The electrophysiology of migraine

The pathophysiology of migraine is far from being understood. Electrophysiological methods are useful to investigate peripheral and central mechanisms underlying this disorder. The purpose of this review is to highlight the results of electrophysiological studies published during the last year and to examine their added value to our previous knowledge.

Studies by visual and auditory evoked potentials and event-related responses suggested that lack of habituation is the principal interictal abnormality of sensory processing in migraineurs. Recently confirmed for somatosensory and laser-evoked cortical potentials and for brainstem responses, it is also responsible for the increased intensity dependence of auditory evoked potentials. This abnormality is possibly caused by a reduced cortical preactivation level due to hypofunctioning subcortico-cortical aminergic pathways. Although studies of cortical excitability by transcranial magnetic stimulation have yielded conflicting results, results obtained using habituation of pattern-reversal visual evoked potentials to explore cortical excitability changes induced by repetitive transcranial magnetic stimulation strongly favour the hypothesis that migraine is characterized by a decreased level of preactivation excitability. With regard to pain mechanisms in migraine, electrophysiological studies of trigeminal pathways using nociceptive blink and corneal reflexes have confirmed that sensitization of central trigeminal nociceptors occurs during the attack, and may even persist interictally.

Scientific publications over the last year confirmed that electrophysiological methods are particularly suited to unravelling some of the pathophysiological mechanisms of migraine. To improve their future contribution, they need to be better standardized and to be correlated with behavioural, metabolic and genetic studies.