الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The World Health Organization (WHO) has described the ischemic stroke as acute focal dysfunction of brain which is originating from vessels and can last for more than 24 hrs.
The 1st 24hr-period of a stroke is referred to as an acute stroke. If a focal neurological deficit lasts for fewer than 24hrs, it can be recognized as a transient ischemic attack. Patients with acute ischemic stroke often require ICU- admission for diverse causes such as disturbed consciousness level as well as airway compensation.
During the acute period of a stroke, there is a pathological activation of the sympathetic that results in a spike in catecholamines. The autonomic dysfunction that follows this sympathetic over-activity is an indicator of a poor functional prognosis. In conjunction with heightened cardiac arrhythmia risk, autonomic dysfunction and sympathetic hyper-activation may contribute to the development of stroke-induced immunodepression, hence elevating the risk of infections.
The post-stroke can alter in the immune system, for instance increased number of circulating monocytes, greater anti-inflammatory cytokines levels along with shifting of the generation of Th1 cytokine to Th2. Beta-blockers displayed a protective effect and the capability of blocking and reversing these catecholamine-induced alterations on the immune system. Besides this, beta-blockers have been stated to diminish the infarct size through scavenging characteristics of both antioxidant and free radical.