Neuron-specific enolase as a marker of the severity and outcome of hypoxic ischemic encephalopathy

2004 ◽  
Vol 26 (6) ◽  
pp. 398-402 ◽  
Author(s):  
Coşkun Çeltik ◽  
Betül Acunaş ◽  
Naci Öner ◽  
Özer Pala
Keyword(s):  
Neuron Specific Enolase ◽  
Hypoxic Ischemic Encephalopathy ◽  
Ischemic Encephalopathy

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.

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.

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

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 Hydrogen water reduces NSE, IL-6, and TNF-α levels in hypoxic-ischemic encephalopathy

Open Medicine ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. 399-406 ◽  
Author(s):  
Lin Yang ◽  
Dunchen Li ◽  
Shuying Chen
Keyword(s):  
Neuron Specific Enolase ◽  
Conventional Group ◽  
Hypoxic Ischemic Encephalopathy ◽  
Care Group ◽  
Control Group ◽  
Hydrogen Water ◽  
Water Group ◽  
Tnf Α ◽  
Group 5 ◽  
Ischemic Encephalopathy

AbstractThis study retrospectively analyzed the efficacy of hydrogen water in the treatment of neonatal hypoxic-ischemic encephalopathy (HIE) and its effect on serum neuron-specific enolase (NSE), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels.Forty newborns with HIE who received treatment from April 2014 to April 2015 were divided into a conventional care group and a hydrogen water group according to the different treatment methods applied. Twenty healthy full-term newborns comprised the control group. In the hydrogen water group, 5-mL/kg hydrogen water was orally administered two days after birth daily for 10 days in addition to conventional treatment. After 10 days, efficacy indicators were examined in the HIE groups. The NSE, IL-6, and TNF-α levels were compared among all three groups.The efficacy indicators were significantly lower in the hydrogen water group compared with the conventional group. Before treatment, the serum NSE, IL-6, and TNF-α levels in the HIE groups were higher than those in the control group. After treatment, these levels in the hydrogen water group were lower than those in the conventional group.Hydrogen water lowers serum NSE, IL-6, and TNF-α levels in HIE newborns, thereby exerting a protective effect.

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

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