Treatment of the Term Newborn With Brain Injury: Simplicity As the Mother of Invention

Yager, Jerome Y.; Armstrong, Edward A.; Black, Amy M.

doi:10.1016/j.pediatrneurol.2008.12.002

Cited by 15 publications

(16 citation statements)

References 70 publications

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“…Both experimentally and clinically, reducing body temperature has been shown to be neuroprotective in the immature brain (Busto et al, 1987, Yager et al, 1993, Yager et al, 2009). Thus, a critical question in the model we present here was whether altering body temperature could influence ketamine-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Despite the above argument, body cooling has been shown to prevent injury in other models of neonatal brain injury, such as hypoxia-ischemia (Busto et al, 1987, Yager et al, 1993, Yager et al, 2009). It must be considered however, that traumatic brain injury invokes a number of highly toxic responses (loss of blood flow, inflammation, hemorrhage, blood brain barrier breakdown) that are not found in the NMDAR blockade-induced injury model.…”

Section: Discussionmentioning

confidence: 99%

“…However, the benefit of cooling the brain may be limited to mild or modest hypothermia, as more severe reductions may actually induce injury (Steen et al, 1979, Ditsworth et al, 2003). These mixed experimental outcomes have their clinical correlates (Yager et al, 2009), suggesting that lowering temperature to control ongoing brain injury is a more complex issue than some studies might indicate.…”

Section: Introductionmentioning

confidence: 99%

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Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?

et al. 2010

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General anesthetics have long been thought to be relatively safe but recent clinical studies have revealed that exposure of very young children (4 years or less) to agents that act by blocking the N-methyl-D-aspartate receptor (NMDAR) can lead to cognitive deficits as they mature. In rodent and non-human primate studies, blockade of this receptor during the perinatal period leads to a number of molecular, cellular and behavioral pathologies. Despite the overwhelming evidence from such studies, doubt remains as to their clinical relevance. A key issue is whether the primary injury (apoptotic cell death) is specific to receptor blockade or due to non-specific, patho-physiological changes. Principal to this argument is that loss of core body temperature following NMDAR blockade could explain why injury is observed hours later. We therefore examined the neurotoxicity of the general anesthetic ketamine in P7, P14 and P21 rats while monitoring core body temperature. We found that, at P7, ketamine induced the pro-apoptotic enzyme activated caspase-3 in a dose-dependent manner. As expected, injury was greatly diminished by P14 and absent by P21. However, contrary to expectations, we found that core body temperature was not a factor in determining injury. Our data imply that injury is directly related to receptor blockade and is unlikely to be overcome by artificially changing core body temperature.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?

et al. 2010

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“…After asphyxia, infants may have long-term neurological sequelae such as cerebral palsy, mental retardation, and epilepsy, and it is also associated with attention deficits and hyperactivity in children and adolescents. 4 In the early phase after a HI event, reperfusion brings about the overproduction of free radicals. This event is usually followed by oxidative stress, which plays a substantial role in the pathogenesis of early developmental brain injury, leading to damage of vital cellular components as nucleic acids, cell membranes, and mitochondria resulting in subsequent cell death and also to the stimulation of ischemic cells to secrete inflammatory cytokines and chemokines.…”

Section: Introductionmentioning

confidence: 99%

Apoptotic Cell Death Correlates With ROS Overproduction and Early Cytokine Expression After Hypoxia–Ischemia in Fetal Lambs

et al. 2012

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Despite advances in neonatology, the hypoxic-ischemic injury in the perinatal period remains the single most important cause of brain injury in the newborn, leading to death or lifelong sequelae. Using a sheep model of intrauterine asphyxia, we evaluated the correlation between reactive oxygen species (ROS) overproduction, cytokine expression, and apoptotic cell death. Fetal lambs were assigned to sham group, nonasphyctic animals; and hypoxia-ischemia (HI) group, lambs subjected to 60 minutes of HI) by partial cord occlusion and sacrificed 3 hours later. Different brain regions were separated to quantify the number of apoptotic cells and the same territories were dissociated for flow cytometry studies. Our results suggest that the overproduction of ROS and the early increase in cytokine production after HI in fetal lambs correlate in a significant manner with the apoptotic index, as well as with each brain region evaluated.

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“…After asphyxia, infants may suffer from long-term neurological sequelae such as cerebral palsy, mental retardation and epilepsy. Asphyxia is also associated with attention deficits and hyperactivity in children and adolescents [7,8] . The high incidences of certain kinds of hypoxic-ischemic brain lesions [9,10] can be partly attributed to the fact that the developing brain is especially vulnerable to ischemia [11][12][13][14][15] .…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid as a neuroprotective strategy in perinatal hypoxic-ischemic injury

2011

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Perinatal hypoxia-ischemia remains the single most important cause of brain injury in the newborn, leading to death or lifelong sequelae. Because of the fact that there is still no specific treatment for perinatal brain lesions due to the complexity of neonatal hypoxic-ischemic pathophysiology, the search of new neuroprotective therapies is of great interest.In this regard, therapeutic possibilities of the endocannabinoid system have grown lately. The endocannabinoid system modulates a wide range of physiological processes in mammals and has demonstrated neuroprotective effects in different paradigms of acute brain injury, acting as a natural neuroprotectant. Concerning perinatal asphyxia, the neuroprotective role of this endogenous system is emerging these years. The present review mainly focused on the current knowledge of the cannabinoids as a new neuroprotective strategy against perinatal hypoxic-ischemic brain injury.

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Treatment of the Term Newborn With Brain Injury: Simplicity As the Mother of Invention

Cited by 15 publications

References 70 publications

Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?

Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?

Apoptotic Cell Death Correlates With ROS Overproduction and Early Cytokine Expression After Hypoxia–Ischemia in Fetal Lambs

Cannabinoid as a neuroprotective strategy in perinatal hypoxic-ischemic injury

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