The exact pathophysiological mechanisms leading to the activation and sensitization of the trigeminovascular pathway, which in turns results in the migraine attack, are not completely elucidated. It is likely that direct activation by cortical spreading depression, together with dysfunctional central control of pain, plays a major role in the onset and spreading of the migraine attack. This review focuses on recent structural and functional neuroimaging studies that investigated the role of subcortical and cortical structures in modulating nociceptive input in migraine, which outlined the presence of an imbalance between inhibitory and excitatory modulation of pain processing in the disease.