Cortical Inhibition During Visual Perception in Migraine
Cortical Inhibition During Visual Perception in Migraine
批准号:
6889721
负责人:
Yue Cao
金额:
$5.89万
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-04-05 至 2005-03-31
中文摘要
点击翻译按钮获取中文摘要
英文摘要
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.
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