Piper R D, Edvinsson L, Ekman R, Lambert G A
Institute of Neurological Sciences, Prince Henry Hospital, University of New South Wales, Sydney, Australia.
Cephalalgia. 1993 Jun;13(3):180-3; discussion 149. doi: 10.1046/j.1468-2982.1993.1303180.x.
There is circumstantial evidence that cortical spreading depression (SD) may account for the scotoma and the "spreading cortical oligemia" seen during migraine with aura. It has been shown that calcitonin gene-related peptide (CGRP) is increased in blood taken from the external jugular vein (EJV) in humans during migraine and after stimulation of the trigeminal ganglion. To test the hypothesis that cortical SD may elevate the concentration of this vasoactive peptide in the EJV during migraine, we have measured its concentration in the external jugular vein of cats during cortical SD. This study demonstrates that SD has no effect on the concentration of CGRP either during the passage of a wave of spreading depression across the cortex or, 60 min later, during the period of post-SD cortical oligemia.
有间接证据表明,皮层扩散性抑制(SD)可能是偏头痛伴先兆期间出现暗点和“皮层扩散性低灌注”的原因。研究表明,在偏头痛发作期间及刺激三叉神经节后,人体颈外静脉(EJV)血液中的降钙素基因相关肽(CGRP)会增加。为了验证皮层SD可能会在偏头痛期间提高EJV中这种血管活性肽浓度的假说,我们测量了猫在皮层SD期间颈外静脉中CGRP的浓度。这项研究表明,无论是在扩散性抑制波穿过皮层期间,还是在60分钟后的SD后皮层低灌注期,SD对CGRP的浓度均无影响。