ObjectiveChronic subdural hematoma (CSDH) is a typical disease that is encountered frequently in neurosurgical practice. The medications which could cause coagulopathies were known as one of the risk factors of CSDH, such as anticoagulants (ACs) and antiplatelet agents (APs). Recently, the number of patients who are treated with ACs/APs is increasing, especially in the elderly population. With widespread use of these drugs, there is a need to study the changes in risk factors of CSDH patients.MethodsWe retrospectively reviewed 290 CSDH patients who underwent surgery at our institute between 1996 and 2010. We classified them into three groups according to the time of presentation (Group A : the remote period group, 1996-2000, Group B : the past period group, 2001-2005, and Group C : the recent period group, 2006-2010). Also, we performed the comparative analysis of independent risk factors between three groups.ResultsAmong the 290 patients, Group A included 71 patients (24.5%), Group B included 98 patients (33.8%) and Group C included 121 patients (41.7%). Three patients (4.2%) in Group A had a history of receiving ACs/APs, 8 patients (8.2%) in Group B, and 19 patients (15.7%) in Group C. Other factors such as head trauma, alcoholism, epilepsy, previous neurosurgery and underlying disease having bleeding tendency were also evaluated. In ACs/APs related cause of CSDH in Group C, significantly less proportion of the patients are associated with trauma or alcohol compared to the non-medication group.ConclusionIn this study, the authors concluded that ACs/APs have more importance as a risk factor of CSDH in the recent period compared to the past. Therefore, doctors should prescribe these medications carefully balancing the potential risk and benefit.

The authors present the clinical, radiological, pathological features, and autopsy findings of a patient with malignant triton tumor of the acoustic nerve, which probably arose from a pre-existing acoustic schwannoma. The term "malignant triton tumor" is applied to malignant schwannomas with rhabdomyoblastic differentiation. A cerebellopontine angle tumor with spinal drop metastasis occurred in this patient 10 months after near-total removal of the original tumor.

Background-Paclitaxel has been shown to inhibit vascular smooth muscle cell migration and proliferation contributing to neointimal formation. This study tested whether novel oral formulations of paclitaxel can prevent neointimal formation in a rat carotid artery injury model. Methods and Results-Oral formulations of paclitaxel (0, 5, 7.5, or 10 mg/kg) were administered to 40 rats by gavage for 5 days after injury. The peak plasma levels of paclitaxel administered at 5, 7.5, and 10 mg/kg were 61Ϯ16, 89Ϯ22, and 108Ϯ28 nmol/L, respectively. Treatment effects were assessed 11 days after injury. The angiographic minimum luminal diameters of the oral paclitaxel groups treated at 5, 7.5, and 10 mg/kg were 6.28Ϯ2.09, 6.97Ϯ1.79, and 7.97Ϯ1.57 AU, and these were significantly larger than that of the control group (4.67Ϯ1.45 AU). The oral paclitaxel groups (5, 7.5, 10 mg/kg; 0.05Ϯ0.05, 0.04Ϯ0.03, 0.05Ϯ0.03 mm 2 ) showed significant neointimal formation reductions versus the control group (0.13Ϯ0.05 mm 2 ). All rats survived to study completion. Only 2 animals in the 10 mg/kg group experienced weight loss (Ϸ10%) and loose stools between 4 and 6 days after injury. All other animals appeared healthy during the study. For comparison purposes, intraperitoneal formulations of paclitaxel (0 or 2 mg/kg) were administered by injection to 15 rats. We confirmed that the intraperitoneal administration of paclitaxel also effectively inhibited neointimal formation. Conclusions-Oral formulations of paclitaxel provide an effective means of inhibiting proliferative response to vascular injury in the rat. Thus, oral formulations of paclitaxel may prevent human restenosis without significant toxicity.

It has been shown that green tea catechins (GTC) suppress proliferation of vascular smooth muscle cells (VSMCs) and that epigallocatechin-3-gallate (EGCG), which is a major constituent of GTC, selectively inhibits the platelet-derived growth factor-BB (PDGF-BB)-induced intracellular signaling transduction pathway. Vascular smooth muscle cell proliferation is one of major mechanisms of restenosis following percutaneous coronary intervention. This study tested whether GTC can inhibit VSMC proliferation and prevent neointimal formation in a rat carotid artery injury model. Vascular smooth muscle cell proliferation inhibition was analyzed with [3H]thymidine incorporation. Green tea catechins were applied to the endothelium-denuded carotid arteries of rats for 20 min. Angiography and morphometric analysis was performed after 2 weeks. Green tea catechins decreased [3H]thymidine incorporation stimulated with PDGF-BB dose dependently. In the absence of PDGF-BB, the decrement of [3H]thymidine incorporation was evident above a concentration of 10 micro g/ml of GTC. Carotid arteriographic evaluation showed that the minimum luminal diameter in the GTC-treated group (n=12) was 5.9 +/- 1.6 arbitrary units (a.u.) and was significantly larger than in the control group (4.3 +/- 1.4 a.u., n=10) ( P <0.05). The GTC-treated group also showed a significant reduction in neointimal formation compared with the control group (0.29 +/- 0.11 vs 0.42 +/- 0.10 mm2, P < 0.05). To identify the active ingredients, we performed a similar experiment using EGCG. The effects of EGCG were similar to those of GTC. Green tea catechins effectively inhibited VSMC proliferation. Neointimal formation was prevented in the rat carotid artery injury model by local delivery of GTC. As EGCG showed similar effects, it may be one of the major constituents of GTC having these effects.