scholarly journals Preconditioning and Postinsult Therapies for Perinatal Hypoxic–Ischemic Injury at Term

2010 ◽  
Vol 113 (1) ◽  
pp. 233-249 ◽  
Author(s):  
Robert D. Sanders ◽  
Helen J. Manning ◽  
Nicola J. Robertson ◽  
Daqing Ma ◽  
A. David Edwards ◽  
...  
Keyword(s):  
Perinatal Period ◽  
Rapid Identification ◽  
Postnatal Period ◽  
Hypoxic Ischemic Encephalopathy ◽  
Current Status ◽  
Neuroprotective Agents ◽  
Period 2 ◽  
Neuroprotective Strategies ◽  
The Brain ◽  
Ischemic Encephalopathy

Perinatal hypoxic-ischemic encephalopathy can be a devastating complication of childbirth. Herein, the authors review the pathophysiology of hypoxic-ischemic encephalopathy and the current status of neuroprotective strategies to ameliorate the injury centering on four themes: (1) monitoring in the perinatal period, (2) rapid identification of affected neonates to allow timely institution of therapy, (3) preconditioning therapy (a therapeutic that reduces the brain vulnerability) before hypoxic-ischemic encephalopathy, and (4) prompt institution of postinsult therapies to ameliorate the evolving injury. Recent clinical trials have demonstrated the significant benefit for hypothermic therapy in the postnatal period; furthermore, there is accumulating preclinical evidence that adjunctive therapies can enhance hypothermic neuroprotection. Advances in the understanding of preconditioning may lead to the administration of neuroprotective agents earlier during childbirth. Although most of these neuroprotective strategies have not yet entered clinical practice, there is a significant hope that further developments will enhance hypothermic neuroprotection.

Evidence of Occurrence of Intradural and Subdural Hemorrhage in the Perinatal and Neonatal Period in the Context of Hypoxic Ischemic Encephalopathy: An Observational Study from Two Referral Institutions in the United Kingdom

2009 ◽  
Vol 12 (3) ◽  
pp. 169-176 ◽  
Author(s):  
Marta C. Cohen ◽  
Irene Scheimberg
Keyword(s):  
Thin Film ◽  
Hypoxic Ischemic Encephalopathy ◽  
Subdural Hemorrhage ◽  
Intrauterine Death ◽  
Venous Plexus ◽  
Neonatal Deaths ◽  
The United Kingdom ◽  
Degrees Of Severity ◽  
The Brain ◽  
Ischemic Encephalopathy

The occurrence of subdural hemorrhage (SDH) on the convexities of the cerebral hemispheres is not an unusual finding in the setting of intrauterine, perinatal, or neonatal deaths, the hemorrhage usually presenting either as a thin film over the occipital poles or as a small infratentorial bleed. Working in 2 referral centers with over 30 000 deliveries per year, we routinely examine the dura macroscopically and histologically in nonmacerated fetuses over 24 weeks in gestation and in neonates. This paper describes our experience of intradural hemorrhage (IDH) and SDH associated with hypoxia. Our series comprises 25 fetuses and 30 neonates with obvious macroscopic intradural hemorrhage and hypoxia of varying degrees of severity diagnosed by systematic examination of the brain. Fetal gestational age ranged from 26–41/40 weeks (all no more than 24 hours from intrauterine death), while the 30 neonates lived for between 1 hour and 19 days. Simultaneously with IDH, frank SDH was seen in 2 of 3 of all cases (16 fetuses and 20 neonates). Intradural hemorrhage was more prominent in the posterior falx and tentorium, most likely because of the existence of 2 venous plexus at these sites. Our findings demonstrate that SDH and cerebral hypoxia are common associations of IDH and that SDH (often seen as a thin film of hemorrhage) almost always occurs in association with diffuse falcine IDH. Diffuse IDH with SDH are more frequently associated with severe or moderate hypoxic ischemic encephalopathy (HIE), while mild or early HIE is more common with focal IDH without SDH.

scholarly journals Perinatal Hypoxic-Ischemic Encephalopathy

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Ming-Chi Lai ◽  
San-Nan Yang
Keyword(s):  
Therapeutic Strategy ◽  
Hypoxic Ischemic Encephalopathy ◽  
Pathophysiological Mechanism ◽  
Perinatal Hypoxia ◽  
Ongoing Research ◽  
Neuroprotective Strategies ◽  
Future Potential ◽  
Clinical Potential ◽  
Ischemic Encephalopathy

Perinatal hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and can result in long-term devastating consequences. Perinatal hypoxia is a vital cause of long-term neurologic complications varying from mild behavioural deficits to severe seizure, mental retardation, and/or cerebral palsy in the newborn. In the mammalian developing brain, ongoing research into pathophysiological mechanism of neuronal injury and therapeutic strategy after perinatal hypoxia is still limited. With the advent of promising therapy of hypothermia in HIE, this paper reviews the pathophysiology of HIE and the future potential neuroprotective strategies for clinical potential for hypoxia sufferers.

scholarly journals Lipid Profiles from Dried Blood Spots Reveal Lipidomic Signatures of Newborns Undergoing Mild Therapeutic Hypothermia after Hypoxic-Ischemic Encephalopathy

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4301
Author(s):  
Rebekah Nixon ◽  
Ting Hin Richard Ip ◽  
Benjamin Jenkins ◽  
Ping K. Yip ◽  
Paul Clarke ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Peripheral Blood ◽  
Univariate Analysis ◽  
Dried Blood Spots ◽  
Hypoxic Ischemic Encephalopathy ◽  
Perinatal Brain Injury ◽  
Blood Spots ◽  
Lipid Species ◽  
The Brain ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is associated with perinatal brain injury, which may lead to disability or death. As the brain is a lipid-rich organ, various lipid species can be significantly impacted by HIE and these correlate with specific changes to the lipidomic profile in the circulation. Objective: To investigate the peripheral blood lipidomic signature in dried blood spots (DBS) from newborns with HIE. Using univariate analysis, multivariate analysis and sPLS-DA modelling, we show that newborns with moderate–severe HIE (n = 46) who underwent therapeutic hypothermia (TH) displayed a robust peripheral blood lipidomic signature comprising 29 lipid species in four lipid classes; namely phosphatidylcholine (PC), lysophosphatidylcholine (LPC), triglyceride (TG) and sphingomyelin (SM) when compared with newborns with mild HIE (n = 18). In sPLS-DA modelling, the three most discriminant lipid species were TG 50:3, TG 54:5, and PC 36:5. We report a reduction in plasma TG and SM and an increase in plasma PC and LPC species during the course of TH in newborns with moderate–severe HIE, compared to a single specimen from newborns with mild HIE. These findings may guide the research in nutrition-based intervention strategies after HIE in synergy with TH to enhance neuroprotection.

scholarly journals Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy

2015 ◽  
Vol 16 (9) ◽  
pp. 22368-22401 ◽  
Author(s):  
Brandon Dixon ◽  
Cesar Reis ◽  
Wing Ho ◽  
Jiping Tang ◽  
John Zhang
Keyword(s):  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Strategies ◽  
Ischemic Encephalopathy

scholarly journals Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead

2020 ◽  
Vol 21 (7) ◽  
pp. 2262 ◽  
Author(s):  
Raquel Boia ◽  
Noelia Ruzafa ◽  
Inês Dinis Aires ◽  
Xandra Pereiro ◽  
António Francisco Ambrósio ◽  
...  
Keyword(s):  
Axonal Regeneration ◽  
Therapeutic Strategy ◽  
Ganglion Cells ◽  
Current Status ◽  
Retinal Ganglion ◽  
Cell Degeneration ◽  
Extrinsic Factors ◽  
Axonal Connections ◽  
Neuroprotective Strategies ◽  
The Brain

The retinal ganglion cells (RGCs) are the output cells of the retina into the brain. In mammals, these cells are not able to regenerate their axons after optic nerve injury, leaving the patients with optic neuropathies with permanent visual loss. An effective RGCs-directed therapy could provide a beneficial effect to prevent the progression of the disease. Axonal injury leads to the functional loss of RGCs and subsequently induces neuronal death, and axonal regeneration would be essential to restore the neuronal connectivity, and to reestablish the function of the visual system. The manipulation of several intrinsic and extrinsic factors has been proposed in order to stimulate axonal regeneration and functional repairing of axonal connections in the visual pathway. However, there is a missing point in the process since, until now, there is no therapeutic strategy directed to promote axonal regeneration of RGCs as a therapeutic approach for optic neuropathies.

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