Immunohistochemistry and serum values of S-100B,  glial fibrillary acidic protein, and hyperphosphorylated  neurofilaments in brain injuries.
BACKGROUND
Traumatic brain injury (TBI) triggers a series of reactions resulting in cytoskeletal-related changes varying between focal and diffuse injuries.


METHODS
The patients (n=38) were divided into group of diffuse axonal injuries (DAI, n=10) and focal (n=28) injuries. Serum hyperphosphorylated neurofilaments (NF-H) and glial fibrillary acidic protein (GFAP) were measured by Biovendor immunoassay, and serum S-100B protein was measured by Cobas e411 (Roche) by immunoassay. Immunohistochemistry was performed with monoclonal antibodies (Chemicon, USA).


RESULTS
The median serum S-100B concentration was higher in patients with focal mass lesions (1.72±0.4 μg/l vs. 0.37±0.1 μg/l, p<0,05) compared to patients with DAI during 10 days of hospitalisation. With respect to all patients, the highest peak of serum S-100B values (4.21±1.1 μg/l) and GFAP (8.58±2.4 μg/l) were found in expansive lesions. The median serum NF-H was higher in DAI compared to focal TBI (0.625±0.14 vs 0.139±0.02 ng/l, p<0.05) during all 10 days after admission. Further, immunohistochemical investigation, in deceased patients with DAI , using NF-H antibody proved positive varicose and waving axons, and retraction balls. Time-dependent profile of serum NF-H demonstrated the increase of values within 4th up to 10th day in both groups. Values ranged from 0.263 up to 1.325 ng/l in DAI, and from 0.103 up to 1.108 ng/l in focal injuries. Patients with expansive contusions had similar levels of serum NF-H as patients without expansive lesions. Immunohistochemistry of cytoskeletal proteins presented strong positive staining of vinculin, vimentin in vessels, GFAP, and S-100B in DAI compared to weak staining in expansive lesions.


CONCLUSIONS
The time-profile kinetics of all markers may reflect different types of pathophysiological changes of the BBB or axonal damage in focal and diffuse injuries.


BACKGROUND
brain contusions - diffuse axonal injury - S-100B protein - GFAP - hyperphosphorylated neurofilaments.
Department of Forensic Medicine and Toxicology, Charles University 1st Medical Faculty, Prague, Poland.
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Vajtr
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Benada
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Linzer
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Sámal
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Springer
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Strejc
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Beran
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Průša
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Zima
D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D020833:Diffuse Axonal Injury / Q000378:metabolism / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D009414:Nerve Growth Factors / Q000097:blood / Q000378:metabolism*; D016900:Neurofilament Proteins / Q000378:metabolism*; D010766:Phosphorylation; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood / Q000378:metabolism*
D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D016900:Neurofilament Proteins; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins