Electrical vestibular stimulation after vestibular deafferentation and in vestibular schwannoma.

Electrical vestibular stimulation after vestibular deafferentation and in vestibular schwannoma.
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DOI:
10.1371/journal.pone.0082078
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Halmagyi GM
Halmagyi GM
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Aw ST;Todd MJ;Lehnen N;Aw GE;Weber KP;Eggert T;Halmagyi GM

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前庭反射是由人类电(电)前庭刺激(EVS)诱发的,被用来评估前庭功能并研究其通路。本研究旨在研究双侧和单侧前庭去传入后的电诱发前庭-眼反射(EVOR)输出,以确定前庭神经鞘瘤等单侧病变的特征。EVOR采用双搜索线圈记录,EVOR为双极100ms阶跃,EVS强度为[0.9,2.5,5.0,7.5,10.0]mA,单极100ms阶跃,EVS强度为5 mA。对5例双侧前庭去传入(BVD)、12例单侧前庭去传入(UVD)、4例单侧前庭神经鞘瘤(UVS)患者和17例健康人进行双极EVS测试,5例UVD单极EVS测试。BVD后,双相EVS不能诱发EVOR。UVD后,一侧正常耳的双极电刺激对阴极电诱发的双向兴奋性eVOR潜伏期为9ms,对负极电刺激的抑制性eVOR则相反,幅度减半,潜伏期为12ms,表现为兴奋抑制不对称。UVS的eVOR模式与UVD的反应一致,证实了病变侧前庭的丢失。出乎意料的是,UVD耳朵的单极电波不是没有反应,而是引起了三分之一的双极EVOR,而正常耳朵的单极EV引起了一半的双相反应。来自UVD的双极EV具有兴奋抑制不对称性和正常侧与病变侧3ms的潜伏期差异,其诱发的双向eVOR可能有助于检测UVS等前庭病变。我们认为,电流扩散可以解释UVD耳的小eVOR到5 mA单极eVS。
Vestibular reflexes, evoked by human electrical (galvanic) vestibular stimulation (EVS), are utilized to assess vestibular function and investigate its pathways. Our study aimed to investigate the electrically-evoked vestibulo-ocular reflex (eVOR) output after bilateral and unilateral vestibular deafferentations to determine the characteristics for interpreting unilateral lesions such as vestibular schwannomas. EVOR was recorded with dual-search coils as binocular three-dimensional eye movements evoked by bipolar 100 ms-step at EVS intensities of [0.9, 2.5, 5.0, 7.5, 10.0]mA and unipolar 100 ms-step at 5 mA EVS intensity. Five bilateral vestibular deafferented (BVD), 12 unilateral vestibular deafferented (UVD), four unilateral vestibular schwannoma (UVS) patients and 17 healthy subjects were tested with bipolar EVS, and five UVDs with unipolar EVS. After BVD, bipolar EVS elicited no eVOR. After UVD, bipolar EVS of one functioning ear elicited bidirectional, excitatory eVOR to cathodal EVS with 9 ms latency and inhibitory eVOR to anodal EVS, opposite in direction, at half the amplitude with 12 ms latency, exhibiting an excitatory-inhibitory asymmetry. The eVOR patterns from UVS were consistent with responses from UVD confirming the vestibular loss on the lesion side. Unexpectedly, unipolar EVS of the UVD ear, instead of absent response, evoked one-third the bipolar eVOR while unipolar EVS of the functioning ear evoked half the bipolar response. The bidirectional eVOR evoked by bipolar EVS from UVD with an excitatory-inhibitory asymmetry and the 3 ms latency difference between normal and lesion side may be useful for detecting vestibular lesions such as UVS. We suggest that current spread could account for the small eVOR to 5 mA unipolar EVS of the UVD ear.