From different neurophysiological methods to conflicting pathophysiological views in migraine: a critical review of literature.

Abnormal increased cortical responsivity to various types of stimuli plays a major role in migraine pathogenesis. Neurophysiological studies, however, have provided ambiguous findings of either hypo or hyper cortical excitability. This is why the term "dysexcitability" has been recently proposed to indicate a more general dysregulation of cortical excitability. The aims of this review are: (1) to provide existing knowledge and research advances in migraine pathophysiology; (2) to propose a unitary interpretation of apparently conflicting neurophysiological findings. Data of studies conducted in migraine through various evoked potentials techniques and non-invasive brain stimulation methods are reviewed, and in some cases reinterpreted according to more recent findings on migraine pathophysiology. In particular, we emphasize the concept that various methods of testing brain excitability may induce different degrees of cortical activation depending on the stimulus parameters used (e.g., intensity, frequency, and duration of stimulation), so shedding light on different pathophysiological aspects. Finally, we try to reconcile apparently conflicting neurophysiological data in the light of a unitary pathophysiological model, suggesting that a condition of interictal cortical hyperresponsivity, possibly due to a glutamatergic dysfunction, could represent the primum movens of migraine pathogenesis.