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Typus
Verschleierung
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Hindemith
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Untersuchte Arbeit:
Seite: 5, Zeilen: 1-30
Quelle: Granz 2009
Seite(n): 8, 9, Zeilen: 8: 23ff; 9: 1ff
[Direct modulation of electrical activity of cortical neurons by the locally] spreading wave can lead to neurological symptoms (e.g. the aura phase of migraine). These same neuronal processes can also alter the neurochemistry of cortical and subcortical structures, modulating oxygen distribution and cell survival in these structures and change the behaviour. These problem has not been addressed before, mainly because SD induces such a short depression in each cortical loci, that transient neurochemical changes cannot be examined with conventional approaches, for example by microdialysis.

A) SD and migraine with aura: A few years before discovery of SD, Lashley (1941) explained his visual aura associated with his own ophthalmic migraine attacks as bright scintillations moving across the visual field leaving a blind area in his visual field. Mapping the trajectory of his scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 2-3 mm/min (Lashley, 1941; Milner, 1958). This report accordingly suggested a possible physiological mechanism for migraine aura in the visual cortex. Thus, it may be suggested that the scintillations represent the excitatory phase, while the pursuing blind spot is the inhibitory process of a SD wave. Similar conclusions were suggested from blood flow studies (Lauritzen, 1984) that demonstrated that the oligaemia associated with the spread of SD from the occipital cortex showed a very similar propagation velocity to that of the SD itself. 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 closed to SD propagation velocity (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 about fifteen minutes, both BOLD signals and MR stimulus-induced [response recovered.]

Direct modulation of electrical activity of cortical neurons by the locally spreading wave can lead to neurological symptoms (e.g. the aura phase of migraine). These same neuronal processes can also alter the neurochemistry of subcortical structures, modulating oxygen distribution, cell survival in these structures and behavior. This problem has not been addressed before, mainly because SD induces such a short depression in each cortical loci, that transient neurochemical changes cannot be examined with conventional approaches, for example by microdialysis.

[page 9]

a) SD and migraine with aura

SD and migraine with aura: A few years before, Lashley (1941) explained the visual aura associated with his own ophthalmic migraine attacks as bright scintillations moving across his visual field leaving a blind area in his visual field. Mapping the trajectory of this scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 3 mm/min (Lashley, 1941; Milner, 1958). This report accordingly suggested a possible physiological mechanism for migraine aura in the visual cortex. Thus, one may suggest that the scintillations represent the excitatory phase, while the pursuing blind spot is the inhibitory process of a SD event. Similar conclusions were suggested from blood flow studies (Lauritzen, 1984) that demonstrated that the oligaemia associated with the spread of SD from the occipital cortex showed a very similar propagation velocity to that of the SD itself. [...] 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.

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