Imaging patterns of brain injury in term-birth asphyxia

2009 ◽  
Vol 98 (3) ◽  
pp. 586-592 ◽  
Author(s):  
Renate Swarte ◽  
Maarten Lequin ◽  
Perumpillichira Cherian ◽  
Alexandra Zecic ◽  
Johannes van Goudoever ◽  
...  
2012 ◽  
Vol 123 (8) ◽  
pp. 1631-1638 ◽  
Author(s):  
Renate M.C. Swarte ◽  
Perumpillichira J. Cherian ◽  
Maarten Lequin ◽  
Gerhard H. Visser ◽  
Paul Govaert

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Pia Wintermark

Despite major advances in monitoring technology and knowledge of fetal and neonatal pathophysiology, neonatal hypoxic-ischemic encephalopathy (HIE) remains one of the main causes of severe adverse neurological outcome in children. Until recently, there were no therapies other than supportive measures. Over the past several years, mild hypothermia has been proven to be safe to treat HIE. Unfortunately, this neuroprotective strategy seems efficient in preventing brain injury in some asphyxiated newborns, but not in all of them. Thus, there is increasing interest to rapidly understand how to refine hypothermia therapy and add neuroprotective or neurorestorative strategies. Several promising newer treatments to treat birth asphyxia and prevent its devastating neurological consequences are currently being tested. In this paper, the physiopathology behind HIE, the currently available treatment, the potential alternatives, and the next steps before implementation of these other treatments are reviewed.


2011 ◽  
Vol 32 (2) ◽  
pp. 232-241 ◽  
Author(s):  
Zoya V Niatsetskaya ◽  
Pradeep Charlagorla ◽  
Dzmitry A Matsukevich ◽  
Sergey A Sosunov ◽  
Korapat Mayurasakorn ◽  
...  

Reperfusion triggers an oxidative stress. We hypothesized that mild hypoxemia in reperfusion attenuates oxidative brain injury following hypoxia-ischemia (HI). In neonatal HI-mice, the reperfusion was initiated by reoxygenation with room air (RA) followed by the exposure to 100%, 21%, 18%, 15% oxygen for 60 minutes. Systemic oxygen saturation (SaO2), cerebral blood flow (CBF), brain mitochondrial respiration and permeability transition pore (mPTP) opening, markers of oxidative injury, and cerebral infarcts were assessed. Compared with RA-littermates, HI-mice exposed to 18% oxygen exhibited significantly decreased infarct volume, oxidative injury in the brain mitochondria and tissue. This was coupled with improved mitochondrial tolerance to mPTP opening. Oxygen saturation maintained during reperfusion at 85% to 95% was associated ( r=0.57) with the best neurologic outcome. Exposure to 100% or 15% oxygen significantly exacerbated brain injury and oxidative stress. Compared with RA-mice, hyperoxia dramatically increased reperfusion CBF, but exposure to 15% oxygen significantly reduced CBF to values observed during the HI-insult. Mild hypoxemia during initial reperfusion alleviates the severity of HI-brain injury by limiting the reperfusion-driven oxidative stress to the mitochondria and mPTP opening. This suggests that at the initial stage of reperfusion, a slightly decreased systemic oxygenation (SaO2 85% to 95%) may be beneficial for infants with birth asphyxia.


1991 ◽  
Vol 7 (2) ◽  
pp. 86-90 ◽  
Author(s):  
Sarah C. Muttitt ◽  
Margot J. Taylor ◽  
Jeffrey S. Kobayashi ◽  
Lynn MacMillan ◽  
Hilary E. Whyte

2017 ◽  
Vol 45 (5) ◽  
pp. 1067-1076 ◽  
Author(s):  
Claire Thornton ◽  
Ana A. Baburamani ◽  
Anton Kichev ◽  
Henrik Hagberg

Birth asphyxia in term neonates affects 1–2/1000 live births and results in the development of hypoxic–ischaemic encephalopathy with devastating life-long consequences. The majority of neuronal cell death occurs with a delay, providing the potential of a treatment window within which to act. Currently, treatment options are limited to therapeutic hypothermia which is not universally successful. To identify new interventions, we need to understand the molecular mechanisms underlying the injury. Here, we provide an overview of the contribution of both oxidative stress and endoplasmic reticulum stress in the development of neonatal brain injury and identify current preclinical therapeutic strategies.


Epilepsia ◽  
2020 ◽  
Author(s):  
Tommi Ala‐Kurikka ◽  
Alexey Pospelov ◽  
Milla Summanen ◽  
Aleksander Alafuzoff ◽  
Samu Kurki ◽  
...  

2021 ◽  
Vol 22 (5) ◽  
pp. 2524
Author(s):  
Marta Reyes-Corral ◽  
Noelia Sola-Idígora ◽  
Rocío de la Puerta ◽  
Joan Montaner ◽  
Patricia Ybot-González

Neonatal hypoxia–ischemia (HI) is a brain injury caused by oxygen deprivation to the brain due to birth asphyxia or reduced cerebral blood perfusion, and it often leads to lifelong limiting sequelae such as cerebral palsy, seizures, or mental retardation. HI remains one of the leading causes of neonatal mortality and morbidity worldwide, and current therapies are limited. Hypothermia has been successful in reducing mortality and some disabilities, but it is only applied to a subset of newborns that meet strict inclusion criteria. Given the unpredictable nature of the obstetric complications that contribute to neonatal HI, prophylactic treatments that prevent, rather than rescue, HI brain injury are emerging as a therapeutic alternative. Nutraceuticals are natural compounds present in the diet or used as dietary supplements that have antioxidant, anti-inflammatory, or antiapoptotic properties. This review summarizes the preclinical in vivo studies, mostly conducted on rodent models, that have investigated the neuroprotective properties of nutraceuticals in preventing and reducing HI-induced brain damage and cognitive impairments. The natural products reviewed include polyphenols, omega-3 fatty acids, vitamins, plant-derived compounds (tanshinones, sulforaphane, and capsaicin), and endogenous compounds (melatonin, carnitine, creatine, and lactate). These nutraceuticals were administered before the damage occurred, either to the mothers as a dietary supplement during pregnancy and/or lactation or to the pups prior to HI induction. To date, very few of these nutritional interventions have been investigated in humans, but we refer to those that have been successful in reducing ischemic stroke in adults. Overall, there is a robust body of preclinical evidence that supports the neuroprotective properties of nutraceuticals, and these may represent a safe and inexpensive nutritional strategy for the prevention of neonatal HI encephalopathy.


2016 ◽  
Vol 39 (1-4) ◽  
pp. 248-256 ◽  
Author(s):  
Jennifer K. Lee ◽  
Andrea Poretti ◽  
Jamie Perin ◽  
Thierry A.G.M. Huisman ◽  
Charlamaine Parkinson ◽  
...  

Background: Therapeutic hypothermia provides incomplete neuroprotection for neonatal hypoxic-ischemic encephalopathy (HIE). We examined whether hemodynamic goals that support autoregulation are associated with decreased brain injury and whether these relationships are affected by birth asphyxia or vary by anatomic region. Methods: Neonates cooled for HIE received near-infrared spectroscopy autoregulation monitoring to identify the mean arterial blood pressure with optimized autoregulatory function (MAPOPT). Blood pressure deviation from MAPOPT was correlated with brain injury on MRI after adjusting for the effects of arterial carbon dioxide, vasopressors, seizures, and birth asphyxia severity. Results: Blood pressure deviation from MAPOPT related to neurologic injury in several regions independent of birth asphyxia severity. Greater duration and deviation of blood pressure below MAPOPT were associated with greater injury in the paracentral gyri and white matter. Blood pressure within MAPOPT related to lesser injury in the white matter, putamen and globus pallidus, and brain stem. Finally, blood pressures that exceeded MAPOPT were associated with reduced injury in the paracentral gyri. Conclusions: Blood pressure deviation from optimal autoregulatory vasoreactivity was associated with MRI markers of brain injury that, in many regions, were independent of the initial birth asphyxia. Targeting hemodynamic ranges to optimize autoregulation has potential as an adjunctive therapy to hypothermia for HIE.


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