Cerebral Ischemia by Werner Hacke MD, Herman J. Gelmers MD, Michael Hennerici MD,

By Werner Hacke MD, Herman J. Gelmers MD, Michael Hennerici MD, Günter Krämer MD (auth.)

Despite a world relief in its occurrence, stroke is still some of the most universal ailments mostly and crucial reason behind untimely and chronic incapacity within the industrialized nations. the main widespread explanation for stroke is a localized disturbance of cerebral circulate, i.e., cerebral ischemia. much less universal are spon­ taneous intracerebral and subarachnoid hemorrhages and sinus ve­ nous thromboses. The creation of recent diagnostic approaches akin to cranial computed tomography, magnetic resonance imaging, digi­ tal subtraction radiologic suggestions, and numerous ultrasound tech­ niques has resulted in amazing advances within the analysis of stroke. during the deliberate software of those strategies, it's even attainable to spot the pathogenetic mechanisms underlying focal cerebral ischemia in people. notwithstanding, those diagnostic advances have made the distance among diagnostic accuracy and healing implications even more than earlier than. This truth should be simply defined. long ago, healing experiences needed to be according to the indications and temporal points of stroke; it was once very unlikely for early investigations to think about a few of the pathogeneses of cerebral ischemia. necessarily, stroke sufferers have been taken care of as being affected by a uniform disease.

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It is assumed that specific functional metabolic factors, such as a high supply of excitatory transmitter substances, may be responsible for this variable reaction (Siesj6 1981). Globally, the resting cerebral circulation amounts on average to about 50-60 ml each minute per 100 g of brain tissue. A reduction in the circulation to some 20 ml per minute per 100 g may not lead to observable consequences, although even here electrophysiologic studies may show a slowing of the EEG. A further reduction in circulation then leads to features of neurologic deficit, the functional or ischemic threshold (the terms are synonymous) having been passed.

Calculations in the general population are without an adequate diagnostic basis; the most representative data appear to be those of the Framingham study, summarized in Fig. 3 (Wolf et al. 1983). --. 200 ~~ --~~~ 160 ~~ ~~ ~~ ~~ ...... 120 ~------ 80 1945-49 50-54 55-59 60-64 65-69 Men ...................... ________~w~omen 70-74 75-79 Years Fig. 2. Mean annual incidence of all first stroke episodes in Rochester, Minnesota, at 5-year intervals per 100000 inhabitants. (From Whisnant 1983) 70 % Stroke episode 60 OMen 50 Women 40 30 20 10 Atherothrombotic cerebral infarct Embolic cerebral infarct SubIntraarachnoid cerebral hemorrhage hemorrhage Transient ischemic attacks only Other Fig.

In: Meyer JS, Lechner H, Reivich M, Ott EO, Arabinar A ,(eds) Cerebral vascular disease, vol 3. Excerpta Medica, Amsterdam, p 3 Katzmann R, Pappius HM (1973) Brain electrolytes and fluid metabolism. Williams and Wilkins, Baltimore Langfitt TW, Weinstein JD, Kassell NF (1965) Cerebral vasomotor paralysis produced by intracranial hypertension. Neurology 15:622 Lassen NA (1961) The luxury perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet II:1113 Lassen NA, Palv6lgyi R (1968) Cerebral steal during hypercapnia and inverse reaction during hypocapnia observed by the 133-xenon technique in man.

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