The neurological and cognitive sequelae of cardiac arrest

Lim, Chun Soo; Alexander, Michael P.; Lafleche, Ginette; Schnyer, David M.; Verfaellie, Mieke

doi:10.1212/01.wnl.0000144189.83077.8e

Cited by 204 publications

(144 citation statements)

References 32 publications

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“…Cerebral HR is a central component of many disorders or conditions affecting cognition. These include stroke (Kalaria and Ballard, 2001), cardiac arrest (Lim et al, 2004), postoperative cognitive dysfunction (Caza et al, 2008), acute respiratory distress syndrome (Hopkins et al, 2006), obstructive sleep apnea (El-Ad and Lavie, 2005), high-altitude cerebral edema, and acute mountain sickness (Hackett, 1999).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Increases Blood–Brain Barrier Permeability and Induces Alterations in Occludin during Hypoxia–Reoxygenation

Lochhead

McCaffrey

Quigley

et al. 2010

J Cereb Blood Flow Metab

278

185

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The blood-brain barrier (BBB) has a critical role in central nervous system homeostasis. Intercellular tight junction (TJ) protein complexes of the brain microvasculature limit paracellular diffusion of substances from the blood into the brain. Hypoxia and reoxygenation (HR) is a central component to numerous disease states and pathologic conditions. We have previously shown that HR can influence the permeability of the BBB as well as the critical TJ protein occludin. During HR, free radicals are produced, which may lead to oxidative stress. Using the free radical scavenger tempol (200 mg/kg, intraperitoneal), we show that oxidative stress produced during HR (6% O 2 for 1 h, followed by room air for 20 min) mediates an increase in BBB permeability in vivo using in situ brain perfusion. We also show that these changes are associated with alterations in the structure and localization of occludin. Our data indicate that oxidative stress is associated with movement of occludin away from the TJ. Furthermore, subcellular fractionation of cerebral microvessels reveals alterations in occludin oligomeric assemblies in TJ associated with plasma membrane lipid rafts. Our data suggest that pharmacological inhibition of disease states with an HR component may help preserve BBB functional integrity.

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Section: Introductionmentioning

confidence: 99%

Oxidative Stress Increases Blood–Brain Barrier Permeability and Induces Alterations in Occludin during Hypoxia–Reoxygenation

Lochhead

McCaffrey

Quigley

et al. 2010

J Cereb Blood Flow Metab

278

185

View full text Add to dashboard Cite

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“…In most patients referred to neuropsychological examination for memory deficits the cognitive impairment is a combination of memory and executive and mild motor deficits. 23 Cognitive impairment is not uncommon after surviving a critical illness. A recent study examining cognitive performance and specifically executive function in a population of general intensive care survivors found these functions to be very significantly impaired at least three months after discharge from ICU.…”

Section: Discussionmentioning

confidence: 99%

Cognitive and Neurophysiological Outcome of Cardiac Arrest Survivors Treated With Therapeutic Hypothermia

Tiainen

Poutiainen

Kovala

et al. 2007

Stroke

105

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Background and Purpose-Cognitive deficits are common in survivors of cardiac arrest (CA). The aim of this study was to examine the effect of therapeutic hypothermia after CA on cognitive functioning and neurophysiological outcome. Methods-A cohort of 70 consecutive adult patients resuscitated from out-of-hospital ventricular fibrillation CA were randomly assigned to therapeutic hypothermia of 33°C for 24 hours accomplished by external cooling or normothermia.Neuropsychological examination was performed to 45 of the 47 conscious survivors of CA (27 in hypothermia and 18 in normothermia group) 3 months after the incident. Quantitative electroencephalography (Q-EEG) and auditory P300 event-related potentials were studied on 42 patients at the same time point. Results-There were no differences between the 2 treatment groups in demographic variables, depression, or delays related to the resuscitation. No differences were found in any of the cognitive functions between the 2 groups. 67% of patients in hypothermia and 44% patients in normothermia group were cognitively intact or had only very mild impairment.Severe cognitive deficits were found in 15% and 28% of patients, respectively. All Q-EEG parameters were better in the hypothermia-treated group, but the differences did not reach statistical significance. The amplitude of P300 potential was significantly higher in hypothermia-reated group. Conclusions-The use of therapeutic hypothermia was not associated with cognitive decline or neurophysiological deficits after out-of-hospital CA.

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“…These patients show neurological injury, delayed hippocampal damage, neurological deficits and impairment of learning and memory. 24) Present study demonstrates the neuroprotective effect of trolox in bilateral carotid arteries occlusion (BCAO) model of global cerebral ischemia in gerbils. Mongolian gerbils were selected for inducing global ischemia.…”

Section: Discussionmentioning

confidence: 76%

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

Gupta

Sharma

2006

Biological & Pharmaceutical Bulletin

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Stroke is the third leading cause of death and a major cause of long-term disability in industrialized countries. Dramatic reduction of oxygen in stroke may lead to ischemia of the whole brain (global ischemia) or of defined cerebral territories (focal ischemia) depending on the cerebral artery occluded.1) Global cerebral ischemia is commonly an outcome of a range of clinical conditions, which comprises cardiac arrest, closed head injury, coronary artery bypass surgery etc. The most affected brain area as a consequence of global ischemia is CA1 neurons of the hippocampus. Neuronal death in global ischemia precedes 1-3 d after insult, a process referred as delayed neuronal death. 2-4)The pathophysiological mechanisms leading to neuronal injury in ischemic stroke are complex and multifactorial. Ischemia induced brain damages are accompanied by biochemical alterations and neurological sequelae.1) There are substantial experimental evidences that reactive oxygen species (ROS) are produced in the brain during ischemia and reperfusion injury.5) ROS such as superoxide radical, hydroxyl radical and hydrogen peroxide contributes to ischemic brain damage.5) Superoxide can react with nitric oxide to form peroxynitrite, a potent oxidant. It has been proposed that many of the toxic effects of nitric oxide are due to the generation of peroxynitrite. Peroxynitrite can directly react with target biomolecules like DNA, protein, via one or two electron oxidations. 5-7)Antioxidants such as (Ϫ)-epigallocatechin gallate, melatonin, curcumin, FeTMPyP and FeTPPS have been demonstrated to ameliorate neuronal damage in cerebral ischemic reperfusion injury. 3,[8][9][10][11] Antioxidant activity of trolox (6-hydroxy-2,5,7,8-tetramethyl chroman-2-carboxylic acid) a cellpermeable, water-soluble derivative of vitamin E has been established in vitro and in vivo conditions. 12-15) However its neuroprotective effects have not been investigated in global cerebral ischemia. Therefore, in the present study, the neuroprotective potential of trolox was investigated in bilateral carotid artery occlusion induced global cerebral ischemia in Mongolian gerbils. MATERIALS AND METHODS AnimalsAdult male Mongolian gerbils (Meriones unguiculatus) weighing 60-80 g were obtained from Central Animal Facility (CAF), NIPER for this study. They were provided with standard diet and water ad libitum and were maintained at 22Ϯ2°C and a 12 : 12 h light : dark cycle. All the procedures used in this study were approved by Institutional Animal Ethics Committee (IAEC), NIPER.Materials Trolox was purchased from Calbiochem Inc., U.S.A. Cresyl violet and malondialdehyde were purchased from Sigma Chemical Company, U.S.A. Rest of the chemicals were of analytical grade and were purchased from commercial suppliers.Treatment Schedule Gerbils were divided into sham, vehicle-treated ischemic and trolox-treated (3, 10, 30 mg/kg i.p.) ischemic groups. Phosphate buffer saline (pH 7.4) was used as a vehicle for trolox. Trolox was administered 30 min before occlusion.Induction of Transie...

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The neurological and cognitive sequelae of cardiac arrest

Cited by 204 publications

References 32 publications

Oxidative Stress Increases Blood–Brain Barrier Permeability and Induces Alterations in Occludin during Hypoxia–Reoxygenation

Oxidative Stress Increases Blood–Brain Barrier Permeability and Induces Alterations in Occludin during Hypoxia–Reoxygenation

Cognitive and Neurophysiological Outcome of Cardiac Arrest Survivors Treated With Therapeutic Hypothermia

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

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