Stroke cerebral blood flow

Sorensen AG, Copen WA, 0stergaard L, Buonanno FS, Gonzalez RG, Rordorf G, Rosen BR, Schwamm LH, Weisskoff RM, Koroshetz WJ. Hyperacute stroke simultaneous measurement of relative cerebral blood volume, relative cerebral blood flow, and mean tissue transit time. Radiology 1999 210 519-527. 

Parsons MW, Yang Q, Barber PA, Darby DG, Desmond PM, Gerraty RP, Tress BM, Davis SM. Perfusion magnetic resonance imaging maps in hyperacute stroke relative cerebral blood flow most accurately identifies tissue destined to infarct. Stroke 2001 32 1581-1587. 

Wintermark M, Reichhart M, Thiran JP, Maeder P, Chalaron M, Schnyder P, Bogous-slavsky J, MeuU R. Prognostic accuracy of cerebral blood flow measurement by perfusion computed tomography, at the time of emergency room admission, in acute stroke patients. Ann Neurol 2002 51 417-432. 

Grandin CB, Duprez TP, Smith AM, Mataigne F, Peeters A, Oppenheim C, Cosnard G. Usefulness of magnetic resonance-derived quantitative measurements of cerebral blood flow and volume in prediction of infarct growth in hyperacute stroke. Stroke. 2001 32 1147-1153. 

Elevated blood pressure should remain untreated in the acute period (first 7 days) after ischemic stroke because of the risk of decreasing cerebral blood flow and worsening symptoms. The pressure should be lowered if it exceeds 220/120 mm Hg or there is evidence of aortic dissection, acute myocardial infarction, pulmonary edema, or hypertensive encephalopathy. If blood pressure is treated in the acute phase, short-acting parenteral agents (e.g., labetalol, nicardipine, nitroprusside) are preferred. 

Neuromuscular symptoms include altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia can mimic a stroke or CNS tumor by producing headache, papilledema, focal paresis, and abnormal reflexes. CNS symptoms are caused by increased cerebral blood flow and are variable, depending in part on the acuity of onset. 

Ischaemic stroke is the third leading cause of death in industrialized countries. The debilitating or lethal consequences of transient or temporary reductions in cerebral blood flow are not only caused by necrosis in the infarct zone itself, but also by pathophysiological events in the peri-infarct zone [14]. Apparently, the release of inflammatory mediators such as cytokines and NO contributes to tissue inflammatory injury. There is also evidence for apoptosis in the peri-infarct zone. These processes offer novel targets for therapeutic strategies. In this respect, the potential of neurotrophic factor treatment is described in Section 2.4.2.6. 

Atherosclerosis is a condition of the organism characterized by elevated levels of atherogenic lipoproteins in blood plasma, lipid deposits (including cholesterol) in the form of esters inside walls of the arterial system, and it is expressed by a gradual difficulty of blood circulation. The most appropriate name for this disease is lipoproteinemia. Clinically, it is manifested in the form of ischemic heart disease, stroke, abnormal cerebral blood flow, and peripheral ischemia. 

Two types of circulatory perturbations contribute to different types of ischemic injury to the brain (reviewed by Lipton 1999) (1) stroke (a complete occlusion of a cerebral artery) irreversibly kills the neurons in its core region and severely damages others in the penumbral region and (2) reversible circulatory arrest, with a transient total stop of cerebral blood flow, selectively kills vulnerable cell populations. These clinical conditions can be studied in animals, with focal ischemic models replicating stroke and global ischemic models replicating cardiac arrest. 

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. 

Lin W, Lee JM, Lee YZ, Vo KD, Pilgram T, Hsu CY (2003) Temporal relationship between apparent diffusion coefficient and absolute measurements of cerebral blood flow in acute stroke patients. Stroke 34 64-70... 

Morawetz RB, DeGirolami U, Ojemann RG, Marcoux FW, Crowell RM (1978) Cerebral blood flow determined by hydrogen clearance during middle cerebral artery occlusion in unanesthetized monkeys. Stroke 9 143-149 Moseley ME, Cohen Y, Mintorovitch J, Chileuitt L, Shimizu H, Kucharczyk JF, Wendland ME, Weinstein PR (1990) Early detection of regional cerebral ischemia in cats comparison of diffusion- and T2-weighted MRI and spectroscopy. Magn Reson Med 14 330-346... 

Schmidt-Kastner R, Paschen W, Ophoff BG, Hossmann KA (1989) A modified four-vessel occlusion model for inducing incomplete forebrain ischemia in rats. Stroke 20 938-946 Schmitz B, Bottiger BW, Hossmann KA (1997) Functional activation of cerebral blood flow after cardiac arrest in rat. J Cereb Blood FlowMetab 17 1202-1209 Schmitz B, Bock C, Hoehn-Berlage M, Kerskens CM, Bottiger BW, Hossmann KA (1998) Recovery of the rodent brain after cardiac arrest a functional MRI study. Magn Reson Med 39 783-788... 

Fiehler J, von Bezold M, Kucinski T et al (2002) Cerebral blood flow predicts lesion growth in acute stroke patients. Stroke 33 2421-2425... 

Fig. 7.2. Relationship between relative (rADC) and cerebral blood flow (CBF). ADC drops to below normal at CBF values around 15-24 ml/min/100 g, as shown in a pixel-wise comparison between diffusion and perfusion imaging in acute stroke patients. A lower threshold (15 ml/min/100 g) was found for patients imaged earlier (up to 4 h ) compared to the value (24 ml/min/100 g) of those patients imaged between 4.5 and 6.5 h ( ).The data show that the ADC threshold increases with time. [Reproduced with permission from Lin et al. (2003)]...

Earliest proof of an ischemic situation on MRI can be obtained within seconds after stroke onset by perfusion imaging (PI), depicting the area of reduced cerebral blood flow (Fig. 8.2 see also Chap. 6). This is followed within minutes by a rapid delineation of the early ischemic injury (cytotoxic edema) on DWI. Focus of this chapter will be on data acquired in animal ischemia models, using PD-w, Tl-w, and T2-w MRI, and their correlation with histopathology. 

Bose B, Jones SC, Lorig R, Friel HT, Weinstein M, Little JR (1988) Evolving focal cerebral ischemia in cats spatial correlation of nuclear magnetic resonance imaging, cerebral blood flow, tetrazolium staining, and histopathology. Stroke 19 28-37... 

Paschen W, Mies G, Hossmann KA (1992) Threshold relationship between cerebral blood flow, glucose utilization, and energy metabolites during development of stroke in ger-bils. Exp.Neurol 117 325-333... 

The longer the neurological deficit lasts and the later in the course of the stroke symptoms CT or DWI are performed, the higher the likelihood of a positive finding. Moderate decreases of cerebral perfusion as defined by increased relative mean transit times (rMTT), decreased relative cerebral blood flow (rCBF) but normal relative cerebral blood volume (rCBV) are typically found in DWI negative TIA or stroke patients (Ay et al. 1999b). 

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