Infarct brain

Edavarone acute infarction study group. Effect of a novel free radical scavenger, edaravone (mci-186), on acute brain infarction. Randomized, placebo-controlled, double-blind study at multicenters. Cerebrovasc Dis 2003 15 222-229. 

Martz, D., Rayos, G., Schielke, G.P. and Betz, A.L. (1989). Allopurinol and dimethylthiourea reduce brain infarction following middle cerebral artery occlusion in rats. Stroke 20, 488-494. 

Brain infarction was the first clinical application of SPECT. Decreases in relative cerebral perfusion were imaged by SPECT for diagnosis. Decreased rCBF is visualized in the form of decreased signal on SPECT and PET. The sensitivity and specificity of brain SPECT for infarct localization are 85.5% and 97.6%, respectively [99]. Blood-flow imaging is useful in the evaluation of response to therapy in patients with cerebrovascular diseases [100]. 

Some reflecf a pafhologic process and are, at least, candidate surrogates (e.g., brain appearance in Alzheimer s disease, brain infarct size, and various radiographic or isotopic function tests). 

Rail up 20 X 10 ) Opportunistic meningoencephaUtis Diabetic polyneuropadiy Brain infarction Cortical atrophy... 

Sanchez-Guerra M, Valle N, Blanco LA, Combarros O, Pascual J. Brain infarction after postcoital contraception in a migraine patient. J Neurol 2002 249 774. 

Because it is necessary for the stroke patient to receive prompt treatment before brain cell death occurs, any useful drug must be effective even when there is considerable time lapse (often several hours) between the occurrence of the stroke and the onset of treatment. The term "therapeutic window" refers to the critical time of intervention between the onset of the ischaemia and occurrence of brain infarction. Some of the drugs that have been developed and shown to be effective in the treatment of various animal models of stroke are listed in Table 14.5. It should be emphasized that none of these drugs is currently marketed for the treatment of stroke. All have been developed on animal models and recent positron emission tomography and magnetic resonance imaging studies have shown that the therapeutic window may be much more variable and prolonged in man than in such models. Only extensive double-blind clinical trials (estimated... 

Systemic (i.p.) administration of the GPx inhibitor MS (1.5-150 mg/kg) dose-dependently reduced brain infarct area and volume produced by 2 h MCAo, as assessed by TTC staining 22 h after reperfusion (Fig. 1A-C). A representative image of the infarcted (pale) areas throughout the brain of rats treated with MS (150 mg/kg) or vehicle (PBS, 1 ml/kg), administered i.p. 15 min before MCAo, is... 

Fig. 1. Systemic administration of MS dose-dependently reduces brain infarct damage produced by transient MCAo in rat. Brain infarct areas (A) and volumes (B) were measured in TTC-stained brain coronal sections from rats treated with mercaptosuccinate (MS), i.p., 15 min before transient (2 h) MCAo. Brain damage was evaluated after 22 h of reperfusion. Values are expressed as mean + S.E.M. indicates P < 0.05 versus vehicle (one-way ANOVA followed by Dunnett s posttest n — 4—6 rats per experimental group). (C) Representative brain coronal sections (2 mm thick), stained with TTC, showing the infarct area (unstained) in rats treated with MS (150 mg/kg) or vehicle (PBS, 1 ml/kg) i.p., 15 min before transient (2 h) MCAo followed by 22 h reperfusion. Compared to vehicle-treated animals, MS...

Neuroprotection was only observed when MS was administered 15 min before MCAo. In fact, administration of the drug 1 h before the induction of ischemia or at the beginning of reperfusion resulted in an infarct volume which was not significantly different from vehicle treated animals (Fig. 2). This suggests that a limited time-window exists to provide reduction of brain infarct damage by GPx inhibition. 

Compared to normotensives, hypertensive persons develop a marked excess of the major cardiovascular diseases. In the age group 45-74, they develop at least twice as much occlusive peripheral artery disease, about three times as much coronary disease, more than four times as much congestive [heart] failure and over seven times the incidence of brain infarction as normotensives. 

Fig. 4.12. Mismatch concept of diffusion lesion (smaller) and perfusion deficit (larger) in human territorial brain infarction. Acute MCA territory ischemia/oligemia with a smaller, centrally located diffusion disturbance showing the relationship between infarct core, ischemic penumbra and changes in DWI and PI. DWI, diffusion-weighted imaging PI, perfusion imaging ADC, apparent diffusion coefficient ATP, high energy phosphates MCA, middle cerebral artery...

Hata R, Maeda K, Hermann D, Mies G, Hossmann KA (2000) Evolution of brain infarction after transient focal cerebral ischemia in mice. J Cereb Blood Flow Metab 20 937-946 HeissW-D (1983) Flow thresholds to functional and morphological damage of brain tissue. Stroke 14 329-331 Heiss W-D, Rosner G (1983) Functional recovery of cortical neurons as related to degree and duration of ischemia. Ann Neurol 14 294-301... 

Hossmann KA, Schuier FJ (1980) Experimental brain infarcts in cats. I. Pathophysiological observations. Stroke... 

Kohno K, Hoehn-Berlage M, Mies G, Back T, Hossmann KA (1995) Relationship between diffusion-weighted MR images, cerebral blood flow, and energy state in experimental brain infarction. Magn Reson Imaging 13 73-80 Lansberg MG, O Brien MW, Norbash AM, Moseley ME, Morrell... 

Fig.8.6a-d. Various subareas within and outside of the final brain infarction as determined by PET measurements of CBF and flu-mazenil (FMZ) binding on benzodiazepine receptors extension of final infarct as seen on MRI3 weeks post-insult (a) subarea with severely decreased FMZ binding (b) subarea with CBF < 14 ml/100 g/min combination of (a), (b) and (c) showing infarct subareas with decreased FMZ binding and reduced CBF in relation to final infarction. [Reproduced with permission from Heiss et al. (2001)]... 

Chuaqui R, Tapia J (1993) Histologic assessment of the age of recent brain infarcts in man. J Neuropathol Exp Neurol 52 481-489... 

Mokri B (2001) The Monro-Kellie hypothesis applications in CSF volume depletion. Neurology 56 1746-1748 Naruse S, Horikawa Y, Tanaka C, Hirakawa K, Nishikawa H, Yoshizaki K (1982) Proton nuclear magnetic resonance studies on brain edema. J Neurosurg 56 747-752 Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the borderzone around old small human brain infarcts. Stroke 17 1129-1137... 

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