Morphological Changes in Rat Hippocampus after Brain Injury

We performed morphological analysis of the structure of rat hippocampus after ablation of the left sensorimotor cortex. Four experimental groups were formed: two control groups (intravenous and intracerebral injections of the culture medium) and two experimental groups (intravenous and intracerebral transplantation of MSC). Ten weeks after surgery, disturbed cytoarchitectonics and great number of dead neurons were found in all zones of the hippocampus in animals of the control groups. In animals receiving cell therapy, no pathological changes in the structure of the hippocampus were found: hyperchromatic neurons were absent and the cells had regular shape and closely adjoined to each other.     

Neuroprotective Effect of Plasminogen Activator Inhibitor-1 Antagonist in the Rat Model of Mild Traumatic Brain Injury

Inflammation - Plasminogen activator inhibitor-1 (PAI-1) antagonists are known for their neuroprotective effects. In this study, it was aimed to investigate the possible protective effects of PAI-1...     

Malingering and Defensiveness in the Neuropsychological Assessment of Mild Traumatic Brain Injury

A balanced approach to the detection of malingering and defensiveness in the neuropsychological assessment of mild traumatic brain injury (MTBI) is suggested, while genuine neurobehavioral and psychopathological sequelae are documented. The absence of neuroradio-loglcal evidence and heavy reliance on patient report and neuropsychological test data make malingering and defensiveness issues that are critical in forensic contexts and for the credibility of neuropsychology. Deficiencies in interview data collection and the relative strengths and weaknesses of the MMPI (Minnesota Muttiphasic Personality Inventory) are reviewed. The potential independence of malingering and defensiveness and of MMPI and neuropsychological data are noted. The equivocal research on malingering is reviewed, with particular emphasis on assessment of memory deficits as one of the most common complaints in MTBI. Arguably, malingering is more similar to than different from other diagnoses, but it has not been so treated in clinical practice. The need for developing sophisticated malingering probes is acknowledged, but the quest for a single malingering test is criticized and preference given to approaches that rely on evaluating data patterns indicating malingering.     

大鼠脑缺血再灌注后微血管通透性变化

目的 :了解大鼠脑缺血再灌注后微血管通透性的变化。方法 :用暂时性脑缺血的大鼠模型 ,以右旋糖酐分子为示踪剂对缺血再灌注后微血管通透性的变化进行观察。结果 :电镜下见缺血 1h和再灌注后 1、2、3、4、6、9、12h各时点均可见右旋糖酐颗粒穿出血管外 ,微血管通透性增高有二个高峰 ,一是单纯缺血 1h ,另一是再灌注 6h以后。胞浆内出现的大量吞饮小泡 ,细胞间连接的增宽和开放 ,内皮细胞胞膜表面的凹陷及多量微绒毛的出现是微血管通透性增高的结构基础。结论 :单纯缺血和再灌注损伤都可引起微血管通透性的改变 ,但超微结构的变化提示有不同的机制参与通透性变化的调节。     

Effect of Mild Traumatic Brain Injury on Behavioral Reactions and Neocortical Morphology in Rats

Bulletin of Experimental Biology and Medicine - The original weight-drop model was employed to examine the effect of mild traumatic brain injury (TBI) on behavioral phenotype and neocortical...     

长期慢性脑外伤大鼠脑线粒体功能的变化

研究长期慢性轻度脑外伤对大鼠脑线粒体功能的影响。大鼠连续1、5、10、15、20、25、30d轻度闭合性颅脑撞击后分离脑线粒体,测定线粒体肿胀度、膜流动性、膜磷脂含量、呼吸功能、线粒体呼吸酶、超氧化物歧化酶(SOD)、丙二醛(MDA)和Ca2 等指标以显示线粒体功能、抗氧化能力的变化。结果显示,第15、20、25、30d大鼠脑线粒体明显肿胀,膜磷脂降解,膜流动性下降,呼吸功能衰减,呼吸酶、SOD活性降低,Ca2 、MDA含量升高。由此认为,经常性头部撞击可造成大鼠脑线粒体功能受损,其机制可能与脑线粒体膜损伤后继发的自由基生成增加、脑线粒体能量代谢障碍有关。     

周期蛋白依赖性激酶-5在创伤性脑损伤中的表达变化研究

目的:探讨周期蛋白依赖性激酶-5 (cyclin-dependent kinase-5,CDK5)在创伤性脑损伤(traumatic brain injury,TBI)组织中的表达变化及其意义.方法:建立成年SD(Sprague-Dawley) 大鼠TBI模型,应用免疫荧光方法检测CDK5在大鼠脑组织中的细胞定位,Western blot和RT-PCR方法检测大鼠脑组织中CDK5蛋白和mRNA的时间表达变化.结果:免疫荧光双标结果显示,CDK5与小胶质细胞的标记物CD11b、神经元的标记物NeuN共定位.CDK5在大鼠脑组织损伤后蛋白表达迅速升高,在3d升至最高点,之后逐渐降低,7d达到最低,14d后趋于平稳; RT-PCR的结果与Western blot相似.结论:急性脑损伤可诱导CDK5的表达变化和mRNA表述,这种改变可能参与脑损伤后小胶质细胞的活化和增殖过程,并与神经元的凋亡有关.     

Are the Pathobiological Changes Evoked by Traumatic Brain Injury Immediate and Irreversible?

Traumatic brain injury has long been thought to evoke immediate and irreversible damage to the brain parenchyma and its intrinsic vasculature. In this review, we call into question the correctness of this assumption by citing two traumatically related brain parenchymal abnormalities that are the result of a progressive, traumatically induced perturbation. In this context, we first consider the pathogenesis of traumatically induced axonal damage to show that it is not the immediate consequence of traumatic tissue tearing. Rather, we illustrate that it is a delayed consequence of complex axolemmal and/or cytoskeletal changes evoked by the traumatic episode which then lead to cytoskeletal collapse and impairment of axoplasmic transport, ultimately progressing to axonal swelling and disconnection. Second, we consider the traumatized brain's increased neuronal sensitivity to secondary ischemic insult by showing that even after mild traumatic brain injury, CA1 neuronal cell loss can be precipitated by the induction of sublethal ischemic insult within 24 hrs of injury. In demonstrating this increased sensitivity to secondary insult, evidence is provided that it is triggered by the neurotransmitter storm evoked by traumatic brain injury, allowing for sublethal neuroexcitation. In relation to this phenomenon, the protective effect of receptor antagonists are discussed, as well as the concept that this relatively prolonged posttraumatic brain hypersensitivity offers a potential window for therapeutic intervention. Collectively, it is felt that both examples of the brain parenchyma's response to traumatic brain injury show that the resulting pathobiology is much more complex and progressive than previously envisioned, and as such, rejects many of the previous beliefs regarding the pathobiology of traumatic brain injury.     

大鼠创伤性脑损伤后海马细胞凋亡及bcl-2、NGF-R阳性细胞的变化

目的：探讨大鼠创伤性脑损伤后不同时相海马细胞凋亡及。bcl-2、NGF—R阳性细胞的变化规律。方法：采用大鼠自由落体脑损伤模型，伤后1、2、3、4、5、7、10d取脑切片，作：Nissl染色，用TUNEL法检测细胞凋亡，免疫组化染色观察bcl-2、NGF-R阳性细胞。结果：Nissl染色可见损伤侧海马CA2、CA3区锥体细胞层细胞消失或排列紊乱。损伤侧海马凋亡细胞伤后5d达到高峰，正常侧海马各时相点均未见到凋亡细胞。损伤侧海马bcl-2阳性细胞数量下降，伤后3d至最低点；NGF—R阳性细胞数量增加，伤后5d达到高峰。结论：大鼠创伤性脑损伤后损伤侧海马细胞凋亡数量的变化与伤后时程有关。伤后细胞bcl-2表达下降、NGF-R表达增加是导致细胞凋亡的因素。     

Long-Term Executive Functioning Outcomes for Complicated and Uncomplicated Mild Traumatic Brain Injury Sustained in Early Childhood

This study investigated long-term executive functioning following early mild traumatic brain injury (TBI), differentiating between complicated (n = 34) and uncomplicated injuries (n = 18). Children post mild TBI were compared to 33 controls at least 7-years post-injury. The complicated mild TBI group performed significantly worse on divided attention compared to both groups, with younger age at injury and neurological symptoms predictors of outcome. No significant group differences existed on speed of information processing, selective attention, working memory, or goal setting. These findings indicate that specific aspects of executive function are compromised by early complicated mild TBI and argue for a stratified definition of mild TBI.     

The WRAIR Projectile Concussive Impact Model of Mild Traumatic Brain Injury: Re-design,Testing and Preclinical Validation

The WRAIR projectile concussive impact (PCI) model was developed for preclinical study of concussion. It represents a truly non-invasive closed-head injury caused by a blunt impact. The original design, however, has several drawbacks that limit the manipulation of injury parameters. The present study describes engineering advancements made to the PCI injury model including helmet material testing, projectile impact energy/head kinematics and impact location. Material testing indicated that among the tested materials, ‘fiber-glass/carbon’ had the lowest elastic modulus and yield stress for providing an relative high percentage of load transfer from the projectile impact, resulting in significant hippocampal astrocyte activation. Impact energy testing of small projectiles, ranging in shape and size, showed the steel sphere produced the highest impact energy and the most consistent impact characteristics. Additional tests confirmed the steel sphere produced linear and rotational motions on the rat’s head while remaining within a range that meets the criteria for mTBI. Finally, impact location testing results showed that PCI targeted at the temporoparietal surface of the rat head produced the most prominent gait abnormalities. Using the parameters defined above, pilot studies were conducted to provide initial validation of the PCI model demonstrating quantifiable and significant increases in righting reflex recovery time, axonal damage and astrocyte activation following single and multiple concussions.     

高压氧治疗对急性脑外伤大鼠神经功能修复及BDNF表达的影响

目的探讨高压氧治疗对急性脑外伤大鼠神经行为功能及脑源性神经营养因子(BDNF)表达的影响。方法成年SD大鼠24只,随机分配为3组:假手术组、脑外伤组及高压氧治疗组。假手术组仅行开颅手术不致脑外伤;脑外伤组采用Alice打击法制作脑外伤模型;高压氧治疗组在脑外伤基础上行高压氧治疗1个疗程,即每天1次,治疗10天。伤后第14天对大鼠进行神经功能缺损评分,然后处死大鼠,获取脑组织,采用RT-PCR方法测定BDNF mRNA的表达,用免疫组织化学结合图像分析技术确定BDNF光密度值变化。结果与脑外伤组比较,高压氧治疗组NSS评分明显降低,差异均有统计学意义(P<0.01)。同时,高压氧治疗组BDNF mRNA明显增高,差异有统计学意义(P<0.05)。结论高压氧治疗能明显改进急性脑外伤大鼠神经功能并增加BDNF表达。     

创伤性脑损伤活体脑片不同时相的脂质过氧化损伤

目的 观测创伤性脑损伤后不同时间大鼠脑组织的脂质过氧化损伤。方法 70只SD大鼠随机分为假损伤组（n=10）和脑损伤组，损伤组按伤后1、6、24、48、72和168h观察时间点分为6个亚组（n=10）。用Feeney氏自由落体撞击法制作重型颅脑损伤模型。利用激光扫描共聚焦显微镜观察损伤后不同时间荧光探剂2，7-二氯氢化荧光素（H2DCFDA）与碘化丙啶（PI）标记的活体脑片细胞内脂质过氧化物的动态变化和细胞死亡程度。结果 ①1、6、24h损伤组脂质过氧化物明显增加（P〈0．05），48h达到峰值，之后下降，72h已显著下降（P〈0．05），168h恢复正常水平。②1、6h损伤组神经细胞死亡明显增加（P〈0．05），24h达到峰值，之后维持不变，24、48、72及168h各损伤组之间细胞死亡无明显差异（P〉0．05）。③脂质过氧化物引起神经细胞死亡。结论 创伤性脑损伤早期（〈72h）脑组织即发生脂质过氧化反应引起神经细胞死亡，并且将持续一周。脂质过氧化物在创伤性脑损伤的继发损害中起重要作用。     

小脑缺血再灌注损伤后形态学及NGF、BDNF表达的研究

目的研究缺血再灌注损伤(IRI)不同时间青年大鼠小脑皮质结构的改变和NGF、BDNF表达的变化,进一步探讨NGF、BDNF对小脑IRI的神经营养保护作用。方法健康雄性SD大鼠56只随机分成正常组、对照组和模型组,模型组分为IRI 6h、24h、2d、4d和7d组,用HE染色和电镜观察缺血再灌注不同时间段小脑皮质神经元的形态改变,用免疫组织化学检测NGF、BDNF表达的改变。结果 IRI后2d小脑形态的病理损伤最为严重。正常大鼠小脑浦肯野细胞NGF有少量表达,IRI后6h表达增加,2d达高峰,主要表达在浦肯野细胞和颗粒层,分子层少量表达,髓质无表达;正常大鼠浦肯野细胞BDNF有少量表达,IRI后6h表达增加,2d达高峰,主要表达在浦肯野细胞和颗粒层,分子层少量表达,髓质无表达。结论 NGF和BDNF参与了小脑IRI的病理过程,发挥了神经保护作用。     

Sports Neuropsychology: Assessment and Management of Traumatic Brain Injury

The speed of information processing was examined in a group of patients in the early stages of Alzheimer's disease (AD) and in a group of healthy, age‐and educationally matched controls. Subjects were tested on auditory simple‐reaction time (RT), visual choice‐RT, and combined simple‐ and choice‐RT tasks. The choice‐RT task required elementary linguistic or visuoperceptual matching of successively presented stimuli. AD patients had normal simple RTs but had delayed RTs on the matching tasks, suggesting a slower rate of processing for the component mental operations of the matching tasks. Estimates of the attentional demands or costs of these mental operations—stimulus encoding, decision making, and response selection—were obtained by combining the matching task with the simple‐RT task (probe‐RT). AD patients again showed a significant slowing in choice‐RT, although they exhibited normal accuracy or performance outcome. AD patients also showed increased attentional cost for letter encoding (as reflected in increased probe‐RT) but not for the other constituent mental operations. The results suggest that the differential slowing of choice‐RT in AD is related to the complexity and attentional demands associated with coordinating and executing the matching tasks.