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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.   

yes
Fußnoten    yes
Fragmente    4


Fragmente der Quelle:
[1.] Clg/Fragment 008 01 - Diskussion
Zuletzt bearbeitet: 2014-05-10 18:18:16 Singulus
Clg, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Untersuchte Arbeit:
Seite: 8, Zeilen: 1-4, 7-9
Quelle: Gorji 2001
Seite(n): 34, Zeilen: left col. 44-46 - right col. 1-7
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. [...] Given the widespread potential signaling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and 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].

[231] PE. Kunkler, R.P. Kraig, Calcium waves precede electrophysiological changes of spreading depression in hippocampal organ cultures, J. Neurosci. 18 (1998) 3416-3425.

[299] M. Nedergaard, Direct signaling from astrocytes to neurons in cultures of mammalian brain cells, Science 263 (1994) 1768-1771.

[332] V. Parpura, T.A. Basarsky, F. Liu, K. Jeftinija, S. Jeftinia, P.G. Haydon, Glutamate-mediated astrocyte-neuron signaling, Nature 369 (1994) 744-747.

[440] A. Van Harreveld, Two mechanisms for spreading depression in the chicken retina, J. Neurobiol. 9 (1978) 419-431.

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[2.] Clg/Fragment 009 11 - Diskussion
Zuletzt bearbeitet: 2014-05-10 18:42:49 Singulus
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Untersuchte Arbeit:
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Seite(n): 35, 36, Zeilen: 35:right col. 35-44; 36:left col. 42-56 - right col. 1-14
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 patients with migraine, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals (Welch et al, 1993). A recent study strongly supports the link between SD and the aura period in human visual cortex. High-field functional magnetic resonance imaging (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 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 (Hadjikhani et al., 2001). The most common symptoms during the aura phase in migraine are visual. As mentioned, spreading oligemia and excitation wave of aura symptoms start in occipital lobe and propagate anteriorly. Altering the ionic makeup of the extracellular fluid reversibly raises or lowers the susceptibility to SD. Glial cells act as spatial buffer explicitly for potassium by taking potassium up and carrying it from regions of high concentration to neighbouring regions of low concentration. In human the lowest glial-neuronal ratio is in the primary visual cortex (Fig. 2; Gorji, 2001).

Gorji A (2001); Spreading depression: a review of the clinical relevance. Brain Res Brain Res Rev. 38(1-2):33-60.

Hadjikhani N, Sanchez Del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RB, Sorensen AG, Moskowitz MA (2001) Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci U S A 10; 98 (8): 4687-92.

Welch KM, Barkley GL, Tepley N, Ramadan NM (1993) Central neurogenic mechanisms of migraine. Neurology 43(6 Suppl 3):S21-5.

[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]

A recent study strongly supports the link between SD and the aura period in human visual cortex. 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 who suffer from migraine with aura, they found that the signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as CSD did not cross prominent sulci [162].

The most common symptoms during the aura phase in migraine are visual. As mentioned, spreading oligemia and excitation wave of aura symptoms start in occipital lobe and propagate anteriorly. Altering the ionic makeup of the extracellular fluid reversibly raises or lowers the susceptibility to SD. Glial cells act as spatial buffer explicitly for potassium by taking potassium up and carrying it from regions of high concentration to neighboring regions of low concentration [324]. In human the lowest glial-neuronal ratio is in the primary visual cortex [20].


[20] P. Baily, G. von Bonin, in: The Isocortex of Man, University of Illinois Press, Urbana, IL, 1951.

[162] N. Hadjikhani, M. Sanchez Del Rio, O. Wu, D. Schwartz, D. Bakker, B. Fischl, K.K. Kwong, F.M. Cutrer, B.R. Rosen, R.B. Tootell, A.G. Sorensen, M.A. Moskowitz, Mechanisms of migraine aura revealed by functional MRI in human visual cortex, Proc. Natl. Acad. Sci. USA 98 (2001) 4687–4692.

[324] R.K. Orkand, J.G. Nicholls, S.W. Kuffler, Effect of nerve impulses on the membrane potential of glial cells in the central nervous system of amphibia, J. Neurophysiol. 29 (1966) 788–806.

[455] K.M. Welch, G.L. Barkley, N. Tepley, N.M. Ramadan, Central neurogenic mechanisms of migraine, Neurology 43 (1993) S21–S25.

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[3.] Clg/Fragment 011 19 - Diskussion
Zuletzt bearbeitet: 2014-05-11 00:49:34 Schumann
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Quelle: Gorji 2001
Seite(n): 43, Zeilen: right col. 11ff
The damage to cerebral tissue depends on a complex series of physiological responses and degradative cellular cascades involving a dynamic interplay among the various cells in the region of damaged tissue. Experimental studies of focal ischemic stroke in animals and human support the concept that there is a core of severe ischemia, the ‘ischemic core’ which is surrounded by a region of reduced perfusion, the ‘ischemic penumbra’. Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable (Olesen et al., 1986). The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core.

Olesen J (1986) Regional cerebral blood flow (rCBF) studies in migraine and epilepsy. Funct Neurol 1(4):369-74.

The damage to cerebral tissue depends on a complex series of physiological responses and degradative cellular cascades involving a dynamic interplay among the various cells in the region of damaged tissue. Experimental studies of focal ischemic stroke in animals and human support the concept that there is a core of severe ischemia, the ‘ischemic core’, that is surrounded by a region of reduced perfusion, the ‘ischemic penumbra’. Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable [13,322]. The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core.

[13] J. Astrup, L. Symon, N.M. Branston, N.A. Lassen, Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia, Stroke 8 (1) (1977) 51-57.

[321] J. Olesen, Regional cerebral blood flow (rCBF) studies in migraine and epilepsy, Funct. Neurol. 1 (1986) 369-374.

[322] T.S. Olsen, Regional cerebral blood flow after occlusion of the middle cerebral artery, Acta Neurol. Scand. 73 (1986) 321-337.

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[4.] Clg/Fragment 012 01 - Diskussion
Zuletzt bearbeitet: 2014-05-11 00:50:24 Schumann
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Seite(n): 43, 44, Zeilen: 43: r.col: 33ff - 44: l.col: 1ff
[There is a suggestion that the high potassium concentration] in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard and Astrup, 1986). Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex (Hossmann, 1996). A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia (Koroleva et al., 1998). Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological or metabolic damage. However, it is believed that when SD repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade (Somjen et al., 1990). The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating SD in oxygen/glucose-deprived tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity (Obeidat and Andrew, 1998).

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non- NMDA receptor antagonist and by hypothermia (Mies et al., 1993; Mies et al., 1994).


Hossmann KA (1996) Periinfarct depolarizations. Cerebrovasc Brain Metab Rev 8(3):195-208.

Koroleva VI, Vinogradova LV, Korolev OS (1998) The persistent negative potential provoked in different structures of the rat brain by a single wave of spreading cortical depression. Zh Vyssh Nerv Deiat Im I P Pavlova. 48(4):654-63.

Mies G, Iijima T, Hossmann KA (1993) Correlation between peri-infarct DC shifts and ischaemic neuronal damage in rat. Neuroreport 4(6):709-11.

Mies G, Kohno K, Hossmann KA (1994) Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat. J Cereb Blood Flow Metab. 14(5):802-7.

Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the border zone around old small human brain infarcts. Stroke 17(6):1129-37.

Obeidat AS, Andrew RD (1998) Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation. Eur J Neurosci 10(11):3451-61.

Somjen GG, Aitken PG, Balestrino M, Herreras O, Kawasaki K (1990) Spreading depression-like depolarization and selective vulnerability of neurons. A brief review. Stroke 21(11 Suppl):III179- 83.

There is a suggestion that the high potassium concentration in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia [301,395]. Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex [179]. A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia [218]. Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional

[page 44]

release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological [404] or metabolic [148,170] damage. However, it is believed that when SD repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade [180,404]. The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating SD in oxygen/glucose-deprived tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity [311].

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia [218,219]. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non-NMDA receptor antagonist and by hypothermia [281,282,359].


[148] N.A. Gorelova, J. Krivanek, J. Bures, Functional and metabolic correlates of long series of cortical spreading depression waves in rats, Brain Res. 404 (1987) 379-381.

[170] A.J. Hansen, M. Nedergaard, Brain ion homeostasis in cerebral ischemia, Neurochem. Pathol. 9 (1988) 195-209.

[179] K.A. Hossmann, Periinfarct depolarizations, Cerebrovasc. Brain Metab. Rev. 8 (1996) 195-208.

[180] K.A. Hossmann, Mechanisms of ischemic injury: is glutamate involved?, in: J. Krieglstein, H. Oberpichler-Schwenk (Eds.), Pharmacology of Cerebral Ischemia, Medpharm Scientific, Stuttgart, 1994, pp. 239-251.

[218] VI. Koroleva, J. Bures, TPe use of spreading depression waves for acute and long-term monitoring of the penumbra zone of focal ischemic damage in rats, Proc. Natl. Acad. Sci. USA 93 (1996) 3710-3714.

[219] VI. Koroleva, O.S. Korolev, E. Loseva, J. Bures, TPe effect of MK-801 and of brain-derived polypeptides on the development of ischemic lesion induced by photothrombotic occlusion of the distal middle cerebral artery in rats, Brain Res. 786 (1998) 104-114.

[281] G. Mies, K. Kohno, K.A. Hossmann, MK-801, a glutamate antagonist, lowers flow threshold for inhibition of protein synthesis after middle cerebral artery occlusion of rat, Neurosci. Lett. 155 (1993) 65-68.

[282] G. Mies, K. Kohno, K.A. Hossmann, Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat, J. Cereb. Blood Flow Metab. 14 (1994) 802-807.

[301] M. Nedergaard, J. Astrup, Infarct rim: effect of hyperglycemia on direct current potential and [14C]2-deoxyglucose phosphorylation, J. Cereb. Blood Flow Metab. 6 (1986) 607-615.

[311] A.S. Obeidat, R.D. Andrew, Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation, Eur. J. Neurosci. 10 (1998) 3451-3461.

[359] K. Revett, E. Ruppin, S. Goodall, J.A. Reggia, Spreading depression in focal ischemia: a computational study, J. Cereb. Blood Flow Metab. 18 (1998) 998-1007.

[395] B.K. Siesjo, F. Bengtsson, Calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a unifying hypothesis, J. Cereb. Blood Flow Metab. 9 (1989) 127-140.

[404] G.G. Somjen, P.G. Aitken, M. Balestrino, O. Herreras, K. Kawasaki, Spreading depression-like depolarization and selective vulnerability of neurons. A brief review, Stroke 21 (11 S) (1990) III-179-183.

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