Subarachnoid hemorrhage (SAH) elicits an inflammatory response in the subarachnoid space, which is mediated by the release of various cytokines. To assess their involvement in post-hemorrhagic complications, we determined the source and time-course of the release of inflammatory cytokines and acute-phase proteins in cerebrospinal fluid (CSF) following SAH. Concentrations of interleukin (IL)- 1beta, IL-6, transforming growth factor-beta1 (TGF-beta1) and C-reactive protein (CRP) in CSF of 36 patients with SAH were measured by enzyme-linked immunoabsorbent assay (ELISA). Floating cells collected from the CSF were centrifuged four to six days after SAH, and examined immunohistochemically. Intracellular IL-1beta and IL-6 were examined by flow cytometric analysis. The molecular weight of TGF-beta1 in CSF of 30 patients was examined by Western blot analysis. The TGF-beta1 levels of patients who had undergone ventriculoperitoneal (VP) shunt (n = 19) was significantly higher than nonshunt group (n = 16). The CRP levels of VP shunt group was significantly higher than nonshunt group. IL-6 concentration was maximal within day 0-1 and it was secreted by neutrophils and monocytes. ELISA showed consistently low levels of IL-1beta, whereas a proportion of monocytes and lymphcytes were IL- 1beta-positive by flow cytometric analysis. TGF-beta1 levels were also maximal on day 0-1 according to ELISA, although it tended to be in the inactive form derived from platelets. A 25 kDa band of TGF-1 was detectable for at least 13 days after SAH, which may have been secreted in part by neutrophils and monocytes. CRP levels in CSF peaked on day 2-3. The present results suggest that leukocytes induced by SAH play an important role in post-hemorrhagic inflammation in the subarachnoid space by releasing IL-6 and TGF-beta1. The CRP and TGF-beta1 levels in CSF are strongly concerned with communicating hydrocephalus after SAH.
Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional polypeptide that controls the production of extracellular matrix protein. Platelets store a large quantity of TGF-beta 1, which is released at hemorrhage. We recently reported that human recombinant TGF-beta 1 induced communicating hydrocephalus in mice. The aim of this study was to determine whether TGF-beta 1 is related to the development of communicating hydrocephalus after subarachnoid hemorrhage (SAH).
TGF-beta 1 in the cerebrospinal fluid of 24 patients with SAH was measured with enzyme-linked immunosorbent assay. The levels were compared between hydrocephalic and nonhydrocephalic groups. Western blot analysis was performed to determine active TGF-beta 1 in the cerebrospinal fluid.
TGF-beta 1 rapidly decreased from the onset of SAH. The level of TGF-beta 1 of 13 patients showing ventricular dilatation with periventricular low density on computed tomographic scan was 1.07 +/- 0.37 ng/mL on days 12 through 14, which was significantly higher than 0.52 +/- 0.21 ng/mL in patients without ventricular dilatation (P < .02). Furthermore, the TGF-beta 1 level of patients who had undergone ventriculoperitoneal shunt (n = 11) was 1.11 +/- 0.09 ng/mL on days 12 through 14, which was also higher than the level of the nonshunt group (n = 13) (0.56 +/- 0.22 ng/mL; P < .01). A 25-kD band was demonstrated by Western blot analysis in the cerebrospinal fluid of a patient with SAH.
Our results strongly suggest that TGF-beta 1 plays an important role in generating communicating hydrocephalus after SAH.
The factors related to poor outcomes were, age of 60 years or over, pre-operative Hunt & Kosnik grade II or more, Fisher Scale 3 or more, aneurysm size over 15 mm in diameter, and location at and around the basilar artery bifurcation. The results presented in this study show the status of our direct surgical management of subarachnoid haemorrhage in a large series with standardized surgical principles and procedures.
The authors reviewed 47 cases of infantile subdural fluid collection with regard to diagnosis and postoperative course after placement of a subdural-peritoneal shunt. CT scan with contrast enhancement proved to be an important diagnostic modality, showing vessels in the subarachnoid space as high-density spots. Utilizing this technique, we were able to differentiate the following varieties of fluid collection: (1) subdural fluid collection, in which enhancing vessels were seen on the brain surface, (2) subarachnoid fluid collection, in which vessels were on the inner table of the cranium, and (3) coexistence of subdural and subarachnoid fluid collections, in which vessels were between the inner table of the cranium and the brain surface. The postoperative course of subdural fluid collection was characterized as follows: (1) the subdural fluid collection decreased first, with increased subarachnoid fluid collection; (2) the subarachnoid fluid collection remained after the disappearance of subdural fluid collection; and (3) the brain expanded again later. Subdural fluid collection disappeared about 1 month after the shunt operation, which could lead occlusion of the shunt system. Postoperative enlargement of the subarachnoid space was an early indicator of the efficacy of the subdural-peritoneal shunt.
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