Infarct cortical

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

Nudo RJ (2007). Post infarct cortical plasticity and behavioural recovery. Stroke 38 840-845 Outpatient Service Trialists (2003). Therapy-based rehabilitation services for stroke patients at home Cochrane Database of Systematic Reviews 1 CD002925 Pariente J, Loubinoux I, Carel C et al. (2001). Lluoxetine modulates motor performance and cerebral activation of patients recovering from stroke. Annab of Neurology 50 718-729... 

Anderson RE, Tan WK, Martin HS, Meyer FB. Effects of glucose and Pa02 modulation on cortical intracellular acidosis, NADH redox state, and infarction in the ischemic penumbra. Stroke 1999 30(1) 160-170. 

N-Nitro-L-arginine methyl ester (L-NAME) is an inhibitor of NOS L-NAME reportedly reduces the volume of cortical and striatal infarct after middle cerebral artery occlusion in the rat. This protection can be reversed by co-injection of L-arginine. L-NAME also reduced the excitotoxic damage induced by NMDA injection. Finally, the authors showed that L-NAME reduced glutamate efflux produced by ischaemic injury in rats. The authors concluded that NOS induced by NMDA receptor overstimulation is a key event in the neuronal injury cascade (Buisson eta/., 1993). 

Laursen H, Hansen A, Sheardown M. 1993. Cerebrovascular permeability and brain edema after cortical photochemical infarcts in the rat. Acta Neuropathologica 86(4) 378-385. 

Contraindications Uncontrolled adrenal cortical insufficiency, untreatedthyrotoxico-sis, treatment of obesity, uncontrolled angina, uncontrolled hypertension, uncontrolled myocardial infarction, and hypersensitivity to any component of the formulations... 

Many pathological conditions, including ischemia/reperfusion, inflammation, and sepsis may induce tissues to simultaneously produce both superoxide and nitric oxide. For example, ischemia allows intracellular calcium to accumulate in endothelium (Fig. 20). If the tissue is reperfused, the readmission of oxygen will allow nitric oxide as well as superoxide to be produced (Beckman, 1990). For each 10-fold increase in the concentration of nitric oxide and superoxide, the rate of peroxynitrite formation will increase by 100-fold. Sepsis causes the induction of a second nitric oxide synthase in many tissues, which can produce a thousand times more nitric oxide than the normal levels of the constitutive enzyme (Moncada et al., 1991). Nitric oxide and indirectly peroxynitrite have been implicated in several important disease states. Blockade of nitric oxide synthesis with N-methyl or N-nitroarginine reduces glutamate-induced neuronal degeneration in primary cortical cultures (Dawson et al., 1991). Nitroarginine also decreases cortical infarct volume by 70% in mice subjected to middle cerebral artery occlusion (Nowicki et al., 1991). Myocardial injury from a combined hy-... 

Diagnosed, but uncorrected adrenal cortical insufficiency Untreated thyrotoxicosis Hypersensitivity to any component of drug Myocardial infarction... 

Gold AE, Marshall SM. Cortical blindness and cerebral infarction associated with severe hypoglycemia. Diabetes Care 1996 19(9) 1001-3. 

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... 

Disturbances of proton diffusion are not unique to cerebral ischemia. Reduced diffusion has also been found in various experimental conditions including spreading depression (Busch et al. 1995) and peri-infarct depolarizations (Gyngell et al. 1994 Rother et al. 1996), hypoglycemia (Hasegawa et al. 1996), following cortical application of noxious substances [blockers of the Na+-/K+-ATPase (Benveniste et al. 1992), excitotoxins (Verheul et al. 1994)] and... 

Many individuals with LA also harbor lacunar and/or cortical infarcts. Presence of LA serves as an intermediate surrogate both for ischemic stroke and intracerebral hemorrhage as they all share similar risk factors and similar pathophysiological mechanisms (Inzitari 2003). LA is widely found in dementing illnesses, such as Alzheimer s disease, vascular dementia, and cerebral autosomal dominant arteri-opathy with subcortical infarcts and leukoencepha-lopathy (CADASIL). Failure of blood supply in the... 

Histopathological features of white matter lesions include diffuse myelin pallor (sparing the U-fibers, that are supplied by cortical branches), astrocytic gliosis, widening of perivascular spaces, and loss of oligodendrocytes leading to rarefaction, spongiosis, as well as loss of myelin and axons without definite necrosis, which has also been described as incomplete white matter infarction, which may finally... 

While physicians may not recognize up to 80% of lacunes (Tuszynski et al. 1989), several clinical syndromes have been correlated with relevant lacunes detected at subsequent autopsy. Five of these are regarded as the classic lacunar syndromes pure motor hemiparesis, sensorimotor stroke, pure sensory hemiparesis, dysarthria clumsy hand syndrome, and ataxic hemiparesis (Donnan et al. 2002 Fisher 1982 Bamford 2001). Pure motor stroke is the commonest lacunar syndrome in clinical practice, while pure sensory stroke is encountered less frequently. The involvement of the face, arm and leg of one side is the characteristic feature of the first three syndromes while reductions of consciousness, cognitive or visual field defects are absent. Even though lacunar infarcts have been linked to lacunar syndromes, the latter are of course not specific for this stroke subtype and mimicked by cortical infarcts, intracerebral hematomas, and non-vascular causes (Bogousslavsky et al. 1988 Bamford 2001). 

MCA infarcts are mainly caused by cardioembolism, internal carotid artery (ICA) thrombosis, dissection or embolism and rarely (in Caucasians) by intrinsic MCA disease. MCA atherothrombotic territory infarctions related to intrinsic MCA disease often cause concomitant small cortical (territorial or borderzone) and subcortical infarcts (Min et al. 2000). 

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