Deterioration in Acute Ischemic Stroke as the Target for Neuroprotection

Serena, Joaquı́n; Rodríguez‐Yáñez, Manuel; Castellanos, Mar

doi:10.1159/000091707

Cited by 41 publications

(38 citation statements)

References 68 publications

(82 reference statements)

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“…Although several clinical, radiological, and biochemical factors have been associated with early neurological deterioration, most of them have a low predictor value [145][146]. Regarding our patients with lacunar stroke, about 20% of our patients did not have visible infarction on CT or MRI, which is similar to the results of previous studies [147,148].…”

Section: Inflammation In Acute Stroke Subtypessupporting

confidence: 89%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

127

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Determining the cause of stroke does influence choices for management. categorization of subtypes of ischemic stroke has had considerable study, but definitions are hard to formulate and their application for diagnosis in an individual patient is often problematic. Cerebral ischemia initiates a complex cascade of events at genomic, molecular, and cellular levels, and inflammation is important in this cascade. In 1993 for For the Trial of Org 10172 in Acute Stroke Treatment (TOAST), Adams et al] conducted a placebo-controlled, randomized, blinded study of the low-molecular-weight heparinoid given to patients within 24 hours after stroke and developed a system for diagnosis of subtype of ischemic stroke that uses components of existing diagnostic schemes. The type of acute ischemic stroke was classified according to the TOAST classification: 1) Large Artery AtheroSclerosis (LAAS); 2) CardioEmbolic Infarct (CEI); 3) LACunar infarct (LAC); 4) stroke of Other Determined Etiology (ODE); 5) stroke of UnDetermined Etiology (UDE) (see Fig. (1)). On the basis of pathophysiologic differences of each stroke subtype it's possible to hypothesize a different pattern of immuno-inflammatory activation in relation of ischemic stroke subtype. A nonspecific systemic inflammatory response occurs after both ischemic and hemorrhagic stroke, either as part of the process of brain damage or in response to complications such as deep venous thrombosis. Several studies have reported that higher levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) are associated with worse outcome after ischemic stroke.Our group reported that patients with cardioembolic subtype showed significantly higher median plasma levels of TNF-, IL-6, IL-1 whereas the lacunar subtype showed significantly lower median plasma levels of TNF-, IL-6 and IL-1 . Our findings underlined the significant association was noted between the severity of neurological deficit at admission, the diagnostic subtype and some inflammatory variables.

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Section: Inflammation In Acute Stroke Subtypessupporting

confidence: 89%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

127

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“…EIW may result from numerous biochemical and hemodynamic mechanisms [6][7][8][9][10] that may converge to produce damaging …”

Section: Discussionmentioning

confidence: 99%

Uric Acid Therapy Prevents Early Ischemic Stroke Progression

Amaro¹,

Laredo²,

Renú³

et al. 2016

Stroke

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Background and Purpose— Identification of neuroprotective therapies in acute ischemic stroke is imperative. We report a predefined analysis of the URICO-ICTUS trial (Efficacy Study of Combined Treatment With Uric Acid and r-tPA in Acute Ischemic Stroke) assessing the efficacy of uric acid (UA) compared with placebo to prevent early ischemic worsening (EIW) and the relevance of collateral circulation. Methods— URICO-ICTUS was a double-blind, placebo-controlled, phase 2b trial where a total of 411 patients treated with alteplase within 4.5 hours of stroke onset were randomized (1:1) to receive UA 1000 mg (n=211) or placebo (n=200) before the end of alteplase infusion. EIW defined an increment ≥4 points in the National Institutes of Health Stroke Scale score within 72 hours of treatment in the absence of hemorrhage or recurrent stroke. Logistic regression models assessed the interaction between therapy and the collateral circulation in 112 patients who had a pretreatment computed tomographic angiography. Results— EIW occurred in 2 of 149 (1%) patients with good outcome and 23 of 262 (9%) patients with poor outcome (χ 2 ; P =0.002). EIW occurred in 7 of 204 (3%) patients treated with UA and in 18 of 200 (9%) patients treated with placebo (χ 2 ; P =0.01). There was a significant interaction between the efficacy of UA to prevent EIW and collaterals ( P =0.029), with lower incidence in patients with good collaterals treated with UA compared with placebo (2% versus 15%, respectively; P =0.048). Conclusions— UA therapy may prevent EIW after acute stroke in thrombolysed patients. Optimal access of UA to its molecular targets through appropriate collaterals may modify the magnitude of the neuroprotective effect. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00860366.

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“…13,16 However, as will be seen, the latter may sometimes facilitate the occurrence of END through hemodynamic disturbances or by influencing neuronal viability in hypoperfused areas.…”

Section: Pathophysiological Mechanisms Of End and Factors Influencingmentioning

confidence: 99%

“…Genetic polymorphism in the excitatory amino acids carriers has been suggested as one potential mechanism. 13 Another possibility is that the role of excitotoxic factors is important in determining the fate of hypoperfused tissue surviving on perfusion levels just above the penumbral threshold. Indeed, excitation of this tissue will have detrimental effects, because any increase in energy metabolism would not be sustained by increased oxygen supply due to autoregulation failure, whereas oxygen extraction fraction is already maximal.…”

Section: Biochemical and Biological Mechanisms Excitotoxicitymentioning

confidence: 99%

“…The clinical and biochemical predictors of END, and END secondary to symptomatic intracranial hemorrhage, are not discussed here; the interested reader is referred to topical reviews. [13][14][15][16][17] The neuroimaging predictors of malignant middle cerebral artery infarction (MMI), a distinct form of END, is addressed separately. In the second section, we address putative mechanisms of END focusing on perfusion abnormalities.…”

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confidence: 99%

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Hemodynamic Factors and Perfusion Abnormalities in Early Neurological Deterioration

Alawneh

Moustafa

Baron

2009

Stroke

110

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Background and Purpose-Early neurological deterioration (END) is a relatively common unfavorable course after anterior circulation ischemic stroke that can lead to worse clinical outcome. None of the END predictors identified so far is sufficiently reliable to be used in clinical practice and the mechanisms underlying END are not fully understood. We review the evidence from the literature for a role of hemodynamic and perfusion abnormalities, more specifically infarction of the oligemia, in END. Summary of Review-After an overview of the neuroimaging, including perfusion imaging, predictors of END, we review the putative mechanisms of END with a special focus on hemodynamic factors. The evidence relating perfusion abnormalities to END is addressed and potential hemodynamic mechanisms are suggested. Conclusions-Hemodynamic factors and perfusion abnormalities are likely to play a critical role in END. Infarction of the oligemic tissue surrounding the penumbra could be the putative culprit leading to END as a result of perfusion, but also physiological and biochemical abnormalities. Further studies addressing the role of the oligemia in END and developing measures to protect its progression to infarction are now needed. (Stroke. 2009;40:e443-e450.)

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Deterioration in Acute Ischemic Stroke as the Target for Neuroprotection

Cited by 41 publications

References 68 publications

Inflammation in Ischemic Stroke Subtypes

Inflammation in Ischemic Stroke Subtypes

Uric Acid Therapy Prevents Early Ischemic Stroke Progression

Hemodynamic Factors and Perfusion Abnormalities in Early Neurological Deterioration

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