The MDR1C3435T polymorphism was also found to be a higher risk factor for topiramate treatment failure in a comparison of the number of days with migraine (β2=1.152, p=0.015).
Our findings demonstrated that prematurity ([OR = 4.99 (95% CI 1.34-18.68), P = 0.017]), history of measles and mumps ([OR = 1.60 (95% CI 1.05-2.45), P = 0.029; OR = 1.85 (95% CI 1.22-2.78), P = 0.003, respectively]), breast feeding [OR = 2.90 (95% CI 1.49-5.65), P = 0.002], head trauma in childhood ([OR = 8.21 (95% CI 1.56-43.06), P = 0.013]), vaccination in adulthood ([OR = 4.57 (95% CI 1.14-18.41), P = 0.032, respectively]), migraine ([OR = 3.50 (95% CI 1.61-7.59), P = 0.002]), family history of MS, IBD, migraine, and collagen vascular diseases ([OR = 2.73 (95% CI 1.56-4.78), P < 0.001], [OR = 3.14 (95% CI 1.460-6.78), P = 0.004; OR = 3.18 (95% CI 1.83-5.53), P < 0.001; OR = 1.81 (95% CI 1.03-3.20), P = 0.040, respectively]), stressful events ([OR = 32.57 (95% CI 17.21-61.64), P < 0.001]), and microwave exposure ([OR = 3.55 (95% CI 2.24-5.63), P ≤0.001]) were more in the MS group.
Clinical studies have suggested that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be effective in migraine prophylaxis.
Our data suggest that although the ACE I/D polymorphism is not a direct risk factor for migraine, the ACE I/I genotype may influence the clinical feature of this disease being associated with reduced use of prophylactic agents in patients with migraine with aura and in those with chronic migraine.
Susceptibility to any type of migraine (migraine with aura, migraine without aura, and both types combined) was neither increased by each polymorphism on its own, nor in combination (MTHFR: X(2) = 0.18 [P = .91]; ACE: X(2) = 1.62 [P = .45]; combined: OR = 1.02 [95% CI 0.98-1.05] P = .97).
ACE DD genotype showed significant association in migraine patients with aura (MA) but a marginal significance in female MA patients in comparison with healthy controls.
Of 2461 retrieved articles, 18 included RCT, meta-analysis, systemic reviews, or guidelines published on ACE inhibitors or ARB in the prevention of migraine.
In 302 patients suffering from migraine without aura (at least for 1 year), with no history of cardiovascular diseases and major risk factors for ischemic events, the genotypes of the ACE gene, plasma ACE activity, and the frequency (weekly) and duration of migraine attacks were evaluated.
In Caucasians, the ACE D allele confers a weak independent risk to migraine susceptibility and also appears to act in combination with the C677T variant in the MTHFR gene to confer a stronger influence on the disease.
The MTHFR 677TT genotype is associated with an increased risk for migraine with aura, while the ACE II genotype is protective against both migraine with and without aura.
The inhibitor of AChE neostigmine did not change the firing <i>per se</i> but induced nociceptive activity, sensitive to d-tubocurarine, after pretreatment of meninges with the migraine mediator CGRP.
In conclusion, we identified the functional variant (rs2256368:A>G) affecting ACSL5 exon 20 skipping, as a causal factor linked to the migraine-associated rs12355831:A>G, suggesting that the activation of long-chain fatty acids by the spliced ACSL5-Δ20 molecules, a mitochondrial located enzyme, is involved in migraine pathology.