Angaben zur Quelle [Bearbeiten]
| Autor | Ali Gorji |
| Titel | Spreading Depression Associated Neurological Disorders Part II |
| Zeitschrift | Avicenna. The Iranian Journal of Science and Culture |
| Ausgabe | 4 |
| Jahr | 2005 |
| Nummer | 1 |
| ISSN | 1610-8159 |
| URL | http://ebitik.azerblog.com/anbar/1977.pdf |
Literaturverz. |
no |
| Fußnoten | no |
| Fragmente | 2 |
| [1.] Clg/Fragment 010 01 - Diskussion Zuletzt bearbeitet: 2014-05-11 00:46:20 Schumann | Clg, Fragment, Gesichtet, Gorji 2005, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
|
|
|
| Untersuchte Arbeit: Seite: 10, Zeilen: 1ff (komplett) |
Quelle: Gorji 2005 Seite(n): 26-27, Zeilen: 26:left.col. 20; right col. 31-50 - 27:left col. 1-5 |
|---|---|
| b) SD and epilepsy
SD and epilepsy: regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in migraine. The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red. Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. The small but significant reduction in both of those observed in cerebral hemisphere homolateral to the hypoperfused and hypometabolic areas (Bernardi et al., 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Olesen, 1986). |
[page 26]
2.13. SD, epilepsy and migraine: [...] rCBF changes in epilepsy have some similarities to those changes in migraine. The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red (Dalessio 1980). Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. The small but significant reduction in both of those observed in cereberal hemisphere homolateral to the hypoperfused and hypometabolic areas [page 27] (Bernardi et al. 1983, Bonte et al. 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Frank et al. 1986, Olesen 1986). |
Nothing is marked as a citation. Taken from an at that time four years old article of Clg's Dr-advisor. Can also be found in Quelle:Clg/Gorji 2001. |
|
| [2.] Clg/Fragment 011 01 - Diskussion Zuletzt bearbeitet: 2014-05-11 00:48:35 Schumann | Clg, Fragment, Gesichtet, Gorji 2005, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
|
|
|
| Untersuchte Arbeit: Seite: 11, Zeilen: 1-15 |
Quelle: Gorji 2005 Seite(n): 27, Zeilen: left col. 6ff |
|---|---|
| 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 (Gorji, 2001). 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 (Koroleva and Bures, 1983). CSD penetration into epileptic foci established in different models 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 (Koroleva and Bures, 1983). | 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+ ATP-ase e.g. by ouabain, blocking of Ca2+ channels e.g. by NiCl2 , blocking of GABA receptors e.g. by picrotoxine are the common pathways for eliciting epileptiform burst discharges and SD in experimental models (Leao 1944A, Petsche et al. 1973, Traynelis and Dingledine 1988, Psarropoulou and Avoli 1992, Balestrino et al. 1999, Gorji et al. 2003A). 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 (Koroleva and Bures 1983, Gorji et al. 2000). 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 (Koroleva and Bures 1980, Bures et al. 1975). |
Nothing is marked as a citation. Can also be found in Quelle:Clg/Gorji 2001. |
|