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Brain changes in tinnitus

耳鸣的大脑变化

基本信息

批准号：
7933869
负责人：
JOSEF P RAUSCHECKER
金额：
$ 33.91万
依托单位：
GEORGETOWN UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-09-17 至 2012-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7933869
关键词：
Acetylcysteine Acoustic Nerve Adult Affect Aging American Animals Area Arousal Attention Auditory Auditory area Auditory system Blindness Brain Brain Injuries Central Hearing Loss Cochlea Cognitive Development Devices Disease Esthesia Face Frequencies Functional Magnetic Resonance Imaging Generations Geniculate body structure Goals Hair Cells Hand Human Image Inferior Colliculus Intervention Lead Lesion Magnetic Resonance Imaging Maps Measurable Measurement Medial Methods Modeling Neurons Noise Nucleus Accumbens Ocular Prosthesis Pathway interactions Patients Perception Peripheral Physiological Population Process Psychophysiology Rehabilitation therapy Research Resolution Role Scanning Self-Help Devices Sensory Sensory Process Signal Transduction Sleep Deprivation Somatosensory Cortex Stimulus Stress Structure System Testing Thalamic Nuclei Thalamic structure Time Tinnitus Touch sensation Ventral Striatum auditory pathway base blind experience gray matter hearing impairment morphometry neuromechanism neuropsychological prevent rehabilitation strategy research study response sensory system somatosensory sound transmission process

项目摘要

DESCRIPTION (provided by applicant): Tinnitus, a mostly whistling, buzzing, or hissing phantom sound perceived in the absence of a corresponding external stimulus, is perceived by about 15% of the adult population, and about 75% of all patients with hearing loss. It can cause severe suffering, and to date, no reliable cure has been found. The causes of tinnitus are still poorly understood. The fact that it persists after section of the auditory nerve indicates that its origin lies within the central auditory system. Based on previous research on tinnitus and somatosensory phantom perception in humans and animals, our hypotheses about tinnitus generation are as follows. Damage to the auditory periphery (e.g. as a consequence of loud-noise exposure or aging), which does not even have to manifest itself in a measurable hearing loss, causes some central auditory neurons to lose their input. It is known from research on somatosensory phantom sensations that brain areas that have lost their input due to peripheral damages start responding to stimuli that are normally processed in adjacent areas. We assume that, just like the area of somatosensory cortex that previously processed sensory input from a now amputated hand, starts responding to touches on the face (which are normally processed in an adjacent area of somatosensory cortex), the areas of auditory cortex affected by hearing loss start responding to hearing-loss edge frequencies. This assumption is corroborated by the fact that psychophysical experiments on patients with hearing loss have shown that sensitivity for edge frequencies increases. The resulting imbalance in neuronal activity is mistakenly interpreted as a sound signal - the tinnitus. As not all patients with hearing loss perceive tinnitus, we assume that activity in extra-auditory structures can regulate neuronal auditory activity and prevent tinnitus perception. A likely candidate for such a structure is the paralimbic nucleus accumbens. This part of the ventral striatum has excitatory connections to the reticular thalamic nucleus (RTN), which in turn can inhibit the medial geniculate nucleus (MGN), the thalamic relay between the inferior colliculus and the auditory cortex assumed to be involved with the direction of attention. In tinnitus patients, NAc gray-matter volume is significantly reduced compared to healthy controls. It seems plausible to assume that the volume- reduced NAc of tinnitus patients cannot exert the inhibition necessary to block the excessive activation that ultimately gives rise to the tinnitus percept. It speaks in favor of the assumption of a connection between tinnitus and the NAc that both tinnitus and activity in the subcallosal area (including the NAc) are modulated by stress, arousal, and sleep deprivation. The aims of the proposed research are 1) to provide direct evidence for reorganization of tonotopic maps in central auditory structures by means of high-resolution functional MRI, both in tinnitus patients and in patients matched for hearing loss who do not perceive tinnitus, and 2) to investigate the role of the NAc in tinnitus by a. comparing NAc volume in tinnitus patients and patients matched for hearing loss who do not perceive tinnitus, using high-resolution structural MRI and voxel-based morphometry, and b. comparing, by means of high-resolution functional MRI, activation in central auditory structures and the NAc of patients with intermittent tinnitus in periods during which they do perceive tinnitus and periods during which they do not. Our predictions are that we will find reorganization of tonotopic maps in all patients with hearing loss, but reduced NAc volume and activity only in patients who do (at the time of measurement) perceive tinnitus. These results would guide tinnitus research into a new direction and open up a new point of intervention by emphasizing the modulatory role of extra-auditory structures responsible for the direction of attention.

描述（由申请人提供）：耳鸣是一种主要是口哨、嗡嗡声或嘶嘶声的幻听，在没有相应的外部刺激的情况下，大约15%的成年人和大约75%的听力损失患者都能感觉到。它会造成严重的痛苦，迄今为止，还没有找到可靠的治疗方法。耳鸣的原因仍然知之甚少。它在一段听神经后仍然存在的事实表明它起源于中央听觉系统。根据前人对耳鸣和人、动物体感幻觉的研究，我们对耳鸣产生的假设如下：听觉外围的损伤（例如，由于暴露于大噪音或衰老）甚至不必表现为可测量的听力损失，但会导致一些中枢听觉神经元失去输入。从体感幻感的研究中我们知道，由于外周损伤而失去输入的大脑区域开始对通常在邻近区域处理的刺激做出反应。我们假设，就像先前处理来自截肢手的感觉输入的体感皮层区域开始对面部触摸做出反应（通常在相邻的体感皮层区域处理）一样，听力损失影响的听觉皮层区域开始对听力损失边缘频率做出反应。对听力损失患者进行的心理物理实验表明，边缘频率的敏感性增加，这一事实证实了这一假设。由此导致的神经活动失衡被错误地解释为声音信号——耳鸣。由于并非所有的听力损失患者都能感知耳鸣，我们认为听觉外结构的活动可以调节神经元的听觉活动，从而防止耳鸣的感知。这种结构的一个可能的候选者是旁缘核伏隔核。腹侧纹状体的这一部分与丘脑网状核（RTN）有兴奋性连接，而RTN又可以抑制内侧胫状核（MGN），后者是丘脑下丘和听觉皮层之间的中继，被认为与注意力的方向有关。与健康对照相比，耳鸣患者NAc灰质体积明显减少。似乎有理由认为，耳鸣患者的NAc体积减少不能发挥必要的抑制作用，以阻止最终引起耳鸣的过度激活。它支持耳鸣和胼胝体下区（包括胼胝体下区）的活动都受压力、觉醒和睡眠剥夺调节的假设，即耳鸣和胼胝体下区之间存在联系。本研究的目的是：1)利用高分辨率功能MRI为耳鸣患者和听力损失匹配的无耳鸣患者中枢听觉结构的声位图重组提供直接证据；2)通过比较耳鸣患者和听力损失匹配的无耳鸣患者的NAc体积，探讨NAc在耳鸣中的作用。使用高分辨率结构MRI和基于体素的形态测量，b.通过高分辨率功能MRI，比较间歇性耳鸣患者在耳鸣和不耳鸣期间中枢听觉结构的激活和NAc。我们的预测是，我们将在所有听力损失患者中发现音调图重组，但只有在（测量时）感觉耳鸣的患者中NAc体积和活动减少。这些结果将引导耳鸣研究进入一个新的方向，并开辟一个新的干预点，强调负责注意方向的听觉外结构的调节作用。