Afridi et al1 concluded that activation of the dorsal pons in migraine supports a subcortical site of origin of the disorder. It is simplistic to assume that demonstration of cortical or brainstem activation in patients with migraine through positron emission tomography indicates the primary pathogenetic source.2 More than 5 decades ago, Leão’s3 experiments showed that retinal stimulation can also elicit spreading cortical silence and depression. Second, neuroimaging, however sophisticated, does not record early physiological events in migraine that occur in the prodromal or “preprodromal” periods; although the preprodromal phase is completely subclinical, the prodromal phase is characterized by subtle and protean clinical phenomena.4 Fundamentally, alterations of cerebral circulation or brain activation after onset of migraine aura or headache cannot be construed to reflect primary pathogenetic alterations. Third, inclusion of migraine patients with attacks as frequent as 4 per month1 assumes that cessation of pain indicates return to the basal physiological state by 72 hours; this assumption is erroneous.4 Fourth, Afridi et al1 offer no logical explanation why nonlateralizing ictal brainstem activation should manifest on the right side with brainstem deactivation on the left side regardless of the side of the headache. Fifth, the pathophysiological emphasis on the locus coeruleus1 is debatable; the locus caeruleus (and the dorsal raphe nucleus) does not directly innervate meningeal tissues and its involvement in migraine remains uncertain.5
Gupta VK. Brainstem Activity in Migraine: Primary or Secondary? Arch Neurol. 2006;63(9):1347. doi:10.1001/archneur.63.9.1347-a
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: