Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

Li, Fengpeng; Qiu, Enchao; Dong, Zhao; Liu, Ruozhuo; Wu, Shiwen; Yu, Shengyuan

doi:10.1007/s10194-011-0300-1

Cited by 23 publications

(20 citation statements)

References 48 publications

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“…Although the different compounds used for migraine prevention clearly act at different receptor sites or channels, it has been suggested that they may modulate common pathways or mechanisms implicated in migraine pathogenesis. For example, several migraine preventives such as propranolol, topiramate, valproate, amitriptyline [11], and flunarizine [12], but also CGRP antagonists [13] have been shown to suppress CSD. Other compounds have been suggested to reduce neuronal sensitization [14,15].…”

Section: General Preventive Treatment Principles and Mechanisms Of Acmentioning

confidence: 99%

“…Furthermore, flunarizine acts as a D2 dopamine antagonist and has in this regard been shown to possess (at high doses) comparable antipsychotic efficacy as haloperidol [53]. It has also been shown that flunarizine can reduce the number and duration of CSD waves [12]. Furthermore, it has been suggested that flunarizine can alleviate CSD-induced mitochondrial injury [12].…”

Section: Calcium Antagonistsmentioning

confidence: 99%

“…It has also been shown that flunarizine can reduce the number and duration of CSD waves [12]. Furthermore, it has been suggested that flunarizine can alleviate CSD-induced mitochondrial injury [12]. Finally, flunarizine has also been shown to increase leptin levels [17], which have been suggested to reflect leptin resistance, which may potentially explain the treatment-related weight gain [54].…”

Section: Calcium Antagonistsmentioning

confidence: 99%

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Current Prophylactic Medications for Migraine and Their Potential Mechanisms of Action

Sprenger¹,

Viana²,

Tassorelli

2018

Neurotherapeutics

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A relatively high number of different medications is currently used for migraine prevention in clinical practice. Although these compounds were initially developed for other indications and differ in their mechanisms of action, some general themes can be identified from the mechanisms at play. Efficacious preventive drugs seem to either suppress excitatory nervous signaling via sodium and/or calcium receptors, facilitate GABAergic inhibition, reduce neuronal sensitization, block cortical spreading depression and/or reduce circulating levels of CGRP. We here review such mechanisms for the different compounds.

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Section: General Preventive Treatment Principles and Mechanisms Of Acmentioning

confidence: 99%

Section: Calcium Antagonistsmentioning

confidence: 99%

Section: Calcium Antagonistsmentioning

confidence: 99%

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Current Prophylactic Medications for Migraine and Their Potential Mechanisms of Action

Sprenger¹,

Viana²,

Tassorelli

2018

Neurotherapeutics

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“…Ketamine, a proven blocker of SD, has been shown to stop the neurological aura symptoms in some patients but had no effect on the headache. 120 Many migraine drugs from different pharmacological classes have been tested against SD so far, 50,97,102,110,179,185,[192][193][194][195][196][197][198][199][200][201][202][203][204][205][206][207] and topiramate and flunarizine were most effective since they exerted an inhibitory effect in all of the revised studies.…”

Section: Anti-migraine Drugsmentioning

confidence: 99%

Systematic review of the pharmacological agents that have been tested against spreading depolarizations

Klass

Sánchez-Porras

Santos

2018

J Cereb Blood Flow Metab

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Spreading depolarization (SD) occurs alongside brain injuries and it can lead to neuronal damage. Therefore, pharmacological modulation of SD can constitute a therapeutic approach to reduce its detrimental effects and to improve the clinical outcome of patients. The major objective of this article was to produce a systematic review of all the drugs that have been tested against SD. Of the substances that have been examined, most have been shown to modulate certain SD characteristics. Only a few have succeeded in significantly inhibiting SD. We present a variety of strategies that have been proposed to overcome the notorious harmfulness and pharmacoresistance of SD. Information on clinically used anesthetic, sedative, hypnotic agents, anti-migraine drugs, anticonvulsants and various other substances have been compiled and reviewed with respect to the efficacy against SD, in order to answer the question of whether a drug at safe doses could be of therapeutic use against SD in humans.

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“…Moreover, cerebral mitochondrial injury seems to be related to cortical spreading depression, so assuming that this neuronal phenomenon may precede any form of migraine, independently from the perception of aura symptoms, the NAA reduction may be the consequence of the migraine episodes repetition [28].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Dysfunctions in Patients with Migraine

Alloush¹,

Haroun²,

Shalash³

et al. 2019

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Study Objectives: Migraine is a complex neurovascular disease and is believed to be due to a mixture of genetic and environmental factors. Study design: This was a cross-sectional observational prospective hospital based study conducted on 100 participants. They were divided into two groups; Group A: 50 migrainous patients according to the criteria of the International Classification of Headache Disorders and Group B: 50 healthy subjects both groups were age and sex matched. All subjects underwent a full neurological and psychiatric examination. Full headache evaluation sheet used in headache outpatient clinic in Ain Shams University Hospitals and HIT-6™ Headache Impact Test was used. Assay of serum level of N-acetyl-aspartate (NAA) as mitochondrial function marker was done. Results: There was no significant difference between both groups regarding gender, age or age group, marital state, education, residence and special habits. However, there was a statistical significant difference as regards family history of migraine more in patient group. In this study, serum NAA levels in migraine patients were significantly lower than in healthy controls. Decreased NAA level is generally believed to be a sign of reduced neuronal and glial mitochondrial function. Also, migraine with aura patients showed lower NAA levels when compared to migraine without aura subtypes. However, there was no significant correlation was found between NAA serum levels, and gender, age at onset, age group, type of aura, duration of the illness, type of onset of pain, frequent site of pain, time to max severity, severity of attack, and daily functions (social life, work, psychological wellbeing, sleep and cognition). Conclusions: Findings of this study indicate that NAA in serum may be a marker for neuronal dysfunction predisposing to migraine, probably related to the reduced mitochondria function.

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Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

Cited by 23 publications

References 48 publications

Current Prophylactic Medications for Migraine and Their Potential Mechanisms of Action

Current Prophylactic Medications for Migraine and Their Potential Mechanisms of Action

Systematic review of the pharmacological agents that have been tested against spreading depolarizations

Mitochondrial Dysfunctions in Patients with Migraine

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