Thrombin induced TGF-β1 pathway: a cause of communicating hydrocephalus post subarachnoid hemorrhage

2010 ◽  
Vol 34 (8) ◽  
pp. S19-S19
Author(s):  
Tong Li ◽  
Peng Zhang ◽  
Bin Yuan ◽  
Dongliang Zhao ◽  
Yueqin Chen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Communicating Hydrocephalus ◽  
Tgf Β1

scholarly journals Thrombin-induced TGF-β1 pathway: A cause of communicating hydrocephalus post subarachnoid hemorrhage

2013 ◽  
Vol 31 (3) ◽  
pp. 660-666 ◽  
Author(s):  
TONG LI ◽  
PENG ZHANG ◽  
BIN YUAN ◽  
DONGLIANG ZHAO ◽  
YUEQIN CHEN ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Communicating Hydrocephalus ◽  
Tgf Β1

Human arachnoid villi response to subarachnoid hemorrhage: possible relationship to chronic hydrocephalus

1999 ◽  
Vol 91 (1) ◽  
pp. 80-84 ◽  
Author(s):  
Eric M. Massicotte ◽  
Marc R. Del Bigio
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cellular Proliferation ◽  
Communicating Hydrocephalus ◽  
Csf Flow ◽  
Content Type ◽  
Arachnoid Villi ◽  
Cell Accumulation ◽  
Flow Through ◽  
The Relationship ◽  
Fine Print

Object. The origin of chronic communicating hydrocephalus following subarachnoid hemorrhage (SAH) is not well understood. Fibrosis of the arachnoid villi has been suggested as the cause for obstruction of cerebrospinal fluid (CSF) flow, but this is not well supported in the literature. The goal of this study was to determine the relationship between blood, inflammation, and cellular proliferation in arachnoid villi after SAH.Methods. Arachnoid villi from 50 adult patients were sampled at autopsy. All specimens were subjected to a variety of histochemical and immunohistochemical stains. The 23 cases of SAH consisted of patients in whom an autopsy was performed 12 hours to 34 years post-SAH. Fifteen cases were identified as moderate-to-severe SAH, with varying degrees of hydrocephalus. In comparison with 27 age-matched non-SAH controls, the authors observed blood and inflammation within the arachnoid villi during the 1st week after SAH. Greater mitotic activity was also noted among arachnoid cap cells. The patient with chronic SAH presented with ventriculomegaly 2 months post-SAH and exhibited remarkable arachnoid cap cell accumulation.Conclusions. The authors postulate that proliferation of arachnoidal cells, triggered by the inflammatory reaction or blood clotting products, could result in obstruction of CSF flow through arachnoid villi into the venous sinuses. This does not exclude the possibility that SAH causes generalized fibrosis in the subarachnoid space.

A murine model of communicating hydrocephalus: Role of TGF-β1

1997 ◽  
Vol 4 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Miki Kanaji ◽  
Tsuyoshi Tada ◽  
Shigeaki Kobayashi
Keyword(s):  
Murine Model ◽  
Communicating Hydrocephalus ◽  
Tgf Β1

Abstract T P403: Permanent Ventricular Shunting In Subarachnoid Hemorrhage And Intracerebral Hemorrhage Patients Requiring Temporary Ventriculostomy

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yogesh Moradiya ◽  
Santosh Murthy ◽  
Christa San Luis ◽  
Daniel Hanley ◽  
Wendy Ziai
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracerebral Hemorrhage ◽  
Large Scale ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Communicating Hydrocephalus ◽  
Increasing Trend ◽  
Sample Weighting ◽  
Baseline Characteristics ◽  
Aneurysm Coiling ◽  
Ventricular Shunting

Background and Purpose: Aneurysmal subarachnoid hemorrhage (SAH) and spontaneous intracerebral hemorrhage (ICH) frequently lead to obstructive and/or communicating hydrocephalus. A permanent ventricular shunt is required in cases with failure to wean ventriculostomy. Large-scale studies comparing rates of ventricular shunting after SAH and ICH are lacking. Therefore, we studied the rates of shunting among SAH and ICH requiring ventriculostomy. Methods: We analyzed the Nationwide Inpatient Sample, a 20% sample of non-federal hospitalizations in US from 2002 to 2011 to select adults with ICH (ICD-9 code 431) and SAH (430) undergoing ventriculostomy (02.2, 02.21). We excluded patients surviving <7 days after ventriculostomy. We compared rates of ventricular shunting (02.32-02.34) between SAH and ICH after adjusting for baseline characteristics using logistic regression. Population estimates were obtained using sample weighting. Results: 23,541 cases with ICH (median age 59 y) and 31,883 cases with SAH (median age 56 y) were included. Unadjusted shunting rate was higher in SAH compared to ICH (19.9% vs 11.4%, P<0.001), and it remained higher in SAH in multivariate analysis (adjusted OR: 1.69; 95% CI: 1.45-1.98, P<0.001). There was no difference in the interval between ventriculostomy and shunting between SAH and ICH (mean: 18.9 +/- 11.8 [SD] vs 18.1 +/- 10.9 days, P=0.196). Among SAH cases, shunting rate was higher with coiling compared to clipping (23.8% vs 18.1%, P<0.001). There was a significant trend toward higher shunt utilization over time among SAH patients (16.3% in 2002-03 to 21.4% in 2010-11, trend P<0.001). The shunting rate remained unchanged among ICH patients (11.3% in 2002-03 to 11.5% in 2010-11, trend P=0.363). Patients requiring ventriculostomy within 24 hours of admission comprised 61.8% of all cases, and had higher shunting rate (adjusted OR: 1.17; 95% CI: 1.07-1.28, P=0.001). Conclusions: SAH compared to ICH has higher rates of failure to wean ventriculostomy requiring permanent ventricular shunting. Increasing trend in shunt utilization after SAH is co-incident with increase in aneurysm coiling during recent years.

Lumbar Drain

2019 ◽  
pp. 907-911
Author(s):  
Jamie J. Van Gompel
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cord Blood ◽  
Low Risk ◽  
Communicating Hydrocephalus ◽  
Spinal Cord Blood Flow ◽  
Lumbar Drain ◽  
Csf Leaks

Lumbar drainage has a major role in neurosurgical and neurocritical care procedures. Lumbar drain insertion is a simple and, when done well, low-risk procedure. A lumbar drain is often necessary in the management of perioperative cerebrospinal fluid (CSF) leaks, the most common use, but it may be beneficial for patients with subarachnoid hemorrhage and communicating hydrocephalus and for patients undergoing surgery involving the aorta with possible damage to the spinal cord. CSF removal optimizes spinal cord blood flow. This chapter describes lumbar drain insertion and some of the associated perils and pitfalls.

Ventricular dilatation and communicating hydrocephalus following spontaneous subarachnoid hemorrhage

1979 ◽  
Vol 51 (3) ◽  
pp. 341-351 ◽  
Author(s):  
John Vassilouthis ◽  
Alan E. Richardson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ventricular Dilatation ◽  
Communicating Hydrocephalus ◽  
Content Type ◽  
Clinically Significant ◽  
Definitive Surgery ◽  
Two Phases ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Shunting System ◽  
Ventricular Shunting

✓ Ventricular dilatation following spontaneous subarachnoid hemorrhage (SAH) is a well recognized phenomenon. Its clinical significance, however, remains controversial. Two phases are distinguished, the acute or early, occurring soon after the ictus, and the chronic or late, developing after the second week. The authors studied the ventricular size in 210 patients with spontaneous SAH through the course of their illness and convalescence by means of serial computerized tomography (CT) scans. Their findings suggest that ventricular dilatation soon after SAH is not always clinically significant and does not necessarily require shunting before definitive surgery. Delayed symptomatic ventricular enlargement (communicating hydrocephalus) occurs in 7% of the patients and can be safely diagnosed on the basis of the clinical picture and CT scan appearances. Treatment with a ventricular shunting system is almost invariably rewarding.

Hydrocephalus following spontaneous subarachnoid hemorrhage

1973 ◽  
Vol 39 (4) ◽  
pp. 474-479 ◽  
Author(s):  
M. Gazi Yasargil ◽  
Yasuhiro Yonekawa ◽  
Bruno Zumstein ◽  
Hans-Jürgen Stahl
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Features ◽  
Intracranial Aneurysms ◽  
Communicating Hydrocephalus ◽  
Content Type ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
The Relationship ◽  
Ruptured Intracranial Aneurysms ◽  
Fine Print

✓ Twenty-eight cases of communicating hydrocephalus after subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms are reported. The relationship between the incidence of this complication and the various clinical features of SAH is discussed. The findings of RISA cisternography have little relationship to the findings of pneumoencephalography or the results of shunting procedures. The availability and value of echoencephalography in treating such patients is emphasized.

scholarly journals Transforming Growth Factor-β1 in the Cerebrospinal Fluid of Patients with Subarachnoid Hemorrhage: Titers Derived from Exogenous and Endogenous Sources

2001 ◽  
Vol 21 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Caroline Flood ◽  
James Akinwunmi ◽  
Catherine Lagord ◽  
Matija Daniel ◽  
Martin Berry ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Communicating Hydrocephalus ◽  
Specific Response ◽  
Immunosorbant Assay ◽  
Sequential Samples ◽  
Enzyme Linked Immunosorbant Assay ◽  
Tgf Β1

Transforming growth factor-β1 (TGF-β1) is a fibrogenic cytokine that is involved in postinjury repair and is implicated in the etiology of postsubarachnoid hemorrhage (SAH) chronic communicating hydrocephalus. TGF-β1 was measured by enzyme-linked immunosorbant assay (ELISA) in sequential samples of cerebrospinal fluid (CSF) in 11 patients with hydrocephalus after SAH; levels were seen to be biphasically elevated and sources were investigated. TGF-β1 levels were compared with albumin levels that estimated CSF blood content. Control samples from nonhemorrhagic hydrocephalics were tested similarly. Mean total TGF-β1 levels were elevated to 4400 ± 3435 (±SD) pg/mL greater than control levels of 97 ± 42 at 1 to 2 days posthemorrhage. Thereafter, levels fell to 714 ± 401 by 5 to 6 days posthemorrhage, then rose to a second peak of 1667 ± 774 at 9 to 10 days posthemorrhage, remaining significantly increased until 19 days posthemorrhage ( P = 0.007). The first peak probably derived from extravasated platelets and correlated with increased albumin levels in the CSF. The second TGF-β1 peak rose greater than CSF albumin levels that had stabilized at this time, and thus was attributed to a tissue-specific response rather than a re-bleed. TGF-β1 was detected in the choroid secretory epithelium from controls, but levels were greater in SAH patients at 10 to 12 days posthemorrhage. The authors conclude that the elevated levels of TGF-β1 in CSF after SAH are derived initially from blood and later from endogenous sources such as the choroid plexus.

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