Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy are the main revascularization therapies for acute ischemic stroke. However, ischemia-reperfusion injury after revascularization therapy can result in worsening outcomes. Among all possible pathological mechanisms of ischemia-reperfusion injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play a key role in the process. Free radicals lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in cell death. Additionally, free radical damage has a strong connection with inducing hemorrhagic transformation and cerebral edema, which are the major complications of revascularization therapy, and mainly influencing neurological outcomes due to the disruption of the blood-brain barrier. In order to get a better clinical prognosis, more and more studies focus on the pharmaceutical and nonpharmaceutical neuroprotective therapies against free radical damage. This review discusses the pathological mechanisms of free radicals in ischemia-reperfusion injury and adjunctive neuroprotective therapies combined with revascularization therapy against free radical damage.

Reports of dCA in patients with ICH group are scarce, yet diverse. In a case-control study, a higher gain was observed within 3 days of ICH onset when compared with the healthy controls, indicating a less effective dCA during the acute stage. 7 In a recent study, researchers obtained serial measurements and stated that a higher bilateral gain could last 5 days Background and Purpose-Cerebral autoregulation is crucial in patients with intracerebral hemorrhage. Dynamic cerebral autoregulation is probably altered in acute intracerebral hemorrhage; however, the temporal course of dynamic cerebral autoregulation and its correlation with clinical factors and outcomes are poorly understood. Methods-Forty-three acute supratentorial intracerebral hemorrhage patients (53.7±10.0 years old, 30 men) were enrolled for serial measurements performed on days 1 to 2, 4 to 6, 10 to 12, and 30 days after ictus. Noninvasive continuous cerebral blood flow velocity and arterial blood pressure were recorded simultaneously using transcranial Doppler and a servocontrolled plethysmograph, respectively. Transfer function analysis was used to derive the autoregulatory parameters, including phase difference (PD), gain, and the rate of recovery of cerebral blood flow velocity. Results were compared with healthy controls and correlated with clinical factors and the 90-day outcome. Results-PD did not differ between affected and unaffected hemispheres over time. A significant lower PD (indicating dynamic cerebral autoregulation impaired) was found in bilateral hemispheres on days 1 to 2, 4 to 6, and 10 to 12, followed by later recovery on day 30. Lower bilateral PD on days 1 to 2 was associated with poorer Glasgow Coma Scale score at that time. Lower affected-side PD on days 4 to 6 was an independent predictive value for a poorer modified Rankin Scale at 90 days. Conclusions-In patients with supratentorial intracerebral hemorrhage, dynamic cerebral autoregulation is bilaterally impaired lasting at least 10 to 12 days and recovers within a month. Individual PD value is associated with clinical status at acute stage and affected-side PD on days 4 to 6 can be an independent predictor for clinical outcome. after ictus, whereas a higher gain value was not associated with any clinical factors or outcome. 14 Serial index Mx (reflecting both static and dynamic CA) was also derived within 5 days after ICH onset. Although it was not generally impaired on the first day, a secondary decline between days 3 and 5 could possibly occur mainly on the affected side, and this may be associated with poorer clinical status and outcomes.15 Yet, the above studies all garnered attention toward the early stage after ICH, while ignoring the subacute and recovery stages. This left unresolved whether, when, and to what extent could the altered dCA be restored.Thus, in the present study, we sought to (1) investigate the time course of dCA in ICH patients with serial follow-ups, including 1 to 2 days after ictus and 3 additional time points within a month, and (2) explore th...

ObjectivesEpidemiological studies aimed at stroke and its risk factors can help identify persons at higher risk and therefore promote stroke prevention strategies. We aimed to explore the current prevalence of stroke and its associated risk factors in northeast China.DesignPopulation based cross sectional study.SettingData were collected using a structured precoded questionnaire designed by the Stroke Screening and Prevention Programme of the National Health and Family Planning Commission of China, between January and March 2016.Participants4100 permanent residents, aged 40 years or older, who had lived in Dehui City of Jilin Province for more than 6 months volunteered to participate in the survey, with a response rate of 92.2%. For the purpose of the present analysis, 48 subjects were excluded due to missing values, giving a total of 4052 people included in this analysis.Main outcome measureThe questionnaire included demographic characteristics, stroke related behavioural factors, personal and family medical history of stroke, physical examination and laboratory testing.ResultsThe overall prevalence of stroke in Jilin Province was 7.2% (95% CI 6.3% to 8.2%). Of all stroke cases, 91.7% (95% CI 87.4% to 94.6%) were ischaemic stroke and 8.3% (95% CI 5.4% to 12.6%) were haemorrhagic stroke. The prevalence rates of dyslipidaemia, smoking and hypertension were ranked as the top three cerebrovascular risk factors and were 62.1%, 61.8% and 57.3%, respectively. We found that hypertension, dyslipidaemia and lack of exercise were associated with ischaemic stroke. However, only hypertension (OR=4.064, 95% CI 1.358 to 12.160) was significantly associated with haemorrhagic stroke.ConclusionsThe prevalence of stroke, especially ischaemic stroke, and associated cerebrovascular risk factors among adults aged 40 years or older in northeast China were high. A higher regional prevalence of hypertension, dyslipidaemia and lack of exercise may be responsible.

Background and purpose Lipoxin A4 (LXA4) has been reported to reduce inflammation in several neurological injury models. We studied the effects of LXA4 on neuroinflammation after subarachnoid hemorrhage (SAH) in a rat model. Methods Two hundred and thirty eight Sprague Dawley male rats, weight 280–320 g were used. Exogenous LXA4 (0.3 and 1.0 nmol) were injected intracerebroventricularly at 1.5 hours after SAH. Neurological scores, brain water content and blood-brain barrier were evaluated at 24 hours after SAH; Morris water maze and T-maze tests were examined at 21 days after SAH. The expression of endogenous LXA4 and its receptor formyl peptide receptor 2 (FPR2), as well as p38, IL-1β and IL-6 were studied either by ELISA or western blots. Neutrophil infiltration was observed by myeloperoxidase (MPO) staining. FPR2 siRNA was used to knock down LXA4 receptor. Results The expression of endogenous LXA4 decreased and the expression of FPR2 increased after SAH. Exogenous LXA4 decreased brain water content, reduced Evans blue extravasation, and improved neurological functions and improved the learning and memory ability after SAH. LXA4 reduced neutrophil infiltration and phosphorylation of p38, IL-1β and IL-6. These effects of LXA4 were abolished by FPR2 siRNA. Conclusion Exogenous LXA4 inhibited inflammation by activating FPR2 and inhibiting p38 after SAH. LXA4 may serve as an alternative treatment to relieve early brain injury after SAH.