局部脑桥损伤对人听觉脑干诱发电位和双耳加工的影响

Hillel Pratt , Andrey Polyakov , Vered Aharonson , Amos D. Korczyn , Rina Tadmor , Barbara C. Fullerton , Robert A. Levine , Miriam Furst
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引用次数: 36

摘要

目的和方法:对11例因血管疾病引起的局部小脑桥病变患者(44-80岁)进行四组测量:(1)单耳听觉脑干诱发电位(ABEPs);峰I ~ VI);(2)双耳ABEPs在IV ~ VI峰潜伏期范围内对其双耳相互作用分量(bic)进行处理;(3)脑干磁共振成像(MRI);(4)双耳定位时差测量的心理声学。分析abep和bic的峰值延迟和峰间延迟差异。推导了ABEP和BICs的三通道Lissajous轨迹(3-CLTs),并由此推断了ABEP和BICs等效偶极子的潜伏期和取向。结果:11例患者中仅有3例单侧诱发ABEPs的成分间潜伏期测量异常。11例患者中有9例使用3-CLT测量bic,发现病变部位与神经生理异常之间存在一致的相关性。11例患者中有6例缺少一种或多种BIC成分。11例患者中有7例BICs定向异常,3例潜伏期异常。梯形体(TB)病变(6例)与第一组分偶极子取向缺失(2例为腹侧-尾侧病变)或异常(1例为腹侧-喙侧病变)相关(在ABEPs IV时),并且在中线腹侧结核病变(2例)中保留该组分。在腹侧结核病变中观察到第二个BICs成分(在ABEPs V时)的偏离方向。这些患者的心理声学偏侧倾向于中心。吻侧外侧小丘(LL)病变(3例)与第三个BICs成分(ABEPs VI时)方向缺失(1例)或异常(2例)相关;还有一个带有行为测试的偏侧化。结论:这些结果表明:(1)ABEPs峰IV时的BICs成分依赖于腹尾结核完整性;(2)在ABEPs峰值V时,腹侧TB对BICs成分有贡献;(3)吻侧LL是发生在ABEP峰值VI时的bic成分的贡献发生器。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of localized pontine lesions on auditory brain-stem evoked potentials and binaural processing in humans

Objectives and mehtods: Four sets of measurements were obtained from 11 patients (44–80 years old) with small, localized pontine lesions due to vascular disease: (1) Monaural auditory brain-stem evoked potentials (ABEPs; peaks I to VI); (2) Binaural ABEPs processed for their binaural interaction components (BICs) in the latency range of peaks IV to VI; (3) magnetic resonance imaging (MRI) of the brain-stem; and (4) psychoacoustics of interaural time disparity measures of binaural localization. ABEPs and BICs were analyzed for peak latencies and interpeak latency differences. Three-channel Lissajous' trajectories (3-CLTs) were derived for ABEPs and BICs and the latencies and orientations of the equivalent dipoles of ABEP and BICs were inferred from them.

Results: Intercomponent latency measures of monaurally evoked ABEPs were abnormal in only 3 of the 11 patients. Consistent correlations between sites of lesion and neurophysiological abnormality were obtained in 9 of the 11 patients using 3-CLT measures of BICs. Six of the 11 patients had absence of one or more BIC components. Seven of the 11 had BICs orientation abnormality and 3 had latency abnormalities. Trapezoid body (TB) lesions (6 patients) were associated with an absent (two patients with ventral-caudal lesions) or abnormal (one patient with ventral-rostral lesions) dipole orientation of the first component (at the time of ABEPs IV), and sparing of this component with midline ventral TB lesions (two patients). A deviant orientation of the second BICs component (at the time of ABEPs V) was observed with ventral TB lesions. Psychoacoustic lateralization in these patients was biased toward the center. Rostral lateral lemniscus (LL) lesions (3 patients) were associated with absent (one patient) or abnormal (two patients) orientation of the third BICs component (at the time of ABEPs VI); and a side-biased lateralization with behavioral testing.

Conclusions: These results indicate that: (1) the BICs component occurring at the time of ABEPs peak IV is dependent on ventral-caudal TB integrity; (2) the ventral TB contributes to the BICs component at the time of ABEPs peak V; and (3) the rostral LL is a contributing generator of the BICs component occurring at the time of ABEP peak VI.

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