Neuron Specific Enolase — an Indicator of Brain Damage due to Hypoxia in Newborns and Adults

1983 ◽  
pp. 71-74 ◽  
Author(s):  
J. GROSS ◽  
P.J. MARANGOS ◽  
V. BENDER ◽  
R. DAUBERSCHMIDT ◽  
E.P. ISSEL ◽  
...  
Keyword(s):  
Brain Damage ◽  
Neuron Specific Enolase

scholarly journals Cerebral damage pathogeny peculiarities in local and globalcerebral perfusion impairment models in rats

2017 ◽  
Vol 8 (6) ◽  
pp. 62-71
Author(s):  
Maria A. Zelenenko ◽  
Valeria A. Pechatnikova ◽  
Vassiliy A. Zaplutanov ◽  
Nikolay V. Tsygan ◽  
Nikolay A. Verlov ◽  
...  
Keyword(s):  
Brain Damage ◽  
Vascular Endothelium ◽  
Cerebral Circulation ◽  
Carotid Arteries ◽  
Considerable Increase ◽  
Neuron Specific Enolase ◽  
Experimental Models ◽  
Pronounced Difference ◽  
Damage Site ◽  
S100β Protein

A complex study of clinical and laboratory pathogenic features of cerebrovascular disease has been performed in rats using two experimental models: local ischemia with cerebral infarction and global ischemia caused by acute or chronic impairment of cerebral circulation without verified site of brain damage. A pronounced difference has been demonstrated between the two studied models of cerebral impairment. The development of brain damage site constituting 20-30% of the total cortex of the impaired hemisphere was demonstrated to be accompanied by a considerable increase of basic nervous tissue damage markers (neuron-specific enolase, S100β-protein), development of endothelial dysfunction and hemostasiological disturbances. Irreparable cerebral circulation impairment by ligation of carotid arteries was followed by considerably lower lethality in the experimental animals, neurospecific markers’ moderate dynamics but however side by side with pronounced and inadequately compensated manifestations in the hemostasis system and vascular endothelium caused by brain hypoxia.

SERUM NEURON ??? SPECIFIC ENOLASE AS A PROGNOSTIC MAKER FOR HYPOXIC BRAIN DAMAGE AFTER CARDIAC ARREST IN MAN

Shock ◽  
1995 ◽  
Vol 4 (Supplement) ◽  
pp. 58
Author(s):  
Hitoshi Imaizumi ◽  
Masashi Yoshida ◽  
Morihito Satoh ◽  
Yasuo Shichinohe ◽  
Tomoyuki Kawamata ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Damage ◽  
Neuron Specific Enolase ◽  
Hypoxic Brain Damage ◽  
Hypoxic Brain ◽  
Prognostic Maker ◽  
Serum Neuron Specific Enolase

S-100 protein and neuron-specific enolase in CSF after experimental traumatic or focal ischemic brain damage

1989 ◽  
Vol 71 (5) ◽  
pp. 727-731 ◽  
Author(s):  
Hans-Göran Hårdemark ◽  
Nils Ericsson ◽  
Zbigniew Kotwica ◽  
Gerd Rundström ◽  
Ib Mendel-Hartvig ◽  
...  
Keyword(s):  
Clinical Practice ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Neuron Specific Enolase ◽  
Experimental Models ◽  
Neurological Injury ◽  
Content Type ◽  
Mca Occlusion ◽  
S 100 ◽  
Fine Print

✓ Cerebrospinal fluid (CSF) markers of brain damage are potentially capable of providing quantitative information about the extent of certain neurological injury. The presence of such markers in CSF after brain damage is transient and it is essential to understand their kinetics if they are to be used in clinical practice. In the present study, the CSF concentrations of two neurospecific proteins, S-100 protein and neuron-specific enolase (NSE), were determined in rats before and repeatedly after one of two types of experimental brain damage: traumatic cortical injury and focal cerebral ischemia induced by middle cerebral artery (MCA) occlusion. The two types of experimental brain damage resulted in significant differences in the kinetics of S-100 and NSE concentrations in CSF. Cortical contusion was followed by a rapid increase in both S-100 and NSE and a peak occurred in both after about 7½ hours, at which time the values declined toward normal. A second, smaller peak was seen after about 1½ days. The increase and decrease in S-100 and NSE levels in CSF was slower after MCA occlusion; a peak was seen after 2 to 4 days. Furthermore, S-100 was generally higher than NSE after trauma, whereas after MCA occlusion the NSE concentration was slightly higher than the S-100 value. These results support the use of CSF markers for estimation of the extent of brain damage in experimental models and forms a basis for the understanding of their kinetics, which is important for their use in clinical practice.

scholarly journals NEURON SPECIFIC ENOLASE (NSE)IN PRETERM BABIES WITH BRAIN DAMAGE

1992 ◽  
Vol 32 (5) ◽  
pp. 630-630 ◽  
Author(s):  
Adelina Pellicer ◽  
Fernando Cabanas ◽  
Alfredo García-Alix ◽  
Angel Hernanz ◽  
Tom A Stiris ◽  
...  
Keyword(s):  
Brain Damage ◽  
Neuron Specific Enolase ◽  
Preterm Babies

Increased serum creatine kinase BB and neuron specific enolase following head injury indicates brain damage

1992 ◽  
Vol 115 (3-4) ◽  
pp. 106-111 ◽  
Author(s):  
I. M. Skogseid ◽  
H. K. Nordby ◽  
P. Urdal ◽  
E. Paus ◽  
F. Lilleaas
Keyword(s):  
Creatine Kinase ◽  
Head Injury ◽  
Brain Damage ◽  
Neuron Specific Enolase ◽  
Serum Creatine Kinase ◽  
Creatine Kinase Bb

scholarly journals Brain injury markers (S100B and NSE) in chronic cocaine dependents

2007 ◽  
Vol 29 (2) ◽  
pp. 134-139 ◽  
Author(s):  
Felix Henrique Paim Kessler ◽  
George Woody ◽  
Luís Valmor Cruz Portela ◽  
Adriano Bretanha Lopes Tort ◽  
Raquel De Boni ◽  
...  
Keyword(s):  
Brain Damage ◽  
Illicit Drugs ◽  
Cell Injury ◽  
Neuron Specific Enolase ◽  
Serum Levels ◽  
Blood Levels ◽  
Probabilistic Sampling ◽  
Chronic Cocaine ◽  
Cocaine Users ◽  
Serum Neuron Specific Enolase

OBJECTIVE: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs. METHOD: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay. RESULTS: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 ± 0.04 µg/l among cocaine users and 0.08 ± 0.04 µg/l among controls. Mean serum neuron specific enolase level was 9.7 ± 3.5 ng/l among cocaine users and 8.3 ± 2.6 ng/l among controls. CONCLUSIONS: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.

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