在1月在线出版的《自然—神经科学》期刊上，研究人员分析光线加剧了偏头疼患者疼痛的可能性。他们提出了眼睛中的光敏感细胞与大脑中某种神经细胞之间的一种新联系，这种神经细胞是偏头疼患者感觉疼痛的关键所在。

Rami Burstein和同事发现，许多盲人偏头疼患者也在努力避免光照。然而，完全失去视力的盲人患者却没有这样的问题。这表明，在眼睛中感觉到的光线确实加剧了偏头疼，科学家们因此指出，可以预设这是一种控制白天生物钟节奏的光敏感视网膜神经细胞，但这种细胞并不参与视力功能。

为了测试这个想法，研究人员以老鼠为对象，寻找视网膜与大脑中疼感区域的直接联系。他们发现，包括光敏感神经在内的视网膜神经轴突确实与大脑中一组神经细胞群有联系，这些神经细胞群被称为丘脑，该区域负责接受和传递与偏头疼相关的疼痛。这种联系也许可以解释光线如何加剧了偏头疼患者的疼痛。

原始出处：

Nature Neuroscience 10 January 2010 | doi:10.1038/nn.2475

A neural mechanism for exacerbation of headache by light

Rodrigo Noseda1, Vanessa Kainz1, Moshe Jakubowski1, Joshua J Gooley2, Clifford B Saper2,3, Kathleen Digre4 & Rami Burstein1,3

The perception of migraine headache, which is mediated by nociceptive signals transmitted from the cranial dura mater to the brain, is uniquely exacerbated by exposure to light. We found that exacerbation of migraine headache by light is prevalent among blind individuals who maintain non–image-forming photoregulation in the face of massive rod/cone degeneration. Using single-unit recording and neural tract tracing in the rat, we identified dura-sensitive neurons in the posterior thalamus whose activity was distinctly modulated by light and whose axons projected extensively across layers I–V of somatosensory, visual and associative cortices. The cell bodies and dendrites of such dura/light-sensitive neurons were apposed by axons originating from retinal ganglion cells (RGCs), predominantly from intrinsically photosensitive RGCs, the principle conduit of non–image-forming photoregulation. We propose that photoregulation of migraine headache is exerted by a non–image-forming retinal pathway that modulates the activity of dura-sensitive thalamocortical neurons.

1 Department of Anesthesia, Boston, Massachusetts, USA.
2 Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
3 Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA.
4 Department of Neurology and Ophthalmology, Moran Eye Center, University of Utah, Salt Lake City, Utah, USA.