Since the first electroencephalographic recordings obtained by Golla and Winter in 1959, researchers have used a variety of neurophysiological techniques to determine the mechanisms underlying recurrent migraine attacks. Neurophysiological methods have shown that the brain during the interictal phase of an episodic migraine is characterized by a general hyperresponsiveness to sensory stimuli, a malfunction of the monoaminergic brainstem circuits, and by functional alterations of the thalamus and thalamocortical loop. All of these alterations vary plastically during the phases of the migraine cycle and interictally with the days following the attack. Both episodic migraineurs recorded during an attack and chronic migraineurs are characterized by a general increase in the cortical amplitude response to peripheral sensory stimuli; this is an electrophysiological hallmark of a central sensitization process that is further reinforced through medication overuse. Considering the large-scale functional involvement and the main roles played by the brainstem-thalamo-cortical network in selection, elaboration, and learning of relevant sensory information, future research should move from searching for one specific primary site of dysfunction at the macroscopic level, to the chronic, probably genetically determined, molecular dysfunctions at the synaptic level, responsible for short- and long-term learning mechanisms.
Keywords: Brainstem; Cortex; Event-related potentials; Evoked potentials; Migraine; Neuromodulation; Thalamus.
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