Mitochondrial Dysfunction in Migraine

Yorns, William R.; Hardison, H. Huntley

doi:10.1016/j.spen.2013.09.002

Cited by 97 publications

(84 citation statements)

References 61 publications

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“…Mitochondrial dysfunction occurred during migraine. [56][57][58] It has been showed that mitochondrial ATP depletion results in MMP drop. 59 Normal MPT pore may be affected and opened by ROS formation.…”

Section: Lipid Peroxides Productionmentioning

confidence: 99%

Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity

Fard¹,

Hamzeiy²,

Sattari³

et al. 2016

Adv Pharm Bull

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Section: Lipid Peroxides Productionmentioning

confidence: 99%

Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity

Fard¹,

Hamzeiy²,

Sattari³

et al. 2016

Adv Pharm Bull

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“…It has been reported in clinical studies that riboflavin may reduce the pain in humans [21,22], although recent papers did not support the prophylactic effects of riboflavin [23,24]. More recent studies have suggested that at least some subtypes of migraines may be related to a mitochondria defect.…”

Section: Introductionmentioning

confidence: 99%

“…More recent studies have suggested that at least some subtypes of migraines may be related to a mitochondria defect. Different types of evidence support a relationship between mitochondria and migraines [21,22]. Riboflavin works as a coenzyme in the mitochondrial electron transport chain [21].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Riboflavin and Selenium on Brain Microsomal Ca2+-ATPase and Oxidative Damage Caused by Glyceryl Trinitrate in a Rat Headache Model

Nazıroğlu

Çelik

Uğuz

et al. 2014

Biol Trace Elem Res

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Migraine headaches are considered to be associated with increased mitochondrial energy metabolism. Mitochondrial oxidative stress is also important in migraine headache pathophysiology although riboflavin and selenium (Se) induced a modulator role on mitochondrial oxidative stress in the brain. The current study aimed to determine the effects of Se with/without riboflavin on the microsomal membrane Ca(2+)-ATPase (MMCA), lipid peroxidation, antioxidant, and electroencephalography (EEG) values in glyceryl trinitrate (GTN)-induced brain injury rats. Thirty-two rats were randomly divided into four groups. The first group was used as the control, and the second group was the GTN group. Se and Se plus oral riboflavin were administered to rats constituting the third and fourth groups for 10 days prior to GTN administration. The second, third, and fourth groups received GTN to induce headache. Ten hours after the administration of GTN, the EEG records and brain cortex samples were obtained for all groups. Brain cortex microsomes were obtained from the brain samples. The brain and microsomal lipid peroxidation levels were higher in the GTN group compared to the control group, whereas they were decreased by selenium and selenium + riboflavin treatments. Vitamin A, vitamin C, vitamin E, and reduced glutathione (GSH) concentrations of the brain and MMCA, GSH and glutathione peroxidase values of microsomes were decreased by the GTN administration, although the values and β-carotene concentrations were increased by Se and Se + riboflavin treatments. There was no significant change in EEG records of the four groups. In conclusion, Se with/without riboflavin administration protected against GTN-induced brain oxidative toxicity by inhibiting free radicals and the modulation of MMCA activity and supporting the antioxidant redox system.

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“…In adults with mitochondrial disease, CNS involvement includes progressive cognitive decline,7 migraine,8 and epilepsy. Some genotypes produce relatively specific CNS syndromes.…”

mentioning

confidence: 99%

Epilepsy in adults with mitochondrial disease: A cohort study

Whittaker

Devine

Gorman

et al. 2015

Annals of Neurology

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ObjectiveThe aim of this work was to determine the prevalence and progression of epilepsy in adult patients with mitochondrial disease.MethodsWe prospectively recruited a cohort of 182 consecutive adult patients attending a specialized mitochondrial disease clinic in Newcastle upon Tyne between January 1, 2005 and January 1, 2008. We then followed this cohort over a 7‐year period, recording primary outcome measures of occurrence of first seizure, status epilepticus, stroke‐like episode, and death.ResultsOverall prevalence of epilepsy in the cohort was 23.1%. Mean age of epilepsy onset was 29.4 years. Prevalence varied widely between genotypes, with several genotypes having no cases of epilepsy, a prevalence of 34.9% in the most common genotype (m.3243A>G mutation), and 92.3% in the m.8344A>G mutation. Among the cohort as a whole, focal seizures, with or without progression to bilateral convulsive seizures, was the most common seizure type. Conversely, all of the patients with the m.8344A>G mutation and epilepsy experienced myoclonic seizures. Patients with the m.3243A>G mutation remain at high risk of developing stroke‐like episodes (1.16% per year). However, although the standardized mortality ratio for the entire cohort was high (2.86), this ratio did not differ significantly between patients with epilepsy (2.96) and those without (2.83).InterpretationEpilepsy is a common manifestation of mitochondrial disease. It develops early in the disease and, in the case of the m.3243A>G mutation, often presents in the context of a stroke‐like episode or status epilepticus. However, epilepsy does not itself appear to contribute to the increased mortality in mitochondrial disease. Ann Neurol 2015;78:949–957

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Mitochondrial Dysfunction in Migraine

Cited by 97 publications

References 61 publications

Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity

Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity

Protective Effects of Riboflavin and Selenium on Brain Microsomal Ca2+-ATPase and Oxidative Damage Caused by Glyceryl Trinitrate in a Rat Headache Model

Epilepsy in adults with mitochondrial disease: A cohort study

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