Mechanisms of ischemic brain injury

Janardhan, Vallabh; Qureshi, Adnan I.

doi:10.1007/s11886-004-0009-8

Cited by 113 publications

(59 citation statements)

References 46 publications

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“…7,20,23,28,38 However, inclusion of perfusion data may have been useful to identify the "no reflow" phenomenon, whereby recanalization is not associated with reperfusion. 39 Finally, we were unable to detect an effect of collateral circulation on clinically meaningful outcome despite prior reports of such an interaction. 40,41 It is possible that the narrow scoring range of the collateral score used in this study underestimates the effect of collaterals on outcome.…”

Section: Discussionmentioning

confidence: 55%

Factors Influencing Clinically Meaningful Recanalization after IV-rtPA in Acute Ischemic Stroke

Murphy

Symons²,

Hopyan

et al. 2012

AJNR Am J Neuroradiol

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Section: Discussionmentioning

confidence: 55%

Factors Influencing Clinically Meaningful Recanalization after IV-rtPA in Acute Ischemic Stroke

Murphy

Symons²,

Hopyan

et al. 2012

AJNR Am J Neuroradiol

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“…However, differences in underlying pathophysiology among stroke subtypes mandates different management strategies. Ischemic stroke results from occlusion of an artery with subsequent reduction in regional cerebral blood flow (rCBF) within the affected region [27]. However, the reduction in rCBF is not homogenous but is demarcated into regions of severe reduction (core) and moderate reduction (penumbra).…”

Section: Discussionmentioning

confidence: 99%

Prevalence of elevated blood pressure in 563704 adult patients with stroke presenting to the ED in the United States

Qureshi¹,

Ezzeddine²,

Nasar³

et al. 2007

The American Journal of Emergency Medicine

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374

238

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Purpose-To estimate the prevalence of elevated blood pressure in adult patients with acute stroke in the United States (U.S.).Methods-Stroke patients were classified by initial systolic blood pressure into four categories using demographic, clinical, and treatment data from the National Hospital Ambulatory Medical Care Survey, the largest study of utilization and provision of emergency department services in the U.S. We also compared the age-, sex-, and ethnicity-adjusted rates of elevated blood pressure strata comparable with stages 1 and 2 hypertension in the U.S. population.Results-Of the 563,704 stroke patients evaluated, initial systolic blood pressure was <140 mm Hg in 173,120 patients (31%), 140-184 mm Hg in 315,207 patients (56%), 185-219 mm Hg in 74,586 patients (13%), and ≥220 mm Hg in 791 patients (0.1%). The mean time interval between presentation and evaluation was 40 ± 55, 33 ± 39, 25 ± 27, and 5 ± 1 minutes for increasing systolic blood pressure strata (p=0.009). A 3-and 8-fold higher rate of elevated blood pressure strata was observed in acute stroke than the existing rates of stages 1 and 2 hypertension in the U.S. population. Labetalol and hydralazine were used in 6,126 (1%) and 2,262 (0.4%) patients, respectively. Thrombolytics were used in 1,283 patients (0.4%), but only in those with SBP of 140-184 mm Hg.Conclusions-In a nationally representative large dataset, elevated blood pressure was observed in over 60% of the patients presenting with stroke to the emergency department. Elevated blood pressure was associated with an earlier evaluation, however, the use of thrombolytics was restricted to ischemic stroke patients with systolic blood pressure <185 mm Hg.

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“…This response results in an increase in toxic inflammatory mediators including, but not limited to, interleukin (IL)-1b, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-a). 21 An increase in these molecules is sufficient to induce neuronal apoptosis within the infarcted tissue, ultimately causing irreversible brain damage. In addition to the presence of these classic inflammatory molecules, nitric oxide is dramatically increased after ischemia.…”

Section: Inflammation In the Mammalian Brainmentioning

confidence: 99%

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

Tobin

Bonds

Minshall

et al. 2014

J Cereb Blood Flow Metab

292

219

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This review covers the pathogenesis of ischemic stroke and future directions regarding therapeutic options after injury. Ischemic stroke is a devastating disease process affecting millions of people worldwide every year. The mechanisms underlying the pathophysiology of stroke are not fully understood but there is increasing evidence demonstrating the contribution of inflammation to the drastic changes after cerebral ischemia. This inflammation not only immediately affects the infarcted tissue but also causes long-term damage in the ischemic penumbra. Furthermore, the interaction between inflammation and subsequent neurogenesis is not well understood but the close relationship between these two processes has garnered significant interest in the last decade or so. Current approved therapy for stroke involving pharmacological thrombolysis is limited in its efficacy and new treatment strategies need to be investigated. Research aimed at new therapies is largely about transplantation of neural stem cells and using endogenous progenitor cells to promote brain repair. By understanding the interaction between inflammation and neurogenesis, new potential therapies could be developed to further establish brain repair mechanisms.

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Mechanisms of ischemic brain injury

Cited by 113 publications

References 46 publications

Factors Influencing Clinically Meaningful Recanalization after IV-rtPA in Acute Ischemic Stroke

Factors Influencing Clinically Meaningful Recanalization after IV-rtPA in Acute Ischemic Stroke

Prevalence of elevated blood pressure in 563704 adult patients with stroke presenting to the ED in the United States

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

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