scholarly journals Efficacy of different treatment times of mild cerebral hypothermia on oxidative factors and neuroprotective effects in neonatal patients with moderate/severe hypoxic–ischemic encephalopathy

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094377
Author(s):  
Tingting Yang ◽  
Shan Li
Keyword(s):  
Mild Hypothermia ◽  
Neuron Specific Enolase ◽  
The Other ◽  
Hypoxic Ischemic Encephalopathy ◽  
Psychomotor Development ◽  
Controlled Study ◽  
Neurological Assessment ◽  
Neuroprotective Effects ◽  
Assessment Scores ◽  
Ischemic Encephalopathy

Objective To investigate the efficacy of different treatment times of mild cerebral hypothermia for treating moderate/severe hypoxic–ischemic encephalopathy (HIE) in neonatal patients and its effects on oxidative factors. Methods This prospective, randomized, controlled study included 92 neonatal patients with moderate/severe HIE and 30 controls. The patients with HIE received routine treatment, 48 hours of hypothermia, or 72 hours of hypothermia. Results Superoxide dismutase (SOD) values were significantly lower and malondialdehyde (MDA) and neuron-specific enolase (NSE) values were higher in patients with HIE than in controls before the study. After 24, 48, and 72 hours of treatment, SOD values in all patients with HIE gradually increased and MDA and NSE values gradually decreased. At 3, 7, and 10 days, the Neonatal Behavioral Neurological Assessment scores were highest in the mild hypothermia for 72 hours group than in the other groups. The Mental and Psychomotor Development Indices scores of the Bayley Scales were significantly higher in the mild hypothermia for 72 hours group than in the other groups. Conclusion Hypothermia treatment of 72 hours is better than 48 hours for improving oxidative conditions, reducing NSE values, and improving neurological behavior and development for neonates with moderate/severe HIE.

scholarly journals Neural Function Recovery and Safety of Mild Hypothermia Therapy Combined with Monosialotetrahexosylganglioside on Neonatal Asphyxia Complicated by Hypoxic Ischemic Encephalopathy

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Jingjing Ge ◽  
Xiaoling Jiao ◽  
Fanlin Qi ◽  
Hui Li
Keyword(s):  
Mild Hypothermia ◽  
Clinical Signs ◽  
Neuron Specific Enolase ◽  
The Other ◽  
Hypoxic Ischemic Encephalopathy ◽  
Combination Group ◽  
Neural Function ◽  
Neonatal Asphyxia ◽  
Function Recovery ◽  
Ischemic Encephalopathy

Objective. To explore the effect and safety of mild hypothermia therapy combined with monosialotetrahexosylganglioside (GM1) on neural function recovery of neonatal asphyxia complicated by hypoxic ischemic encephalopathy (HIE). Methods. The clinical data of 90 neonates with HIE were retrospectively analyzed. According to the treatment methods, the neonates were divided into a routine group, a mild hypothermia group, and a combination group, with 30 cases in each group. The differences in neural function recovery, biochemical indexes, clinical signs recovery, efficacy, and complications were observed in the three groups after treatment. Results. After treatment, the score of neonatal behavioral neurological assessment (NBNA) and level of superoxide dismutase (SOD) in the combination group were higher than those of the other two groups ( P < 0.05 ). The levels of neuron-specific enolase (NSE), S-100β protein, and plasma neuropeptide Y (NPY) in the combination group were lower than those in the other two groups, and the recovery time of consciousness, muscle tension, and reflex was shorter ( P < 0.05 ). The combination group showed higher total effective rate and lower incidence of complications as compared with the other two groups ( P < 0.05 ). Conclusion. Mild hypothermia therapy combined with GM1 for the treatment of neonatal asphyxia complicated by HIE can promote the recovery of neural function and reduce the incidence of complications in neonates.

scholarly journals Early Neurological Assessment in Infants with Hypoxic Ischemic Encephalopathy Treated with Therapeutic Hypothermia

2019 ◽  
Vol 8 (8) ◽  
pp. 1247
Author(s):  
Domenico M. Romeo ◽  
Sarah Bompard ◽  
Francesca Serrao ◽  
Giuseppina Leo ◽  
Gianpaolo Cicala ◽  
...  
Keyword(s):  
Neurological Examination ◽  
Motor Impairment ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neurological Assessment ◽  
Neurodevelopmental Outcomes ◽  
Good Tool ◽  
Motor Disabilities ◽  
High Risk Infants ◽  
Ischemic Encephalopathy

Early neurological assessment in infants with hypoxic ischemic encephalopathy (HIE) treated with hypothermia has not been systematically explored. The aims of the present study were to assess whether the Hammersmith Infant Neurological Examination (HINE) is a good tool to predict later neurodevelopmental outcomes at 2 year from birth in this population of infants. A total of 41 term born infants with HIE treated with hypothermia performed the HINE at 12 months and a neurodevelopmental assessment at 24 months. All the infants who had a global HINE score between 67 and 78 were able to walk independently at 2 years and reported a normal developmental quotient; language disorders were observed in a limited number of infants. HINE scores <67 were always associated with motor impairment. In conclusion, the HINE confirms its role as one of the early neurological examination tools for the diagnosis of high risk infants, even in infants with HIE treated with hypothermia. These results can be useful for clinicians involved in the follow up of these infants for early identification of motor disabilities and in planning appropriate intervention.

scholarly journals Current Controversies in Newer Therapies to Treat Birth Asphyxia

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Pia Wintermark
Keyword(s):  
Brain Injury ◽  
Neurological Outcome ◽  
Mild Hypothermia ◽  
Birth Asphyxia ◽  
Hypoxic Ischemic Encephalopathy ◽  
Monitoring Technology ◽  
The Past ◽  
Neuroprotective Strategy ◽  
Ischemic Encephalopathy

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.

scholarly journals Environmental Enrichment Enhances Cav 2.1 Channel-Mediated Presynaptic Plasticity in Hypoxic–Ischemic Encephalopathy

2021 ◽  
Vol 22 (7) ◽  
pp. 3414
Author(s):  
Suk-Young Song ◽  
Soonil Pyo ◽  
Sungchul Choi ◽  
Hee Sang Oh ◽  
Jung Hwa Seo ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Hypoxic Condition ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Effects ◽  
Y Maze ◽  
Behavioral Assessments ◽  
The Right ◽  
Vesicle Cycle ◽  
Ischemic Encephalopathy ◽  
Presynaptic Proteins

Hypoxic–ischemic encephalopathy (HIE) is a devastating neonatal brain condition caused by lack of oxygen and limited blood flow. Environmental enrichment (EE) is a classic paradigm with a complex stimulation of physical, cognitive, and social components. EE can exert neuroplasticity and neuroprotective effects in immature brains. However, the exact mechanism of EE on the chronic condition of HIE remains unclear. HIE was induced by a permanent ligation of the right carotid artery, followed by an 8% O2 hypoxic condition for 1 h. At 6 weeks of age, HIE mice were randomly assigned to either standard cages or EE cages. In the behavioral assessments, EE mice showed significantly improved motor performances in rotarod tests, ladder walking tests, and hanging wire tests, compared with HIE control mice. EE mice also significantly enhanced cognitive performances in Y-maze tests. Particularly, EE mice showed a significant increase in Cav 2.1 (P/Q type) and presynaptic proteins by molecular assessments, and a significant increase of Cav 2.1 in histological assessments of the cerebral cortex and hippocampus. These results indicate that EE can upregulate the expression of the Cav 2.1 channel and presynaptic proteins related to the synaptic vesicle cycle and neurotransmitter release, which may be responsible for motor and cognitive improvements in HIE.

Metabolic Encephalopathy - Part I

2019 ◽  
Author(s):  
Rick Gill ◽  
Matthew McCoyd ◽  
Sean Ruland ◽  
José Biller
Keyword(s):  
Neuron Specific Enolase ◽  
Hypoxic Ischemic Encephalopathy ◽  
Temperature Management ◽  
Initial Assessment ◽  
Acute Confusional State ◽  
Confusional State ◽  
Metabolic Encephalopathy ◽  
Key Words Encephalopathy ◽  
Toxic Exposures ◽  
Ischemic Encephalopathy

Encephalopathy can range from the acute confusional state to frank coma, and is broadly defined as a constellation of symptoms and signs reflecting diffuse cerebral dysfunction.  The potential causes of encephalopathy are vast requiring a thorough initial assessment and systematic diagnostic approach.  Obtaining a comprehensive history may be challenging and ancillary sources of information are often helpful in narrowing the differential diagnosis.  The general examination may provide hints as to the cause of encephalopathy and the neurologic examination can guide both acute management and focus the diagnostic investigations on specific etiologies which fit the clinical presentation.  The systemic manifestations of infection and toxic exposures are common causes of encephalopathy.  In sepsis, not only is brain perfusion compromised, multi system dysfunction is common and additional factors related to the specific infection such as hypoxia in pneumonia or secondary CNS involvement can complicate management.  An understanding of the common physical examination findings of toxic exposures can aid in the diagnosis and rapid treatment of reversible toxic encephalopathies such as narcotics, benzodiazepines or environmental toxins.  Cardiopulmonary dysfunction can lead to hypoxic-ischemic encephalopathy and advances in critical care, and particularly targeted temperature management following cardiac arrest, have improved the neurologic outcome in these patients.   This review contains 2 figures, 3 tables, and 25 references. Key words: encephalopathy, delirium, ascending reticular activating system, acute confusional state, subclinical seizures, Glasgow Coma Scale, Full Outline of Unresponsiveness (FOUR) Score , hypoxic-ischemic encephalopathy, neuroleptic malignant syndrome, serum neuron-specific enolase

Biomarkers of Hypoxic-Ischemic Encephalopathy in Newborns

2020 ◽  
Author(s):  
Mahmood Noorishadkam ◽  
Shekoofeh Savabieh ◽  
Mohammad Emad Sharifi
Keyword(s):  
Brain Mri ◽  
Neuron Specific Enolase ◽  
Hypoxic Ischemic Encephalopathy ◽  
Growth Outcomes ◽  
Target Organs ◽  
Specific Proteins ◽  
Brain Specific Proteins ◽  
Ischemic Encephalopathy ◽  
Neonatal Brain Damage

Biomarkers are particles that are released from target organs during tissue hypoxia injury. Recognizing biomarkers released from the damaged brain helps physicians determine the extent of tissue damage and the use of protective techniques in clinical treatment.  Previous studies revealed that biomarkers such as brain-specific proteins (neuron-specific enolase (NSE), S100B, ubiquitincarboxy-terminal hydrolase-L1, total Tau) and cytokines, including IL-6, IL-1β, IL-10, IL-13, interferon-gamma, TNF alpha and brain-derived neurotrophic factor are useful in diagnosing hypoxic-ischemic encephalopathy (HIE) and predicting nerve growth outcomes. However, optimal sensitivity and specificity of these biomarkers have not been achieved, which has limited their clinical application. This review focuses on biomarkers such as lactate, LDH, NRBC, NSE, S100B, GFAP, CPK-BB, IL-6, NPBI, UCHL-1. More sensitive and accurate instruments such as brain imaging (such as brain MRI), brain function (such as NIRS, aEEG), and long-term neuroassay should be used in the future to confirm biomarkers of neonatal brain damage.

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