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上行通路损伤后丘脑高频振荡与感觉诱发电位慢成分的分离

Dissociation of thalamic high frequency oscillations and slow component of sensory evoked potentials following damage to ascending pathways.

作者信息

Hanajima Ritsuko, Dostrovsky Jonathan O, Lozano Andres M, Chen Robert

机构信息

Toronto Western Research Institute, University Health Network, University of Toronto, Toronto, Ont. Canada.

出版信息

Clin Neurophysiol. 2006 Apr;117(4):906-11. doi: 10.1016/j.clinph.2005.12.002. Epub 2006 Feb 21.

DOI:10.1016/j.clinph.2005.12.002
PMID:16495148
Abstract

OBJECTIVE

Somatosensory evoked potentials (SEPs) recorded from the thalamus have a slow component and high frequency (approximately 1000 Hz) oscillations (HFOs). In this study, we examined how lesions in the sensory afferent pathway affect these components.

METHODS

Thalamic SEPs to contralateral median nerve stimulation were recorded from deep brain stimulation electrodes in two patients. Patient 1 had spinal cord injury at the C4/5 level. Patient 2 had multiple sclerosis with mid brain lesions. Seven patients with no brain or cervical spinal cord lesions served as controls.

RESULTS

In both patients, the low frequency component of the SEP (LF SEP) was delayed and/or prolonged and greatly decreased in amplitude compared with controls. HFOs were recorded in both patients. The latencies of onset and peak of the HFOs were approximately the same as those of the LF SEPs and their amplitudes were similarly reduced. However, their frequency was similar to that of the control group. Cortical SEPs were absent in both patients.

CONCLUSIONS

Normal frequencies of thalamic HFOs in association with increased peak latencies, and decreased amplitudes provide further evidence that the HFOs are likely due to intrinsic oscillations in the thalamus rather than high frequency synchronous inputs.

SIGNIFICANCE

Thalamic HFOs are closely associated with the LF SEP but are generated by a different mechanism.

摘要

目的

从丘脑记录的体感诱发电位(SEP)有一个慢波成分和高频(约1000赫兹)振荡(HFO)。在本研究中,我们研究了感觉传入通路中的损伤如何影响这些成分。

方法

从两名患者的脑深部刺激电极记录对侧正中神经刺激时的丘脑SEP。患者1在C4/5水平有脊髓损伤。患者2患有伴有中脑病变的多发性硬化症。七名无脑或颈脊髓病变的患者作为对照。

结果

与对照组相比,两名患者SEP的低频成分(LF SEP)均延迟和/或延长,且波幅大幅降低。两名患者均记录到HFO。HFO的起始和峰值潜伏期与LF SEP大致相同,其波幅也同样降低。然而,其频率与对照组相似。两名患者均未记录到皮层SEP。

结论

丘脑HFO的正常频率与峰值潜伏期增加和波幅降低相关,这进一步证明HFO可能是由于丘脑的固有振荡而非高频同步输入所致。

意义

丘脑HFO与LF SEP密切相关,但由不同机制产生。

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