Cortical Inhibition During Visual Perception in Migraine

描述 偏头痛是一种常见的神经系统疾病，影响美国近12%的人口，女性发病率较高。偏头痛的疼痛可以消失几个小时到几天，并导致相当大的不适，残疾和工作损失的日子视觉症状是深刻的偏头痛。视觉先兆可以发生在偏头痛发作之前。畏光和视力模糊与 大多数偏头痛发作，有或没有先兆。神经元过度兴奋， 特别是在视觉皮层，是偏头痛的一个普遍假设， 病理生理学皮质过度兴奋的一种机制可能 γ-氨基丁酸（GABA）能中间神经元的抑制不足。在 初级视皮层，GABA能神经元形成弥漫性水平网络， IV层，并且很可能选择性地易受 在偏头痛发作期间发生的低灌注/缺氧。 作为对PA-98-050的响应，申请人提出探索一种创新的解决方案。 有视觉先兆偏头痛患者视皮层兴奋性的研究 通过检查视觉感知过程中的兴奋性和抑制性相互作用。 具体来说，他们将开发强大的心理物理方法来确定 视觉皮层抑制的程度，在偏头痛受试者和 非头痛对照组，在视觉掩蔽期间。他们将开发功能磁共振成像方法， 确定皮质对未设盲（未抑制）和设盲 （抑制）视觉目标在非头痛和偏头痛的个人。的 假设：（1）非头痛患者的视觉靶点是不可见的（抑制的） 控件可见（非抑制）或部分可见（部分 非抑制性）至具有视觉先兆的偏头痛患者， （2）偏头痛患者的非抑制性视觉靶点 诱导初级视觉皮层中的神经元反应， 在非头痛对照中靶点不引起神经元反应。为了 为了验证这些假设，他们将开发新的功能磁共振成像方法， 对视觉刺激的反应时间短暂（20 ms至100 ms），以及 尺寸小（对向0.5至4度的视角）。有 与视觉掩蔽相关的参数。成功开发这些新 方法不仅对拟议的研究至关重要，而且 对其他大脑研究很有价值。此外，提出的科学概念 这可能会导致一种创新方法来研究视觉 偏头痛的功能/功能障碍，并可能提供一个新的见解偏头痛 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.