Relevant bibliographies by topics / Hypoxic ischaemic brain injury

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Hypoxic ischaemic brain injury'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Hypoxic ischaemic brain injury"

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Howard, R. S., P. A. Holmes, and M. A. Koutroumanidis. "Hypoxic-ischaemic brain injury." Practical Neurology 11, no. 1 (January 13, 2011): 4–18. http://dx.doi.org/10.1136/jnnp.2010.235218.

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Gresoiu, Mihaela, and Silvana Christou. "Hypoxic ischaemic brain injury." Anaesthesia & Intensive Care Medicine 21, no. 6 (June 2020): 298–304. http://dx.doi.org/10.1016/j.mpaic.2020.03.009.

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Gray, Peter H., David I. Tudehope, John P. Masel, Yvonne R. Burns, Heather A. Mohay, Michael J. OʼCallaghan, and Gail M. Williams. "Perinatal Hypoxic-Ischaemic Brain Injury." Obstetrical & Gynecological Survey 49, no. 6 (June 1994): 389–90. http://dx.doi.org/10.1097/00006254-199406000-00010.

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Rocha-Ferreira, Eridan, and Mariya Hristova. "Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury." Neural Plasticity 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/4901014.

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Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI) of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity.
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Hage, Lory, Dusha Jeyakumaran, Jon Dorling, Shalini Ojha, Don Sharkey, Nicholas Longford, Neena Modi, Cheryl Battersby, and Chris Gale. "Changing clinical characteristics of infants treated for hypoxic-ischaemic encephalopathy in England, Wales and Scotland: a population-based study using the National Neonatal Research Database." Archives of Disease in Childhood - Fetal and Neonatal Edition 106, no. 5 (February 4, 2021): 501–8. http://dx.doi.org/10.1136/archdischild-2020-319685.

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BackgroundTherapeutic hypothermia is standard of care for babies with moderate/severe hypoxic-ischaemic encephalopathy and is increasingly used for mild encephalopathy.ObjectiveDescribe temporal trends in the clinical condition of babies diagnosed with hypoxic-ischaemic encephalopathy who received therapeutic hypothermia.DesignRetrospective cohort study using data held in the National Neonatal Research Database.SettingNational Health Service neonatal units in England, Wales and Scotland.PatientsInfants born from 1 January 2010 to 31 December 2017 with a recorded diagnosis of hypoxic-ischaemic encephalopathy who received therapeutic hypothermia for at least 3 days or died in this period.Main outcomesPrimary outcomes: recorded clinical characteristics including umbilical cord pH; Apgar score; newborn resuscitation; seizures and treatment on day 1. Secondary outcomes: recorded hypoxic-ischaemic encephalopathy grade.Results5201 babies with a diagnosis of hypoxic-ischaemic encephalopathy received therapeutic hypothermia or died; annual numbers increased over the study period. A decreasing proportion had clinical characteristics of severe hypoxia ischaemia or a diagnosis of moderate or severe hypoxic-ischaemic encephalopathy, trends were statistically significant and consistent across multiple clinical characteristics used as markers of severity.ConclusionsTreatment with therapeutic hypothermia for hypoxic-ischaemic encephalopathy has increased in England, Scotland and Wales. An increasing proportion of treated infants have a diagnosis of mild hypoxic-ischaemic encephalopathy or have less severe clinical markers of hypoxia. This highlights the importance of determining the role of hypothermia in mild hypoxic-ischaemic encephalopathy. Receipt of therapeutic hypothermia is unlikely to be a useful marker for assessing changes in the incidence of brain injury over time.
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Wyatt, JS. "Hypoxic-ischaemic injury of the neonatal brain." Fetal and Maternal Medicine Review 8, no. 2 (May 1996): 95–108. http://dx.doi.org/10.1017/s0965539500001522.

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Despite advances in obstetric and neonatal care, hypoxia-ischaemia remains as probably the commonest cause of severe disabling brain injury which occurs in the perinatal period. Although for the population as a whole, congenital brain abnormality and early fetal events are the most frequent antecedent of permanent neurodevelopmental disability, perinatal brain injury is an important and potentially preventable cause of severe and permanent handicap in both developed and developing countries.
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Howard, Robin S. "Hypoxic–ischaemic brain injury following cardiac arrest." Anaesthesia & Intensive Care Medicine 15, no. 4 (April 2014): 176–80. http://dx.doi.org/10.1016/j.mpaic.2014.01.014.

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Howard, Robin S. "Hypoxic–ischaemic brain injury following cardiac arrest." Anaesthesia & Intensive Care Medicine 18, no. 5 (May 2017): 244–48. http://dx.doi.org/10.1016/j.mpaic.2017.02.005.

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de Vries, Linda S., and Floris Groenendaal. "Patterns of neonatal hypoxic–ischaemic brain injury." Neuroradiology 52, no. 6 (April 14, 2010): 555–66. http://dx.doi.org/10.1007/s00234-010-0674-9.

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Gadian, D. G. "Developmental amnesia associated with early hypoxic-ischaemic injury." Brain 123, no. 3 (March 1, 2000): 499–507. http://dx.doi.org/10.1093/brain/123.3.499.

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Dissertations / Theses on the topic "Hypoxic ischaemic brain injury"

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Peden, Carol J. "Proton and phosphorus spectroscopy of hypoxic, ischaemic and haemorrhagic perinatal brain injury." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21460.

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Proton magnetic resonance spectroscopy was investigated as a non-invasive technique to observe biochemical changes in the brains of children who had sustained perinatal hypoxic, ischaemic and haemorrhagic brain injury. Methods: Proton spectra were acquired from the centre of the brain in premature infants, and from the parieto-occipital region in older children. Phosphorus spectra were also collected and compared with the proton spectra. Unlocalized phosphorus spectra were acquired at different repetition times. Some children had localized phosphorus spectroscopy examinations with two and four dimensional chemical shift imaging. The children were between 33 weeks post-conceptional age and four years and three months postnatal age at the time of their initial spectroscopy examination. The ability of early proton spectroscopy to predict outcome was considered in relation to the clinical neurological state at eighteen months or more. Because certain assumptions were made about the proton spectra (e.g. no T2 measurements were made), proton spectra were acquired from adults with central nervous system tumours. At surgery, biopsies were taken from the tumours and from normal brain and were analysed with in vitro spectroscopy, histology and established biochemical techniques. The metabolite ratios were compared with those from the in vivo spectra. Modifications were made to commercially available monitoring and ventilation equipment to provide the same standards of care within the magnetic field for sick patients, as on the neonatal or intensive care units. Results: All the proton spectra had peaks attributable to N-Acetyl aspartate (NAA), choline containing compounds (Cho) and creatine plus phosphocreatine (Cr). The NAA/Cho and NAA/Cr peak height ratios increased with age, while the Cho/Cr ratio decreased. The NAA/Cr ratios were significantly decreased in all children with an abnormal neurological outcome when compared with the NAA/Cr ratios from children with a normal outcome. The NAA/Cho ratios were significantly decreased in those children with a moderate outcome but not in those with a severe neurological outcome. There were no significant changes in the Cho/Cr ratios. The phosphorus spectra showed changes; phosphocreatine (PCr) to inorganic phosphate (Pi) decreased after injury and there was a marked increase in pH in the children with the poorest outcome. The apparent Tl of Pi was increased in the first month after birth in the children with a severe outcome. Few changes were seen with localized phosphorus spectroscopy in children who had focal lesions. Phosphorus spectra returned to normal within weeks of birth, while the proton spectra remained abnormal. The adult tumour proton spectra compared well with the in vitro spectra and histology of the biopsies. The concentrations changes of metabolites in vivo, were consistent with the measurements made with established biochemical techniques. Discussion: Hypoxic-ischaemic injury produced changes in the proton spectrum from neonatal brain. These changes persisted with time. Some of these changes correlated with outcome. Phosphorus spectra showed acute changes in response to injury, but the changes resolved within weeks. NAA is located in neurons; the decrease in NAA could be due to failure of neurons to develop normally, or to areas of neuronal loss and gliosis resulting from hypoxic-ischaemic damage. Phosphorus spectra may return to normal because neurons and glia have similar phosphorus metabolite ratios. Proton spectroscopy combined with magnetic resonance imaging, may become a useful technique for studying the anatomy and biochemistry of the brain in children who have suffered brain injury.
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Pennell, Craig Edward. "The role of lactate measurement in the prediction of fetal hypoxic-ischaemic brain injury during labour." University of Western Australia. School of Women's and Infants' Health, 2004. http://theses.library.uwa.edu.au/adt-WU2003.0037.

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[Truncated abstract] In this thesis the role of lactate measurement has been evaluated in intrapartum assessment of fetal wellbeing. Specifically, I have addressed the question of whether fetal lactate measurement is better than the assessment of fetal heart rate patterns or the measurement of pH at predicting fetal brain injury after intrapartum asphyxia. Using an ovine model of repeated umbilical cord occlusion designed to mimic events which may occur during human labour, I have shown that the measurement of fetal lactate levels after repeated cord occlusion is significantly associated with the severity of brain injury after the asphyxial insult. No significant associations were identified with fetal pH measurements or with the duration of decelerative or compound fetal heart rate patterns; however, this is the first study to describe an association between the duration of both increased fetal heart rate variability and fetal heart rate overshoot with the severity of subsequent brain injury. Although no significant association was identified between fetal arterial pressure measured between umbilical cord occlusions and the grade of brain injury, the studies performed in this thesis are the first to show a strong correlation between the duration of specific arterial pressure responses during cord occlusions and the grade of brain injury, accounting for approximately 90% of the variability seen in the severity of injury. The mechanism responsible for the improved ability of lactate measurement to predict fetal brain injury is unknown. It may be because fetal lactate levels are a more stable marker of anaerobic metabolism of glucose than fetal pH levels, which are influenced by both increasing levels of carbon dioxide and anaerobic metabolism of amino-acids and fatty acids. In addition fetal pH levels can be rapidly normalised through placental exchange of carbon dioxide whereas fetal lactate levels are slow to normalise across the placenta as they rely on facilitated diffusion.
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Wilkinson, Dominic James Clifford. "Ethical issues in the use of magnetic resonance imaging of the brain in newborn infants with hypoxic-ischaemic encephalopathy : neuroimaging and decision-making for brain injured newborns." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:d61e4318-3568-4310-bf92-c7d70f2cb3da.

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Infants with hypoxic-ischaemic encephalopathy (birth asphyxia) have a high risk of death or disability. Those with poor prognosis are sometimes allowed to die after withdrawal of intensive care. In recent years, doctors have used new types of brain scan, magnetic resonance imaging (MRI), to predict the type and severity of impairment if the infant survives and to help with such decisions. In this thesis, I analyse the issues arising from the use of MRI for prognostication and decision-making in newborn infants. I argue that previous prognostic research has been hampered by a failure to identify and focus on the most important practical question and that this contributes to uncertainty in practice. I outline recommendations for improving research. I then look at existing guidelines about withdrawal of life-sustaining treatment. I identify several problems with these guidelines; they are vague and fail to provide practical guidance, they provide little or no genuine scope for parental involvement in decisions, and they give no weight to the interests of others. I argue that parental interests should be given some weight in decisions for newborn infants. I develop a new model of decision-making that, using the concept of a Restricted Life, attempts to set out clearly the boundaries of parental discretion in decision-making. I argue that where infants are predicted to have severe cognitive or very severe physical impairment parents should be permitted to request either withdrawal or continuation of treatment. I justify this model on the basis of overlapping interests, (prognostic, experiential and moral) uncertainty, asymmetrical harms, and the burden of care. In the conclusion, I set out a guideline for the use of MRI in newborn infants with hypoxic-ischaemic encephalopathy. I suggest that this guideline would provide a more robust, coherent and practical basis for decision-making in newborn intensive care.
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Fairlie, John. "Neuronal and microvascular adaptions to hypoxic/ischaemic injury in animal models." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427287.

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Flynn, Liam Martin Clint. "Physiological responses to brain tissue hypoxia and blood flow after acute brain injury." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31268.

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This thesis explores physiological changes occurring after acute brain injury. The first two chapters focus on traumatic brain injury (TBI), a significant cause of disability and death worldwide. I discuss the evidence behind current management of secondary brain injury with emphasis on partial brain oxygen tension (PbtO2) and intracranial pressure (ICP). The second chapter describes a subgroup analysis of the effect of hypothermia on ICP and PbtO2 in 17 patients enrolled to the Eurotherm3235 trial. There was a mean decrease in ICP of 4.1 mmHg (n=9, p < 0.02) and a mean decrease in PbtO2 (7.8 ± 3.1 mmHg (p < 0.05)) in the hypothermia group that was not present in controls. The findings support previous studies in demonstrating a decrease in ICP with hypothermia. Decreased PbtO2 could partially explain worse outcomes seen in the hypothermia group in the Eurotherm3235 trial. Further analysis of PbtO2 and ICP guided treatment is needed. The third chapter focuses on delayed cerebral ischaemia (DCI) after aneurysmal subarachnoid haemorrhage (aSAH), another form of acute brain injury that causes significant morbidity and mortality. I include a background of alpha-calcitonin gene-related peptide (αCGRP), a potential treatment of DCI, along with results from a systematic review and meta-analysis of nine experimental models investigating αCGRP. The meta-analysis demonstrates a 40.8 ± 8.2% increase in cerebral vessel diameter in those animals treated with αCGRP compared with controls (p < 0.0005, 95% CI 23.7 to 57.9). Neurobehavioural scores were reported in four publications and showed a Physiological responses to brain tissue hypoxia and blood flow after acute brain injury standardised mean difference of 1.31 in favour of αCGRP (CI -0.49 to 3.12). I conclude that αCGRP reduces cerebral vessel narrowing seen after SAH in animal studies but note that there is insufficient evidence to determine its effect on functional outcomes. A review of previous trials of αCGRP administration in humans is included, in addition to an original retrospective analysis of CSF concentrations of αCGRP in humans. Enzyme-linked immunosorbent assay of CSF (n = 22) was unable to detect αCGRP in any sample, which contrasts with previous studies and was likely secondary to study methodology. Finally, I summarise by discussing a protocol I designed for a dose-toxicity study involving the intraventricular administration of αCGRP to patients with aSAH and provide some recommendations for future research. This protocol was based upon the systematic review and was submitted to the Medical Research Council's DPFS funding stream during the PhD.
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Rutherford, Mary. "Magnetic resonance imaging of hypoxic-ischaemic brain lesions in the term infant." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262817.

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Lim, Ta. "The role of hypoxia-inducible factor-1α in xenon preconditioning versus hypoxic-ischaemic organ injury." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/7663.

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Background: The anaesthetic gas xenon provides long-lasting preservation of neuronal function when given several hours prior to neuronal injury. This phenomenon is described as preconditioning. However, little is known of the mechanisms by which xenon preconditioning mediates its protective effect. Interest has focused on the involvement of hypoxia-inducible factor-1α (HIF-1α) in preconditioning because: (i) Hypoxia activates HIF-1α and is an effective preconditioning stimulus; (ii) HIF-1α is a regulator of adaptive responses promoting cellular survival; (iii) Several genes that have hypoxia-responsive elements (HRE) for HIF-1 in the promoter region are capable of mediating preconditioning (e.g., erythropoietin). Therefore, this study speculates on the role of HIF-1α in xenon preconditioning. Method: Separate cohorts of male adult C57/BL6 mice were preconditioned by exposure to 75% xenon/25 % oxygen for 2 hours and thereafter immediately sacrificed for organ harvesting at 0-24 hours after xenon preconditioning. Semi-quantitative study of HIF-1α and EPO protein expression was performed by Western blot analysis, and RT-PCR was used as a measure of gene transcription. Results: Xenon preconditioning provokes a time-dependent increase in HIF-1α protein in brain as well as kidney. Xenon preconditioning also caused a time-dependent increase in EPO (a HIF-1 target gene) transcription and protein expression in a corresponding time course to xenon-induced HIF-1α. To elucidate the mechanisms of xenon-induced HIF-1α accumulation, the effect of xenon preconditioning on HIF-1α transcription, translation and degradation was studied. Xenon preconditioning does not induce a change in HIF-1α mRNA expression, nor does it significantly attenuate the expression of the PHD2 enzyme, required for HIF-1α degradation. To explore translation-dependent pathways, mice were treated with rapamycin before xenon preconditioning, to inhibit translation of HIF-1α through the mTOR pathway. Inhibition of this pathway prevented the xenon-induced increase of HIF-1α protein. To ascertain whether HIF-lα is required for xenon preconditioning, siRNA was used to knockdown HIF-lα expression in the kidney and xenon's renoprotective properties were shown to be abolished. Conclusions: Over the same time course as xenon's protection against subsequent injury in both brain and kidney, xenon preconditioning induces expression of HIF-1α. Increased HIF-1α expression is also associated with increased activity as evidenced by enhanced transcription and translation of the downstream effector, EPO. Xenon preconditioning does not regulate HIF-1α at the transcriptional level, nor does it inhibit HIF-lα degradation. However, these results suggest that xenon preconditioning upregulates expression of HIF-1α through translation-dependent mechanisms. Furthermore, xenon's action on HIF-1α is shown to be causally related to its organ protective effect. If these data can be extrapolated to the clinical setting, exposure to xenon would be beneficial prior to procedures in which organ perfusion is interrupted, preventing hypoxic-ischaemic as well as ischaemic-reperfusion injury.
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Whiteley, Tara. "Mitochondria and secondary ischaemic neural injury after head trauma." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285401.

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Rocha, Ferreira E. "The role of infection/inflammation, the TNF family of cytokines and myeloid cells in perinatal hypoxia-ischaemia brain injury." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1447553/.

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Synergy between materno-foetal infection and hypoxic-ischaemic insult around the time of birth is a known contributing factor to perinatal brain damage. This is a common precursor to cerebral palsy and other neurological deficits, affecting 2 to 5 per 1000 live births. Endotoxin up-regulates several molecules, including the TNF cluster of pro-inflammatory cytokines. Our group has explored the role of this cluster and shown that its deletion abolishes LPS sensitization to neonatal hypoxic-ischaemic insult. In this study we wanted to first investigate the effects of LPS-mediated sensitization across multiple wild type strains (C57BL/5, 129SVJ, BALB/c, CD1 and FVB) in order to then further characterize the TNF cluster, by studying the individual effects of TNFα, LTα and LTβ members of this cluster, using either global gene deletion, or peripheral myeloid/macrophage-specific deletion of the floxed TNFα allele with MLys::Cre (MLys+). Additionally, we decided to also look at the acquired cellular immune system, using the athymic nude mouse model of T cell deficiency (nu). At P7, littermates for each of the wild type strains, wild-type and homozygous knock-out offspring of heterozygous animals listed above underwent hypoxic-ischaemic insult, consisting of unilateral carotid occlusion followed 2 hours recovery before being placed in a hypoxic chamber for 30min with continuous 8% oxygen exposure. 12 hours prior, animals received a single intraperitoneal injection of 0.6µg/g LPS or saline as a control. 1/3 of animals in the wild type strains group underwent hypoxia-ischaemia alone as a control for saline treatment. LPS pre-treatment resulted in substantial increase inflammation, neuronal injury and infarct in all wild type strains, as well as in the phenotypically wild type littermates of the homozygous mutant animals. Mice lacking both copies of the LTα gene revealed a clear reduction in LPS-mediated sensitization. In reverse, global deletion of LTβ had a detrimental effect, with significant increase in brain damage. Global deletion of TNFα showed a trend towards greater damage, but deletion just in MLys+ macrophages was strongly protective, pointing to a dual role for the TNFα gene depending on in which cell-type it is expressed. Finally, nude animals (nu/nu) demonstrated a complete lack of LPS-mediated sensitization to subsequent hypoxic-ischaemic insult, suggesting that LPS sensitization may require T cell function.
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Crooks, Suzanne. "Long-term neuropsychological and psychosocial outcomes of hypoxic-ischemic brain injury." Thesis, Queen's University Belfast, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.676279.

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Purpose: This study aimed to identify the long-term cognitive impairments arising from Hypoxic Ischaemic Brian Injury (HIBI) in a group of patients at least one year post insult. The long term psycho-social impact and carer burden associated with HIBI were also investigated. Method: A case series design was employed to facilitate detailed analysis of individual profiles. A battery of neuropsychological measures was administered to all participants. Cognitive domains assessed included premorbid and current IQ, visual and auditory recognition, immediate and delayed recall, auditory and visual attention, divided attention, executive functioning and visuo-spatial ability. HIBI survivors and a nominated family member also completed questionnaires relating to depression, anxiety, quality of life and caregiver strain. Results: Participants performed largely within estimated levels of premorbid functioning and any impairment was distributed across domains. Clinically significant symptoms of depression and anxiety were reported in both carers and HIBI smvivors and the carers' response suggested a high level of strain associated with caring. Conclusions: Results provide further support for the HIBI- bimodal distribution hypothesis. The use of premorbid measures and the inclusion of a caregiver assessment in neurorehabilitation interventions are indicated.
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Books on the topic "Hypoxic ischaemic brain injury"

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Mishra, Om P. Mechanisms of hypoxic brain injury in the newborn and potential strategies for neuroprotection. Trivandrum,Kerala, India: Transworld Research Network, 2007.

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Koutroumanidis, Michalis, and Robin Howard. Encephalopathy, central nervous system infections, and coma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0032.

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This chapter provides an overview of the indications for and the diagnostic and prognostic value of acute video-electroencephalogram (EEG) and continuous video-EEG monitoring in patients with encephalopathies, encephalitides, and coma. Particular emphasis is placed on the detection of non-convulsive seizures and non-convulsive status epilepticus secondary to acute and sub-acute cerebral insults, including post-cardiac arrest hypoxic-ischaemic brain injury, and on the related pitfalls and uncertainties. It also discusses key technical aspects of the EEG recording, including artefact identification and limitation, timing and type of external stimulation and assessment of EEG reactivity, and highlights the main relevant pitfalls. Finally, it explores the role of evoked potentials (EPs) in outcome prediction and the value of Cognitive EPs and quantitative EEG in the assessment of chronic disorders of consciousness.
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Aisiku, Imoigele, and Claudia S. Robertson. Epidemiology and pathophysiology of traumatic brain injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0341.

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Although medical management of traumatic brain injury (TBI) may have improved in developed countries, TBI is still a major cause of mortality and morbidity. The demographics are skewed towards the younger patient population, and affects males more than females, but in general follow a bimodal distribution with peaks affecting young adults and the elderly. As a result, the loss of functional years is devastating. Pathology due to brain trauma is a complex two-hit phenomenon, frequently divided into ‘primary’ and ‘secondary’ injury. Hypoxia, ischaemia, and inflammation all play a role, and the importance of each component varies between patients and in an individual patient over time. The initial injury may increase intracranial pressure and reduce cerebral perfusion due to the presence of mass lesions or diffuse brain swelling. Further secondary insults, such as hypotension, reduced cerebral perfusion pressure, hypoxia, or fever may exacerbate swelling and inflammation, and further compromise cerebral perfusion. Although there are currently no specific effective treatments for TBI, an improved understanding of the pathophysiology may eventually lead to treatments that will reduce mortality and improve long-term functional outcome.
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Hanrahan, John Donncha. The use of magnetic resonance spectroscopy in infants following perinatal hypoxic-ischaemic injury. 1997.

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Chang, Eugene. Neuroprotection for Premature Birth and Neonatal Brain Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0014.

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Preterm birth is associated with increased risk of perinatal brain injury. Although there has been little headway made in reducing preterm birth rates, survival of infants born prematurely has improved greatly. Because of this, the neurodevelopmental consequences related to prematurity have become significant issues, especially in those infants born at less than 32 weeks gestation. Hypoxic-ischemic encephalopathy commonly leads to neonatal brain injury both before and after delivery. While perinatal birth asphyxia accounts for a proportion of neonatal brain injury in neonates younger than 37 weeks, preterm birth is the more significant risk factor. This chapter explores the neurodevelopmental consequences associated with preterm birth, the pathophysiology of perinatal brain injury, and the imaging modalities used to assess the newborn brain. Finally, various neuroprotective interventions in clinical use and in development will be described.
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Ferioli, Simona, and Lori Shutter. Normal anatomy and physiology of the brain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0219.

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An understanding of the normal anatomy of the brain is essential to the diagnosis of a number of conditions that may be encountered in patients in the intensive care unit (ICU). Common structural cerebral conditions causing patients to be admitted to the ICU include cerebral trauma (traumatic brain injury), cerebrovascular accidents (both ischaemic and haemorrhagic), and infections. Cerebral conditions with a structural basis occurring after admission to the ICU are not as common as functional abnormalities, such as delirium, and peripheral complications, such as critical illness neuropathy and myopathy. An understanding of brain physiology, in particular factors that control or influence intracranial pressure (ICP) and cerebral blood flow (CBF) underpin much of the theory behind the management of acute brain injuries and syndromes.
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Chong, Ji Y., and Michael P. Lerario. Cardiac Arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0028.

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Hypoxic–ischemic brain injury is common following cardiopulmonary arrest and is associated with high rates of mortality and morbidity. Therapeutic hypothermia has been helpful in increasing survival and functional outcomes in these patients. The neurological examination, neuroimaging studies, and ancillary serological and neurophysiological testing can be helpful in prognostication post-arrest.
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De Deyne, Cathy, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0016.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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De Deyne, Cathy, Ward Eertmans, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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Shein, Steven L., and Robert S. B. Clark. Neurocritical Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0009.

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Brain injury is the most common proximate cause of death in pediatric intensive care units. For children who survive critical illness, long-standing brain damage and residual brain dysfunction can affect quality of life significantly. Therefore, minimizing neurological injury to improve patient outcomes is a priority of neurocritical care. This may be accomplished by implementing specific targeted therapies, avoiding pathophysiological conditions that exacerbate neurological injury, and using a multidisciplinary team that focuses on contemporary care of children with neurological injury and disease. This chapter reviews pertinent anatomy and physiology; general principles of pediatric neurocritical care; and specifics for caring for children with traumatic brain injury, hypoxic–ischemic encephalopathy, status epilepticus, meningitis/encephalitis, stroke, and acute hydrocephalus.
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Book chapters on the topic "Hypoxic ischaemic brain injury"

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Russell-Buckland, Joshua, P. Kaynezhad, S. Mitra, G. Bale, C. Bauer, I. Lingam, C. Meehan, et al. "Systems Biology Model of Cerebral Oxygen Delivery and Metabolism During Therapeutic Hypothermia: Application to the Piglet Model." In Advances in Experimental Medicine and Biology, 31–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_5.

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AbstractHypoxic ischaemic encephalopathy (HIE) is a significant cause of death and disability. Therapeutic hypothermia (TH) is the only available standard of treatment, but 45–55% of cases still result in death or neurodevelopmental disability following TH. This work has focussed on developing a new brain tissue physiology and biochemistry systems biology model that includes temperature effects, as well as a Bayesian framework for analysis of model parameter estimation. Through this, we can simulate the effects of temperature on brain tissue oxygen delivery and metabolism, as well as analyse clinical and experimental data to identify mechanisms to explain differing behaviour and outcome. Presented here is an application of the model to data from two piglets treated with TH following hypoxic-ischaemic injury showing different responses and outcome following treatment. We identify the main mechanism for this difference as the Q10 temperature coefficient for metabolic reactions, with the severely injured piglet having a median posterior value of 0.133 as opposed to the mild injury value of 5.48. This work demonstrates the use of systems biology models to investigate underlying mechanisms behind the varying response to hypothermic treatment.
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Ordidge, R., J. Thornton, M. Clemence, S. Punwani, E. Cady, J. Penrice, P. Amess, and J. Wyatt. "NMR Studies of Hypoxic-Ischaemic Injury in Neonatal Brain Using Imaging and Spectroscopy." In Advances in Experimental Medicine and Biology, 539–44. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5399-1_76.

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Bale, Gemma, Ajay Rajaram, Matthew Kewin, Laura Morrison, Alan Bainbridge, Linshan Liu, Udunna Anazodo, Mamadou Diop, Keith St Lawrence, and Ilias Tachtsidis. "Multimodal Measurements of Brain Tissue Metabolism and Perfusion in a Neonatal Model of Hypoxic-Ischaemic Injury." In Advances in Experimental Medicine and Biology, 203–8. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_32.

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AbstractThis is the first multimodal study of cerebral tissue metabolism and perfusion post-hypoxic-ischaemic (HI) brain injury using broadband near-infrared spectroscopy (bNIRS), diffuse correlation spectroscopy (DCS), positron emission tomography (PET) and magnetic resonance spectroscopy (MRS). In seven piglet preclinical models of neonatal HI, we measured cerebral tissue saturation (StO2), cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), changes in the mitochondrial oxidation state of cytochrome c oxidase (oxCCO), cerebral glucose metabolism (CMRglc) and tissue biochemistry (Lac+Thr/tNAA). At baseline, the parameters measured in the piglets that experience HI (not controls) were 64 ± 6% StO2, 35 ± 11 ml/100 g/min CBF and 2.0 ± 0.4 μmol/100 g/min CMRO2. After HI, the parameters measured were 68 ± 6% StO2, 35 ± 6 ml/100 g/min CBF, 1.3 ± 0.1 μmol/100 g/min CMRO2, 0.4 ± 0.2 Lac+Thr/tNAA and 9.5 ± 2.0 CMRglc. This study demonstrates the capacity of a multimodal set-up to interrogate the pathophysiology of HIE using a combination of optical methods, MRS, and PET.
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Shima, K., K. Ohashi, H. Umezawa, H. Chigasaki, Y. Karasawa, S. Okuyama, H. Araki, and S. Otomo. "Post-ischaemic Treatment with the Prostacycline Analogue TTC-909 Reduces Ischaemic Brain Injury." In Brain Edema VIII, 242–44. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9115-6_81.

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Dugan, Laura L., M. Margarita Behrens, and Sameh S. Ali. "Oxidative Stress in Hypoxic-Ischemic Brain Injury." In Brain Hypoxia and Ischemia, 239–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-579-8_12.

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Carroll, James. "Stem Cell Therapy for Neonatal Hypoxic–Ischemic Brain Injury." In Cell Therapy for Brain Injury, 307–20. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15063-5_16.

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Hayakawa, Masahiro. "Pathophysiology and Pathology of Neonatal Hypoxic-Ischemic Encephalopathy." In Cell Therapy for Perinatal Brain Injury, 25–35. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-1412-3_3.

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Strong, A. J., and R. Dardis. "Depolarisation Phenomena in Traumatic and Ischaemic Brain Injury." In Advances and Technical Standards in Neurosurgery, 3–49. Vienna: Springer Vienna, 2005. http://dx.doi.org/10.1007/3-211-27208-9_1.

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Teasdale, G. "Pathological and Clinical Evidence of Ischaemic Damage in Brain Trauma." In Ischaemia in Head Injury, 21–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80172-3_3.

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Matić, Vladimir, Perumpillichira J. Cherian, Devy Widjaja, Katrien Jansen, Gunnar Naulaers, Sabine Van Huffel, and Maarten De Vos. "Heart Rate Variability in Newborns with Hypoxic Brain Injury." In Oxygen Transport to Tissue XXXV, 43–48. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7411-1_7.

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Conference papers on the topic "Hypoxic ischaemic brain injury"

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Bale, Gemma, Ajay Rajaram, Matthew Kewin, Laura Morrison, Alan Bainbridge, Linshan Liu, Udunna Anazodo, Mamadou Diop, Keith St. Lawrence, and Ilias Tachtsidis. "Multimodal measurements of brain tissue metabolism and perfusion in a neonatal model of hypoxic-ischaemic injury." In Diffuse Optical Spectroscopy and Imaging, edited by Hamid Dehghani and Heidrun Wabnitz. SPIE, 2019. http://dx.doi.org/10.1117/12.2526729.

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Doyle, O. M., A. Temko, D. M. Murray, G. Lightbody, W. Marnane, and G. B. Boylan. "Predicting the neurodevelopmental outcome in newborns with hypoxic-ischaemic injury." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626736.

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McAllister, J., A. Mahaveer, and R. Gottstein. "G487(P) Fact or fiction? brain herniation after hypoxic-ischaemic events in neonatal patients." In Royal College of Paediatrics and Child Health, Abstracts of the Annual Conference, 24–26 May 2017, ICC, Birmingham. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313087.479.

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Wu, Dan, Anastassios Bezerianos, David Sherman, Xiaofeng Jia, and Nitish V. Thakor. "Causal interactions between thalamic and cortical LFPs following hypoxic-ischemic brain injury." In 5th International IEEE/EMBS Conference on Neural Engineering (NER 2011). IEEE, 2011. http://dx.doi.org/10.1109/ner.2011.5910518.

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Warpsinski, Gabriela, Salil Srivastava, Thomas P Keeley, Paul Fraser, and Giovanni E Mann. "17 Establishing a physiologically relevant in vitro model for ischaemic stroke injury in brain endothelial cells." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.28.

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Bakalov, V., J. Hertel, A. Ku, and B. E. DiSilvio. "Significant Recovery in Functional Capacity After Hypoxic-Ischemic Brain Injury in Young Female Patient." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6633.

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Dandan Zhang, M. Hathi, Zeng-Jin Yang, Haiyan Ding, R. Koehler, and N. Thakor. "Hypoxic-ischemic brain injury in neonatal piglets with different histological outcomes: An amplitude-integrated EEG study." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333439.

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Mauro, I., A. Franz, E. Baraldi, V. Carnielli, G. Paterlini, M. Napolitano, P. Faldini, et al. "The Albino Trail Effect of Allopurinol in Addition to Hypothermia for Hypoxic-Ischemic Brain Injury on Neurocognitive Outcome." In 7th International Conference on Clinical Neonatology—Selected Abstracts. Thieme Medical Publishers, 2018. http://dx.doi.org/10.1055/s-0038-1647082.

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Lee, Sung Jin, Jingjing Sun, Michael King, Huikai Xie, and Malisa Sarntinoranont. "Viscoelastic Property Changes of Acute Rat Brain Tissue Slices as a Function of Cell Viability." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53909.

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Changes in mechanical properties within brain tissues after losses in cell viability have not been well investigated. Lack of oxygen and nutrient transport can induce hypoxic neuronal injury and increase cell membrane permeability, and cell membranes and matrix components can lose their structural and mechanical integrity. These physical changes may have an effect on mechanical properties of brain tissue [1]. In this study, the viscoelastic behavior of two anatomical regions (cerebral cortex and hippocampus) in acute rat brain tissue slices were measured as a function of cell viability using indentation combined with optical coherence tomography (OCT). Neuronal viability in brain tissue slices was determined by measuring Fluoro-Jade C (FJC) staining to assay neuronal death or degeneration as a function of incubation time. OCT-measured deformation depths were compared with finite element (FE) simulations to estimate the relaxation of shear modulus. Measured equilibrium shear modulus (μ∞) after 8 hrs incubation was lower than μ∞ measured after 2 hrs incubation in the cerebral cortex (μ∞, 2hrs = 225 Pa, μ∞, 8hrs = 62 Pa) and hippocampus regions (μ∞, 2hrs = 170 Pa, μ∞, 8hrs = 33 Pa). Instantaneous shear modulus (μ0) after 8 hrs incubation was also an order of magnitude lower than μ0 after 2 hrs incubation in cortex (μ0, 2hrs = 1600 Pa, μ0, 8hrs = 100 Pa) and hippocampus regions (μ0, 2hrs = 370 Pa, μ0, 8hrs = 70 Pa). The results of this study provide a timeline for measuring mechanical properties of brain tissues ex vivo and provide better understanding of changes in brain modulus after injury or cell death.
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