Stroke pathophysiology

Furlan A, Higashida R. Intra-arterial thrombolysis in acute ischemic Stroke. In Mohr JP, Choi DW, Grotta JC, et al., eds. Stroke Pathophysiology, Diagnosis, and Management. 4th ed. Philadelphia, PA Churchill Livingstone 2004 p. 943-951. 

OXIDATIVE STRESS IN STROKE PATHOPHYSIOLOGY VALIDATION OF HYDROGEN PEROXIDE METABOLISM AS A PHARMACOLOGICAL TARGET TO AFFORD NEUROPROTECTION... 

Up or downregulation of specific glutamate receptor subunits contribute to stroke pathophysiology in different ways [7], For example, after global cerebral ischemia, there is a relative reduction of calcium-... 

On the pathophysiological side, hyperactive nNOS has been implicated in A/-methyl-D-aspartate (NMDA)-receptor-mediated neuronal death in cerebrovascular-stroke. Some disturbances of smooth muscle tone within the gastrointestinal tract (e.g., gastroesophageal reflux disease) may also be related to an overproduction of NO by nNOS in peripheral nitrergic nerves. 

Darby DG, Barber PA, Gerraty RP, Desmond PM, Yang Q, Parsons M, Li T, Tress BM, Davis SM. Pathophysiological topography of acute ischemia by combined diffusion-weighted and perfusion MRI. Stroke 1999 30 2043-2052. 

Since functional outcome and risk of recurrent stroke are, in part, predictable based on the pathophysiologic subtype of stroke, the ability to accurately classify patients based on emergency clinical and imaging data would provide valuable predictive information. Unfortunately, misclassifications of stroke subtypes based on clinical data and a noncontrast CT scan are common. The final subtyping of stroke is made with all available clinical data, but is heavily influenced by neuroimaging studies that identify the location, size, and vascular distribution of the infarct, or that establish that the arteries supplying the region of stroke are stenotic or occluded. 

A basic grasp of normal cardiac function sets the stage for understanding the pathophysiologic processes leading to HF and selecting appropriate therapy for HF. Cardiac output is defined as the volume of blood ejected per unit of time (liters per minute) and is a major determinant of tissue perfusion. Cardiac output is the product of heart rate (HR) and stroke volume (SV) CO = HR x SV. The following describes how each parameter relates to CO. 

The pathophysiology of hemorrhagic stroke is not as well studied as that of ischemic stroke however, it is a more complex process than previously thought. Much of the process is related to the presence of blood in the brain tissue and/or surrounding... 

FIGURE 32-2. Treatment algorithm for Alzheimer s disease. A. Cognitive treatment. B. Treatment of psychiatric or behavioral symptoms. AD, Alzheimer s disease MMSE, Mini Mental Status Examination NINCDS-ADRDA National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer s Disease and Related Disorders Association. (From Faulkner JD, Bartlett J, Hicks P. Alzheimer s disease. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 1164, with permission.)... 

CVD is a generic denomination mainly integrated by coronary heart disease (CHD) and stroke. Although not considered as a form of CVD in some instances, venous thromboembolic disease (VTED) shares with the other forms of CVD the territorial assignment, the vascular tree, although clear differences exist in the main pathophysiological mechanisms. In most CVD forms, however, thrombus formation plays a crucial role. 

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. 

Danysz W, Parsons CG, Mobius HJ, et al (2000) Neuroprotective and symptomatological action of memantine relevant for Alzheimer s disease—an unified glutamatergic hypothesis on the mechanism of action. Neurotox Res 2 85-97 Davis SM, Lees KR, Albers GW, et al (2000) Selfotel in acute ischemic stroke possible neurotoxic effects of an NMDA antagonist. Stroke 31 347-354 DeKeyser J (1991) Excitotoxic mechanisms may be involved in the pathophysiology of tardive dyskinesia. Clin Neuropharmacol 14 562-565 Del Dotto P, Pavese N, Gambaccini G, et al (2001) Intravenous amantadine improves levodopa-induced dyskinesias an acute double-blind placebo-controlled study. Mov Disord 16 515-520... 

Sildenafil was the first oral treatment for ED and is the most extensively evaluated (35). Overall success rates in patients with cardiovascular disease of 80% or greater have been recorded with no evidence of tolerance, Patients with diabetes with or without additional risk factors, with their more complex, and extensive pathophysiology, have an average success rate of 60%. In randomized trials to date, open-label or outpatient monitoring studies the use of sildenafil is not associated with any excess risk of myocardial infarction, stroke, or mortality (38-40), In patients with stable angina pectoris there is no evidence of an ischemic effect due to coronary steal, and in one large, double-blind, placebo-controlled, exercise study sildenafil 100 mg increased exercise time and diminished ischemia (41), A study of the hemodynamic effects in men with severe CAD identified no adverse cardiovascular effects and a potentially beneficial effect on coronary blood flow reserve (42), Studies in patients with and without diabetes have demonstrated improved endothelial function acutely and after long-term oral dose administration, which may have implications beyond... 

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