Ischemic Stroke is defined by World Health Organization (WHO) as acute focal dysfunction of brain, originating from vessels lasting for more than 24 hours.
An acute stroke refers to the first 24-hour- period of a stroke. Focal neurological deficit lasting less than 24 hours known as transient ischemic attack. Acute ischemic stroke patients often need Intensive Care Unit (ICU) admission for different causes like disturbed level of consciousness and airway compensation. A pathological sympathetic activation with a surge in catecholamines occurs in the acute phase of stroke, and both the sympathetic over-activation and the subsequent autonomic dysfunction are predictors of poor functional outcome. In addition to increasing the risk of cardiac arrhythmias, the autonomic dysfunction and sympathetic over-activation may have a role in the development of stroke-induced immunodepression, which could increase the risk of infections. The post-stroke changes in the immune system include an increased number of circulating monocytes, higher levels of anti-inflammatory cytokines and a shift from Th1 to Th2 cytokine production. Beta-blockers showed a protective effect and an ability to block and reverse these catecholamine induced changes on the immune system. In addition to this, beta-blockers have been reported to reduce infarct size by antioxidant and free radical scavenging properties.