脑损伤后神经内分泌改变研究进展

神经系统和内分泌系统是机体中相互制约和相互协调的两大调节系统.脑损伤后由于存在应激反应,以及脑组织的解剖结构发生改变,可引起下丘脑和垂体的直接和间接损伤,导致垂体内分泌功能发生变化,垂体分泌的各种激素也会受到影响,使机体产生一系列的代谢紊乱,出现各种并发症.近年来,脑损伤患者的死亡率呈上升趋势,研究脑损伤后神经内分泌改变,可以指导临床有针对性地治疗,为脑损伤患者康复治疗提供了新的方向.     

脑出血恢复期内分泌激素异常的研究

目的 探讨脑出血恢复期患者内分泌激素变化情况.方法 用放射免疫法测定90例脑出血患者发病后3个月,6个月,12个月周围静脉血中FT3、FT4、TSH、GH、ACTH、Cor、PRL、T、E2、FSH、LH、P的浓度.分析内分泌异常的发生率及其与出血量、有无并发症及恢复时间的关系.结果 内分泌激素异常在发病后3个月时发生率11.1％,6个月时发生率8.9％,12个月时发生率7.8％.随着恢复时间的延长逐渐下降,出血量越大分泌异常发生率越高,发病当时有并发症者恢复期内分泌激素异常发病率高.结论 脑出血恢复期内分泌异常有一定的发生率,有必要对恢复期患者进行常规的内分泌激素水平检查,并用于指导治疗.     

自体神经干细胞原位激活与缺血性脑损伤

缺血性脑血管病是严重威胁人类健康的常见病和多发病,已经成为当今第三大致死疾病及首位致残原因犤1犦。其病理过程涉及复杂的时间和空间级联反应,虽然对其机制的了解越来越深入,但有效的治疗手段仍然缺乏。对于大多数脑缺血患者,神经元死亡不可避免,是治疗难以取得满意效果的主要原因。近年来,已经从胚胎及成年的脑组织分离出具有自我更新、能够分化成神经元和神经胶质细胞的神经干细胞(neuralstemcell,NSC)。因为NSC能促进神经元再生及损伤脑组织恢复,许多学者开始研究NSC移植对脑缺血的治疗作用,并取得了一定进展,但由于免疫排斥及技…     

合并多器官功能衰竭的急性脑血管病患者神经内分泌的改变

本实验动态测定了急性脑血管病（ＡＣＶＤ）并发多器官功能衰竭（ＭＯＦ）患者血清生长激素（ＧＨ）、泌乳素（ＰＲＬ）、促黄体生长素（ＬＨ）、促滤泡成熟激素（ＦＳＨ）、睾酮（Ｔ）、孕酮（Ｐ）、雌二醇（Ｅ２）、皮质醇（Ｆ）和血浆促肾上腺皮质激素（ＡＣＴＨ）水平的变化，并与ＡＣＶＤ各疾病组对比。结果发现：ＧＨ、ＰＲＬ、ＡＣＴＨ、Ｆ及ＦＳＨ水平显著升高；ＡＣＶＤ并发ＭＯＦ重型患者（ＭＯＦ积分＞４分）ＰＲＬ、ＧＨ、Ｆ水平显著高于轻型患者（ＭＯＦ积分≤４分）。结果提示ＰＲＬ、ＧＨ和Ｆ可能参与了ＡＣＶＤ并ＭＯＦ的病理生理过程     

强迫症的神经内分泌研究

对探讨强迫症患者的下丘脑－垂体－肾上腺皮质系统的功能状态及强迫症与抑郁症的生物联系，作者对３０例未服药的强迫症患者的基础血浆皮质醇、地塞米松抑制试验（ＤＳＴ）及氯丙咪嗪治疗前后的血催乳素含量进行测定，并以２０例健康志愿者的血浆皮质醇、ＤＳＴ和血催乳素测定值作对照。结果显示：强迫症患者基础血浆皮质醇和基础血催乳素含量高于对照组，但ＤＳＴ无一例呈脱抑制反庆；患者经氯丙咪嗪治疗后，血浆催乳素含量明显升高     

ECT后神经内分泌的变化

近十几年,国外许多研究者用不同方法对ECT治疗引起的神经内分泌变化进行了大量的研究,并提出了若干假设。本文扼要介绍这方面的研究及结果。     

神经干细胞与缺血性脑损伤

介绍神经干细胞及其在缺血性脑损伤中的作用     

皮肤神经内分泌癌一例报告

患者,女,53岁,于2001年无明显诱因发现头顶有一拇指大小肿物,质地软,不痛,皮肤颜色、感觉无异常,无脱屑、破溃等异常。未予特殊处理。2005年9月起肿物迅速增大,质地软,不痛,皮肤颜色、感觉无异常,予膏药外敷后,皮肤出现破溃、     

神经干细胞治疗缺血性脑损伤研究进展

缺血性脑血管病是严重威胁人类健康的常见病和多发病,其病理过程涉及复杂的时间和空间级联反应,虽然对其机制的了解越来越深入,但有效的治疗手段仍然缺乏.对于大多数脑缺血患者,神经元死亡不可避免,是治疗难以取得满意效果的主要原因.近年来,已经从胚胎及成年的脑组织分离出具有自我更新、能够分化成神经元和胶质细胞的神经干细胞(neural stem cells, NSCs).因为NSCs能促进神经元再生及损伤脑组织恢复,许多学者开始研究NSCs对脑缺血的治疗作用,已经取得了重大进展.NSCs治疗缺血性脑损伤主要有两个途径:NSCs移植和自体NSCs原位激活.     

创伤性脑损伤后垂体前叶功能减退及临床意义

创伤性颅脑损伤(traumatic brain injure,TBI)后出现神经内分泌功能紊乱并不少见,TBI与神经内分泌的关系日益受到关注,垂体前叶功能减退可以显著影响颅脑损伤患者功     

垂体前叶黄体生成素对重度颅脑创伤病情及预后的监测与评估

目的研究急性颅脑创伤病人垂体前叶黄体生成素（luteinizing hormone,LH）的动态变化及其对病情及预后的评估.方法随机选取1999年12月至2001年6月间急性颅脑创伤住院病人50例,按照GCS分数、GOS不同的预后、不同的创伤类型、CT中线移位程度等因素分别进行了分析研究.同时设立对照组12例.结果颅脑创伤组LH值明显高于正常对照组.颅脑创伤的程度越重,伤后即刻的LH值越高,而动态观察则快速下降,波动幅度大,其伤后入院即刻检测值与入院第3天的检测值之比值也就越大.如GCS 3～5分组,死亡组,重度中线移位组,脑挫伤组的情况都是如此.伤情较轻者,黄体生成素升高的程度较小,且伤后48 h逐渐恢复正常,波动幅度小,其伤后入院即刻检测值与伤后入院第3天的检测值之比值也就越小.结论颅脑创伤病人伤后LH的动态变化可以作为伤情判断和判断预后的重要指标之一.凡伤后LH明显升高而48 h后明显降低者,入院检测的LH值与入院后72 h所检测的LH比值大于3者,预示伤情严重且预后不良.     

经亚低温治疗的重型脑损伤患者外周血NSE的动态变化及临床意义

目的研究经亚低温治疗的重型脑损伤患者其外周血神经元特异性烯醇化酶(NSE)的动态变化及其临床意义。方法52例重型脑损伤患者随机分为亚低温组和对照组,前者进行亚低温治疗,后者除了不进行亚低温治疗外其他治疗方法与前者相同,分别于手术的次日、第2、3、5、7天测其外周血的NSE,满3个月进行GOS预后评分。结果发现经过一定时间的亚低温治疗,亚低温组外周血的NSE与对照组比较有明显的差异,满3个月进行GOS预后评分,亚低温组明显优于对照组(P＜0．05)。结论亚低温的确是治疗重型颅脑损伤的有效手段之一,其外周血NSE的动态变化能够准确反映治疗效果,而且简便易行,是评价重型脑损伤患者伤情及预后的客观指标之一。     

脑外伤后的注意、记忆和信息处理能力障碍及其恢复

用划消测验、同步听觉系列加法测验及临床记忆量表对105例脑外伤患者进行了测查,以观察脑外伤后患者的注意、记忆和信息处理能力受损程度,并在伤后5个月左右进行复查,以观察上述障碍的恢复情况。49名年龄和文化水平相当的正常人作为对照组。结果表明脑外伤后注意、记忆、信息处理能力均显著受损。5个月左右后中型脑外伤患者上述障碍已基本恢复。重型脑外伤患者上述心理功能虽有明显恢复,但尚未恢复到正常水平。     

Myelinated and unmyelinated axons of the corpus callosum differ in vulnerability and functional recovery following traumatic brain injury

Traumatic axonal injury (TAI), a common feature of traumatic brain injury, is associated with postinjury morbidity and mortality. However, TAI is not uniformly expressed in all axonal populations, with fiber caliber and anatomical location influencing specific TAI pathology. To study differential axonal vulnerability to brain injury, axonal excitability and integrity were assessed in the corpus callosum following fluid percussion injury in the rat. In brain slice electrophysiological recordings, compound action potentials (CAPs) were evoked in the corpus callosum, and injury effects were quantified separately for CAP waveform components generated by myelinated axons (N1 wave) and by unmyelinated axons (N2 wave). Ultrastructural analyses were also conducted of TAI-induced morphological changes in these axonal populations. The two populations of axons differed in response to brain injury, and in their functional recovery, during the first week postinjury. Amplitudes of N1 and N2 were significantly depressed at 3 h, 1 day, and 3 days survival. N1 amplitudes exhibited a recovery to control levels by 7 days postinjury. In contrast, N2 amplitudes were persistently suppressed through 7 days postinjury. Strength-duration properties of evoked CAPs further differentiated the effects of injury in these axonal populations, with N2 exhibiting an elevated strength-duration time constant postinjury. Ultrastructural observations revealed degeneration of myelinated axons consistent with diffuse injury sequelae, as well as previously undocumented pathology within the unmyelinated fiber population. Collectively, these findings demonstrate differential vulnerabilities of axons to brain injury and suggest that damage to unmyelinated fibers may play a significant role in morbidity associated with brain injury.     

Focal traumatic brain injury causes widespread reductions in rat brain norepinephrine turnover from 6 to 24 h

The effect of right sensorimotor traumatic brain injury (TBI) in male Sprague-Dawley rats on brain norepinephrine (NE) turnover was assessed by measuring the decline of endogenous NE levels following tyrosine hydroxylase inhibition produced with α-methyl-p-tyrosine. Right sensorimotor cortex contusions were produced by a pneumatically driven piston which depressed the dural surface by 2 mm at 3.2 m/s. TBI rats were compared to uninjured, anesthetized controls at 6 h and 24 h after surgery. While NE turnover was not affected at the lesion site at 6 h after TBI, it was either abolished or decreased by 33–75% bilaterally in the hypothalamus and in the cerebral cortex surrounding and rostral to the lesion site. In the cortex caudal to the lesion site, NE turnover was completely abolished. NE turnover in cerebral cortex opposite the lesion site and in the contralateral cerebellum was decreased by 51 and 43%, respectively, at 6 h. At 24 h, NE turnover was either abolished or decreased bilaterally by 45–92% in all cortical areas, in the hypothalamus, cerebellum, locus coeruleus and medulla. Thus, right sensorimotor cortex contusion causes a marked, early and widespread depression of brain NE turnover. Since amphetamine increases NE turnover, this may explain the dramatic improvement in behavioral deficits which occurs following amphatamine administration at 24 h after such lesions.     

颅脑损伤后大鼠脑皮质中神经丝的改变Calpain活性的变化及两者之间的关系研究

目的观察颅脑损伤后大鼠脑皮质中神经丝的改变,同时检测Calpain活性的变化,探讨两者之间的关系及其对治疗颅脑损伤的意义。方法 25只雄性Wistar大鼠,随机分为正常对照组、颅脑损伤组(颅脑损伤后6h、12h、24h、72h)共5组,每组5只。采用Myneurolab脑立体定向仪和Benchmark颅脑损伤撞击器制作创伤性颅脑损伤模型。应用免疫组化法检测上述时间点损伤灶周围皮层中神经丝的形态改变,检测Calpain活性的变化。结果颅脑损伤后,神经丝的结构紊乱,降解逐渐增多,伤后24h时降解达到最高点,随后降解的神经丝逐渐减少。颅脑损伤后Calipain活性随时间逐渐升高,伤后24h时活性达到最高点,随后逐渐降低。结论颅脑损伤后神经丝降解的机制可能与Calipain活性的变化有关。     

弥漫性脑损伤微血管形态学研究

目的 运用形态计量学方法研究弥漫性脑损伤（DBI）大鼠模型的微循环及胶质细胞形态学改变，并观察萘呋胺酯（NF）对DBI的治疗作用。方法 采用Marmarou的DBI模型，光镜下测量顶叶皮质内微血管及其周围水肿区的截面面积，电镜下半定量测定皮质区毛细血管周的水肿范围及胶质细胞胞体的肿胀程度。结果 外伤后2、6、24小时平均微血管截面面积与对照组比较无显著缩小，6、24小时微血管周水肿明显增加。NF组伤后2小时微血管无扩张，但其周围水肿增加，24小时两者均改善。电镜下2、24小时毛细血管周水肿明显；胶质细胞胞体肿胀在2小时明显，24小时无显著差异；NF在2小时能减轻胶质细胞肿胀程度，但对毛细血管周水肿范围影响不大。结论 形态计量学方法能准确反映脑外伤后微循环及脑水肿改变。外伤早期慎用血管扩张药物。     

颅脑损伤后脑脊液C-反应蛋白与颅内压相关性及临床意义

目的探讨颅脑损伤后脑脊液C-反应蛋白(CRP)与颅内压变化的关系。方法颅脑损伤患者65例,按GCS评分分为轻型组15例,中型组20例,重型组30例。腰椎穿刺检测脑脊液压力,同时采集其伤后1 d内至4 w的脑脊液,以免疫比浊法测定脑脊液中CRP的含量,将脑脊液中CRP的含量与颅内压变化进行比较。结果伤后轻、中、重型各组脑脊液CRP与颅内压变化存在组间差异(P0.01);CRP含量的变化与颅内压变化呈正相关。结论脑脊液中CRP的含量是反映颅脑损伤急性期脑组织损伤的敏感指标,能反映颅脑损伤后颅内压变化趋势。     

Clinical significance of skull base fracture in patients after traumatic brain injury

About 4% of all head injuries include skull base fractures. Most of these fractures (90%) are secondary to closed head trauma; the remainder are due to penetrating trauma. We reviewed the records from January 2006 through December 2008 of all patients older than 18 years of age who arrived at Soroka Medical Center in Be’er-Sheva, Israel, with skull base fractures following a traumatic brain injury (TBI). We identified 107 patients with a mean age of 42 years at the time of TBI. Glasgow Coma score on arrival predicted the clinical outcome. We observed temporal fractures in 30% of these patients, occipital fractures in 20%, pyramidal fractures in 19%, anterior skull base fractures in 17%, and multiple fractures in 14%. Cerebrospinal fluid (CSF) leak was observed in 16 patients (15%). Of the patients experiencing CSF leaks, otorrhea occurred in 10 (62%) and rhinorrhea occurred in six (37%). Three patients required surgical intervention to repair the leak. Meningitis occurred in four patients with clinically evident CSF leak. Multiple skull base fractures are associated with poor neurological outcome. The low rate of meningitis in this patient sample implies that there is no indication to administer prophylactic antibiotics to patients with skull base fractures.     

中性粒细胞弹性蛋白酶在脂多糖致幼鼠感染性脑损伤中的表达及意义

目的 通过建立脂多糖(LPS)致幼鼠感染性脑损伤模型,观察中性粒细胞弹性蛋白酶(NE)的表达变化,探讨其作用机制. 方法 将1月龄SD大鼠80只按随机数字表法分为2组:LPS组(n=40),颈外动脉注射LPS建立感染性脑损伤模型;对照组(NS组,n=40),颈外动脉注射等量生理盐水.2组按LPS注射后不同时间点分为24 h、48 h 2个时间点(各时间点n=20).于相应时间点抽血检测NE的表达,并处死幼鼠取脑组织,甲酰胺法测定伊文思蓝(EB)含量,酶联免疫吸附法测定NE含量. 结果 LPS组24 h、48 h脑组织EB、NE含量以及血清NE含量均高于NS组,比较差异有统计学意义(P＜0.05).LPS组24 h、48 h脑组织NE含量与EB含量呈正相关关系(r=.903,P＜0.001;r=.908,P＜0.001). 结论 NE参与了幼鼠感染性脑损伤的发展过程,且与血脑屏障损伤程度呈正相关性.