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Neural plasticity expressed in central auditory structures with and without tinnitus

机译:在有或没有耳鸣的中央听觉结构中表达的神经可塑性

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摘要

Sensory training therapies for tinnitus are based on the assumption that, notwithstanding neural changes related to tinnitus, auditory training can alter the response properties of neurons in auditory pathways. To assess this assumption, we investigated whether brain changes induced by sensory training in tinnitus sufferers and measured by electroencephalography (EEG) are similar to those induced in age and hearing loss matched individuals without tinnitus trained on the same auditory task. Auditory training was given using a 5 kHz 40-Hz amplitude-modulated (AM) sound that was in the tinnitus frequency region of the tinnitus subjects and enabled extraction of the 40-Hz auditory steady-state response (ASSR) and P2 transient response known to localize to primary and non-primary auditory cortex, respectively. P2 amplitude increased over training sessions equally in participants with tinnitus and in control subjects, suggesting normal remodeling of non-primary auditory regions in tinnitus. However, training-induced changes in the ASSR differed between the tinnitus and control groups. In controls the phase delay between the 40-Hz response and stimulus waveforms reduced by about 10° over training, in agreement with previous results obtained in young normal hearing individuals. However, ASSR phase did not change significantly with training in the tinnitus group, although some participants showed phase shifts resembling controls. On the other hand, ASSR amplitude increased with training in the tinnitus group, whereas in controls this response (which is difficult to remodel in young normal hearing subjects) did not change with training. These results suggest that neural changes related to tinnitus altered how neural plasticity was expressed in the region of primary but not non-primary auditory cortex. Auditory training did not reduce tinnitus loudness although a small effect on the tinnitus spectrum was detected.
机译:耳鸣的感觉训练疗法是基于这样的假设,即尽管与耳鸣有关的神经变化,听觉训练仍会改变听觉通路中神经元的反应特性。为了评估该假设,我们调查了由耳鸣患者的感官训练诱导并通过脑电图(EEG)进行测量的大脑变化是否与年龄和听力损失匹配的个体(未接受相同听觉训练的耳鸣的个体)相似。使用位于耳鸣受试者耳鸣频率范围内的5 kHz 40 Hz调幅(AM)声音进行听觉训练,并能够提取已知的40 Hz听觉稳态响应(ASSR)和P2瞬态响应分别定位于初级和非初级听觉皮层。在训练过程中,耳鸣参与者和对照组的P2振幅均等增加,表明耳鸣非主要听觉区域的正常重塑。但是,耳鸣组和对照组在训练中引起的ASSR变化有所不同。在控制中,经过训练后,在40 Hz响应和刺激波形之间的相位延迟减少了约10°,这与以前在年轻的正常听力个体中获得的结果一致。然而,尽管有些参与者表现出与对照相似的相移,但耳鸣组的训练并未使ASSR阶段发生显着变化。另一方面,耳鸣组的训练会导致ASSR振幅增加,而在对照组中,这种反应(在年轻的正常听力受试者中很难重塑)不会随训练而改变。这些结果表明,与耳鸣有关的神经变化改变了在原发性而非非原发性听觉皮层区域中神经可塑性的表达方式。听觉训练并没有降低耳鸣响度,尽管对耳鸣谱的影响很小。

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