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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）：耳鸣是一种在没有相应外部刺激的情况下感知到的主要为哨声、嗡嗡声或嘶嘶声的幻声，约15%的成年人群和约75%的听力损失患者感知到耳鸣。耳鸣的病因有哪些？耳鸣的病因有哪些？它在听神经切断后仍然存在的事实表明它的起源位于中枢听觉系统内。根据以往的研究耳鸣和躯体感觉幻象知觉在人类和动物，我们的假设耳鸣的产生如下。听觉外围的损伤（例如，由于噪音暴露或老化），甚至不必表现为可测量的听力损失，导致一些中枢听觉神经元失去输入。从对躯体感觉幻感觉的研究中得知，由于外周损伤而失去输入的大脑区域开始对相邻区域正常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躯体感觉皮层区域开始对面部的触摸做出反应（通常在躯体感觉皮层的相邻区域进行处理）一样，受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学实验表明，边缘频率的敏感性增加，这一事实证实了这一假设。由此产生的神经元活动的不平衡被错误地解释为声音信号-耳鸣。由于并非所有听力损失患者都能感觉到耳鸣，我们假设听觉外结构的活动可以调节神经元的听觉活动并防止耳鸣感知。这种结构的一个可能的候选者是核边缘核。腹侧纹状体的这一部分与丘脑网状核（RTN）有兴奋性联系，而丘脑网状核又可以抑制内侧膝状体核（MGN），这是下丘和听觉皮层之间的丘脑中继，被认为与注意力的方向有关。在耳鸣患者中，NAc灰质体积与健康对照组相比显着减少。这似乎是合理的假设，耳鸣患者的体积减少的NAc不能发挥必要的抑制作用，以阻止过度激活，最终引起耳鸣的感觉。它支持耳鸣和NAc之间存在联系的假设，即耳鸣和胼胝体下区域（包括NAc）的活动都受到压力，唤醒和睡眠剥夺的调节。本研究的目的是：1）通过高分辨率功能MRI为耳鸣患者和听力损失匹配但未感知耳鸣的患者的中枢听觉结构的音调定位图的重组提供直接证据; 2）通过a.使用高分辨率结构MRI和基于体素的形态测定法比较耳鸣患者和匹配听力损失但未感知耳鸣的患者的NAc体积，以及B.通过高分辨率的功能性磁共振成像，比较间歇性耳鸣患者在感觉到耳鸣和感觉不到耳鸣的时期中枢听觉结构和NAc的激活情况。我们的预测是，我们将发现所有听力损失患者的音调图重组，但只有在（测量时）感知耳鸣的患者中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，并通过强调负责注意方向的听觉外结构的调节作用，开辟了一个新的干预点。