Management of Acute Stroke.
- Author:
Jei KIM
1
Author Information
1. Department of Neurology, College of Medicine, Chungnam National University, Korea.
- Publication Type:Original Article
- Keywords:
Stroke;
Thrombolytic therapy;
Anticoagulant therapy;
Antiplatelet agent;
Penumbral area
- MeSH:
Animals;
Blood Pressure;
Calcium;
Calcium Channels;
Cerebral Infarction;
Consensus;
Free Radicals;
Humans;
Ion Channels;
Models, Animal;
Neurons;
Oxygen;
Phlebitis;
Population Characteristics;
Positron-Emission Tomography;
Pressure Ulcer;
Prognosis;
Reperfusion;
Stroke*;
Thrombolytic Therapy
- From:Journal of the Korean Academy of Rehabilitation Medicine
1997;21(4):633-642
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
New insights in the pathophysiology of stroke have been developed in the past few years. The progress in this area has led the development of diagnostic devices and new treatments. No specific therapy has proven efficacious in treating acute ischemic stroke, because of major differences between animal models and human stroke, the heterogeneity of stroke pathogenesis, and the lack of consensus on stroke management in each subtypes of stroke. A good general management is an important factor for the better prognosis than specific therapy in different types of stroke. General management of stroke includes cardiac and pulmonary care, metabolic maintenance, blood pressure control, and prevention of bedsores and phlebitis. Thrombolytic therapy, anticoagulation and antiplatelet agent therapy are kinds of specific therapies in acute ischemic stroke. It has to be emphasized that patients be referred early. In animal studies, focal ischemic insult requires 3-4 hours to progress to cerebral infarction. Six hours after onset of stroke has been arbitrarily defined as the limit to initiate reperfusion on positron emission tomography in human. The entry of calcium into the cells via receptor-mediated membrane channels is an important factor in ischemic neuronal death. Oxygen free radical is an another factor in the ischemic damage. Calcium channel antagonists and scavengers of oxygen free radicals will have beneficial roles to prevent ischemic neuronal injury.
