Excerpt
Migraine is the most prevalent among disabling neurological disorders. In its episodic form, it is characterized by ictal phases alternating with periods of wellness, lasting from few to many days. Although many efforts have been made in the last decades to unravel what makes the migrainous brain susceptible to migraine attacks, no consistent and permanent structural disturbances have been found. Migraine pathophysiology is thus supposed to be originated by a central nervous system (CNS) dysfunction, where several neuronal structures play major or minor roles, such as the cerebral cortex, the brainstem (periaqueductal gray matter, aminergic nuclei), and both peripheral and central components of the trigeminovascular system. Clinical neurophysiology methods have been used since many years to study migraine pathophysiology, because they are versatile, non-invasive, easy to replicate also in a standard clinical setting, and relatively not much expensive. Almost every electrophysiological technique has been used, usually by applying more or less sophisticated analysis tools: electroencephalography, event-related potentials, evoked potentials (VEP, AEP, SEP, LEPs), magnetoencephalography, transcranial magnetic stimulation, and blink reflex. Among them, the tests that have provided the most relevant informations for the understanding of migraine pathophysiology are evoked potentials. By using the very simple ploy of analyzing the cortical evoked responses to repetitive external stimulations by consecutive block averages, instead of by a global average, every modality of stimulation—delivered in episodic migraine patients during the interictal period—showed a particular response pattern, which is a deficit of habituation of cortical responses to repeated stimuli. Normally, when a stimulus is delivered repetitively, the amplitude of cortical evoked potentials gradually decreases (i.e., habituates). This phenomenon, known as “habituation,” is supposed to protect the brain from sensory overload and to save attentional resources for meaningful and potentially dangerous novel stimuli. However, in episodic migraine sufferers, the amplitude of cortical responses remains unchanged or increases (i.e., potentiates) between attacks [
1]. It has been demonstrated particularly by the mean of pattern-reversal visual evoked potentials, but it was successfully replicated also by the mean of auditory evoked potentials, somatosensory evoked potentials, laser evoked potentials, visual evoked magnetoencephalographic (MEG) responses, and also by tests where responses are not mediated at a cortical level, such as nociceptive trigeminal evoked responses. Surprisingly, the habituation of cortical responses normalizes just before and during the attack, and it shows a normal behavior in chronic migraine patients [
2]. Although at the present no instrumental test is available for diagnosing migraine, this electrophysiologic pattern is so relevant and prevalent in migraineurs that it has been recently proposed as a possible diagnostic tool for episodic migraine [
3]. …
