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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 . . . [Full Text of this Article]

AUTHOR INFORMATION

Vinod Kumar Gupta, MBBS, MD

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