Dysfunctional ionic and metabolic regulation is evident in migraine, preceeding behavioral onset of pain and culminating in the extensive clinical (pre, peri and post-ictal) features presented in migraine. It, therefore, stands to reason that the ionic and metabolic abnormalities may induce microvascular blood flow changes in brain tissue, with altered perfusion not as an inciting event but as a response underlying ionic impacts. To elucidate the timing of hemodynamic effects in migraine, the overarching aim of this study is to investigate perfusion changes that potentially follow triggered migraine.
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