Tinnitus, Diminished Sound-Level Tolerance, and Elevated Auditory Activity in Humans With Clinically Normal Hearing Sensitivity
Tinnitus, Diminished Sound-Level Tolerance, and Elevated Auditory Activity in Humans With Clinically Normal Hearing Sensitivity
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DOI：
10.1152/jn.00226.2010
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发表时间：
2010-12-01
影响因子：
2.5
通讯作者：
Melcher, Jennifer R.
中科院分区：
文献类型：
--
作者：
Gu, Jianwen Wendy;Halpin, Christopher F.;Melcher, Jennifer R.
Gu JW，Halpin CF，Nam E-C，Levine RA，Melcher JR.临床上听力正常的人的耳鸣、声级耐受性降低和听觉活动增加。J Neurophysiol 104：3361-3370，2010.首次发表于2010年9月29日; doi：10.1152/jn.00226.2010。幻影感觉和感觉超敏反应是一种紊乱的知觉，其特征是涉及躯体感觉、视觉和听觉模态的各种顽固性病症。我们报告的生理相关性的两个感知异常的听觉领域：耳鸣，幻影感知的声音，和听觉过敏，降低容忍的声音的基础上响度。在这里，有耳鸣和没有耳鸣的受试者，所有临床听力阈值正常，接受1）行为测试，以评估声级耐受性和2）功能性MRI，以测量中央听觉中心的声音诱发激活。尽管接受相同的声音刺激水平，具有降低的声音水平耐受性的受试者（即，与正常耐受的受试者相比，听觉过敏的受试者显示听觉中脑、丘脑和初级听觉皮层的激活升高。初级听觉皮层，而不是皮层下中心，表现出升高的激活，特别是与耳鸣。研究结果直接将听觉过敏和耳鸣与中枢听觉系统的过度活跃联系起来。我们假设，耳鸣相关的海拔在皮层激活可能反映了过度的注意力吸引到听觉域，解释一致的缺乏耳鸣相关的影响subcortically激活是不太有力的调节注意力状态。这些数据在机械水平上加强了以前在耳鸣/听觉过敏和其他非听觉障碍感知之间的类比，这些感知被认为是由神经过度活跃引起的，如慢性神经性疼痛和恐惧症。疼痛和恐惧症
Gu JW, Halpin CF, Nam E-C, Levine RA, Melcher JR. Tinnitus, diminished sound-level tolerance, and elevated auditory activity in humans with clinically normal hearing sensitivity. J Neurophysiol 104: 3361-3370, 2010. First published September 29, 2010; doi:10.1152/jn.00226.2010. Phantom sensations and sensory hypersensitivity are disordered perceptions that characterize a variety of intractable conditions involving the somatosensory, visual, and auditory modalities. We report physiological correlates of two perceptual abnormalities in the auditory domain: tinnitus, the phantom perception of sound, and hyperacusis, a decreased tolerance of sound based on loudness. Here, subjects with and without tinnitus, all with clinically normal hearing thresholds, underwent 1) behavioral testing to assess sound-level tolerance and 2) functional MRI to measure sound-evoked activation of central auditory centers. Despite receiving identical sound stimulation levels, subjects with diminished sound-level tolerance (i.e., hyperacusis) showed elevated activation in the auditory midbrain, thalamus, and primary auditory cortex compared with subjects with normal tolerance. Primary auditory cortex, but not subcortical centers, showed elevated activation specifically related to tinnitus. The results directly link hyperacusis and tinnitus to hyperactivity within the central auditory system. We hypothesize that the tinnitus-related elevations in cortical activation may reflect undue attention drawn to the auditory domain, an interpretation consistent with the lack of tinnitus-related effects subcortically where activation is less potently modulated by attentional state. The data strengthen, at a mechanistic level, analogies drawn previously between tinnitus/hyperacusis and other, nonauditory disordered perceptions thought to arise from neural hyperactivity such as chronic neuropathic pain and photophobia. pain and photophobia.