Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma

Vascular endothelial growth factor (VEGF), a potent inducer of angiogenesis and vascular permeability in diverse physiological and pathological conditions, may be involved in the pathophysiology of chronic subdural hematoma (CSDH). The present study investigated the source and mechanisms for the induction of VEGF in CSDH by measuring the concentration of VEGF in the hematoma of 102 patients (122 hematomas) using the enzyme-linked immunosorbent assay technique. The relationship between the VEGF concentration in hematoma and the intrahematoma membranous structure confirmed by preoperative T 2 *-weighted magnetic resonance image was examined in 46 of these patients. VEGF and hypoxia-inducible factor-1a (HIF-1a) expression was immunohistochemically studied and microvessel density (MVD) in the outer membrane was identified using anti-CD31 antibody in 30 patients. VEGF and HIF-1a were positive in the outer membranes of all 30 patients. VEGF expression was significantly correlated to HIF-1a expression (r s ＝ 0.651, p ＝ 0.0084) and VEGF concentration in the hematoma (r s ＝ 0.654, p ＝ 0.0013). VEGF concentration in layered hematomas, which have intrahematoma membranous structure, was significantly higher than in non-layered hematomas (p º 0.01). Although MVDs of the outer membranes were comparable to those described in tumors, there was no significant relationship with VEGF expression. The present study suggests that VEGF in CSDH, which may be induced in the neomembrane by HIF-1 release, may give rise to the excessive development of fragile microvessels and hyperpermeability, resulting in the enlargement of CSDH.

Section: Discussionmentioning

confidence: 99%

Involvement of Hypoxia-Inducible Factor-1.ALPHA. and Vascular Endothelial Growth Factor in the Mechanism of Development of Chronic Subdural Hematoma

Nanko

Tanikawa

Mase

et al. 2009

“…Inflammation may be an important element in the pathogenesis of CSH, 4) and eosinophils infiltrating the membrane of the hematoma may contribute to bleeding into the cavity. 3,9) Increased plasma levels of the inflammatory mediator platelet-activating factor (PAF) and anti-PAF immunoglobulin G levels are observed after head injury in patients with CSH but not in patients with other types of head injury or in normal subjects, 1) which suggests the involvement of PAF in the formation of CSH. Further, PAF concentrations are higher in acute than in chronic CSH, whereas PAF acetylhydrolase activity is lower in acute than in chronic CSH.…”

Section: Introductionmentioning

confidence: 99%

Etizolam, an Anti-anxiety Agent, Attenuates Recurrence of Chronic Subdural Hematoma. Evaluation by Computed Tomography.

Hirashima

Kuwayama

Hamada

et al. 2002

Etizolam, an anti-anxiety agent which is an antagonist of platelet-activating factor receptors, was administered to patients with chronic subdural hematoma (CSH) after hematoma removal to assess the effectiveness for preventing recurrence compared with control patients not given the drug after surgery. The remaining volumes of subdural hematomas on brain computed tomography were measured approximately 1 month after removal. Volume in the etizolam group (15 patients) was significantly smaller than in the control group (24 patients). Hematoma recurrence was not detected in the etizolam group 3 months after surgery, but occurred in the control group. The difference was significant. Etizolam administration may be useful for the prevention of recurrence of CSH.

“…8) Repeated hemorrhaging from the outer membrane has been considered to be a causative factor of the chronic subdural hematoma. 6,21) Intravenous infusion of 51 Cr-labeled red blood cells in patients with chronic subdural hematoma resulted in the subsequent presence of labeled cells in the subdural fluid. 7) The presence of 51 Cr-labeled erythrocytes in the chronic subdural hematoma fluid confirms rebleeding from capillaries in the outer membrane as a major source of expansion in the chronic subdural hematoma.…”

Section: Discussionmentioning

confidence: 99%

Subdural Hyperintense Band on Diffusion-Weighted Imaging of Chronic Subdural Hematoma Indicates Bleeding From the Outer Membrane

Kuwahara¹,

Fukuoka²,

Koan³

et al. 2005

The diffusion-weighted magnetic resonance (MR) imaging characteristics of chronic subdural hematoma and the correlation between hematoma liquidity and apparent diffusion coefficient (ADC) were investigated in 26 consecutive patients, 16 males and 10 females aged 42 to 92 years (mean ± SD 73.3 ± 13.1 years), with 31 chronic subdural hematomas. The chronic subdural hematomas were divided into homogeneous, separate, and trabecular types based on diffusion-weighted MR imaging findings. Almost all hematomas were low intensity on diffusion-weighted imaging, and the mean ADC value was 1.81 ± 0.79 × 10 -3 mm 2 /sec. The high intensity areas in the subdural hematomas consisted of several types: high intensity line along the dura mater (subdural hyperintense band), high intensity along the intrahematoma septum, and laminar shape along the inner membrane. The subdural hyperintense bands accounted for almost all high intensity areas in the subdural hematomas. The mean ADC value of the high intensity areas was 0.76 ± 0.24 × 10 -3 mm 2 /sec, close to that of the normal brain. The subdural hyperintense bands were considered to be intracellular and/or extracellular methemoglobin based on the T 1 -and T 2 -weighted imaging and intraoperative findings. The subdural hyperintense band is an important finding indicating relatively fresh bleeding from the outer membrane. Diffusionweighted imaging shows liquid subdural hematoma as low intensity, and measurement of the ADC values can differentiate between liquid and solid components of the chronic subdural hematoma.