Assessment of cerebral S100B levels by proton magnetic resonance spectroscopy after lateral fluid-percussion injury in the rat.
OBJECTIVE
After traumatic brain injury (TBI), S100B protein is released by astrocytes. Furthermore, cerebrospinal fluid (CSF) and serum S100B levels have been correlated to outcome. Given that no data exist about the temporal profile of cerebral S100B levels following TBI and their correlation to serum levels, the authors examined whether proton magnetic resonance (MR) spectroscopy is capable of measuring S100B.


METHODS
Results of in vitro proton MR spectroscopy experiments (2.35-tesla magnet, 25 G/cm, point-resolved spatially localized spectroscopy) revealed an Sl00B-specific peak at 4.5 ppm and confirmed a positive correlation between different S100B concentrations (10 nM-1 microM) and the area under the curve (AUC) for the S100B peak (r = 0.991, p < 0.001). Thereafter, proton MR spectroscopy was performed in male Sprague-Dawley rats (7 X 5 X 5-mm voxel in each hemisphere, TR 3000 msec, TE 30 msec, 256 acquisitions). Exogenously increased CSF S100B levels (approximately 200 ng/ml) through the intraventricular infusion of S100B increased the AUC of the S100B peak from 0.06 +/- 0.02 to 0.44 +/- 0.06 (p < 0.05), whereas serum S100B levels remained normal. Two hours after lateral fluid-percussion injury, serum S100B levels increased to 0.61 +/- 0.09 ng/ml (p < 0.01) and rapidly returned to normal levels, whereas the AUC of the S100B peak increased to 0.19 +/- 0.04 at 2 hours postinjury and 0.41 +/- 0.07 (p < 0.05) on Day 5 postinjury.


CONCLUSIONS
Proton MR spectroscopy proves a strong correlation between the AUC of the S100B peak and S100B concentrations. Following experimental TBI, serum S100B levels increased for only a very short period, whereas cerebral S100B levels were increased up to Day 5 postinjury. Given that experimental data indicate that S100B is actively released following TBI, proton MR spectroscopy may represent a new tool to identify increased cerebral S100B levels in patients after injury, thus allowing its biological function to be better understood.
Kleindienst
Andrea
A
Department of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0508, USA. akleindienst@vcu.edu
Tolias
Christos M
CM
Corwin
Frank D
FD
Müller
Christian
C
Marmarou
Anthony
A
Fatouros
Panos
P
Bullock
M Ross
MR
D000818:Animals; D015415:Biomarkers; D001930:Brain Injuries / Q000097:blood* / Q000175:diagnosis; D005240:Feasibility Studies; D007276:Injections, Intraventricular; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D009414:Nerve Growth Factors / Q000097:blood* / Q000494:pharmacology; D011379:Prognosis; D011522:Protons; D051381:Rats; D017207:Rats, Sprague-Dawley; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood* / Q000494:pharmacology; D012720:Severity of Illness Index
D015415:Biomarkers; D009414:Nerve Growth Factors; D011522:Protons; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; C579158:S100b protein, rat