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Angaben zur Quelle [Bearbeiten]

Autor     Katharina Eikermann-Haerter, Michael A. Moskowitz
Titel    Animal models of migraine headache and aura
Zeitschrift    Current Opinion in Neurology
Jahr    2008
Jahrgang    21
Seiten    294–300
URL    http://www.researchgate.net/publication/5400479_Animal_models_of_migraine_headache_and_aura

Literaturverz.   

no
Fußnoten    no
Fragmente    2


Fragmente der Quelle:
[1.] 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

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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

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Sichter
(Graf Isolan) Schumann

[2.] Amh/Fragment 010 01 - Diskussion
Zuletzt bearbeitet: 2014-05-06 20:27:29 Hindemith
Amh, Eikermann-Haerter and Moskowitz 2008, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 10, Zeilen: 1-19
Quelle: Eikermann-Haerter and Moskowitz 2008
Seite(n): 297, Zeilen: left col. 38ff - right col. 1ff
Unlike an epileptic seizure, which spreads asynchronously to activate adjacent brain, SD begins within a synchronously activated brain space.

In experimental animals, SD stimulates ipsilateral trigeminal axons that surround cortical blood vessels. SD causes a breakdown of the blood–brain barrier by mechanisms dependent on matrix metalloproteinase-9. Furthermore, neocortical SD causes ipsilateral extravasation of plasma proteins in dura mater, serving as an experimental marker of trigeminal nerve activation; it also induces c-Fos expression within the trigeminal nucleus caudalis. These findings and a transcription MRI study suggest that intense cortical perturbations like repeated SD can open the blood–brain barrier, thereby activating the trigeminovascular system. SD releases chemicals such as H+, K+, nitric oxide, and neurotransmitters into the extracellular space. It has been hypothesized that released molecules reach the pial surface by diffusion and accumulate in proximity to trigeminovascular afferents. Extracellular K+ levels about 60 mmol/l were measured in the pial space during SD.

Consistent with an upstream role for SD, prolonged application of migraine prophylactic drugs suppresses SD in rats as a proposed mechanism of action. In line with the growing clinical recognition that prolonged administration of prophylactic drugs is important to achieve maximum therapeutic efficacy, treatment extension beyond 3–4 weeks also maximizes the inhibitory effects of topiramate, valproate, methysergide, amitriptyline, and propranolol on SD.

Unlike an epileptic seizure, which spreads asynchronously to activate adjacent brain, CSD begins within a synchronously activated brain space [75].

In experimental animals, CSD stimulates ipsilateral trigeminal axons that surround cortical blood vessels [7]. CSD causes a breakdown of the blood–brain barrier by mechanisms dependent on matrix metalloproteinase-9 [76]. Furthermore, CSD causes ipsilateral extravasation of plasma proteins in dura mater, serving as an experimental marker of trigeminal nerve activation [6]; it also induces c-Fos expression within the trigeminal nucleus caudalis [8]. These findings and a recent transcription MRI study [77] suggest that intense cortical perturbations like repeated CSD can open the blood–brain barrier, thereby activating the trigeminovascular system. CSD releases chemicals such as H+, K+, nitric oxide, and neurotransmitters into the extracellular space. It has been hypothesized that released molecules reach the pial surface by bulk diffusion and accumulate in proximity to trigeminovascular afferents. Extracellular K+ levels greater than 40 mmol/l were measured in the pial space during CSD.

Consistent with an upstream role for CSD, prolonged administration of migraine prophylactic drugs suppresses CSD in rats as a proposed mechanism of action [24]. In line with the growing clinical recognition that prolonged administration of prophylactic drugs is important to achieve maximum therapeutic efficacy, treatment extension beyond 3–4 weeks also maximizes the inhibitory effects of topiramate, valproate, methysergide, amitriptyline, and DL propranolol on CSD [24].


6 Moskowitz MA. Genes, proteases, cortical spreading depression and migraine: impact on pathophysiology and treatment. Funct Neurol 2007;22:133–136.

This work reviews important developments supporting the view of cortical spreading depression as an upstream driver of both migraine aura and pain.

7 Bolay H, Reuter U, Dunn AK, et al. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med 2002; 8:136–142.

8 Moskowitz MA, Nozaki K, Kraig RP. Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. J Neurosci 1993; 13:1167–1177.

24 Ayata C, Jin H, Kudo C, et al. Suppression of cortical spreading depression in migraine prophylaxis. Ann Neurol 2006; 59:652–661.

75 Kunkler PE, Hulse RE, Schmitt MW, et al. Optical current source density analysis in hippocampal organotypic culture shows that spreading depression occurs with uniquely reversing currents. J Neurosci 2005; 25:3952–3961.

76 Gursoy-Ozdemir Y, Qiu J, Matsuoka N, et al. Cortical spreading depression activates and upregulates MMP-9. J Clin Invest 2004; 113:1447–1455.

77 Liu CH, You Z, Ren J, et al. Noninvasive delivery of gene targeting probes to live brains for transcription MRI. FASEB J 2007 [Epub ahead of print].
This study uses an innovative transcription MRI technique to visualize specific cerebral mRNA in vivo. It validates noninvasive delivery of novel magnetic resonance probes to the brains of live animals after acute neurological disorders.

Anmerkungen

Nothing has been marked as a citation, no reference is given.

Sichter
(Graf Isolan) Schumann

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