Neuron-specific enolase as a marker of cerebral tissue lesion in patients with ischemic stroke


  • S.M. Stadnik Military Medical Clinical Center of Western region, Lviv, Ukraine
  • O.V. Saiko Military Medical Clinical Center of Western region, Lviv, Ukraine
  • O.I. Dumchenko Military Medical Clinical Center of Western region, Lviv, Ukraine



ischemic stroke, chronic brain ischemia, neuron-specific enolase, neurologic deficit, cognitive disorders


Background. A promising direction in modern angioneurology is the study of markers of brain tissue damage in the blood serum of patients in the acute period of ischemic stroke and their comparison with the initial level of neurologic deficit and stroke outcome. As a marker of brain tissue damage, the functions of neuron-specific enolase (NSE) are being actively studied. To evaluate the level of NSE in the acute period of ischemic stroke was the purpose of the work. Materials and methods. The clinical trial included 151 patients (mean age 61.5 ± 8.2 years), who were divided into 2 groups: group 1 consisted of 85 patients with acute ischemic stroke; group 2 — of 66 patients with chronic cerebral ischemia. Plasma NSE level was evaluated in all patients. We analyzed the correlations of NSE with the severity of neurologic deficit according to the National Institutes of Health Stroke Scale, functional activity — using Barthel index, the level of disabi­lity — on the modified Rankin scale, and the severity of cognitive impairment — according to the Mini-Mental State Examination. The relationships between the level of NSE and the survival of patients with ischemic stroke were determined. Results. In patients of group 1, the level of NSE exceeded that of the patients in group 2 by 3.8 times (p < 0.001). We established significant differences in the level of NSE depending on the location of the ischemic focus — involving the left middle cerebral artery and the vertebrobasilar bed (p = 0.04). In patients with severe neurologic deficit, NSE level exceeded that of patients with moderate and mild neurologic deficit by 1.3 (p = 0.251) and 2.3 (p = 0.007) times, respectively. A correlation was found between the level of NSE and the severity of neurologic deficit (r = 0.67, p = 0.027), which indicates a direct relationship between the degree of ischemic injury and neurological disorders. In patients with severe cognitive impairment, the level of NSE exceeded that of patients with moderate and mild cognitive impairment by 1.2 (p = 0.444) and 1.9 (p = 0.037) times, respectively. When assessing the relationship between the level of NSE and stroke outcome, a tendency to higher NSE was revealed in the group of deceased people (p = 0.083). The threshold NSE value in the blood of patients with ischemic stroke was determined — 40 ng/ml. Conclusions. Determination of NSE in plasma confirms the degree of damage to neurons and is an informative indicator for the presence of neurologic deficit in patients with acute ischemic stroke. The results indicate the potential role of evaluating the content of NSE in improving the stratification of the risk of death in patients with ischemic stroke.


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