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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A technique for chronic cisternal cerebrospinal fluid (CSF) sampling in conscious rats was used to obtain multiple 50 microliters samples before and up to 7 days after middle cerebral artery occlusion. Neuron-specific enolase (NSE) concentrations were measured by radioimmunoassay using a readily available kit. The volume of infarction was measured by integrating the area of damage on 9 evenly spaced histological sections of the forebrain. This correlated well (r = 0.97, P less than 0.001) with the concentration of CSF neuron-specific enolase integrated over the first 5 days post occlusion, in animals with pure cortical and mixed cortical and striatal lesions. The correlation was maintained in animals given the NMDA antagonist MK-801. There was also a good correlation between the CSF NSE concentration 3 days post-MCAO and the volume of infarction (r = 0.92, P less than 0.01). It is therefore possible that CSF neuron-specific enolase may be useful as a quantitative marker of ischaemic damage in humans and provide a useful adjunct in the assessment of neuroprotective drugs in stroke.
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PMID:CSF neuron-specific enolase as a quantitative marker of neuronal damage in a rat stroke model. 160 99

Changes of neuron-specific enolase (NSE) in cerebrospinal fluid after experimental ischaemic stroke caused by middle cerebral artery occlusion in rat were studied. High enzyme levels were found between the second and seventh day after artery occlusion and they correlated well with the extension of infarct seen in histology. NSE levels in cerebrospinal fluid are sensitive and reliable markers of brain tissue damage during the acute phase of ischaemic stroke.
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PMID:[Usefulness of determining the level of neuron-specific enolase (NSE) in the cerebrospinal fluid as a biochemical indicator of the extent of cerebral ischemic stroke. Experimental study of the rat model of stroke]. 263 19

Neuron-specific enolase concentrations were measured in samples of rat cerebrospinal fluid obtained repeatedly before and after occlusion of the middle cerebral artery. A method for reliable, repeated sampling of cisternal cerebrospinal fluid was developed for this purpose. Occlusion of the middle cerebral artery induced cerebral infarcts of slightly variable size with good correlation to raised neuron-specific enolase concentrations. Sham operation caused only superficial cortical damage at the site of surgery and was followed by an early, slight, and transient increase in neuron-specific enolase concentration. With our technique, the development of cerebral infarcts can be studied in individual rats under experimentally controlled conditions over an extended period of time. Analysis of neuron-specific enolase can be used in trials of drugs for mitigating the effect of ischemia. Information concerning the release of neuron-specific enolase from ischemic cerebral tissue to the cerebrospinal fluid is important because neuron-specific enolase in the cerebrospinal fluid can be determined in patients suffering from cerebrovascular insult.
Stroke 1988 Sep
PMID:Neuron-specific enolase is a marker of cerebral ischemia and infarct size in rat cerebrospinal fluid. 341 12

The development of a radioimmunoassay for S-100 protein is described. This method was used in combination with a recently developed radioimmunoassay for neuron-specific enolase in cerebrospinal fluid and serum from 47 patients with cerebral infarction, transient ischemic attack, intracerebral hemorrhage, subarachnoid hemorrhage, and head injury. In cerebrospinal fluid, increased concentrations of both S-100 and neuron-specific enolase were found after large infarcts, whereas after small infarcts and transient ischemic attacks, only neuron-specific enolase increased. The increased concentrations of S-100 and/or neuron-specific enolase were noted 18 hours to 4 days after cerebral infarction and transient ischemic attacks. Cerebrospinal fluid concentrations of these proteins also reflected the severity of the disease in patients with intracerebral hematoma, subarachnoid hemorrhage, or head injury. Temporal changes in serum S-100 and neuron-specific enolase concentrations reflected the clinical course in 4 patients. In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.
Stroke
PMID:S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system. 362 51

This study relates the level of alpha and gamma enolase in cerebrospinal fluid sampled within 4 days of a stroke to the volume of the cerebral infarct measured on the CT image and to the clinical outcome of the patient. Twenty-eight patients were studied, two with transient ischaemic attacks and 26 with completed stroke due to infarction. The cerebrospinal fluid enolase was raised in the two patients with transient ischaemic attacks and 23 with completed stroke. There was a positive correlation between the volume of the infarct and the level of cerebrospinal fluid alpha and gamma enolase. A high cerebrospinal fluid enolase was always associated with a poor prognosis.
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PMID:Cerebrospinal fluid enolase in stroke. 674 47

In this study levels of neuron-specific enolase (NSE), S-100 protein (S-100) and myelin basic protein (MBP) in cerebrospinal fluid (CSF) of children and adults with distinct neurological disorders were examined. A previous study from our department demonstrated age related reference values for these brain-specific proteins in CSF. The median concentration level of the 3 proteins in 17 different neurological disease groups versus the reference group was compared. Significantly higher MBP values were observed in patients with multiple sclerosis (MS), cerebrovascular accident (CVA), metabolic disorder and infection. Furthermore, significantly higher values were demonstrated for S-100 in CVA and for NSE in metabolic diseases. In CVA, the NSE and S-100 values were significantly related with MBP values, whereas in MS the NSE and S-100 were not related with MBP values.
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PMID:Cerebrospinal neuron-specific enolase, S-100 and myelin basic protein in neurological disorders. 748 80

Neuron-specific enolase (NSE) is a sensitive marker of brain injury after stroke, global ischemia, and coma. We report changes in serum NSE (s-NSE) in 19 patients who sustained status epilepticus. s-NSE peaked within 24 to 48 hours after status epilepticus. The mean peak s-NSE level for the entire group was elevated compared with the levels for normal controls (24.87 ng/ml versus 5.36 ng/ml, p = 0.0001) and for epileptic controls (24.87 ng/ml versus 4.61 ng/ml, p = 0.0001). The mean peak s-NSE level for the 11 subjects without an acute neurologic insult (15.44 ng/ml) was also significantly increased compared with levels for normal and epileptic controls. Further, s-NSE was significantly correlated with outcome and duration. We conclude that s-NSE is a promising in vivo marker of brain injury in status epilepticus and warrants further study in larger populations.
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PMID:Serum neuron-specific enolase in human status epilepticus. 864 98

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in acute ischemic stroke patients as compared with the controls. The altered CSF NSE levels correlated well with the infarct size in CT scan. The CSF NSE levels were higher in 6-multiinfarct dementia (MID) patients who were diagnosed after 6-month follow-up than those in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE in the study of dementia related to ischemic stroke is worth further studies.
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PMID:Neuron-specific enolase in patients with acute ischemic stroke and related dementia. 779 31

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in patients with acute ischemic stroke as compared with the controls. The altered CSF NSE levels were well correlated with the infarct size in CT scan. The CSF NSE levels were higher in 6-patients who were diagnosed as multi-infarct dementia (MID) after 6-month follow-up than in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE for dementia related to ischemic stroke is worth further studying.
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PMID:[Neuro-specific enolase in acute ischemic stroke and related dementia patients]. 920 70

Thirteen patients resuscitated after circulatory arrest due to cardiopulmonary aetiologies were studied with regard to survival and outcome. Exclusion criteria were known central nervous system disorders or death secondary to cerebrovascular accident. The serum level of neuron-specific enolase (NSE), presumably a reliable marker of neuronal death, was measured by enzyme immunoassay in peripheral blood samples over the course of 4 days at 12 h intervals. On the first and third day post-resuscitation, median nerve somatosensory evoked potentials (SSEPs) were recorded and evaluated for the absence of the cortical potential--presently the standard approach for assessing prognosis in terms of post-resuscitation hypoxaemic brain damage. Absent cortical potentials were found in six patients with NSE levels above 140 micrograms l-1. Five of these patients died; one patient survived with loss of cortical functioning. Five patients had normal SSEP findings, and their NSE maximum levels were below 25 micrograms l-1. All five patients survived without neurological deficits. One patient with a peak NSE level of 36 micrograms l-1 on the second day developed a prolonged delirium (according to DSM III-R criteria) and one patient with a peak level of 76 micrograms l-1 on the fourth day developed an acute respiratory distress syndrome; both patients had preserved cortical potentials. In conclusion, pathological SSEPs and increased NSE levels are of comparable prognostic value. They may well be complementary investigations. The neuron-bound enzyme NSE is a biochemical marker which varies with the extent of neuronal damage, while absence of the cortical potentials may indicate neurophysiological loss of function.
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PMID:A comparison of the prognostic value of neuron-specific enolase serum levels and somatosensory evoked potentials in 13 reanimated patients. 942 76


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