终板造瘘对动脉瘤性蛛网膜下腔出血后慢性脑积水的影响

目的:探讨终板造瘘对动脉瘤性蛛网膜下腔出血后慢性脑积水的影响。方法:回顾性分析201例动脉瘤性蛛网膜下腔出血患者的临床资料,将所有患者按动脉瘤夹闭术中是否进行终板造瘘分为两组,随访6个月以上,评价其慢性脑积水的发生率。结果:所有患者慢性脑积水的总发生率为17.4%,终板造瘘组慢性脑积水的发生率7.8%,而单独夹闭组慢性脑积水的发生率为28.1%,显著高于终板造瘘组(P0.05)。在FisherⅠ-Ⅱ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为5.0%、7.7%,两组比较无统计学差异(P0.05);FisherⅢ-Ⅳ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为10.8%、40.3%,单独夹闭组显著高于终板造瘘组(P0.05);而Hunt-HessⅠ-Ⅱ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为7.0%、9.4%,两组比较无统计学差异(P0.05),Hunt-HessⅢ-Ⅳ级中终板造瘘与单独夹闭组慢性脑积水的发生率分别为11.3%、46.5%,单独夹闭组显著高于终板造瘘组(P0.05)。结论:终板造瘘可明显降低Hunt-HessⅢ-Ⅳ级、FisherⅢ、Ⅳ级动脉瘤性蛛网膜下腔出血后患者慢性脑积水的发生率,而对Hunt-HessⅠ-Ⅱ级、FisherⅠ-Ⅱ级的动脉瘤性蛛网膜下腔出血后患者慢性脑积水的发生率影响不明显。     

脑出血后脑积水形成机制研究进展

脑积水是由于颅脑疾患使得脑脊液分泌过多或(和)循环、吸收障碍而致颅内脑脊液量增加,脑室系统扩大或(和)蛛网膜下腔扩大的一种病症。目前多项临床多因素回归分析及前瞻性随机对照研究已证实脑积水是脑出血(intracerebral hemorrhage,ICH)预后不良的独立危险因素。脑积水以脑萎缩及神经功能障碍为主要特征,严重影响人的认知功能和生活质量,给患者家庭及社会带来巨大的经济负担。本人就ICH后脑积水形成机制研究进展做一综述。     

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects

Early brain injury and delayed cerebral vasospasm both contribute to unfavorable outcomes after subarachnoid hemorrhage (SAH). Reproducible and controllable animal models that simulate both conditions are presently uncommon. Therefore, new models are needed in order to mimic human pathophysiological conditions resulting from SAH.This report describes the technical nuances of a rabbit blood-shunt SAH model that enables control of intracerebral pressure (ICP). An extracorporeal shunt is placed between the arterial system and the subarachnoid space, which enables examiner-independent SAH in a closed cranium. Step-by-step procedural instructions and necessary equipment are described, as well as technical considerations to produce the model with minimal mortality and morbidity. Important details required for successful surgical creation of this robust, simple and consistent ICP-controlled SAH rabbit model are described.     

Effects of mouse nerve growth factor in treating cerebral injury in acute period caused by cerebral hemorrhage

ObjectiveTo explore the clinical effects of mouse Nerve Growth Factor (NGF) in treating cerebral injury in acute period caused by cerebral hemorrhage, observe its influences on Natriuretic Peptide (BNP) and NF-kB Level and evaluate its safety and efficiency.Methods96 cases with acute cerebral hemorrhage from January 2016 to January 2017 in our hospital were recruited as this study, they were randomly divided into the control group and the observation group, each 48 cases. The observation group were given NGF on the treatment of the control group. NIHSS, BI score, adverse reactions records were compared in two groups before and after treatment. The clinical effective rate were evaluated. Then BNP and NF-KB Level of patients in two groups before and after treatment were detected by using ELISA.ResultsThere were no significant differences in two groups before treatment with respect to NIHSS and BI score (P > 0.05). After treatment, NIHSS score in the observation group significantly lower than the control group. BI score in the observation group significantly higher than the control group, differences had obvious significance (P < 0.05). The total effective rate in the observation group was 93.75%. The control group was 70.83%. Clinical effective rate of patients in the observation group significantly better than the control group (P < 0.05). There were no significant differences of patients in two groups before treatment with respect to BNP and NF-kB Level (P > 0.05). BNP and NF-kB Level decreased with different levels in two groups after treatment, and the observation group lower than the control group at the same time (P < 0.05).ConclusionNGF is benefit for relieving neurological function injury of patients with acute cerebral hemorrhage in acute period, improving living ability of patients. Patients have good tolerance and no adverse reactions. NGF can lower BNP and NF-kB Level. It has a certain function of inhibiting inflammatory injury caused by cerebral hemorrhage, thus protecting neuron. It is worthy of clinical promotion.     

Exploring the multifaceted roles of heat shock protein B8 (HSPB8) in diseases

HSPB8 is a member of ubiquitous small heat shock protein (sHSP) family, whose expression is induced in response to a wide variety of unfavorable physiological and environmental conditions. Investigation of HSPB8 structure indicated that HSPB8 belongs to the group of so-called intrinsically disordered proteins and possesses a highly flexible structure. Unlike most other sHSPs, HSPB8 tends to form small-molecular-mass oligomers and exhibits substrate-dependent chaperone activity. In cooperation with BAG3, the chaperone activity of HSPB8 was reported to be involved in the delivery of misfolded proteins to the autophagy machinery. Through this way, HSPB8 interferes with pathological processes leading to neurodegenerative diseases. Accordingly, published studies have identified genetic links between mutations of HSPB8 and some kind of neuromuscular diseases, further supporting its important role in neurodegenerative disorders. In addition to their anti-aggregation properties, HSPB8 is indicated to interact with a wide range of client proteins, modulating their maturations and activities, and therefore, regulates a large repertoire of cellular functions, including apoptosis, proliferation, inflammation and etc. As a result, HSPB8 has key roles in cancer biology, autoimmune diseases, cardiac diseases and cerebral vascular diseases.     

Elevation of Platelet Activating Factor,Inflammatory Cytokines,and Coagulation Factors in the Internal Jugular Vein of Patients with Subarachnoid Hemorrhage

The aim of the present study was to examine the changes of inflammatory and coagulation factors in blood of the internal jugular vein, not of peripheral vein, in patients with subarachnoid hemorrhage (SAH). The results show that while interleukin-6 (IL-6) and platelet activating factor (PAF) concentrations increased within first 4 days after SAH and remained elevated up to 14 days, interleukin-1 (IL-1 showed a transient increase between 5–9 days after SAH and tumor necrosis factor- (TNF-) remained unchanged. Also different coagulation factors were increased between 5–9 days after SAH. Moreover, patients with delayed ischemic neurological deficits (DIND) displayed the highest levels of PAF and the coagulation factors, von Willebrand factor (vWF) and thrombin-antithrombin III complex (TAT). These results suggest that elevation of PAF and other inflammatory cytokines following SAH may cause the hypercoagulation state that is associated with cerebral vasospasm and internal jugular vein may be more adequate vessel for sampling blood to examine these factors.     

Circadian variation in clinical features and outcome of intracerebral hemorrhage: The INTERACT studies

Previous studies consistently reported a diurnal variation in the occurrence of intracerebral hemorrhage (ICH), with a morning peak. However, limited knowledge exists on the circadian pattern of ICH severity and outcome. This study aimed to determine possible associations between ICH onset time and admission severity and 90-day outcomes using the combined data set of the pilot and main-phase Intensive blood pressure (BP) reduction in an acute cerebral hemorrhage trial (INTERACT). The ICH onset time was categorized into three groups (1: 00:00–07:59; 2: 08:00–15:59; and 3: 16:00–23:59). We found an association between onset time and low Glasgow Coma Scale score: aOR (time 1: 1.72, 95% CI 1.12–2.66; time 3: 1.95, 95% CI 1.31–2.89, p = 0.003; in comparison to time 2). There was no association between onset time and volume of ICH (adjusted p = 0.354) or 90-day outcomes of death or major disability, and death and major disability separately (all adjusted p > 0.4). The results showed that more severe cases of ICH patients, defined by a reduced level of consciousness, had late afternoon to early morning stroke onset, but this was unrelated to baseline hematoma volume or location. There was no circadian influence on ICH clinical outcome.     

“Timing” of arrival and in-hospital mortality in a cohort of patients under anticoagulant therapy presenting to the emergency departments with cerebral hemorrhage: A multicenter chronobiological study in Italy

Therapy with oral anticoagulants (OACs) is a risk factor for cerebral hemorrhage (CH). Although different studies have been undertaken to investigate the timing of the onset of major cardiovascular events, no data exist on temporal patterns of the onset of CH in subjects treated with OACs. The aim of this study is to evaluate the timing of CH in patients treated with OACs. All patients who developed CH under OACs therapy and admitted to 28 Italian Emergency Departments (EDs) between September 2011 and July 2013 were enrolled. Age, sex, time and location of the hemorrhagic lesion, type of the bleeding events (idiopathic or post-traumatic), anticoagulant therapy (warfarin or new oral anticoagulants - NOAs) and time of ED admission (i.e., hour, day, month and season) were recorded. Five hundred and seventeen patients (63.2% male aged 80 ± 7.9 yrs) with CH were involved. Warfarin was taken by 494 patients (95.6%), and NOAs by 23 (4.4%). In-hospital mortality (IHM) was recorded in 208 cases (40.2%). Cosinor analysis showed a peak of CH arrival between 12:00 and 14:00 h both in the whole population (PR 73.9%, p = 0.002) and the male subgroup (PR 65.2%, p = 0.009), whereas females showed an anticipated morning peak between 08:00 and 10:00 h (PR 65.7%, p = 0.008). A further analysis between idiopathic and post-traumatic CH confirmed the presence of a 24 h pattern with a peak between 12:00 and 14:00 h (PR 58.5%, p = 0.019) and between 08:00 and 10:00 h (PR80.1%, p < 0.001) for idiopathic events and post-traumatic hemorrhages, respectively. Moreover, a seasonal winter peak was identified for idiopathic forms (PR 74%, p = 0.035), and a summer peak for post-traumatic forms (PR 77%, p = 0.025). The present study suggests the presence of a temporal pattern of ED arrivals in CH patients treated with OACs.     

动态监测血清炎症因子和氧化应激产物在急性脑出血患者病情及预后评估中的应用

目的:动态监测急性脑出血患者血清炎症因子和氧化应激产物水平,探讨其与患者病情及预后的关系。方法:采用双抗体夹心酶联免疫吸附法(ELISA法)测定150例急性脑出血患者(病例组)和120例健康志愿者(对照组)发病24 h内、3 d、7 d及14 d时血清炎症因子白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α),采用黄嘌呤氧化酶法(XTO)和硫代巴比妥酸法(TBA)测定两组的血清氧化应激产物超氧歧化酶(SOD)和丙二醛(MDA)水平,并分析血液炎症因子与氧化应激产物与患者病情及预后的关系。结果:病例组血清IL-6、TNF-α、SOD及MDA水平高于对照组,并在发病后7d各指标水平达到最高,发病后14d各指标水平低于发作≤24 h,差异有统计学意义(P0.05)。大量出血组血清IL-6、TNF-α、SOD及MDA水平最高,中量出血组其次,小量出血组各指标水平最低,差异均有统计学意义(P0.05)。重型组血清IL-6、TNF-α、SOD及MDA水平均最高,中型组其次,轻型组各指标水平最低,差异均有统计学意义(P0.05)。结论:动态监测急性脑出血患者血清炎症因子及氧化应激产物水平有助于准确判断患者的病情及评估预后,临床有重要参考价值。