Cortical Inhibition During Visual Perception in Migraine

描述 偏头痛是一种常见的神经疾病，在美国近12%的人口中受到影响，其中女性发病率较高。偏头痛疼痛可持续数小时至数天，并引起相当大的不适、残疾和失去工作的天数。视觉先兆可在偏头痛发作之前出现。畏光和视力模糊与 大多数偏头痛发作，无论有没有先兆。一种神经元的超兴奋性， 尤其是在视觉皮质，是偏头痛的一种普遍假设 病理生理学。导致皮质过度兴奋的一种机制可能是 G-氨基丁酸(GABA)能中间神经元对Be缺乏抑制作用。在 初级视皮层，GABA能神经元形成弥漫的水平网络 并极有可能选择性地易受 偏头痛发作期间出现的低灌注量/低氧。 针对PA-98-050，申请者建议探索一种创新的 研究有视觉先兆的偏头痛患者视觉皮质兴奋性的方法 通过检查视觉知觉中的兴奋性和抑制性相互作用。 具体地说，他们将开发强大的心理物理方法来确定 偏头痛受试者和受试者视觉皮质抑制程度 视觉掩蔽期间的非头痛对照。他们将开发fMRI方法来 确定皮层对非屏蔽(非抑制)和屏蔽的反应 (抑制)非头痛和偏头痛患者的视觉目标。这个 假设是：(1)非头痛患者的隐形(抑制)视觉目标 控件为可见(非禁止)或部分可见(部分 非抑制)到有视觉先兆的偏头痛患者，其中视觉皮质 抑制不足；(2)偏头痛患者的非抑制视觉靶点 在初级视皮层和受抑制的视皮层诱导神经元反应 在非头痛对照中，靶点不会引起神经元反应。为了 验证这些假说，他们将在大脑皮质成像中开发新的功能磁共振成像方法 对时间短暂的视觉刺激的反应(20ms至100ms)，以及 尺寸小(视角在0.5到4度之间)。确实有 与可视掩码关联的参数。成功开发这些新产品 方法论不仅对拟议的研究至关重要，而且非常重要。 对其他大脑研究有价值。此外，还提出了科学概念 这可能会导致一种创新的方法来研究视觉 偏头痛的功能/功能障碍，并可能为偏头痛提供新的见解 病理生理学。

DESCRIPTION Migraine is a common neurological disorder, affecting nearly 12% of the populations in the US with a high incidence in females. Migraine headache pain can lost hours to days, and causes considerable discomfort, disability and days lost from work Visual symptoms are profound in migraine. Visual aura can occur prior to the onset of migraine pain. Photophobia and vision blurring are associated with most migraine attacks, with or without aura. A neuronal hyperexcitability, particularly in the visual cortex, is a generalized hypothesis in migraine pathophysiology. One mechanism responsible for cortical hyperexcitability might be deficient inhibition by g-aminobutyric acid (GABA)ergic interneurons. In the primary visual cortex, GABAergic neurons form a diffuse horizontal network in lamina IV and are very likely to be selectively vulnerable to hypoperfusion/hypoxia occurring during migraine attack. In response to PA-98-050, the applicants propose to explore an innovative approach to study visual cortical excitability in migraineuers with visual aura by examining excitatory and inhibitory interaction during visual perception. Specifically, they will develop robust psychophysical methods to determine the extent of visual cortical inhibition, both in migraine subjects and non-headache controls, during visual masking. They will develop fMRI methods to determine cortical response to the un-masked (non-inhibited) and masked (inhibited) visual targets in non-headache and migraine individuals. The hypotheses are: (1) The invisible (inhibited) visual target in non-headache controls is visible (non-inhibited) or partially visible (partially non-inhibited) to migraineurs with visual aura in whom visual cortical inhibition is deficient; (2) The non-inhibited visual target in migraineurs induces a neuronal response in primary visual cortex and the inhibited visual target in non-headache controls does not evoke a neuronal response. In order to test the hypotheses, they will develop new fMRI methodologies in image cortical responses to the visual stimuli that are temporally brief (20ms to 100ms), and dimensionally small (subtending 0.5 to 4 degrees of visual angles). There are parameters associated with visual masking. Successful developing these new methodologies is not only crucial for the proposed study, but also extremely valuable for other brain research. Furthermore, the scientific concept proposed here may lead to an innovative approach to investigate visual function/dysfunction in migraine, and may provide a new insight into migraine pathophysiology.