In fact, the NSE concentration in serum increase 2–3 h after onset of first stroke, afterwards, NSE decreased, followed by a secondary increase until day 5, that is the last measurement in the observation period; the secondary increase indicates further release of NSE, which probably reflects a secondary mechanism of brain damage, ongoing neuronal cell death (98, 99), or persistent disturbance of the blood–brain barrier (131). Here, ENO2 is linked to stroke disorder.