Neuron-specific enolase in cerebrospinal fluid as a biomarker of brain damage in infants with hypoxic-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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Biomarkers of Hypoxic-Ischemic Encephalopathy in Newborns

World Journal of Peri & Neonatology ◽

10.18502/wjpn.v3i1.5063 ◽

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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