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Clin Neurol Neurosurg. 2006 Sep;108(6):558-63. Epub 2006 Feb 2.

Neuron-specific enolase and tau protein as neurobiochemical markers of neuronal damage are related to early clinical course and long-term outcome in acute ischemic stroke.

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Department of Neurology, Otto-von-Guericke-University of Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany.



Analyses of neuron-specific enolase (NSE) and tau protein in patients with hyperacute ischemic stroke, their association with infarct volume, severity of the neurological deficit, the neurovascular status and functional outcome.


In 66 consecutive patients, serial venous blood samples were taken at 3, 6, 12, 18, 24, 48, 72, 96, and 120 h after stroke onset. The neurovascular status was assessed by repetitive extra- and transcranial duplex sonography. Neurological deficits were quantified by the NIH stroke scale, and functional outcome was assessed with the modified Rankin scale (mRS).


After a first rise within 3 h, NSE decreased followed by a secondary increase until Day 5. Tau protein concentrations showed a continuous increase from admission onward. NSE and tau release were highly correlated with severity of neurological deficits and infarct volume (P = 0.001). NSE, but not tau protein, release was associated to the neurovascular status on admission. NSE and tau protein values were significantly correlated with the functional outcome at 3 months (P < 0.001).


Release kinetics of NSE and tau protein are associated with patients' clinical deficits and infarct volume, and may be used as an additional predictor of the early course and functional outcome.

[Indexed for MEDLINE]

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