Ischemia within the posterior circulation has been proposed as a primary mechanism for migraine. Though, in-vivo studies have yet to fully elucidate the underpinnings of this mechanism. In the current study, angiography via time of flight (ToF) MR was used to identify potential structural deficits within the posterior circulation and hypercapnic BOLD fMRI was used to detect functional vascular defects by quantifying cerebral vascular reactivity (CVR). All three MoA subjects demonstrated a negative correlation in BOLD signal within the red nuclei during CO2 challenge whereas the three MA patients demonstrated CVR within the red nuclei that was similar to that of the control subjects. ToF MR angiography images from all MoA subjects showed hypoplasia of bilateral posterior communicating arteries (PCoA) in proximity of the circle of Willis. In contrast only one out of the three MA subjects showed PCoA hypoplasia on ToF images. Our findings of hypoplasia of posterior communicating arteries combined with abnormal CVR responses within the red nuclei provide both structural and functional evidence for differential vascular defects in the migraine samples studied. We suggest that the identified vascular deficits to impose vulnerability in midbrain blood supply that may likely contribute to the migraine pathophysiology.