von Cornelia Larissa Granz
Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
| [1.] Clg/Fragment 009 02 - Diskussion Zuletzt bearbeitet: 2014-05-11 00:44:36 Schumann | Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Smith et al 2006, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 9, Zeilen: 2-11 |
Quelle: Smith et al 2006 Seite(n): 458, Zeilen: l.col: 6-22 |
|---|---|
| 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 few years before, Lashley (1941) described the visual aura associated with his own ophthalmic migraine syndrome as bright scintillations moving across his visual field leaving a blind area in its wake. Mapping the trajectory of this migrainous scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 3 mm min-1 (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 CSD event. Similar conclusions were suggested from blood flow studies (Lauritzen, 1984) that demonstrated that the oligaemia associated with the spread of CSD from the occipital cortex showed a very similar propagation velocity to that of the CSD itself. |
The source is not given. |
|
| [2.] Clg/Fragment 009 11 - Diskussion Zuletzt bearbeitet: 2014-05-10 18:42:49 Singulus | BauernOpfer, Clg, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop |
|
|
|
| Untersuchte Arbeit: Seite: 9, Zeilen: 11-34 |
Quelle: Gorji 2001 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. |
Nothing has been marked as a citation. |
|
Letzte Bearbeitung dieser Seite: durch Benutzer:Schumann, Zeitstempel: 20140511004558