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      Epilepsy and migraine—Are they comorbidity?

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          Abstract

          Epilepsy and migraine often co-occur. From the clinical symptoms, they often have some signs of symptoms before onset; from the pathogenesis of epilepsy and migraine, both of them have a high degree of neuronal excitement and ion channel abnormalities; in terms of treatment, many antiepileptic drugs are work in migraine. All of this indicates that they interact with each other. But it is undeniable that there are interactions and relationships between them, and there are also some differences such as the different clinical episodes, the different ways of neuronal haperexcitability and the different drug treatment programs. And are they comorbidity? If we can better understand the correlation between seizures and migraines, then this will help develop better guidelines for clinical diagnosis and treatment.

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          Most cited references79

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          The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease.

          The term spreading depolarization describes a wave in the gray matter of the central nervous system characterized by swelling of neurons, distortion of dendritic spines, a large change of the slow electrical potential and silencing of brain electrical activity (spreading depression). In the clinic, unequivocal electrophysiological evidence now exists that spreading depolarizations occur abundantly in individuals with aneurismal subarachnoid hemorrhage, delayed ischemic stroke after subarachnoid hemorrhage, malignant hemispheric stroke, spontaneous intracerebral hemorrhage or traumatic brain injury. Spreading depolarization is induced experimentally by various noxious conditions including chemicals such as potassium, glutamate, inhibitors of the sodium pump, status epilepticus, hypoxia, hypoglycemia and ischemia, but it can can also invade healthy, naive tissue. Resistance vessels respond to it with tone alterations, causing either transient hyperperfusion (physiological hemodynamic response) in healthy tissue or severe hypoperfusion (inverse hemodynamic response, or spreading ischemia) in tissue at risk for progressive damage, which contributes to lesion progression. Therapies that target spreading depolarization or the inverse hemodynamic response may potentially treat these neurological conditions.
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            De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy.

            Severe myoclonic epilepsy of infancy (SMEI) is a rare disorder that occurs in isolated patients. The disease is characterized by generalized tonic, clonic, and tonic-clonic seizures that are initially induced by fever and begin during the first year of life. Later, patients also manifest other seizure types, including absence, myoclonic, and simple and complex partial seizures. Psychomotor development stagnates around the second year of life. Missense mutations in the gene that codes for a neuronal voltage-gated sodium-channel alpha-subunit (SCN1A) were identified in families with generalized epilepsy with febrile seizures plus (GEFS+). GEFS+ is a mild type of epilepsy associated with febrile and afebrile seizures. Because both GEFS+ and SMEI involve fever-associated seizures, we screened seven unrelated patients with SMEI for mutations in SCN1A. We identified a mutation in each patient: four had frameshift mutations, one had a nonsense mutation, one had a splice-donor mutation, and one had a missense mutation. All mutations are de novo mutations and were not observed in 184 control chromosomes.
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              Mechanisms of spreading depression and hypoxic spreading depression-like depolarization.

              G Somjen (2001)
              Spreading depression (SD) and the related hypoxic SD-like depolarization (HSD) are characterized by rapid and nearly complete depolarization of a sizable population of brain cells with massive redistribution of ions between intracellular and extracellular compartments, that evolves as a regenerative, "all-or-none" type process, and propagates slowly as a wave in brain tissue. This article reviews the characteristics of SD and HSD and the main hypotheses that have been proposed to explain them. Both SD and HSD are composites of concurrent processes. Antagonists of N-methyl-D-aspartate (NMDA) channels or voltage-gated Na(+) or certain types of Ca(2+) channels can postpone or mitigate SD or HSD, but it takes a combination of drugs blocking all known major inward currents to effectively prevent HSD. Recent computer simulation confirmed that SD can be produced by positive feedback achieved by increase of extracellular K(+) concentration that activates persistent inward currents which then activate K(+) channels and release more K(+). Any slowly inactivating voltage and/or K(+)-dependent inward current could generate SD-like depolarization, but ordinarily, it is brought about by the cooperative action of the persistent Na(+) current I(Na,P) plus NMDA receptor-controlled current. SD is ignited when the sum of persistent inward currents exceeds persistent outward currents so that total membrane current turns inward. The degree of depolarization is not determined by the number of channels available, but by the feedback that governs the SD process. Short bouts of SD and HSD are well tolerated, but prolonged depolarization results in lasting loss of neuron function. Irreversible damage can, however, be avoided if Ca(2+) influx into neurons is prevented.
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                Author and article information

                Contributors
                Journal
                Genes Dis
                Genes Dis
                Genes & Diseases
                Chongqing Medical University
                2352-4820
                2352-3042
                05 May 2018
                June 2018
                05 May 2018
                : 5
                : 2
                : 112-118
                Affiliations
                [a ]Neurology Department at Chongqing Medical University, Chongqing, China
                [b ]Neurology Department at the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Street, Yuanjiagang, Yuzhong District, Chongqing, China
                Author notes
                []Corresponding author. xiaozhenghf@ 123456126.com
                Article
                S2352-3042(18)30007-2
                10.1016/j.gendis.2018.04.007
                6146266
                30258939
                e9857b29-9519-4d63-9a1b-3f4739709c0e
                © 2018 Chongqing Medical University. Production and hosting by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 19 January 2018
                : 17 April 2018
                Categories
                Article

                comorbidity,csd,epilepsy,fhm,migraine
                comorbidity, csd, epilepsy, fhm, migraine

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