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通过减弱中央前庭通路中速度存储的作用来减轻晕船综合征的症状。

Symptom reduction in mal de débarquement syndrome with attenuation of the velocity storage contribution in the central vestibular pathways.

作者信息

Maruta Jun, Cho Catherine, Raphan Theodore, Yakushin Sergei B

机构信息

Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States.

Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, United States.

出版信息

Front Rehabil Sci. 2024 Feb 29;5:1331135. doi: 10.3389/fresc.2024.1331135. eCollection 2024.

DOI:10.3389/fresc.2024.1331135
PMID:38486679
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10937418/
Abstract

BACKGROUND

The velocity storage mechanism of the central vestibular system is closely associated with the vestibulo-ocular reflex (VOR), but also contributes to the sense of orientation in space and the perception of self-motion. We postulate that mal de débarquement syndrome (MdDS) is a consequence of inappropriate sensory adaptation of velocity storage. The premise that a maladapted velocity storage may be corrected by spatial readaptation of the VOR has recently been translated into the development of the first effective treatment for MdDS. However, this treatment's initial impact may be reversed by subsequent re-triggering events. Presently, we hypothesized that MdDS symptoms could alternatively be reduced by attenuating the velocity storage contribution in the central vestibular pathways.

METHODS

Forty-three patients with MdDS (aged 47 ± 14 yo; 36 women) were randomly assigned to two treatment groups and followed for 6 months. The horizontal VOR was tested with chair rotation during laboratory visits, and the strength of velocity storage was quantified with model-based parameters-the time constant (Tc) and the gain of coupling from the vestibular primary afferent signals (g). To attenuate velocity storage, Group 1 underwent a progressively intensifying series of low-frequency earth-vertical oscillatory rotation coupled to conflicting visual stimuli. Group 2 underwent an established protocol combining head tilts and visual stimulation, designed to correct maladapted spatial orientation but not change the velocity storage strength. The symptom severity was self-rated on an 11-point scale and reported before and up to 6 months after the treatment.

RESULTS

In Group 1, velocity storage was modified through reduction of g ( < 0.001) but not Tc. The symptom rating was at least halved initially in 43% of Group 1 ( = 0.04), the majority of whom retained a similar level of improvement during the 6-month follow-up period. In Group 2, no systematic change was induced in the parameters of velocity storage strength, as expected. The symptom rating was at least halved initially in 80% of Group 2 ( < 0.001), but paralleling previous findings, symptoms often returned subsequently.

CONCLUSION

Attenuation of velocity storage shows promise as a lasting remedy for MdDS that can complement the VOR readaptation approach.

摘要

背景

中枢前庭系统的速度存储机制与前庭眼反射(VOR)密切相关,同时也有助于空间定向感和自我运动感知。我们推测,晕船综合征(MdDS)是速度存储的不适当感觉适应的结果。最近,VOR的空间重新适应可以纠正适应不良的速度存储这一前提已转化为第一种有效的MdDS治疗方法的开发。然而,这种治疗的初始效果可能会被随后的重新触发事件逆转。目前,我们假设可以通过减弱中枢前庭通路中速度存储的作用来减轻MdDS症状。

方法

43例MdDS患者(年龄47±14岁;36名女性)被随机分配到两个治疗组,并随访6个月。在实验室就诊期间,通过椅子旋转测试水平VOR,并使用基于模型的参数——时间常数(Tc)和前庭初级传入信号耦合增益(g)来量化速度存储的强度。为了减弱速度存储,第1组接受了一系列逐渐强化的低频地球垂直振荡旋转,并伴有冲突的视觉刺激。第2组接受了既定的方案,包括头部倾斜和视觉刺激,旨在纠正适应不良的空间定向,但不改变速度存储强度。症状严重程度采用11分制自评,并在治疗前及治疗后长达6个月进行报告。

结果

在第1组中,通过降低g(<0.001)而不是Tc来改变速度存储。第1组中43%的患者症状评分最初至少减半(P=0.04),其中大多数患者在6个月的随访期内保持了相似的改善水平。在第2组中,正如预期的那样,速度存储强度参数没有系统性变化。第2组中80%的患者症状评分最初至少减半(<0.001),但与之前的研究结果相似,症状随后经常复发。

结论

减弱速度存储显示出有望成为MdDS的一种持久治疗方法,可以补充VOR重新适应方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/b03ce742bcd0/fresc-05-1331135-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/08689db37cde/fresc-05-1331135-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/cda328adf5d2/fresc-05-1331135-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/237501992322/fresc-05-1331135-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/b03ce742bcd0/fresc-05-1331135-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/08689db37cde/fresc-05-1331135-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/cda328adf5d2/fresc-05-1331135-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/237501992322/fresc-05-1331135-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3f/10937418/b03ce742bcd0/fresc-05-1331135-g004.jpg

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