Abstract
Dear Sir A recent study published in Cephalalgia using positron emission tomography (PET) in migraine without aura (1) stated: ‘In conclusion, we found in migraine without aura (MoA) a posterior hypoperfusion similar to the changes found in other studies in migraine with aura (MA). If this hypoperfusion is specific to migraine, it favours the same pathophysiology in MA and MoA’. The authors prudently added: ‘However, the significance of this hypoperfusion needs to be specified’ (1).
In a recent review in Lancet Neurology (2) it was stated that this study may question central tenets of migraine pathophysiology. Cortical spreading depression is widely thought to be the mechanism that underlies the aura of migraine. The findings of Denuelle et al. suggest that MA and MoA have similar underlying pathophysiological processes (2). The consequence must in our opinion be that a clinical silent cortical spreading depression is present in MoA.
In contrast, several previous single photon emission computed tomography studies, with a lower spatial resolution than PET, found no decrease in regional cerebral blood flow during MoA (3,4). Furthermore, three PET studies in spontaneous (5,6) and nitroglycerin-induced (7) migraine attacks have been performed. These studies concentrated on PET activation in the brainstem, but there is no mention of a decrease in occipital blood flow (5–7).
It would be important if these investigators could confirm that no decrease in occipital flow was present in their studies. If that is the case, there is no need to reinterpret migraine mechanisms, but a need for replication of the French study.