Abstract
Chronic migraine (CM) is the most disabling form of migraine, because pharmacological treatments have low efficacy and cumbersome side effects. New evidence has shown that migraine is primarily a disorder of brain plasticity and migraine chronification depends on a maladaptive process favoring the development of a brain state of hyperexcitability. Due to the ability to induce plastic changes in the brain, researchers started to look at Non-Invasive Brain Stimulation (NIBS) as a possible therapeutic option in migraine field. On one side, NIBS techniques induce changes of neural plasticity that outlast the period of the stimulation (a fundamental prerequisite of a prophylactic migraine treatment, concurrently they allow targeting neurophysiological abnormalities that contribute to the transition from episodic to CM. The action may thus influence not only the cortex but also brainstem and diencephalic structures. Plus, NIBS is not burdened by serious medication side effects and drug–drug interactions. Although the majority of the studies reported somewhat beneficial effects in migraine patients, no standard intervention has been defined. This may be due to methodological differences regarding the used techniques (e.g., transcranial magnetic stimulation, transcranial direct current stimulation), the brain regions chosen as targets, and the stimulation types (e.g., the use of inhibitory and excitatory stimulations on the basis of opposite rationales), and an intrinsic variability of stimulation effect. Hence, it is difficult to draw a conclusion on the real effect of neuromodulation in migraine. In this article, we first will review the definition and mechanisms of brain plasticity, some neurophysiological hallmarks of migraine, and migraine chronification-related (dys)plasticity. Secondly, we will review available results from therapeutic and physiological studies using neuromodulation in CM. Lastly we will discuss the results obtained in these preventive trials in the light of a possible effect on brain plasticity.
Highlights
Chronic migraine (CM) (ICHD-III 1.3) (>15 days of headache per months, with >8 with migraine features for at least 3 months) affects about 2% of the general population and is the more disabling form of migraine, with a disability greater than that of episodic migraine (EM) (Dodick, 2006; Natoli et al, 2010).Managing CM is extremely challenging for several reasons
Significantly different between the sham and active stimulation group; at the end of the open label phase, the group initially assigned to Non-invasive Vagus Nerve Stimulation (nVNS) - i.e., in the randomized phase- showed a significant reduction in headache days respect to baseline
The initial use of vagus nerve stimulation to treat headaches first came from the epilepsy field, following several anecdotal reports of migraine improvement in patients with comorbid epilepsy who had been implanted with the device (Sadler et al, 2002; Hord et al, 2003)
Summary
Chronic migraine (CM) (ICHD-III 1.3) (>15 days of headache per months, with >8 with migraine features for at least 3 months) affects about 2% of the general population and is the more disabling form of migraine, with a disability greater than that of episodic migraine (EM) (Dodick, 2006; Natoli et al, 2010).Managing CM is extremely challenging for several reasons. Trial’s results were almost negative: neither active nor sham stimulation provided an improvement in primary endpoint (migraine attacks). Active stimulation improved migraine-related days (−42.5%), mean duration of attacks (−19.5%) and intensity of pain (−22.6%), only the latter barely differed significantly from the sham treatment (p = 0.05).
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