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Objective: To determine reversion rates from chronic migraine to episodic migraine during long-term erenumab treatment. Methods: A daily headache diary was completed during the 12-week, double-blind treatment phase of a placebo-controlled trial comparing erenumab 70 mg, 140 mg, and placebo, and weeks 1–12, 21–24, 37–40, and 49–52 of the open-label treatment phase. Chronic migraine to episodic migraine reversion rates were assessed over the double-blind treatment phase; persistent reversion to episodic migraine over 24 weeks (double-blind treatment phase through the first 12 weeks in the open-label treatment phase), long-term persistent reversion to episodic migraine over 64 weeks (double-blind treatment phase plus open-label treatment phase); delayed reversion to episodic migraine through the first 12 weeks of the open-label treatment phase among patients remaining in chronic migraine during the double-blind treatment phase. Results: In the double-blind treatment phase, 53.1% (95% confidence interval: 47.8–58.3) of 358 erenumab-treated completers had reversion to episodic migraine; monthly reversion rates to episodic migraine were typically higher among patients receiving 140 mg versus 70 mg. Among 181 completers (receiving erenumab for 64 weeks), 98 (54.1% [95% confidence interval: 46.6–61.6]) had reversion to episodic migraine during the double-blind treatment phase; of those, 96.9% (95% confidence interval: 91.3–99.4) had persistent reversion to episodic migraine, 96.8% (95% confidence interval: 91.1–99.3) of whom had long-term persistent reversion to episodic migraine. Delayed reversion to episodic migraine occurred in 36/83 (43.4% [95% confidence interval: 32.5–54.7]) patients; of these, 77.8% (95% confidence interval: 60.9–89.9) persisted in reversion through week 64. Conclusions: Patients with reversion to episodic migraine at week 12 will likely persist as episodic migraine with longer-term erenumab; others may achieve delayed reversion to episodic migrai

Objective: To determine reversion rates from chronic migraine to episodic migraine during long-term erenumab treatment. Methods: A daily headache diary was completed during the 12-week, double-blind treatment phase of a placebo-controlled trial comparing erenumab 70 mg, 140 mg, and placebo, and weeks 1–12, 21–24, 37–40, and 49–52 of the open-label treatment phase. Chronic migraine to episodic migraine reversion rates were assessed over the double-blind treatment phase; persistent reversion to episodic migraine over 24 weeks (double-blind treatment phase through the first 12 weeks in the open-label treatment phase), long-term persistent reversion to episodic migraine over 64 weeks (double-blind treatment phase plus open-label treatment phase); delayed reversion to episodic migraine through the first 12 weeks of the open-label treatment phase among patients remaining in chronic migraine during the double-blind treatment phase. Results: In the double-blind treatment phase, 53.1% (95% confidence interval: 47.8–58.3) of 358 erenumab-treated completers had reversion to episodic migraine; monthly reversion rates to episodic migraine were typically higher among patients receiving 140 mg versus 70 mg. Among 181 completers (receiving erenumab for 64 weeks), 98 (54.1% [95% confidence interval: 46.6–61.6]) had reversion to episodic migraine during the double-blind treatment phase; of those, 96.9% (95% confidence interval: 91.3–99.4) had persistent reversion to episodic migraine, 96.8% (95% confidence interval: 91.1–99.3) of whom had long-term persistent reversion to episodic migraine. Delayed reversion to episodic migraine occurred in 36/83 (43.4% [95% confidence interval: 32.5–54.7]) patients; of these, 77.8% (95% confidence interval: 60.9–89.9) persisted in reversion through week 64. Conclusions: Patients with reversion to episodic migraine at week 12 will likely persist as episodic migraine with longer-term erenumab; others may achieve delayed reversion to episodic migrai

Non-invasive vagus nerve stimulation (nVNS; gammaCore®) has the potential to prevent migraine days in patients with migraine on the basis of mechanistic rationale and pilot clinical data. This multicentre study included a 4-week run-in period, a 12-week double-blind period of randomised treatment with nVNS or sham, and a 24-week open-label period of nVNS. Patients were to administer two 120-second stimulations bilaterally to the neck three times daily (6-8 hours apart). Of 477 enrolled patients, 332 comprised the intent-to-treat (ITT) population. Mean reductions in migraine days per month (primary outcome) were 2.26 for nVNS (n = 165; baseline, 7.9 days) and 1.80 for sham (n = 167; baseline, 8.1 days) (p = 0.15). Results were similar across other outcomes. Upon observation of suboptimal adherence rates, post hoc analysis of patients with ≥ 67% adherence per month demonstrated significant differences between nVNS (n = 138) and sham (n = 140) for outcomes including reduction in migraine days (2.27 vs. 1.53; p = 0.043); therapeutic gains were greater in patients with aura than in those without aura. Most nVNS device-related adverse events were mild and transient, with application site discomfort being the most common. Preventive nVNS treatment in episodic migraine was not superior to sham stimulation in the ITT population. The "sham" device inadvertently provided a level of active vagus nerve stimulation. Post hoc analysis showed significant effects of nVNS in treatment-adherent patients. Study identification and registration: PREMIUM; NCT02378844

Introduction: Non-invasive vagus nerve stimulation (nVNS; gammaCore®) has the potential to prevent migraine days in patients with migraine on the basis of mechanistic rationale and pilot clinical data. Methods: This multicentre study included a 4-week run-in period, a 12-week double-blind period of randomised treatment with nVNS or sham, and a 24-week open-label period of nVNS. Patients were to administer two 120-second stimulations bilaterally to the neck three times daily (6–8 hours apart). Results: Of 477 enrolled patients, 332 comprised the intent-to-treat (ITT) population. Mean reductions in migraine days per month (primary outcome) were 2.26 for nVNS (n = 165; baseline, 7.9 days) and 1.80 for sham (n = 167; baseline, 8.1 days) (p = 0.15). Results were similar across other outcomes. Upon observation of suboptimal adherence rates, post hoc analysis of patients with ≥ 67% adherence per month demonstrated significant differences between nVNS (n = 138) and sham (n = 140) for outcomes including reduction in migraine days (2.27 vs. 1.53; p = 0.043); therapeutic gains were greater in patients with aura than in those without aura. Most nVNS device-related adverse events were mild and transient, with application site discomfort being the most common. Conclusions: Preventive nVNS treatment in episodic migraine was not superior to sham stimulation in the ITT population. The “sham” device inadvertently provided a level of active vagus nerve stimulation. Post hoc analysis showed significant effects of nVNS in treatment-adherent patients. Study identification and registration: PREMIUM; NCT02378844; https://clinicaltrials.gov/ct2/show/NCT02378844.

Migraina gure gizartean prebalentzia handia duen gaixotasun neurologiko bat da. Berrikuspen bibliografiko honek gaixotasun honi tratamendu prebentibo eraginkor bat topatzea du helburu. Lehenik eta behin tratamendu prebentiboa jasotzeko bete beharreko baldintzak aztertuko dira, era beran tratamenduaren hasieran lagungarriak izan daitezkeen zenbait gomendio emanez. Azken urteotan ikertuak izan diren lau farmako familia dira nagusienak: betablokeanteak, antiepilekektikoak, antidrepesiboak eta kaltzioaren kanal blokeatzaileak. Hala ere farmako talde hauetako medikamentu guztiak ez dira lehen mailako aukerako farmakoak izango. Betablokeanteen artean propanolol eta metoprolol nagusitzen dira migrainen tratamendu profilaktikotzat erabiltzeko orduan. Antiepilektikoen artean topiramato eta azido valproikoa gailentzen dira. Eta azkenik lehen mailako farmakotzat flunarazina, kaltzio kanal blokeatzailea nabarmentzen da. Bigarren mailako farkamoak amitryptilina eta venlafaxina antidepresiboak, bisoprolol eta timolol betablokeatzaileak izan daitezke. Azkenik, hirugarren mailako aukerako farmakoak migrainen profilaxiarako candasartan, lisinopril, toxina botilunikoa, ferverfew, magnesioa, koentzina Q10 eta rivoflavin proposatzen dira. Hala ere, tratamendu farmakologikoaz gain, terapia naturalen eraginkortasuna aztertu nahi da berrikuspen honetan. Emaitza positiboak agertu dira zenbait tratamendu ez farmakologikoetan, haien artean: biofeedback, akupuntura eta dietaren maneiua. Azkenik erizainak pazientearen heziketan izan dezakeen garrantzia aztertuko da. Alde batetik gaixotasuna eta tratamenduari erlazionatutako heziketa emanez, eta bestetik migrainan eragina izan dezaketen zenbait bizi ohituren aldaketa sustatuz.

Migraina gure gizartean prebalentzia handia duen gaixotasun neurologiko bat da. Berrikuspen bibliografiko honek gaixotasun honi tratamendu prebentibo eraginkor bat topatzea du helburu. Lehenik eta behin tratamendu prebentiboa jasotzeko bete beharreko baldintzak aztertuko dira, era beran tratamenduaren hasieran lagungarriak izan daitezkeen zenbait gomendio emanez. Azken urteotan ikertuak izan diren lau farmako familia dira nagusienak: betablokeanteak, antiepilekektikoak, antidrepesiboak eta kaltzioaren kanal blokeatzaileak. Hala ere farmako talde hauetako medikamentu guztiak ez dira lehen mailako aukerako farmakoak izango. Betablokeanteen artean propanolol eta metoprolol nagusitzen dira migrainen tratamendu profilaktikotzat erabiltzeko orduan. Antiepilektikoen artean topiramato eta azido valproikoa gailentzen dira. Eta azkenik lehen mailako farmakotzat flunarazina, kaltzio kanal blokeatzailea nabarmentzen da. Bigarren mailako farkamoak amitryptilina eta venlafaxina antidepresiboak, bisoprolol eta timolol betablokeatzaileak izan daitezke. Azkenik, hirugarren mailako aukerako farmakoak migrainen profilaxiarako candasartan, lisinopril, toxina botilunikoa, ferverfew, magnesioa, koentzina Q10 eta rivoflavin proposatzen dira. Hala ere, tratamendu farmakologikoaz gain, terapia naturalen eraginkortasuna aztertu nahi da berrikuspen honetan. Emaitza positiboak agertu dira zenbait tratamendu ez farmakologikoetan, haien artean: biofeedback, akupuntura eta dietaren maneiua. Azkenik erizainak pazientearen heziketan izan dezakeen garrantzia aztertuko da. Alde batetik gaixotasuna eta tratamenduari erlazionatutako heziketa emanez, eta bestetik migrainan eragina izan dezaketen zenbait bizi ohituren aldaketa sustatuz.

IMPORTANCE OF THE FIELD: Migraine and cluster headache (CH) are disabling syndromes that often require prophylactic treatment. Valproate semisodium ER (VPS ER) is FDA-approved for the treatment of epilepsy, acute mania in bipolar disorder and migraine prophylaxis. AREAS COVERED IN THIS REVIEW: We reviewed literature regarding VPS ER pharmacokinetics and its use in migraine and CH prophylaxis. WHAT THE READER WILL GAIN: VPS ER is well studied and effective in the preventive treatment of migraine and CH. This article reviews the evidence for its use, describes how to administer and dose this medication, and reviews important safety precautions. TAKE HOME MESSAGE: VPS ER is effective in the prophylactic treatment of migraine and CH. This once-a-day dosing formulation may increase compliance.

Background.-Impaired mitochondrial phosphorylation potential may play a role in migraine pathogenesis. Metabolic enhancers, such as riboflavin or coenzyme Q, are effective in migraine prophylaxis and quasi-devoid of adverse effects. Thioctic acid (-lipoic acid) is another substance known to enhance energy metabolism in mitochondria and to be beneficial in diabetic neuropathy. Objective.-After an open pilot study suggesting its therapeutic antimigraine potentials, we embarked therefore in a randomized controlled trial of thioctic acid (Thioctacid) in migraine prophylaxis steered by the Belgian Headache Society. Methods.-Five Belgian centers recruited 54 migraineurs (43 migraine without aura, 11 with aura; mean age 38 +/- 8 years; 7 males). After a 1-month single-blinded run-in period, 44 patients received either placebo (n = 18) or thioctic acid 600 mg p.o./day (n = 26) for 3 months. Results.-Statistical analysis was carried out on an intention-to-treat basis. Monthly attack frequency tended to be reduced between run-in and the 3rd month of treatment in the thioctic acid group compared to placebo (P = .06). The proportion of 50% responders was not significantly different between thioctic acid (30.8%) and placebo (27.8%). Within-group analyses showed a significant reduction of attack frequency (P = .005), headache days (P = .009), and headache severity (P=.03) in patients treated with thioctic acid for 3 months, while these outcome measures remained unchanged in the placebo group. No adverse effects were reported. For logistical reasons this trial was interrupted before the planned 80 patients were enrolled. Conclusion.-Albeit underpowered, this study tends to indicate that thioctic acid may be beneficial in migraine prophylaxis. Before any firm conclusion can be drawn, however, a large multicenter trial is necessary.