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Angaben zur Quelle [Bearbeiten]

Autor     Ali Gorji
Titel    Spreading depression: a review of the clinical relevance
Zeitschrift    Brain Research Reviews
Verlag    Elsevier
Ausgabe    38
Jahr    2001
Seiten    33-60
URL    http://www.sciencedirect.com/science/article/pii/S0165017301000819

Literaturverz.   

no
Fußnoten    no
Fragmente    6


Fragmente der Quelle:
[1.] Amh/Dublette/Fragment 007 14 - Diskussion
Zuletzt bearbeitet: 2014-05-07 19:01:26 Klgn
Amh, Dublette, Fragment, Gesichtet, Gorji 2001, KeineWertung, SMWFragment, Schutzlevel sysop

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Seite: 7, Zeilen: 14-19
Quelle: Gorji 2001
Seite(n): 34, Zeilen: l. col. 44ff
No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the propagation of SD probably involves the release of different chemical mediators, most likely K+ and glutamate into the interstitial fluid. Given the widespread potential signalling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves may also play a role in SD propagation. No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the spread of SD probably involves the release and diffusion of the chemical mediators, most likely K+ and glutamate into the interstitial fluid [440]. Given the widespread potential signaling capacities of Ca2+ waves [332], observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation [231,299].

[...]

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[2.] Amh/Fragment 005 01 - Diskussion
Zuletzt bearbeitet: 2014-05-06 21:40:09 Schumann
Amh, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 5, Zeilen: 1-3, 5-15
Quelle: Gorji 2001
Seite(n): 34, Zeilen: l.col: 1-4, 7-23
Introduction

Spreading depression (SD) is a propagating wave of depolarisation associated by a depression of the neuronal bioelectrical activity for a period of minutes. [...] SD appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression. A crucial manifestation of SD is a propagating negative potential with an amplitude of 10–30 mV and a duration of more than 0.5–1 min, which may be preceded or succeeded by a positive fluctuation of variable amplitude and duration. Underlying this cellular depolarisation is a dramatic change in the distribution of micromilieu ions between extra- and intracellular compartments. Potassium and proton release from the cells, while sodium, calcium and chloride enter together with water causing cells to swell and the volume of the extracellular compartment to be decreased. SD is accompanied by an increase of glucose utilization and O2 consumption. Recovery of SD depends on energy metabolism.

1. Introduction

Spreading depression (SD) is a self-propagating front of depolarization associated by a depression of the neuronal bioelectrical activity for a period of minutes. [...] It appears first at the stimulated site and spreads out in all directions at the velocity of 2-3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression [243]. A necessary manifestation of SD is a propagating extracellular negative potential with an amplitude of 10-30 mV and a duration of more than 0.5-1 min, which may be preceded or succeeded by a positive deflection of variable amplitude and duration. Underlying this neuro-glial depolarization is a dramatic change in the distribution of ions between extra- and intracellular spaces. K+ and H+ release from the cells, while Na+, Ca2+ and Cl- enter together with water [152,166,222] causing cells to swell and the volume of the extracellular compartment to be reduced. SD is accompanied by an increase of glucose utilization and O2 consumption [47,283]. Recovery of SD depends on energy metabolism [47].


[...]

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[3.] Amh/Fragment 005 25 - Diskussion
Zuletzt bearbeitet: 2014-05-06 21:41:28 Schumann
Amh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Seite(n): 34, Zeilen: l.col: 24-29, 33-38
This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under different experimental conditions. It has been also observed in human neocortical tissue in vitro and in human hippocampus as well as striatum and neocortex in vivo. SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold. This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under various experimental conditions [47]. It has been also observed in human neocortical tissue in vitro [16,17,149] and in human hippocampus as well as striatum [408] and neocortex [272] in vivo.[...]

SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold.


[...]

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[4.] Amh/Fragment 006 01 - Diskussion
Zuletzt bearbeitet: 2014-05-06 21:41:59 Schumann
Amh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Quelle: Gorji 2001
Seite(n): 34, Zeilen: l.col.: 38-43
Conversely, the susceptibility of SD initiation is lowered or the occurrence of SD is prevented in previously susceptible tissue by solution with increased Mg2+ or NaCl, or with the Na+ replaced by certain other cations. SD also is triggered by various modes of mechanical, chemical and electrical stimulation. Conversely, the susceptibility of SD initiation is lowered or the occurrence of SD is prevented in previously susceptible tissue by solution with increased Mg2+ or NaCl, or with the Na+ replaced by certain other cations. SD also is triggered by various modes of mechanical, chemical and electrical stimulation [47].

[...]

Anmerkungen

The source is not mentioned.

The passage starts on the previous page: Amh/Fragment_005_25

Sichter
(Hindemith) Schumann

[5.] Amh/Fragment 008 02 - Diskussion
Zuletzt bearbeitet: 2014-05-06 21:42:54 Schumann
Amh, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 8, Zeilen: 2-4
Quelle: Gorji 2001
Seite(n): 34, Zeilen: r.col: 8-11
SD belongs in the domain of the pathophysiology of the brain, and there are reasons to believe that it is involved in different clinical disorders, including migraine, cerebrovascular diseases, head injury and transient global amnesia. SD belongs in the domain of the pathophysiology of the brain, and there are reasons to believe that it is involved in some clinical disorders, including migraine, cerebrovascular diseases, head injury and transient global amnesia.
Anmerkungen

The source is not mentioned. The passage starts on the previous page: Amh/Fragment_007_14.

Sichter
(Hindemith) Schumann

[6.] Amh/Fragment 009 04 - Diskussion
Zuletzt bearbeitet: 2014-05-06 20:25:56 Singulus
Amh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Untersuchte Arbeit:
Seite: 9, Zeilen: 4-25
Quelle: Gorji 2001
Seite(n): 34, 35, 36, Zeilen: 34:right col. 33-41; 35: right col. 35-44; 36:left col. 43ff - right col. 1-4
The designation migraine with aura denotes the syndrome of headache associated with characteristic sensory, motor, or visual symptoms, usually gradually developed over 5–20 min and lasting less than 60 min. The most common symptoms in aura phase are visual arising from dysfunction of occipital lobe neurons. The positive (stimulative) neurological symptoms, e.g., flashing lights are usually followed by negative (suppressive) ones, e.g., scotoma or hemianopia in this phase. Magnetoencephalographic studies in human revealed that the magnetic signals were seen in migraine patients but not in patients suffering from other forms of headache or normal controls. Three distinctive signal patterns; suppression of spontaneous cortical activity, slow field changes and large-amplitude waves, were observed strictly in migraine patients. In some migraine patients, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals. High-field functional MRI was used to detect blood oxygenation level-dependent (BOLD) changes during visual aura in three migraineurs. A focal increase in BOLD signals developed first in extrastriate cortex and spread at the velocity of 3.5 ± 1.1 mm/min over occipital cortex. These initial BOLD features were consistent with scintillations and paralleled by decreases in the stimulus-driven MR oscillations. Increasing in BOLD signals was followed by a decrease in the mean signal. This phase appeared to correspond to the localized scotoma and MR stimulus-induced response remained suppressed. Within 15 ± 3 min, both BOLD signals and MR stimulus-induced response recovered. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as neocortical SD did not cross prominent sulci. [page 34]

The designation migraine with aura denotes the syndrome of headache associated with characteristic sensory, motor, or visual symptoms, usually gradually developed over 5–20 min and lasting less than 60 min. The most common symptoms in aura phase are visual arising from dysfunction of occipital lobe neurons. The positive (stimulative) neurological symptoms, e.g., flashing lights are usually followed by negative (suppressive) ones, e.g., scotoma or hemianopia in this phase.

[page 35]

Magnetoencephalographic studies in human revealed that the magnetic signals were seen in migraine patients but not in patients suffering from other forms of headache or normal controls. Three distinctive signal patterns; suppression of spontaneous cortical activity, slow field changes and large-amplitude waves, were observed strictly in migraine patients. In some migraineurs, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals [455].

[page 36]

High-field functional MRI was used to detect blood oxygenation level-dependent (BOLD) changes during visual aura in enhanced in three migraineurs. A focal increase in BOLD signals developed first in extrastriate cortex and spread at the velocity of 3.5 ± 1.1 mm/min over occipital cortex. These initial BOLD features were consistent with scintillations and paralleled by decreases in the stimulus-driven MR oscillations. Increasing in BOLD signals was followed by a decrease in the mean MR signal. This phase appeared to correspond to the localized scotoma and MR stimulus-induced response remained suppressed. Within 15 ± 3 min, both BOLD signals and MR stimulus-induced response recovered. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as CSD did not cross prominent sulci [162].


[...]

Anmerkungen

Not marked as a citation, the source is not mentioned.

Sichter
(Graf Isolan), Hindemith

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