Ischemic brain tissue

Junghans U, Seitz RJ, Ritzl A, Wittsack HJ, Fink GR, Freund HJ, Siebler M. Ischemic brain tissue salvaged from infarction by the GP Ilb/IIIa platelet antagonist tirofiban. Neurology 2002 58 474- 76. 

Ay H, Koroshetz WJ, Vangel M et al. (2005). Conversion of ischemic brain tissue into infarction increases with age. Stroke 36 2632-2636... 

Berger C, Fiorelli M, Steiner T et al. (2001). Hemorrhagic transformation of ischemic brain tissue asymptomatic or symptomatic Stroke 32 1330-1335... 

Dzialowski I, Klotz E, Goericke S, Doerfler A, Forsting M, von Kummer R (2007) Ischemic brain tissue water content CT monitoring during middle cerebral artery occlusion and reperfusion in rats. Radiology 243 720-726... 

Inflammatory cells infiltrating postischemic tissue are considered to contribute to disability after cerebral ischemia [5,8,17]. Identification of factors involved in the selective recruitment and accumulation of inflammatory cells into ischemic brain tissue and the mechanisms behind the entry of leukocytes through the blood-brain barrier into sites of ischemia are not completely understood [5,8]. Locally produced proinflammatory cytokines such as TNF-a, IL-1 P, and IL-6 initiate the inflammatory process. TNF-a and IL-1 P mRNA elevate in the brain after experimental middle cerebral artery occlusion [5,51,81]. While, IL-1 p and TNF-a play a major role in promoting adhesion between endothelial cells and leukocytes, they are poor attractants for polymorphonuclear leukocytes and monocytes [7]. Astrocytes and endothelial cells can respond in vitro to such proinflammatory cytokines with enhanced expression of chemokines, which results in the influx of leukocytes to areas of inflammation [5,8,103]. 

Importantly, the identification of ischemic brain tissue by CT not only defines regions likely to infarct, but also may predict outcome and response to intravenous (IV) or intra-arterial (lA) thrombolytic therapy [13]. CT scanning is most commonly used to exclude the presence of intracranial hemorrhage and a large established infarction. In addition, unenhanced CT findings... 

The biophysical basis for the rapid decrease in apparent diffusion coefficients of acutely ischemic brain tissue is complex (Table 7.1). Cytotoxic edema induced with acute hyponatremic encephalopathy is associated with decreased diffusion [3] and is therefore thought to contribute to the decreased diffusion associated with acute stroke. Furthermore, there is decreased Na-t/K-t ATPase activity without a significant increase in brain water [4] when decreased diffusion is present in acutely... 

In animal studies, experimental middle cerebral artery occlusion is followed by ADC values 16-68% below those of normal tissue as measured at 10 min to 2 h [15-21]. Diffusion coefficients pseudonormalize (i.e., the ADCs are similar to those of normal brain tissue though the tissue is not viable) at approximately 48 h and are elevated thereafter. In humans, the time course is longer (Table 7.2) (Fig. 7.7). Decreased diffusion in ischemic brain tissue is observed as early as 11 min after vascular occlusion [22-26]. The ADC continues to decrease with peak signal reduction at 1 days. This decreased diffusion is markedly hyperintense on DW images (a combination of T2 and diffusion weighting), less hyperintense on exponential images, and hypointense on ADC... 

In non-ischemic brain tissue, the CBF value is about 50-80 ml blood per 100 mg brain per minute. Flow reductions below 10-15 ml/100 mg/min usually lead to irreversible infarction after a few minutes. CBF val-... 

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