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Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 10, Zeilen: 1ff (complete page)
Quelle: Gorji 2001
Seite(n): 40-41, Zeilen: 40:right col. 46ff - 41:left col. 1ff
SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models. By all aforementioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes. CSD penetration into the epileptic foci was established in different model of epilepsy. However, it ould be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy.

Although in above-mentioned studies spontaneous SD is a concomitant phenomenon with epileptic burst discharges, inducing of SD by known stimulus such as KCl application drops the incidence of seizure in some in vitro and in vivo epilepsy models. CSD can reduce the seizure appearance in audiogenic epileptic seizure. Eliciting CSD prior to increasing of the susceptibility for audiogenic epilepsy, e.g., by metrazol decreases the seizure appearance and increases the latencies of the running fit onset. Functional decortications induced by KCl application abolish the epileptic bursts of generalized penicillin epilepsy in cats. Induction of unilateral SD completely suppresses the bilateral electrographic and clonic convulsive seizures and produces only a brief electrographic seizure by stimulation of the ipsilateral kindled amygdala. Interestingly, SD can also reduce the threshold for seizures under certain conditions and acts as an epileptogenic factor.

[page 40]

SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+-K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models [22,149,150,243,337,344,433]. By all aforemen-

[page 41]

tioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes [150,217]. CSD penetration into epileptic foci established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy [50,215,217]. Although in above-mentioned studies spontaneous SD is a concomitant phenomenon with epileptic burst discharges, inducing of SD by known stimulus such as KCl application drops the incidence of seizure in some in vitro and in vivo epilepsy models. CSD can reduce the seizure appearance in audiogenic epileptic seizure. Eliciting CSD prior to increasing of the susceptibility for audiogenic epilepsy, e.g., by metrazol decreases the seizure appearance and increases the latencies of the running fit onset [42,78,209,452]. Functional decortication induced by KCl application abolishes the epileptic bursts of generalized penicillin epilepsy in cats [138]. Induction of unilateral SD, completely suppresses the bilateral electrographic and clonic convulsive seizures and produces only a brief electrographic seizure by stimulation of the ipsilateral kindled amygdala [208]. Interestingly, SD can also reduce the threshold for seizures under certain conditions and acts as an epileptogenic factor.

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Sichter
(Graf Isolan) Schumann

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