TY - JOUR
T1 - Comparison of cerebrospinal fluid biomarkers between idiopathic normal pressure hydrocephalus and subarachnoid hemorrhage-induced chronic hydrocephalus
T2 - A pilot study
AU - Lee, Jeong Hyun
AU - Park, Dong Hyuk
AU - Back, Dong Bin
AU - Lee, Jea Young
AU - Lee, Chang In
AU - Park, Kyung Jae
AU - Kang, Shin Hyuk
AU - Cho, Tai Hyoung
AU - Chung, Yong Gu
PY - 2012
Y1 - 2012
N2 - Background: We examined the cerebrospinal fluid (CSF) markers of subarachnoid hemorrhage (SAH)-induced and idiopathic normal pressure hydrocephalus (INPH) to investigate the pathophysiology and mechanism of communicating hydrocephalus compared to obstructive hydrocephalus. Material/Methods: We obtained CSF samples from 8 INPH, 10 SAH-induced hydrocephalus, and 6 unmatched patients with non-hemorrhagic obstructive hydrocephalus during their ventriculoperitoneal shunt operations. Transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-a, vascular endothelial growth factor (VEGF), and total tau in the CSF were analyzed via enzyme-linked immunosorbent assay. Results: The mean VEGF levels in the CSF of patients with SAH-induced hydrocephalus, INPH, and obstructive hydrocephalus were 239±131, 239±75, and 163±122 pg/mL, respectively. The total tau concentrations in the CSF of the groups were 1139±1900, 325±325, and 1550±2886 pg/mL, respectively. TNF-α values were 114±34, 134±38, and 55±16 pg/mL, respectively. TGF-β1 values were 953±430, 869±447, and 136±63 pg/mL, respectively. A significant difference in TNF-α and TGF-β1 levels was observed only between SAH-induced and chronic obstructive hydrocephalus, and between INPH and chronic obstructive hydrocephalus (p<0.01). Conclusions: No significant differences in the 4 CSF biomarker levels were observed between INPH and SAHinduced hydrocephalus, whereas CSF TNF-α and TGF-β1 levels were increased compared to those in patients with chronic obstructive hydrocephalus. Post-SAH hydrocephalus and INPH are probably more destructive to neural tissues, and then stimulate the inflammatory reaction and healing process, compared with obstructive hydrocephalus.
AB - Background: We examined the cerebrospinal fluid (CSF) markers of subarachnoid hemorrhage (SAH)-induced and idiopathic normal pressure hydrocephalus (INPH) to investigate the pathophysiology and mechanism of communicating hydrocephalus compared to obstructive hydrocephalus. Material/Methods: We obtained CSF samples from 8 INPH, 10 SAH-induced hydrocephalus, and 6 unmatched patients with non-hemorrhagic obstructive hydrocephalus during their ventriculoperitoneal shunt operations. Transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-a, vascular endothelial growth factor (VEGF), and total tau in the CSF were analyzed via enzyme-linked immunosorbent assay. Results: The mean VEGF levels in the CSF of patients with SAH-induced hydrocephalus, INPH, and obstructive hydrocephalus were 239±131, 239±75, and 163±122 pg/mL, respectively. The total tau concentrations in the CSF of the groups were 1139±1900, 325±325, and 1550±2886 pg/mL, respectively. TNF-α values were 114±34, 134±38, and 55±16 pg/mL, respectively. TGF-β1 values were 953±430, 869±447, and 136±63 pg/mL, respectively. A significant difference in TNF-α and TGF-β1 levels was observed only between SAH-induced and chronic obstructive hydrocephalus, and between INPH and chronic obstructive hydrocephalus (p<0.01). Conclusions: No significant differences in the 4 CSF biomarker levels were observed between INPH and SAHinduced hydrocephalus, whereas CSF TNF-α and TGF-β1 levels were increased compared to those in patients with chronic obstructive hydrocephalus. Post-SAH hydrocephalus and INPH are probably more destructive to neural tissues, and then stimulate the inflammatory reaction and healing process, compared with obstructive hydrocephalus.
KW - Cerebrospinal fluid
KW - Normal pressure hydrocephalus
KW - Subarachnoid hemorrhage
KW - Total tau
KW - Transforming growth factor-β1
KW - Tumor necrosis factor-α
KW - Vascular endothelial growth factor
UR - http://www.scopus.com/inward/record.url?scp=84874777168&partnerID=8YFLogxK
U2 - 10.12659/msm.883586
DO - 10.12659/msm.883586
M3 - Article
C2 - 23197244
AN - SCOPUS:84874777168
SN - 1234-1010
VL - 18
SP - BR19-BR25
JO - Medical Science Monitor
JF - Medical Science Monitor
IS - 12
ER -