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The role of spreading depression in focal ischemia evaluated by diffusion mapping.

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TLDR
It is demonstrated that ischemia‐related and induced SDs increase significantly ischemic lesion volume in vivo, supporting the hypothesis for a causative role of SD in extending focal ischema injury.
Abstract
This study investigated the role of spontaneous and induced spreading depression (SD) on the evolution of focal ischemia in vivo. We induced focal ischemia in 12 rats using the middle cerebral artery suture occlusion (MCAO) method. Chemical stimulation of nonischemic ipsilateral cortex by potassium chloride application (KCl group; n = 7) and saline (NaCl group; n = 5) was performed at 15, 30, 45, and 60 minutes following MCAO, and SD was detected electrophysiologically. Ischemic lesion volumes assessed over 15-minute intervals, evaluated by continuous apparent diffusion coefficient (ADC) of water mapping, demonstrated that the ischemic region increased significantly during 15-minute time epochs with a single SD episode (36.5 +/- 12.9 mm3, mean +/- SD) or multiple SD episodes (39.8 +/- 22.3) compared with those without SD (13.9 +/- 11.5) (p = 0.0009). Infarct volume at postmortem 24 hours after MCAO was significantly larger in the KCl group, with more total SDs (237.8 +/- 13.8) than the NaCl group (190.5 +/- 12.6) (p = 0.0001). This study demonstrates that ischemia-related and induced SDs increase significantly ischemic lesion volume in vivo, supporting the hypothesis for a causative role of SD in extending focal ischemic injury.

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Journal ArticleDOI

The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease

TL;DR: Therapies that target spreading depolarization or the inverse hemodynamic response may potentially treat neurological conditions such as aneurismal subarachnoid hemorrhage or traumatic brain injury.
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Acute ischemic stroke: overview of major experimental rodent models, pathophysiology, and therapy of focal cerebral ischemia.

TL;DR: Various rodent animal models, pathogenic mechanisms, and promising therapeutic approaches of ischemic stroke are focused on.
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Interplay between Cortical Spreading Depolarization and Seizures

TL;DR: Manipulations in the occurrence and nature of CSD can potentially alter the threshold for seizure activity, and perhaps minimize immediate and long-term sequelae associated with epilepsy.
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The ischemic penumbra Operationally defined by diffusion and perfusion MRI

TL;DR: These MR indexes may allow the identification and quantification of viable but ischemically threatened cerebral tissue amenable to therapeutic interventions in the hyperacute care of stroke patients.
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Enlargement of human cerebral ischemic lesion volumes measured by diffusion-weighted magnetic resonance imaging

TL;DR: Evidence is provided that substantial enlargement of human cerebral ischemic lesion volumes can occur beyond the first 6, 12 or 24 hours after onset and a mismatch acutely between the region of hypoperfusion (larger) and the area of diffusion abnormality (smaller) may be predictive of ischeic lesion enlargement.
References
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Journal ArticleDOI

Spin diffusion measurements : spin echoes in the presence of a time-dependent field gradient

TL;DR: In this article, a derivation of the effect of a time-dependent magnetic field gradient on the spin-echo experiment, particularly in the presence of spin diffusion, is given.
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Spreading depression of activity in the cerebral cortex

TL;DR: In this article, an interesting response elicited by electrical stimulation was noticed in the cortex of rabbits, and the distinctive feature of this response was a marked, enduring reduction of the "spontaneous" electrical activity of the cortex.
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Early detection of regional cerebral ischemia in cats: comparison of diffusion- and T2-weighted MRI and spectroscopy.

TL;DR: Diffusion‐weighted hyperintensity in ischemic tissues may be temperature‐related, due to rapid accumulation of diffusion‐restricted water in the intracellular space (cytotoxic edema) resulting from the breakdown of the transmembrane pump and/or to microscopic brain pulsations.
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Viability thresholds and the penumbra of focal ischemia.

TL;DR: It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of tissue hypoxia, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply.
Journal ArticleDOI

Calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a unifying hypothesis.

TL;DR: The hypothesis predicts that loss of cellular calcium ho­ meostasis underlies selective neuronal vulnerability in ischemia, hypoglycemia, and epileptic seizures and that some cells are more vulner­ able than others because they have a higher density of calcium channels in their plasma membranes.
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