title: Release of neurobiochemical markers of brain damage is related to the neurovascular status on admission and the site of arterial occlusion in acute ischemic stroke.
abstract: OBJECTIVE
  The study aimed at an analysis of the kinetics of protein S100B and neuron-specific enolase (NSE) and their relation to the site of arterial occlusion in patients with acute ischemic stroke.
  
  
  METHODS
  We investigated 32 consecutive patients admitted within 6 h after stroke onset. Serial venous blood samples were taken hourly between 1 and 6 h, and at 12, 18, 24, 48, 72, 96, and 120 h after stroke onset. The neurovascular status was assessed on admission and monitored by repetitive extracranial and transcranial duplex sonography. In all patients, infarct volume was calculated. The neurological deficit was quantified by the National Institutes of Health stroke scale score, and functional outcome after 3 months was assessed with the modified Rankin Scale.
  
  
  RESULTS
  Patients with normal flow velocities in basal cerebral arteries at admission showed significantly less S100B release than those with main stem or multiple branch occlusions (p<0.01). S100B cut-off values of 0.15 microg/l (between 6 and 18 h), 0.21 microg/l (between 24 and 48 h) and 0.5 microg/l (from 72 to 120 h) differentiated best between patients with initially normal and pathological sonographic vessel findings. The release of S100B and NSE was highly correlated with the severity of the corresponding neurological deficit as well as with the final infarct volume. S100B concentrations from 6 h on were associated with the functional outcome. S100B values 48 h after stroke above 0.2 microg/l indicated a poor functional status 3 months after stroke.
  
  
  CONCLUSIONS
  Protein S100B may serve as a monitoring parameter in acute ischemic stroke, especially with respect to the neurovascular status. Furthermore, S100B obtains additional information about functional outcome.
authors.affiliation: Department of Neurology, Otto-von-Guericke-University Magdeburg, Germany. Michael.Wunderlich@medizin.uni-magdeburg.de
authors.forename: Michael T
authors.initials: MT
authors.lastname: Wunderlich
authors.forename: Claus-W
authors.initials: CW
authors.lastname: Wallesch
authors.forename: Michael
authors.initials: M
authors.lastname: Goertler
mesh_terms: D000328:Adult; D000368:Aged; D019540:Area Under Curve; D015415:Biomarkers / Q000097:blood; D001923:Brain Chemistry; D001930:Brain Injuries / Q000097:blood* / Q000209:etiology; D002539:Cerebral Arterial Diseases / Q000150:complications*; D003710:Demography; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009414:Nerve Growth Factors / Q000097:blood; D010751:Phosphopyruvate Hydratase / Q000097:blood; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood; D018709:Statistics, Nonparametric; D020521:Stroke / Q000097:blood* / Q000145:classification / Q000150:complications; D013997:Time Factors
chemical_list: D015415:Biomarkers; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; C579160:S100B protein, human; D010751:Phosphopyruvate Hydratase