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Alistair J. Gunn - One of the best experts on this subject based on the ideXlab platform.
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Status epilepticus after prolonged umbilical cord occlusion is associated with greater Neural Injury fetal sheep at term-equivalent
PloS one, 2014Co-Authors: Paul P. Drury, Laura Bennet, Joanne O. Davidson, Eleanor R. Gunn, Lindsea C. Booth, Lotte G. Van Den Heuij, Guido Wassink, Alistair J. GunnAbstract:The majority of pre-clinical studies of hypoxic-ischemic encephalopathy at term-equivalent have focused on either relatively mild insults, or on functional paradigms of cerebral ischemia or hypoxia-ischemia/hypotension. There is surprisingly little information on the responses to single, severe ‘physiological’ insults. In this study we examined the evolution and pattern of Neural Injury after prolonged umbilical cord occlusion (UCO). 36 chronically instrumented fetal sheep at 125–129 days gestational age (term = 147 days) were subjected to either UCO until mean arterial pressure was < = 8 mmHg (n = 29), or sham occlusion (n = 7). Surviving fetuses were killed after 72 hours for histopathologic assessment with acid-fuchsin thionine. After UCO, 11 fetuses died with intractable hypotension and 5 ewes entered labor and were euthanized. The remaining 13 fetuses showed marked EEG suppression followed by evolving seizures starting at 5.8 (6.8) hours (median (interquartile range)). 6 of 13 developed status epilepticus, which was associated with a transient secondary increase in cortical impedance (a measure of cytotoxic edema, p
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Introduction: This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic–ischemic Injury in the immature brain. Results: Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min ( P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h ( P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. Discussion: EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Methods: Chronically instrumented fetal sheep at 0.7 gestation (101–104 days; term is 147 days) received either 15-min ( n = 13) or 25-min ( n = 13) of complete umbilical cord occlusion. The Δ (0–3.9 Hz), θ (4–7.9 Hz), α (8–12.9 Hz), and β (13–22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep.
Pediatric research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic-ischemic Injury in the immature brain. Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min (P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h (P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Chronically instrumented fetal sheep at 0.7 gestation (101-104 days; term is 147 days) received either 15-min (n = 13) or 25-min (n = 13) of complete umbilical cord occlusion. The Δ (0-3.9 Hz), θ (4-7.9 Hz), α (8-12.9 Hz), and β (13-22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
Sigrid C. Veasey - One of the best experts on this subject based on the ideXlab platform.
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C/EBP homologous binding protein (CHOP) underlies Neural Injury in sleep apnea model.
Sleep, 2013Co-Authors: Yu-ting Chou, Guanxia Zhan, Yan Zhu, Polina Fenik, Lori Panossian, Jing Zhang, Sigrid C. VeaseyAbstract:STUDY OBJECTIVES Obstructive sleep apnea (OSA) is associated with cognitive impairment and neuronal Injury. Long-term exposure to intermittent hypoxia (LTIH) in rodents, modeling the oxygenation patterns in sleep apnea, results in NADPH oxidase 2 (Nox2) oxidative Injury to many neuronal populations. Brainstem motoneurons susceptible to LTIH Injury show uncompensated endoplasmic reticulum stress responses with increased (CCAAT/enhancer binding protein homologous protein (CHOP). We hypothesized that CHOP underlies LTIH oxidative Injury. In this series of studies, we first determined whether CHOP is upregulated in other brain regions susceptible to LTIH oxidative Nox2 Injury and then determined whether CHOP plays an adaptive or injurious role in the LTIH response. To integrate these findings with previous studies examining LTIH Neural Injury, we examined the role of CHOP in Nox2, hypoxia-inducible factor-1α (HIF-1α) responses, oxidative Injury and apoptosis, and neuron loss. DESIGN Within/between mice subjects. SETTING Laboratory setting. PARTICIPANTSSUBJECTS: CHOP null and wild-type adult male mice. INTERVENTIONS LTIH or sham LTIH. MEASUREMENTS AND MAIN RESULTS Relative to wild-type mice, CHOP-/- mice conferred resistance to oxidative stress (superoxide production/ carbonyl proteins) in brain regions examined: cortex, hippocampus, and motor nuclei. CHOP deletion prevented LTIH upregulation of Nox2 and HIF-1α in the hippocampus, cortex, and brainstem motoneurons and protected mice from neuronal apoptosis and motoneuron loss. CONCLUSIONS Endogenous CHOP is necessary for LTIH-induced HIF-1α, Nox2 upregulation, and oxidative stress; CHOP influences LTIH-induced apoptosis in neurons and loss of neurons. Findings support the concept that minimizing CHOP may provide neuroprotection in OSA.
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Neural Injury in Sleep Apnea
Current Neurology and Neuroscience Reports, 2010Co-Authors: Sigrid C. VeaseyAbstract:Sleepiness has long been recognized as a presenting symptom in obstructive sleep apnea syndrome, but persistent neurocognitive Injury from sleep apnea has been appreciated only recently. Although therapy for sleep apnea markedly improves daytime symptoms, cognitive impairments may persist despite long-term therapy with continuous positive airway pressure. We know now that certain groups of neurons, typically those that are more metabolically active, are more vulnerable to Injury than others. Animal models of sleep apnea oxygenation patterns have been instrumental in elucidating mechanisms of Injury. The hypoxia/reoxygenation events result in oxidative, inflammatory, and endoplasmic reticulum stress responses in susceptible Neural groups. With molecular pathways being fleshed out in animal models, it is time to carefully and systematically examine Neural Injury in humans and test the applicability of findings from animal models. To succeed, however, we cannot view sleep apnea as an isolated process. Rather, Injury in sleep apnea is more likely the consequence of overlapping injuries from comorbid conditions. The progress in elucidating mechanisms of Neural Injury is palpable, and it now seems we indeed are closer to developing therapies to prevent and treat Neural Injury in obstructive sleep apnea.
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Comprar Oxidative Neural Injury | Veasey, Sigrid C. | 9781603273411 | Springer
2009Co-Authors: Sigrid C. VeaseyAbstract:Tienda online donde Comprar Oxidative Neural Injury al precio 207,47 € de Veasey, Sigrid C., tienda de Libros de Medicina, Libros de Medicina Familiar y Comunitaria/General - Medicina general
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Insight from Animal Models into the Cognitive Consequences of Adult Sleep-Disordered Breathing
ILAR journal, 2009Co-Authors: Sigrid C. VeaseyAbstract:Obstructive sleep apnea (OSA) affl icts tens of millions of Americans and hundreds of millions of people worldwide, and the possibility that the disease may cause permanent Neural Injury is therefore a signifi cant concern. Numerous comorbidities—including diabetes, cardiovascular disease, and obesity—are associated with the disease, and it is quite diffi cult, if not impossible, in clinical studies to determine whether they increase the propensity for Neural Injury or whether OSA alone causes such Injury. It is nonetheless clear that the severity of hypoxemia in sleep apnea correlates with the severity of cognitive impairments, and animal models of OSA have been instrumental in elucidating the potential for this disease to elicit neurobehavioral impairment independent of comorbidities. At present, there is no animal model of severe OSA with which to explore mechanisms of Neural Injury. Because oxyhemoglobin saturation patterns correlate with Neural Injury, researchers have used rodent models of the oxygenation patterns of severe sleep apnea to study mechanisms of Neural Injury and cognitive impairment, and these models have provided tremendous insight into the molecular mechanisms by which sleep apnea oxygenation patterns injure neurons. Oxidative, infl ammatory, and organelle Injury all contribute to Neural dysfunction. Moreover, molecular targets of Injury have now been identifi ed for many neuronal groups injured in sleep apnea. Researchers are poised to use this knowledge to develop pharmacotherapies that may prevent or partially reverse Neural Injury from sleep apnea.
Michael J. Keogh - One of the best experts on this subject based on the ideXlab platform.
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Introduction: This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic–ischemic Injury in the immature brain. Results: Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min ( P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h ( P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. Discussion: EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Methods: Chronically instrumented fetal sheep at 0.7 gestation (101–104 days; term is 147 days) received either 15-min ( n = 13) or 25-min ( n = 13) of complete umbilical cord occlusion. The Δ (0–3.9 Hz), θ (4–7.9 Hz), α (8–12.9 Hz), and β (13–22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep.
Pediatric research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic-ischemic Injury in the immature brain. Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min (P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h (P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Chronically instrumented fetal sheep at 0.7 gestation (101-104 days; term is 147 days) received either 15-min (n = 13) or 25-min (n = 13) of complete umbilical cord occlusion. The Δ (0-3.9 Hz), θ (4-7.9 Hz), α (8-12.9 Hz), and β (13-22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
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049 The association between seizure activity and Neural Injury following endotoxin exposure and hypoxic-ischaemic insults in a preterm ovine model
Journal of Neurology Neurosurgery & Psychiatry, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Joanne O. Davidson, Lindsea C. Booth, S Maathi, L Bennet, A J GunnAbstract:Introduction Neonatal seizures following hypoxic-ischaemic insults at birth are common. Additional exposure to endotoxins (LPS) prior to ischaemia has been shown to be able to increase or decrease Neural Injury, though whether this is achieved through altering seizure activity is unknown. Methods Fetal sheep (aged 103–104 days gestation) were given a 5-day infusion of normal saline (n=9) or 250 ng/kg/24 h of lipopolysaccharide (a gram negative endotoxin) (n=10) prior to 15 min of umbilical cord ischaemia. Fetal EEG activity was recorded from 6 h before infusion to 5 days post ischaemia and analysed through visual and quantitative spectral methods. Result Neural Injury was lower in the group given LPS prior to ischaemia (p Discussion LPS appears to ‘pre-condition’ the brain to subsequent hypoxic-ischaemic insults, whilst paradoxically increasing seizure activity. Whether exposure to in utero infection confers long-term seizure susceptibility and long-term ability to withstand hypoxic-ischaemic insults remains unclear but may be a promising area of future research.
Colin J. Saldanha - One of the best experts on this subject based on the ideXlab platform.
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Glial aromatization decreases Neural Injury in the zebra finch (Taeniopygia guttata): influence on apoptosis.
Journal of neuroendocrinology, 2004Co-Authors: Ryan D. Wynne, Colin J. SaldanhaAbstract:Emerging evidence suggests a neuroprotective role for oestrogens following damage to the vertebrate brain. Aromatase (oestrogen synthase) is rapidly transcribed and translated in glial cells around areas of Neural damage in several vertebrates. However, the potential neuroprotection afforded by locally up-regulated glial aromatase immediately surrounding the Injury remains to be tested. Towards this end, individual birds sustained penetrating mechanical injuries via a needle that contained either vehicle or the aromatase inhibitor fadrozole into contralateral hemispheres. Seventy-two hours later, the size of Neural Injury (as assessed by the extent of necrotic tissue) and the number of apoptotic cells around the injuries were evaluated. The size of Injury in the hemisphere injected with fadrozole was significantly larger than the Injury caused by vehicle injection. Furthermore, a greater number of apoptotic nuclei were found around the fadrozole-associated lesion relative to vehicle. Finally, constitutively expressed, neuronal aromatase close to the Injury site did not differ between hemispheres. We conclude that local inhibition of glial aromatase immediately around the site of Injury plays a neuroprotective role in the songbird brain and this protection involves apoptotic pathways. Local up-regulation of glial aromatase may play a pivotal role in the limitation of secondary damage and/or the acceleration of restorative processes following Injury to the vertebrate brain.
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Rapid Upregulation of Aromatase mRNA and Protein Following Neural Injury in the Zebra Finch (Taeniopygia guttata)
Journal of neuroendocrinology, 2001Co-Authors: R. Scott Peterson, Colin J. Saldanha, Barney A. SchlingerAbstract:The expression of aromatase (oestrogen synthase) within the vertebrate central nervous system (CNS) is key in the provision of local oestrogens to Neural circuits. Aromatase expression appears to be exclusively neuronal under normal conditions. However, some in vitro studies suggest the presence of astrocytic aromatase in songbirds and mammals. Recently, aromatase in reactive astrocytes has been demonstrated in response to Neural Injury in the mammalian CNS. Since the glial aromatase expression first documented in cultures of the songbird telencephalon may reflect processes similar to those in response to mammalian Neural Injury, we investigated whether Injury alters the pattern of aromatase-expression in the zebra finch, a species with very high levels of forebrain aromatase expression. Adult males received a penetrating Neural Injury to the right hemisphere and were killed either 24 or 72 h later. Controls were anaesthetized and otherwise unmanipulated. We determined the expression of aromatase mRNA and protein using in situ hybridization and immunocytochemistry, respectively. Both the transcription and translation of aromatase is dramatically upregulated around the lesion site in response to Neural Injury in the zebra finch forebrain. This effect is robust and rapid, occurring within 24 h of the Injury itself. Cells that upregulate aromatase appear to be reactive astrocytes based upon morphology. The hemisphere contralateral to the Injury and both hemispheres in control birds showed the normal, exclusively neuronal pattern of aromatase expression. The upregulation of aromatase in astrocytes may provide high levels of oestrogen available to modulate processes such as CNS repair. Injury-induced upregulation of astrocytic aromatase may be a general characteristic of the injured vertebrate brain.
Paul P. Drury - One of the best experts on this subject based on the ideXlab platform.
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Status epilepticus after prolonged umbilical cord occlusion is associated with greater Neural Injury fetal sheep at term-equivalent
PloS one, 2014Co-Authors: Paul P. Drury, Laura Bennet, Joanne O. Davidson, Eleanor R. Gunn, Lindsea C. Booth, Lotte G. Van Den Heuij, Guido Wassink, Alistair J. GunnAbstract:The majority of pre-clinical studies of hypoxic-ischemic encephalopathy at term-equivalent have focused on either relatively mild insults, or on functional paradigms of cerebral ischemia or hypoxia-ischemia/hypotension. There is surprisingly little information on the responses to single, severe ‘physiological’ insults. In this study we examined the evolution and pattern of Neural Injury after prolonged umbilical cord occlusion (UCO). 36 chronically instrumented fetal sheep at 125–129 days gestational age (term = 147 days) were subjected to either UCO until mean arterial pressure was < = 8 mmHg (n = 29), or sham occlusion (n = 7). Surviving fetuses were killed after 72 hours for histopathologic assessment with acid-fuchsin thionine. After UCO, 11 fetuses died with intractable hypotension and 5 ewes entered labor and were euthanized. The remaining 13 fetuses showed marked EEG suppression followed by evolving seizures starting at 5.8 (6.8) hours (median (interquartile range)). 6 of 13 developed status epilepticus, which was associated with a transient secondary increase in cortical impedance (a measure of cytotoxic edema, p
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Introduction: This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic–ischemic Injury in the immature brain. Results: Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min ( P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h ( P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. Discussion: EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Methods: Chronically instrumented fetal sheep at 0.7 gestation (101–104 days; term is 147 days) received either 15-min ( n = 13) or 25-min ( n = 13) of complete umbilical cord occlusion. The Δ (0–3.9 Hz), θ (4–7.9 Hz), α (8–12.9 Hz), and β (13–22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
Pediatric Research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep
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Limited predictive value of early changes in EEG spectral power for Neural Injury after asphyxia in preterm fetal sheep.
Pediatric research, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Laura Bennet, Joanne O. Davidson, Sam Mathai, Eleanor R. Gunn, Lindsea C. Booth, Alistair J. GunnAbstract:This study examined whether spectral analysis of the electroencephalogram (EEG) can discriminate between mild and severe hypoxic-ischemic Injury in the immature brain. Total EEG power was profoundly suppressed after umbilical cord occlusion and recovered to baseline by 5 h after 15-min of occlusion, in contrast with transient recovery in the 25-min (P < 0.05). Power spectra were not different between groups in the first 3 h; α and β power were significantly higher in the 15-min group from 4 h, and Δ and θ power from 5 h (P < 0.05). The 25-min group showed severe neuronal loss in hippocampal regions and basal ganglia at 3 days, in contrast with no/minimal Injury in the 15-min group. EEG power after asphyxia did not discriminate between mild and severe Injury in the first 3 h in preterm fetal sheep. Severe subcortical Neural Injury was associated with persistent loss of high-frequency activity. Chronically instrumented fetal sheep at 0.7 gestation (101-104 days; term is 147 days) received either 15-min (n = 13) or 25-min (n = 13) of complete umbilical cord occlusion. The Δ (0-3.9 Hz), θ (4-7.9 Hz), α (8-12.9 Hz), and β (13-22 Hz) components of the EEG were determined by power spectral analysis. Brains were taken at 3 days for histopathology.
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049 The association between seizure activity and Neural Injury following endotoxin exposure and hypoxic-ischaemic insults in a preterm ovine model
Journal of Neurology Neurosurgery & Psychiatry, 2012Co-Authors: Michael J. Keogh, Paul P. Drury, Joanne O. Davidson, Lindsea C. Booth, S Maathi, L Bennet, A J GunnAbstract:Introduction Neonatal seizures following hypoxic-ischaemic insults at birth are common. Additional exposure to endotoxins (LPS) prior to ischaemia has been shown to be able to increase or decrease Neural Injury, though whether this is achieved through altering seizure activity is unknown. Methods Fetal sheep (aged 103–104 days gestation) were given a 5-day infusion of normal saline (n=9) or 250 ng/kg/24 h of lipopolysaccharide (a gram negative endotoxin) (n=10) prior to 15 min of umbilical cord ischaemia. Fetal EEG activity was recorded from 6 h before infusion to 5 days post ischaemia and analysed through visual and quantitative spectral methods. Result Neural Injury was lower in the group given LPS prior to ischaemia (p Discussion LPS appears to ‘pre-condition’ the brain to subsequent hypoxic-ischaemic insults, whilst paradoxically increasing seizure activity. Whether exposure to in utero infection confers long-term seizure susceptibility and long-term ability to withstand hypoxic-ischaemic insults remains unclear but may be a promising area of future research.
