasticity of the medial vestibular nuclei that mediate the horizontal vestibulo-ocular reflex. Studies range from a cellular level in vitro to a functional level in vivo. Taken together, results from such studies have contributed greatly to what is known of vestibular compensation today. This article summarises evidence for several plasticity mechanisms that drive the recovery of spontaneous nystagmus, one of which is dependent on an endocrine stress-response. In the long run, such knowledge might influence the management and treatment of patients with balance disorders.

摘要

外周前庭输入突然单侧丧失会导致急性头晕和失衡发作,伴有自发性眼球震颤、姿势不稳和恶心。幸运的是,由于中枢神经可塑性变化(统称为“前庭代偿”),即使未经治疗,这些症状也会迅速改善。这一概念已成为研究损伤诱导可塑性的广泛接受的研究模型。最近的研究特别关注介导水平前庭眼反射的内侧前庭核的可塑性。研究范围从体外细胞水平到体内功能水平。综合来看,这些研究结果对当今已知的前庭代偿做出了巨大贡献。本文总结了几种驱动自发性眼球震颤恢复的可塑性机制的证据,其中一种机制依赖于内分泌应激反应。从长远来看,这些知识可能会影响平衡障碍患者的管理和治疗。

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