Olsen T S, Friberg L, Lassen N A
Bispebjerg Hospital, København, klinisk fysiologisk/nuklearmedicinsk afdeling.
Ugeskr Laeger. 1990 May 21;152(21):1507-9.
During the migraine-aura cerebral blood flow (CBF) is reduced in areas corresponding to the neurological deficits and symptoms. Whether this CBF reduction is the primary cause of the neurological deficits (the vascular theory) or a secondary result of primary neuronal dysfunction in particular "spreading depression" (SD) (the neurogenic theory) is still under discussion. The latter theory is supported by CBF investigations performed during attacks of migraine with aura (MA). The CBF reduction was found to be modest (20-35%) and not sufficient to cause ischemia which usually demands reduction of CBF by more than 50%. In addition the low-flow area appeared to "spreading" in the same manner as that seen in SD in the rat ("spreading oligemia"). Recent studies indicate, however, that the CBF reduction in most cases, after all, is sufficient to cause ischemia and that "spreading oligemia" might be an artifact caused by "scattered radiation". Persistent neurological deficits, EEG abnormalities and infarcts on CT-scans are seen after MA, thus further supporting the theory of vascular dysfunction (vasospasm) and ischemia as the cause of the migraine-aura.
在偏头痛先兆期间，与神经功能缺损和症状相对应的区域脑血流量（CBF）减少。这种CBF减少是神经功能缺损的主要原因（血管理论）还是原发性神经元功能障碍特别是“扩散性抑制”（SD）的继发性结果（神经源性理论）仍在讨论中。后一种理论得到了有先兆偏头痛（MA）发作期间进行的CBF研究的支持。发现CBF减少幅度适中（20% - 35%），不足以引起缺血，而缺血通常需要CBF减少超过50%。此外，低血流区域似乎以与大鼠SD中所见相同的方式“扩散”（“扩散性低血容量”）。然而，最近的研究表明，毕竟大多数情况下CBF减少足以引起缺血，并且“扩散性低血容量”可能是由“散射辐射”引起的假象。MA后可见持续性神经功能缺损、脑电图异常和CT扫描上的梗死灶，从而进一步支持血管功能障碍（血管痉挛）和缺血是偏头痛先兆原因的理论。
