Stroke · 2008
Cerebrospinal fluid tenascin-C increases preceding the development of chronic shunt-dependent hydrocephalus after subarachnoid hemorrhage.
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Suzuki Hidenori, Kinoshita Noriaki, Imanaka-Yoshida Kyoko, Yoshida Toshimichi, Taki Waro
Аннотация
BACKGROUND AND PURPOSE: The possible cause of chronic hydrocephalus after subarachnoid hemorrhage (SAH) has been reported to be meningeal fibrosis. We examined whether the induction of tenascin-C (TN-C), an extracellular matrix glycoprotein known to promote tissue fibrosis, was associated with chronic hydrocephalus after SAH.
METHODS: We prospectively measured cerebrospinal fluid TN-C levels in 7 control patients with unruptured cerebral aneurysms and in 29 consecutive patients with aneurysmal SAH on days 1 to 12.
RESULTS: Cerebrospinal fluid TN-C levels were less than the diagnostic threshold level in control patients but markedly increased after SAH. Higher TN-C levels were observed in patients with more severe SAH on admission CT, ventricular drainage for acute obstructive hydrocephalus, and a worse outcome. Independent of these factors, however, cerebrospinal fluid TN-C levels were significantly higher in patients with than without subsequent chronic shunt-dependent hydrocephalus on days 1 to 9.
CONCLUSIONS: These findings suggest the possible involvement of TN-C in the development of chronic hydrocephalus after SAH and encourage further studies.
METHODS: We prospectively measured cerebrospinal fluid TN-C levels in 7 control patients with unruptured cerebral aneurysms and in 29 consecutive patients with aneurysmal SAH on days 1 to 12.
RESULTS: Cerebrospinal fluid TN-C levels were less than the diagnostic threshold level in control patients but markedly increased after SAH. Higher TN-C levels were observed in patients with more severe SAH on admission CT, ventricular drainage for acute obstructive hydrocephalus, and a worse outcome. Independent of these factors, however, cerebrospinal fluid TN-C levels were significantly higher in patients with than without subsequent chronic shunt-dependent hydrocephalus on days 1 to 9.
CONCLUSIONS: These findings suggest the possible involvement of TN-C in the development of chronic hydrocephalus after SAH and encourage further studies.