氨基胍对胶原酶诱导脑出血大鼠模型的影响

目的研究氨基胍对脑出血的影响。方法以Ⅶ胶原酶诱导脑出血大鼠模型,观察动物行为学和脑内血肿的变化,用Western blot检测诱导型一氧化氮合酶蛋白表达的变化。结果氨基胍能明显加快脑出血大鼠行为缺陷的恢复,但对于血肿吸收没有明显影响;Western blot显示:氨基胍能明显抑制脑出血大鼠患侧皮质和基底节诱导型一氧化氮合酶蛋白表达。结论通过广泛抑制脑内诱导型一氧化氮合酶的表达,氨基胍能促进脑出血大鼠的运动功能恢复。     

血府逐瘀汤对实验性脑出血大鼠活化Caspase-3表达的影响

目的观察血府逐瘀汤对脑出血模型大鼠颅内血肿周围神经元活化Caspase-3的干预作用。方法用Ⅶ胶原酶注射诱导大鼠脑出血模型,免疫组化检测血肿周围活化Caspase-3的表达。结果Ⅶ胶原酶造模后模型组血肿周围于6h出现Caspase-3阳性表达细胞,1d阳性细胞计数达高峰,以后逐渐下降,与假手术组差异明显(P<0.01)。血府逐瘀汤治疗组组与模型组比较:6h计数无明显差异,1d,3d,5d三个时间点,给药组阳性细胞数量显著减少,细胞着色变浅。(P<0.01)。结论血府逐瘀汤下调脑出血大鼠血肿周围活化Caspase-3的表达,抑制神经细胞凋亡,可能是其疗效机理之一。     

Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international normalized ratio (INR) of 2.5–6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5–2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation. Received: 1 September 1999/Received in revised form: 28 October 1999/Accepted: 19 November 1999     

单发脑实质转移瘤的CT诊断与鉴别诊断(附34例分析)

目的:探讨单发脑内转移瘤的CT表现,诊断与鉴别诊断.方法:34例经临床和手术病理证实的单发脑内转移瘤,均行CT平扫和增强扫描.原发肿瘤以肺癌最多见(61.8%),40岁以上32例(94.1%).结果:转移瘤均位于皮质和皮质下区,好发于额顶叶.病灶直径在3cm以上者25例(78.1%).平扫呈等或稍低、稍高密度,增强后病灶表现为两种形式:当肿瘤为实质性,呈均匀强化,占58.8%;当转移瘤内出现坏死囊变,则呈环形强化,表现薄壁或不规整厚壁强化.转移瘤主要需与胶质瘤、脑膜瘤和脑脓肿等鉴别.结论:掌握本病的CT表现特点,结合临床资料,对单发脑内转移瘤的诊断和鉴别诊断有重要意义.     

34例高血压脑出血术后再出血的临床分析

目的总结高血压脑出血术后再出血的原因、诊断及防治经验,提高对本病的认识,以便及时发现处理。方法回顾我院1999年1月～2004年12月高血压脑出血术后再出血34例的临床资料。结果高血压脑出血术后再出血发生率11.9%(34/286),手术二次手术清除血肿者24例,保守治疗7例,预后良好率61.8%(21/34),预后不良率38.2%(13/34)。结论高血压脑出血术后再出血预后不良率很高,预防高血压脑出血术后再出血是治疗的关键。     

Chronic subdural hematoma associated with dural metastasis leads to early recurrence and death: A single-institute,retrospective cohort study

The prevalence of chronic subdural hematoma (CSDH) associated with dural metastasis is uncertain, and appropriate treatment strategies have not been established. This study aimed to investigate the characteristics of and appropriate treatment strategies for CSDH associated with dural metastasis. We retrospectively reviewed the charts of 214 patients who underwent surgery for CSDH. The patients were divided into the dural metastasis group (DMG; n = 5, 2.3%) and no dural metastasis group (No-DMG; n = 209, 97.3%). Patient characteristics, treatment, and outcomes were compared between the two groups. Active cancer was detected in 31 out of 214 patients, 5 of whom (16.1%) had dural metastasis. In-hospital death (80.0% vs. 0%; p < 0.001) and recurrence within 14 days (80.0% vs. 2.9%; p < 0.001) and 60 days (80.0% vs. 13.9%; p = 0.002) were significantly prevalent in the DMG. All patients in the DMG developed subdural hematoma re-accumulation requiring emergent surgery because of brain herniation, and patients in the DMG had significantly worse recurrence-free survival (p < 0.001). This relationship remained significant (p < 0.001) even when the analysis was limited to the active cancer cohort (n = 31). CSDH associated with dural metastasis leads to early recurrence and death because of the difficulty in controlling subdural hematoma re-accumulation by common drainage procedures. Depending on the primary cancer status, withdrawal of active treatment and change to palliative care should be discussed after diagnosing CSDH associated with dural metastasis.     

Acute aortic syndromes: aortic dissections,penetrating aortic ulcers and intramural aortic hematomas

Acute aortic syndromes, including dissections, intramural hematomas and penetrating aortic ulcers, are a catastrophic clinical entity that are relatively uncommon. A high index of clinical suspicion along with proper imaging modalities are critical in making a prompt and accurate diagnosis for immediate management and to improve survival of the patient.     

Expression of the TGF-β–ALK-1 Pathway in Dura and the Outer Membrane of Chronic Subdural Hematomas

Neovascularization of the outer membrane plays a critical role in the development and enlargement of chronic subdural hematomas (CSHs) and vascular endothelial growth factor (VEGF) may promote their progression. However, the precise mechanisms remain to be determined. We focused on the signaling pathway upstream of VEGF, transforming growth factor β (TGF-β), and activin receptor-like kinase 1 (ALK-1) to identify the mechanisms underlying the neovascularization of the outer membrane of CSH. Retrospective comparative study was conducted on 15 consecutive patients diagnosed as CSH with burr-hole drainage. Dura and the outer membrane were collected. We immunohistochemically examined the expression of VEGF, integrin-α, TGF-β, and ALK-1 on the outer membrane and dura of CSH and compared our findings with control samples and the signal intensity of hematomas on computed tomography (CT) scans. VEGF and integrin-α expression was markedly up-regulated in both the dura and outer membrane of CSH, the expression of TGF-β and ALK-1 in the dura was slightly increased in the dura and markedly up-regulated in the outer membrane. There was no significant correlation between their expression and CT density. Here we first report the expression of TGF-β and ALK-1 in the outer membrane and dura mater of CSH. We suggest that the TGF-β–ALK-1 pathway and VEGF affect neovascularization and the progression of CSH.