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Reconsolidation: The effects of dopamine receptors on spreading depression in rat neocortical tissues

von Dr. Anna Maria Haarmann

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

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
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

[2.] Amh/Fragment 009 26 - Diskussion
Zuletzt bearbeitet: 2014-05-06 20:27:26 Hindemith
Amh, Eikermann-Haerter and Moskowitz 2008, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 9, Zeilen: 26-31
Quelle: Eikermann-Haerter and Moskowitz 2008
Seite(n): 297, Zeilen: left col. 26-38
Recent investigations provide early insights into mechanisms that lead to trigeminovascular activation. SD is the first endogenous event identified upstream to trigeminovascular activation that appears to be noxious in experimental models. Neocortical SD, originally described by Leão. The slow spread of SD at 3–5 mm/min matches the propagation velocity of wave fronts in the Belousov–Zhabotinsky reaction, that is, a thermodynamic chemical reaction that shows the properties of a nonlinear chemical oscillator even in a Petri dish. Recent studies provide early insights into endogenous mechanisms that lead to trigeminovascular activation. CSD is the first endogenous event identified upstream to trigeminovascular activation that appears to be noxious in experimental models. CSD, originally described by Leão [73], is an intense depolarization of neuronal and glial membranes accompanied by a massive disruption of ionic gradients and loss of membrane resistance [5]. The slow spread of CSD at 3–5 mm/min matches the propagation velocity of wave fronts in the Belousov–Zhabotinsky reaction, that is, a thermodynamic chemical reaction that shows the properties of a nonlinear chemical oscillator even in a Petri dish [74].

3 Eikermann-Haerter K, Moskowitz MA. Pathophsyiology of aura. In: Silberstein BR, editor. Wolff’s headache and other head pain. 2007. pp. 121–132.
This chapter gives a comprehensive overview on pathophysiology of migraine aura and summarizes important findings in both basic and clinical research.

73 Leão AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944; 7:359–390.

74 Biosa G, Bastianoni S, Rustici M. Chemical waves. Chemistry 2006; 12:3430–3437.

Anmerkungen

Nothing has been marked as a citation, no reference given. Some part is missing from the text, resulting in an incomplete sentence.

Sichter
(Graf Isolan) Schumann


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