Stroke is the second leading cause of death, after ischemic heart disease, and accounts for 9% of deaths worldwide. According to the World Health Organization [WHO], 15 million people suffer stroke worldwide each year. Of these, more than 6 million die and another 5 million are permanently disabled. Reactive oxygen species [ROS] have been implicated in brain injury after ischemic stroke. There is evidence that a rapid increase in the production of ROS immediately after acute ischemic stroke rapidly overwhelm antioxidant defences, causing further tissue damage. These ROS can damage cellular macromolecules leading to autophagy, apoptosis, and necrosis. Moreover, the rapid restoration of blood flow increases the level of tissue oxygenation and accountsfor a second burst of ROS generation, which leads to reperfusion injury. Current measures to protect the brain against severe stroke damage are insufficient. Thus, it is critical to investigate antioxidant strategies that lead to the diminution of oxidative injury. The antioxidant vitamins C and E, the polyphenol resveratrol, the xanthine oxidase [XO] inhibitor allopurinol, and other antioxidant strategies have been reviewed in the setting of strokes. This review focuses on the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of ischemic stroke, and the novel therapeutic strategies to be tested to reduce the cerebral damage related to both ischemia and reperfusion.

No abstract

No abstract

Background: The incidence of intracerebral haemorrhage (ICH) in Hispanics is high, especially of non-lobar ICH. Our aim was to ascertain prospectively the incidence of first-ever spontaneous ICH (SICH) stratified by localisation in a Hispanic-Mestizo population of the north of Chile. Methods: Between July 2000 and June 2002 all possible cases of ICH were ascertained from multiple overlapping sources. The cases were allocated according to localisation. Those with vascular malformations or non-identifiable localisations were excluded. Results: We identified a total of 69 cases of first-ever ICH. Of these, 64 (92.7%) had SICH, of which we allocated 58 cases (84%) to non-lobar or lobar localisation. The mean age was 57.3 ± 17 years, and 62.3% of the subjects were male. The age-adjusted incidence rates were 13.8 (non-lobar) and 4.9 (lobar) per 100,000 person-years. Non-lobar SICH was more frequent in young males and lobar SICH in older women. The non-lobar-to-lobar ratio was similar to previous findings in Hispanics. Hypertension was more frequent in non-lobar SICH and in diabetes, heavy drinking and antithrombotic use in lobar SICH, but in none significantly. There was no association between localisation and prognosis. Conclusions: The incidence of non-lobar SICH was high, but lower than in most non-white populations. This lower incidence could be due to a lower population prevalence of risk factors, a higher socioeconomic level in this population, or chance.

Introduction Uric acid has gained considerable attention as a potential neuroprotective agent in stroke during the last decades, however, its role in the pathophysiology of ischemic stroke remains poorly understood. A serial evaluation of uric acid levels during the acute phase of stroke and its association with infarct size on magnetic resonance imaging is lacking. Methods We present a cohort study of 31 patients with ischemic stroke who were not candidates for thrombolysis according to current criteria at the time. We performed daily measurements of serum uric acid and total antioxidant capacity of plasma during the first week after symptoms onset and 30 days after. Infarct size was determined in the acute phase by a DWI sequence and the final infarct size with a control MRI (FLAIR) at day 30. Results Uric acid significantly decreases between days 2 to 6 compared to day 1, after adjustment by sex, age and DWI at diagnosis, with a nadir value at 72h. A mixed model analysis showed a negative association between DWI at diagnosis and uric acid evolution during the first week after stroke. Moreover, multivariable linear regression of uric acid values during follow up on DWI volumes demonstrated that DWI volume at diagnosis is negatively associated with uric acid levels at day 3 and 4. There were no significant associations between total antioxidant capacity of plasma and DWI at diagnosis, or FLAIR at any point. Discussion Patients with larger infarcts exhibited a significant decrease in serum uric acid levels, accounting for a more prominent reactive oxygen species scavenging activity with subsequent consumption and decay of this antioxidant. The different kinetics of total antioxidant capacity of plasma and serum uric acid levels suggests a specific role of uric acid in the antioxidant response in ischemic stroke.