Sedley William, Gander Phillip E, Kumar Sukhbinder, Oya Hiroyuki, Kovach Christopher K, Nourski Kirill V, Kawasaki Hiroto, Howard Matthew A, Griffiths Timothy D
Human Brain Research Laboratory, Department of Neurosurgery, The University of Iowa, Iowa City, IA 52242, USA; Auditory Group, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, Tyne and Wear NE2 4HH, UK.
Human Brain Research Laboratory, Department of Neurosurgery, The University of Iowa, Iowa City, IA 52242, USA.
Curr Biol. 2015 May 4;25(9):1208-14. doi: 10.1016/j.cub.2015.02.075. Epub 2015 Apr 23.
Tinnitus can occur when damage to the peripheral auditory system leads to spontaneous brain activity that is interpreted as sound [1, 2]. Many abnormalities of brain activity are associated with tinnitus, but it is unclear how these relate to the phantom sound itself, as opposed to predisposing factors or secondary consequences [3]. Demonstrating "core" tinnitus correlates (processes that are both necessary and sufficient for tinnitus perception) requires high-precision recordings of neural activity combined with a behavioral paradigm in which the perception of tinnitus is manipulated and accurately reported by the subject. This has been previously impossible in animal and human research. Here we present extensive intracranial recordings from an awake, behaving tinnitus patient during short-term modifications in perceived tinnitus loudness after acoustic stimulation (residual inhibition) [4], permitting robust characterization of core tinnitus processes. As anticipated, we observed tinnitus-linked low-frequency (delta) oscillations [5-9], thought to be triggered by low-frequency bursting in the thalamus [10, 11]. Contrary to expectation, these delta changes extended far beyond circumscribed auditory cortical regions to encompass almost all of auditory cortex, plus large parts of temporal, parietal, sensorimotor, and limbic cortex. In discrete auditory, parahippocampal, and inferior parietal "hub" regions [12], these delta oscillations interacted with middle-frequency (alpha) and high-frequency (beta and gamma) activity, resulting in a coherent system of tightly coupled oscillations associated with high-level functions including memory and perception.
当外周听觉系统受损导致大脑自发活动并被解读为声音时，耳鸣就会发生[1,2]。许多大脑活动异常都与耳鸣有关，但目前尚不清楚这些异常与幻听本身的关系，以及它们与易感因素或继发后果的关系[3]。要证明“核心”耳鸣相关因素（即耳鸣感知所必需且充分的过程），需要对神经活动进行高精度记录，并结合一种行为范式，即让受试者操纵并准确报告耳鸣感知情况。在动物和人类研究中，这一点此前一直无法实现。在此，我们展示了一位清醒、有耳鸣症状的患者在接受声刺激后（残余抑制）耳鸣响度的短期变化过程中的大量颅内记录[4]，从而能够对核心耳鸣过程进行有力的特征描述。正如预期的那样，我们观察到了与耳鸣相关的低频（δ）振荡[5-9]，据认为这是由丘脑的低频爆发触发的[10,11]。与预期相反的是，这些δ变化远远超出了局限的听觉皮层区域，几乎涵盖了整个听觉皮层，以及颞叶、顶叶、感觉运动皮层和边缘皮层的大部分区域。在离散的听觉、海马旁回和顶叶下部“枢纽”区域[12]，这些δ振荡与中频（α）和高频（β及γ）活动相互作用，形成了一个紧密耦合的振荡相干系统，与包括记忆和感知在内的高级功能相关。
