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| [1.] Analyse:Ksh/Fragment 008 03 - Diskussion Bearbeitet: 12. May 2014, 08:07 Singulus Erstellt: 11. May 2014, 23:25 (Graf Isolan) | Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, Ksh, SMWFragment, Schutzlevel |
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| Untersuchte Arbeit: Seite: 8, Zeilen: 3ff |
Quelle: Gorji 2001 Seite(n): 42, Zeilen: left col. 51-52 - right col. 1ff |
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| Migraine and epilepsy are both disorders characterized by transient paroxysmal neurological dysfunction, usually with a normal neurological examination between attacks. The relationship between these disorders has long been suspected. The medieval Iranian practitioner, Rhazes(860–940 A.D.) defines a syndrome in which migraine headache and conjunctivitis preceding epileptic attacks in the headache section of his Al-Hawi. A number of syndromes in which migraine and epilepsy are related have been described. Headaches are observed quite frequently following epileptic attacks and seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics. A number of anticonvulsive drugs have the capacity to stabilize migraine and some anti-migraine drugs increase the epilepsy threshold. Gabapentin is an antiepileptic drug of new generation that enhances brain GABA levels has an effective therapeutic action in the prophylactic treatment of migraine headache. First-generation antiepileptic drug, sodium valproate, is used for the treatment of pain for trigeminal neuralgia and migraine headache. Calcium channel blockers are effective drugs in prophylactic and acute treatment of migraine. Flunarizine produced significant seizure reduction in two trials in therapy-resistant patients. Aura disappeared and post-ictal headache ameliorated in refractive epileptic patients treated with flunarizine. Magnesium which ameliorates migraine headaches is an anticonvulsant compound in eclampsia. It was reported that combination therapy with anticonvulsant and anti-migraine drugs in some intractable epileptics improves seizure control.
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.] |
Migraine and epilepsy are both disorders characterized by transient paroxysmal neurological dysfunction, usually
[right col.] with a normal neurological examination between attacks. The relationship between these disorders has long been suspected. The medieval Iranian practitioner, Rhazes (860–940 A.D.) defines a syndrome in which migraine headache and conjunctivitis preceding epileptic attacks in the headache section of his Al-Hawi [416]. A number of syndromes in which migraine and epilepsy are related have been described [108,249,366]. Headaches are observed quite frequently following epileptic attacks and seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics [376]. A number of anticonvulsive drugs have the capacity to stabilize migraine and some anti-migraine drugs increase the epilepsy threshold. Gabapentin is an antiepileptic drug of new generation that enhances brain GABA levels has an effective therapeutic action in the prophylactic treatment of migraine headache [102]. First-generation antiepileptic drug, sodium valproate, is used for the treatment of pain for trigeminal neuralgia and migraine headache [361]. Calcium channel blockers are an effective drugs in prophylactic and acute treatment of migraine [89,338,406]. Flunarizine produced significant seizure reduction in two trials in therapy-resistant patients [327]. Aura disappeared and post-ictal headache ameliorated in refractive epileptic patients treated with flunarizine [31]. Magnesium which ameliorates migraine headaches is an anticonvulsant compound in eclampsia [380]. It was reported that combination therapy with anticonvulsant and anti-migraine drugs in some intractable epileptics improves seizure control [448]. 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 postconvulsive state were accompanied by widespread vasodilatation of cerebral vessels. |
Nothing has been marked as a citation. All original references have been eliminated. |
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| [2.] Analyse:Ksh/Fragment 009 01 - Diskussion Bearbeitet: 12. May 2014, 07:57 Singulus Erstellt: 11. May 2014, 23:35 (Graf Isolan) | Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, Ksh, SMWFragment, Schutzlevel |
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| Untersuchte Arbeit: Seite: 9, Zeilen: 1-7 (complete page) |
Quelle: Gorji 2001 Seite(n): 42, Zeilen: right col. 32-45 |
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| [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 was observed in cerebral hemisphere homolateral to the hypoperfused and hypometabolic areas. Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus. | An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and postconvulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red [96]. 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 [30,36]. Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus [132,321]. |
Nothing has been marked as a citation; references have been eliminated. |
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| [3.] Analyse:Ksh/Fragment 010 01 - Diskussion Bearbeitet: 13. May 2014, 15:01 Schumann Erstellt: 12. May 2014, 10:00 (Graf Isolan) | Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, Ksh, SMWFragment, Schutzlevel |
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| Untersuchte Arbeit: Seite: 10, Zeilen: 1ff (complete page) |
Quelle: Gorji 2001 Seite(n): 40-41, Zeilen: 40:right col. 46ff - 41:left col. 1ff |
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| 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. |
Nothing has been marked as a citation. All original references have been eliminated |
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| [4.] Analyse:Ksh/Fragment 011 01 - Diskussion Bearbeitet: 15. July 2014, 20:49 Schumann Erstellt: 12. May 2014, 17:02 (Graf Isolan) | BauernOpfer, Fragment, Gesichtet, Gorji 2001, Ksh, SMWFragment, Schutzlevel |
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| Untersuchte Arbeit: Seite: 11, Zeilen: 1-7 |
Quelle: Gorji 2001 Seite(n): 43, Zeilen: left col. 31-42 |
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| [SD may gradually change into spreading] convulsion when repeatedly evoked at brief intervals. Paroxysmal activity instead of depression appears in cortical regions topically treated with acetylcholine or pilocarpine when they are invaded by SD (Gorji 2001).
The first-generation anticonvulsant drug, phenytoin affects the SD elicited by mechanical or chemical stimulation in isolated chick retina. Phenytoin increases the threshold concentration of KCl to initiate this phenomenon; decreases the velocity of propagation and shortens the duration of the slow potential, ionic and volume changes of the extracellular space during SD. Gorji A (2001) Spreading depression: a review of the clinical relevance. Brain Res. Brain Res. Rev.,38, 33 60. |
SD may gradually change into spreading convulsion when repeatedly evoked at brief intervals [457]. Paroxysmal activity instead of depression appears in cortical regions topically treated with acetylcholine or pilocarpine when they are invaded by SD [446].
The first-generation anticonvulsant drug, phenytoin affects the SD elicited by mechanical or chemical stimulation in isolated chick retina. Phenytoin increases the threshold concentration of KCl to initiate this phenomenon; decreases the velocity of propagation and shortens the duration of the slow potential, ionic and volume changes of the extracellular space during SD [74,75]. |
Ksh refers to Gorji (2001) once in between, but as on several pages before he does not mark anything as a citation. All original references have been omitted |
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| Quelle | Autor | Titel | Verlag | Jahr | Lit.-V. | FN |
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| Ksh/Gorji 2001 | Ali Gorji | Spreading depression: a review of the clinical relevance | Elsevier | 2001 | yes | yes |
Übersicht
| Typus | Gesichtet | ZuSichten | Unfertig | Σ |
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| KP | 3 | 0 | 0 | 3 |
| VS | 0 | 0 | 0 | 0 |
| ÜP | 0 | 0 | 0 | 0 |
| BO | 1 | 0 | 0 | 1 |
| KW | 0 | 0 | 0 | 0 |
| KeinP | 0 | 0 | 0 | 0 |
| Σ | 4 | 0 | 0 | 4 |
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