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Brain infarcted regions

Cosmetic filler injections into the glabellar region or nasolabial fold can cause retinal artery occlusion. Iatrogenic ophthalmic artery occlusion is associated with painful blindness, a thin choroid, brain infarction and poor visual outcomes, particularly when autologous fat is used. Ophthalmic examinations and systemic brain magnetic resonance imaging (MRl) should be performed in patients with ocular pain after such injections. [Pg.207]

Hunter GJ, Silvennoinen HM, Hamberg LM, Koroshetz WJ, Buonanno FS, Schwamm LH, Rordorf GA, Gonzalez RG. Whole-brain CT perfusion measurement of perfused cerebral blood volume in acute ischemic stroke probability curve for regional infarction. [Pg.93]

Fig. 1. BEO dose-dependently reduces infarct size after permanent MCAo. Representative images of brain sections from (A) rats in — 5) sacrificed 24 h after permanent occlusion of middle cerebral artery (24 h MCAo) and (B) BEO-treated rats (n — 5) prior to MCAo BEO (0.5 ml/kg) was administered i.p. 1 h before MCAo. Brain sections were stained by TTC the ischemic region appears as a pale-stained area whereas the viable tissue is stained red. (C) Effects of different doses of BEO (0.05—1 ml/kg), administered i.p. 1 h before MCAo, on infarct volume results are expressed as mean S.E.M. (n = 4-6 per group). and Denote P< 0.05 andP< 0.01 versus 24 h MCAo, respectively (ANOVA followed by Dunnett multiple comparisons test). Fig. 1. BEO dose-dependently reduces infarct size after permanent MCAo. Representative images of brain sections from (A) rats in — 5) sacrificed 24 h after permanent occlusion of middle cerebral artery (24 h MCAo) and (B) BEO-treated rats (n — 5) prior to MCAo BEO (0.5 ml/kg) was administered i.p. 1 h before MCAo. Brain sections were stained by TTC the ischemic region appears as a pale-stained area whereas the viable tissue is stained red. (C) Effects of different doses of BEO (0.05—1 ml/kg), administered i.p. 1 h before MCAo, on infarct volume results are expressed as mean S.E.M. (n = 4-6 per group). and Denote P< 0.05 andP< 0.01 versus 24 h MCAo, respectively (ANOVA followed by Dunnett multiple comparisons test).
Especially in models of transient cerebral ischemia, apoptotic cell death has been observed after 3-7 days post insult in selected brain regions in which basal energy metabolism has been preserved (Chen et al. 1997 Du et al. 1996). In the meantime, molecular switches have been identified that gate different populations of neurons with regard to the type of cell death they eventually undergo (Nicotera 2003). However, there is little doubt that in animal stroke the vast majority of cells would die from necrosis or, alternatively, secondary energy failure even in the presence of a pro-apop-totic genetic balance. The concept of thresholds of cerebral blood flow (CBF) for various functions of brain parenchyma (see below) explains why the infarct core suffers from pan-necrosis whereas the peri-infarct border in which function is suppressed, but structure initially preserved (the so-called ischemic penumbra), may show apoptotic cell death or a combination of both. [Pg.43]


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Brain infarct

Brain regions

Infarct

Infarction

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