We developed a protocol for a migraine attack rescue treatment, that is to abort by the rTMS the migraine crisis. However, a first evaluation, before that rescue treatment is needed. The more limiting factor is to be close to our center at the moment of the migraine attack.
Migraine is a very prevalent disease (about 12% in the general population) with a great individual disability and socioeconomic burden due to workday loss or reduced productivity. In about 25% of the cases migraine headache is preceded or associated with transitory neurological symptoms and/or signs (aura) due to temporary dysfunction of cerebral cortex, more frequently represented by visual disturbance. According to the presence or not of such symptoms, migraine is defined as migraine with aura (MwA) or migraine without aura (MwoA).
The precise etiopathogenesis of migraine remains still to be elucidated. The causes of the hyperexcitability of the brain cortex with migraine are probably multiple. However, the cortical spreading depression (CSD) and the activation of the trigeminovascular systems (TVS) are actually considered the most important mechanisms. The aura of migraine is believed to be induced by cortical spreading depression (CSD), while pain is related to the TVS.
First described by Leao (1944), CSD is a wave of intense depolarization-excitation (originating in the occipital lobes) followed by hyperpolarization-hypoactivity (that could be induced in animal models through pinprick or chemical stimulation of cortex). This wave moves slowly across the brain cortex at a velocity of 2–3 mm per minute. This phenomenon would be at the origin of the visual aura. Functional magnetic resonance and magnetoencephalography studies provided evidence of the existence of such a process during an acute attack in patients affected by MwA. CSD could be the first step for activating the TVS. The TVS consists of trigeminalnerve endings on the meningeal vessels, which, by its activation at the beginning of the crisis, could release inflammatory substances that enlarge arteries (which causes a pulsatile pain) that transmit painful sensations fo the trigeminal nucleus caudalis and to the brain.
On this basis, the ability to abort the CSD would represent a critical target for treatment of migraine. Thus, rTMS may be an effective acute treatment for migraine if the cortical current it generates disrupts CSD. rTMS has been shown to inhibit CSD experimentally in animals.
Several studies of which some placebo controlled, randomized and double blind (Clark and colleagues 2006, Mohammad et a. 2006 a and b, Lipton t al. 2010) provided evidence that rTMS over the occipital cortex during the migraine attack is effective in reducing pain (up to 75%) and its recurrence (in 70% of patients) in the following 24 hours. At present in the United States, the only neurological indication approved by the Food and Drug Administration (FDA) for TMS is acute migraine with aura.
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