Stroke by Marc Fisher (Eds.)

By Marc Fisher (Eds.)

This quantity presents a necessary and accomplished source on stroke, together with learn, analysis, prevention, and therapy modalities. Practitioners in those fields will locate important info during this guide, from simple mechanisms of the ailment, to improved diagnostic and healing features for sufferer care.

With the sector of cerebrovascular problems, together with stroke, making quick developments, clinicians will locate illuminating and insightful chapters at the pathophysiological foundation of this disorder.

Advances in our realizing of the biochemical historical past of strokes, coupled with an exam of breakthroughs in epidemiology, genetics, neuroimaging, interventional radiology, surgical procedure, or even scientific psychology also are explored, giving researchers and clinicians a profoundly altered technique to process stroke study, prognosis, and sufferer remedy and care.

* A accomplished source on stroke, prevention strategies, prognosis, and therapy modalities
* Illuminating and insightful details at the pathophysiological foundation of stroke
* a radical exam of the swift developments made within the box of cerebrovascular problems and their functions to stroke

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Evidence supporting a role for programmed cell death in focal cerebral ischemia in rats. Stroke 24: 2002–2009. Lipton P (1999). Ischemic cell death in neurons. Physiol Rev 79: 1431–1568. Lo EH, Dalkara T, Moskowitz MA (2003). Mechanisms, challenges, and opportunities in stroke. Nat Rev Neurosci 4: 399–415. Lo EH, Moskowitz MA, Jacobs TP (2005). Exciting, radical, suicidal. How brain cells die after stroke? Stroke 36: 189–192. McDonald JW, Althomsons SP, Hyra KL, et al. (1998). Oligodendrocytes from forebrain are highly vulnerable to AMPA/kainate receptor mediated excitotoxicity.

Induction of caspase-3like protease may mediate delayed neuronal death in the hippocampus after transient cerebral ischemia. J Neurosci 18: 4914–4928. Clark AW, Krekoski CA, Bou SS, et al. (1997). Increased gelatinase A (MMP-2) and gelatinase B (MMP-9) activities in human brain after focal ischemia. Neurosci Lett 238: 53–56. Connolly ES Jr, Winfree CJ, Springer TA, et al. (1996). Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke.

1999). Similar to gray matter, energy deprivation leads to dysfunction of axons via activation of voltagedependent sodium and calcium channels, and consecutive activation of calcium-dependent disruptive pathways (Goldberg and Ransom, 2003). , 2000). Indeed, the astrocyte glycogen content defines the period of hypoglycemia in which cells are resistant to injury. Particularly vulnerable to ischemic damage are oligodendrocytes, the myelin-forming cells of the central nervous system. , 1998). , 2002).

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