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1.
创伤性脑损伤(TBI)是一类常见且严重威胁公众健康的疾病,国内外对TBI发病机制和治疗方面的研究都有了巨大突破。通过对国内外文献研究发现,TBI后所致神经损害包括原发性和继发性损伤两大类机制,而钙离子(Ca2+)在TBI继发性损伤中扮演着极其重要的角色。本文围绕Ca2+在TBI后继发性损害的致病机制及其治疗展望综述如下。  相似文献   

2.
目的探讨重型颅脑损伤(TBI)病人发生护理干预相关的继发性脑损害的风险预测因子。方法回顾性分析28例重型TBI临床资料,护理干预包括体位护理和卫生护理。预测因子包括基线颅内压(ICP)≥15 mmHg、脑血管压力反应指数(PRx)≥0.3或ICP幅度≥6 mmHg。ICP≥20 mmHg持续5 min以上定义为继发性脑损害。结果 28例共记录67次护理干预,其中体位护理49次,卫生护理18次。12例35次护理干预ICP20 mmHg;10例24次护理干预出现一过性ICP≥20 mmHg;6例8次护理干预出现继发性脑损害,发生率为11.94%(8/67)。基线ICP≥15 mmHg病人继发性脑损害发生率明显增高(P0.05)。基线ICP≥15 mmHg预测护理干预相关性继发性脑损害的特异性为86.4%,敏感性为50.0%,阳性预测值为33.3%,阴性预测值为92.7%。结论基线ICP≥15 mmHg是决定重型颅脑损伤护理干预后继发性脑损害风险的最重要因素。  相似文献   

3.
颅脑创伤(Traumatic Brain Injury,TBI)是世界范围内年轻人和成年人致死、致残的最重要的原因之一,每年 TBI 罹患人数超过1000万[1].TBI 后脑组织的细胞死亡一部分由直接机械损伤(原发性)引起,但是更多是由损伤后一系列生化改变(继发性)引起的.这些继发性损伤包括:细胞因子释放引起的炎性反应,谷氨酸毒性,突触功能障碍,活性氧、活性氧损伤,神经元功能障碍等,这些可进一步引起线粒体功能障碍,也可使细胞死亡信号级联效应放大,最终导致神经元的死亡[2-6].对这些病理生理机制进行深入的研究可为临床的治疗提供理论依据。  相似文献   

4.
颅脑损伤后一氧化氮、一氧化氮合酶和内皮素变化   总被引:2,自引:0,他引:2  
颅脑损伤后继发性脑损害已越来越受到重视,造成继发性损害的因素很多,其中内皮素(endothelin,ET)和一氧化氮(nitric oxide,NO)在继发性损害中所起的作用成为近年研究的热点,并存在很多争论.通过对63例颅脑损伤患者ET、NO和一氧化氮合酶(nitric oxide synthase,NOS)的测定,观察伤后ET、NO及NOS的变化情况,探讨该变化对外伤患者伤情判断的意义.  相似文献   

5.
重型颅脑损伤致残率和死亡率居高不下的重要原因之一是继发性脑损害.研究表明,颅脑损伤后外周血血小板(PLT)参数会发生变化,这与继发性脑损害存在一定的联系~([1]).近年来,我们研究发现早期高压氧(HBO)治疗能有效恢复PLT参数的变化,减少继发性脑损害的程度,提高临床治疗效果,现报告如下.  相似文献   

6.
正颅脑损伤(traumatic brain injury,TBI)是一个全球性的公共卫生问题~([1]),是全球死亡、致残的主要原因。TBI是由外力所致的脑功能的损失或改变。原发性损伤指外部损害导致细胞立即死亡,继发性损伤是原发性损伤周围区域的一系列生物化学变化的结果,进一步导致记忆、认知等功能缺陷。目前的治疗主要集中在减轻继发性损伤的程度,同时增强神经再生。在损伤的早期阶段挽救损伤的脑组织并在恢复期促进再生是可取的。脑源性神经营养因子  相似文献   

7.
颅脑创伤(TBI)是世界范围内年轻人和成年人致残、致死的最重要的原因之一。TBI死亡率 高,而幸存者常伴有身体的残疾、精神障碍等后遗症,为社会发展带来了沉重的负担。星形胶质细胞是 TBI后参与损伤和修复的主要细胞。近年来关于TBI继发性损害机制中反应性星形胶质细胞的研究逐渐 增多,但仍有许多机制有待阐明,现对TBI后反应性星形胶质细胞参与的几种相关机制进行阐述。  相似文献   

8.
近年来,交通事故、军事行动及对抗类体育运动等所导致的颅脑损伤(traumatic brain injury,TBI)的发病率逐年上升。全面了解TBI发病机制对其治疗具有重要意义,其中炎性因子和免疫细胞参与的神经炎性反应在TBI继发性损伤中扮演重要角色,本文将对TBI后神经炎性反应相关机制研究的进展作一综述。  相似文献   

9.
目的 对颅脑损伤影响脑血流及氧代谢进行前瞻性研究。方法 30只Wistar大白鼠分成3组:颅脑损伤1组(TBI1)、2组(TBI2)及3组(TBI3)各10只,分别为轻、中、重型颅脑损伤。用脑阻抗(REG)测定脑血流量,颈内静脉血氧饱和度(SjVO2)反映全脑氧代谢情况。结果 TBI、TBI2及TBI3组影响脑血流和氧代谢程度依次为TBI3>TBI2>TBI1,健侧脑组织含水量各组无明显差异,伤侧脑组织含水量TBI3组最多,其次为TBI2,明显高于TBI1组(P<0.01)。结论 颅脑损伤后脑血流和氧代谢变化取决于损伤程度,脑血流和氧代谢各参数的监测对正确认识脑组织病理生理变化,指导临床治疗,判断预后有重要价值。  相似文献   

10.
<正>颅脑损伤(traumatic brain injury,TBI)是一个全球性问题,涉及病人多、范围广。TBI病理过程包括原发性损伤和继发性损伤,后者是直接损伤造成的一系列细胞及生化级联反应,是TBI致死的主要原因~([1-3]),炎症反应是继发性脑损伤过程中最关键的病理过程~([4,5])。高迁移率族蛋白B1(high mobility group protein B1,HMGB1)释放在TBI后炎症反应中起着重要作用,继发性脑损伤中H1MGB1的作用逐渐引起重视。本文对近年来TBI中HMGB1的研究进展进  相似文献   

11.
Hyperthermia following traumatic brain injury: a critical evaluation   总被引:7,自引:0,他引:7  
Hyperthermia, frequently seen in patients following traumatic brain injury (TBI), may be due to posttraumatic cerebral inflammation, direct hypothalamic damage, or secondary infection resulting in fever. Regardless of the underlying cause, hyperthermia increases metabolic expenditure, glutamate release, and neutrophil activity to levels higher than those occurring in the normothermic brain-injured patient. This synergism may further compromise the injured brain, enhancing the vulnerability to secondary pathogenic events, thereby exacerbating neuronal damage. Although rigorous control of normal body temperature is the current standard of care for the brain-injured patient, patient management strategies currently available are often suboptimal and may be contraindicated. This article represents a compendium of published work regarding the state of knowledge of the relationship between hyperthermia and TBI, as well as a critical examination of current management strategies.  相似文献   

12.
Cerebral inflammation involves molecular cascades contributing to progressive damage after traumatic brain injury (TBI). The chemokine CC ligand-2 (CCL2) (formerly monocyte chemoattractant protein-1, MCP-1) is implicated in macrophage recruitment into damaged parenchyma after TBI. This study analyzed the presence of CCL2 in human TBI, and further investigated the role of CCL2 in physiological and cellular mechanisms of secondary brain damage after TBI. Sustained elevation of CCL2 was detected in the cerebrospinal fluid (CSF) of severe TBI patients for 10 days after trauma, and in cortical homogenates of C57Bl/6 mice, peaking at 4 to 12 h after closed head injury (CHI). Neurological outcome, lesion volume, macrophage/microglia infiltration, astrogliosis, and the cerebral cytokine network were thus examined in CCL2-deficient (−/−) mice subjected to CHI. We found that CCL2−/− mice showed altered production of multiple cytokines acutely (2 to 24 h); however, this did not affect lesion size or cell death within the first week after CHI. In contrast, by 2 and 4 weeks, a delayed reduction in lesion volume, macrophage accumulation, and astrogliosis were observed in the injured cortex and ipsilateral thalamus of CCL2−/− mice, corresponding to improved functional recovery as compared with wild-type mice after CHI. Our findings confirm the significant role of CCL2 in mediating post-traumatic secondary brain damage.  相似文献   

13.
Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.  相似文献   

14.
Hypothermia reduces excitotoxic neuronal damage after seizures, cerebral ischemia and traumatic brain injury (TBI), while hyperthermia exacerbates damage from these insults. Presynaptic release of ionic zinc (Zn2+), translocation and accumulation of Zn2+ ions in postsynaptic neurons are important mechanisms of excitotoxic neuronal injury. We hypothesized that temperature-dependent modulation of excitotoxicity is mediated in part by temperature-dependent changes in the synaptic release and translocation of Zn2+. In the present studies, we used autometallographic (AMG) and fluorescent imaging of N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) staining to quantify the influence of temperature on translocation of Zn2+ into hippocampal neurons in adult rats after weight drop-induced TBI. The central finding was that TBI-induced Zn2+ translocation is strongly influenced by brain temperature. Vesicular Zn2+ release was detected by AMG staining 1 h after TBI. At 30 degrees C, hippocampus showed almost no evidence of vesicular Zn2+ release from presynaptic terminals; at 36.5 degrees C, the hippocampus showed around 20% to 30% presynaptic vesicular Zn2+ release; and at 39 degrees C vesicular Zn2+ release was significantly greater (40% to 60%) than at 36.5 degrees C. At 6 h after TBI, intracellular Zn2+ accumulation was detected by the TSQ staining method, which showed that Zn2+ translocation also paralleled the vesicular Zn2+ release. Neuronal injury, assessed by counting eosinophilic neurons, also paralleled the translocation of Zn2+, being minimal at 30 degrees C and maximal at 39 degrees C. We conclude that pathological Zn2+ translocation in brain after TBI is temperature-dependent and that hypothermic neuronal protection might be mediated in part by reduced Zn2+ translocation.  相似文献   

15.
The neurophysiology of brain injury.   总被引:4,自引:0,他引:4  
OBJECTIVE: This article reviews the mechanisms and pathophysiology of traumatic brain injury (TBI). METHODS: Research on the pathophysiology of diffuse and focal TBI is reviewed with an emphasis on damage that occurs at the cellular level. The mechanisms of injury are discussed in detail including the factors and time course associated with mild to severe diffuse injury as well as the pathophysiology of focal injuries. Examples of electrophysiologic procedures consistent with recent theory and research evidence are presented. RESULTS: Acceleration/deceleration (A/D) forces rarely cause shearing of nervous tissue, but instead, initiate a pathophysiologic process with a well defined temporal progression. The injury foci are considered to be diffuse trauma to white matter with damage occurring at the superficial layers of the brain, and extending inward as A/D forces increase. Focal injuries result in primary injuries to neurons and the surrounding cerebrovasculature, with secondary damage occurring due to ischemia and a cytotoxic cascade. A subset of electrophysiologic procedures consistent with current TBI research is briefly reviewed. CONCLUSIONS: The pathophysiology of TBI occurs over time, in a pattern consistent with the physics of injury. The development of electrophysiologic procedures designed to detect specific patterns of change related to TBI may be of most use to the neurophysiologist. SIGNIFICANCE: This article provides an up-to-date review of the mechanisms and pathophysiology of TBI and attempts to address misconceptions in the existing literature.  相似文献   

16.
The blood–brain barrier (BBB) is an anatomical microstructural unit, with several different components playing key roles in normal brain physiological regulation. Formed by tightly connected cerebrovascular endothelial cells, its normal function depends on paracrine interactions between endothelium and closely related glia, with several recent reports stressing the need to consider the entire gliovascular unit in order to explain the underlying cellular and molecular mechanisms. Despite that, with regard to traumatic brain injury (TBI) and significant events in incidence and potential clinical consequences in pediatric and adult ages, little is known about the actual role of BBB disruption in its diverse pathological pathways. This Mini‐Review addresses the current literature on possible factors affecting gliovascular units and contributing to posttraumatic BBB dysfunction, including neuroinflammation and disturbed transport mechanisms along with altered permeability and consequent posttraumatic edema. Key mechanisms and its components are described, and promising lines of basic and clinical research are identified, because further knowledge on BBB pathological interference should play a key role in understanding TBI and provide a basis for possible therapeutic targets in the near future, whether through restoration of normal BBB function after injury or delivering drugs in an increased permeability context, preventing secondary damage and improving functional outcome. © 2013 Wiley Periodicals, Inc.  相似文献   

17.
Hemodynamic and cerebrovascular factors are crucially involved in secondary damage after traumatic brain injury (TBI). With magnetic resonance imaging, this study aimed to quantify regional cerebral blood flow (CBF) by arterial spin labeling and cerebral blood volume by using an intravascular contrast agent, during 14 days after lateral fluid-percussion injury (LFPI) in rats. Immunohistochemical analysis of vessel density was used to evaluate the contribution of vascular damage. Results show widespread ipsilateral and contralateral hypoperfusion, including both the cortex and the hippocampus bilaterally, as well as the ipsilateral thalamus. Hemodynamic unrest may partly be explained by an increase in blood vessel density over a period of 2 weeks in the ipsilateral hippocampus and perilesional cortex. Furthermore, three phases of perilesional alterations in CBF, progressing from hypoperfusion to normal and back to hypoperfusion within 2 weeks were shown for the first time in a rat TBI model. These three phases were similar to hemodynamic fluctuations reported in TBI patients. This makes it feasible to use LFPI in rats to study mechanisms behind hemodynamic changes and to explore novel therapeutic approaches for secondary brain damage after TBI.  相似文献   

18.
Free radical-induced oxidative damage reactions, and membrane lipid peroxidation (LP), in particular, are among the best validated secondary injury mechanisms in preclinical traumatic brain injury (TBI) models. In addition to the disruption of the membrane phospholipid architecture, LP results in the formation of cytotoxic aldehyde-containing products that bind to cellular proteins and impair their normal functions. This article reviews the progress of the past three decades in regard to the preclinical discovery and attempted clinical development of antioxidant drugs designed to inhibit free radical-induced LP and its neurotoxic consequences via different mechanisms including the O2 ·− scavenger Superoxide dismutase and the lipid peroxidation inhibitor tirilazad. In addition, various other antioxidant agents that have been shown to have efficacy in preclinical TBI models are briefly presented, such as the LP inhibitors U83836E, resveratrol, curcumin, OPC-14177, and lipoic acid; the iron chelator deferoxamine and the nitroxide-containing antioxidants, such as α-phenyl-tert-butyl nitrone and tempol. A relatively new antioxidant mechanistic strategy for acute TBI is aimed at the scavenging of aldehydic LP byproducts that are highly neurotoxic with “carbonyl scavenging” compounds. Finally, it is proposed that the most effective approach to interrupt posttraumatic oxidative brain damage after TBI might involve the combined treatment with mechanistically complementary antioxidants that simultaneously scavenge LP-initiating free radicals, inhibit LP propagation, and lastly remove neurotoxic LP byproducts.  相似文献   

19.
Cytochrome c release and caspase activation after traumatic brain injury   总被引:10,自引:0,他引:10  
Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the primary damage resulting in significant neurological dysfunction. The identification of cell death pathways that mediate this secondary traumatic injury have not been elucidated, however recent studies have implicated a role for apoptosis in the neuropathology of traumatic brain injury. The present study utilized a controlled cortical impact model of brain injury to assess the involvement of apoptotic pathways: release of cytochrome c from mitochondria and the activation of caspase-1- and caspase-3-like proteases in the injured cortex at 6, 12 and 24 h post-injury. Collectively, these results demonstrate cytochrome c release from mitochondria and its redistribution into the cytosol occurs in a time-dependent manner following TBI. The release of cytochrome c is accompanied by a time-dependent increase in caspase-3-like protease activity with no apparent increase in caspase-1-like activity. However, pretreatment with a general caspase inhibitor had no significant effect on the amount of cortical damage observed at 7 days post-injury. Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death.  相似文献   

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