拳击运动伤的诊治和文献回顾

本文总结我科近5年来所诊疗过的拳击运动伤54例,并回顾性分析近10年来的相关文献(因国内相关研究较少,主要为国外的文献)对拳击运动伤诊治和特点略加总结。1资料与方法1.1一般资料男性拳击运动员,年龄分布18～42岁,平均年龄24岁,中位年龄(24.3±6.5)岁。其中门诊18例,主要症状表现为健忘、间断头晕、反应迟缓等,头颅CT均未见明显异常,头颅MR检查可见6例有点状脑软化灶,2例可见脑额颞叶区短T1长T2信号影,考虑为变性改变;急诊36例,均为在比赛或训练时所致损伤,主要为头面部外伤,1例     

颅脑损伤后垂体功能减退的相关危险因素分析

颅脑损伤后引起垂体功能减退的报道日渐增多[1-3],在急性期和恢复期均可发生,从而导致颅脑损伤恢复延迟或阻碍恢复,部分患者甚至因为严重神经内分泌紊乱引起内环境失调而死亡.因此在颅脑损伤的救治中内分泌障碍、内环境失衡应予以重视.本文将对颅脑损伤后相关危险因素结合文献进行临床分析. 资料与方法 1.临床资料:选择2008年12月至2010年6月收治的不同原因外伤所致的颅脑损伤患者119例,其中男87例,女32例;年龄16 ～ 83岁,平均(36.9±14.6)岁.车祸伤61例,坠落伤22例,暴力打击伤15例,摔伤13例,其他伤8例.均有明确头部外伤史,经头颅CT检查确诊,符合国内颅脑损伤诊断标准[4].     

单纯性中型颅脑损伤的临床特征与预后分析

目的总结伤后24h内入院时表现为单纯性中型颅脑损伤病人的临床特征及影响预后的因素。方法对我科78例单纯性中型颅脑损伤病人的临床资料进行了回顾分析。结果78例病人中恢复良好54例（69．2％）,中残11例（14．1％）,重残6例（7．7％）,植物生存2例（2．6％）,死125例（6．4％）。结论中型颅脑损伤有独特的临床特点,重视研究其疾病特征,明确与其预后密切的相关因素,对提高疗效、减少医疗纠纷有着重要意义。     

双额叶脑挫裂伤的临床治疗(附27例分析)

双额叶脑挫裂伤是闭合性颅脑损伤中一种较严重的脑损伤,因为我们县级医院收治颅脑损伤病人较多,所以笔者总结了我院自1989－1997以来收治的双额叶脑挫裂伤27例,对其不同的治疗方法,临床变化及预后进行了临床观察分析,报告如下：1一般资料1．1全组27例,男性23例,女性4例,男女比5．6：1;年龄：20－75岁,平均为46．8岁,以35－45岁多见,车祸伤13例,跌摔伤6例,拳击伤6例,坠落伤2例,受伤部位以枕部最常见。同期收治颅脑损875例,双额叶脑挫伤占3％,1．2诊断方法伤倒入院后头颅0平扫证实,l例因病重,脑疲晚期急行开颅探查证实。…     

颅内压及动态心电图监护在重型颅脑损伤中的应用

对30例重型颅脑损伤病人进行颅内压(ICP,)与动态心电图(DCG)的连续监护.结果显示:3O例重型颅脑损伤患者中,同时有ICP及DCG异常改变者24例,占80%.4例死于特重型颅脑损伤及并发症的患者均有明显的心电图改变,余20例经治疗伤情逐渐平稳、好转及康复,其心电图改变也随病情好转而逐渐恢复至正常或好转.说明重型颅脑损伤的ICP和DCG监护对伤情和预后的判断有较高的临床价值.     

外伤性胼周动脉瘤

报告２例减速性颅脑伤所致的胼周动脉瘤，伤后经治疗症状好转，分别于伤后２５和３３天再次恶化。经头颅ＣＴ和颈动脉造影（ＣＡＧ））确诊后手术。指出患者脑外伤经治疗症状好转或消失，数天或数周后又恶化，ＣＴ发现一侧额叶内血肿伴脑室积血，是外伤性胼周动脉瘤破裂的典型表现，应进一步做ＣＡＧ确诊，及时手术预后良好。文中讨论了胼周动脉损伤的机制。     

颅脑外伤后并发中枢性低钠血症37例临床分析

目的 探讨颅脑外伤后引起中枢性低钠血症的原因、发病机制、诊断及治疗方法.方法 回顾分析本院2009-12-2014-07颅脑外伤后低钠血症患者37例的诊断和治疗.结果 31例经及时正确处理血钠恢复正常,病情好转,4例放弃治疗自动出院,2例因原发性脑干损伤并发MODS而死亡.结论 中枢性低钠血症患者正确分型、快速诊断、及时处理能够达到满意的疗效和预后.     

婴幼儿颅脑损伤临床分析

目的总结分析婴幼儿颅脑损伤的临床特点.方法回顾性研究婴幼儿颅脑损伤患者的致伤原因、损伤类型、临床表现、救治方法和预后状况.结果本组年龄15 d～2岁婴幼儿150例,其中坠落伤79例,跌伤35例,共占76.0%;闭合性颅脑损伤126例;开放性颅脑损伤24例.合并颅内血肿62例(41.30%),并发颅骨骨折62例(41.30%).伤后所有婴幼儿均有不同程度的呼吸、心率变化;伤后意识障碍147例( 98%);16例(10.70%)有大面积脑缺血表现.本组手术治疗54例,保守治疗96例.格拉斯哥预后评级(GOS):恢复良好131例(87.33%);中残8例(5.33%);重残6例(4.0%);植物生存1例(0.67%);死亡4例,死亡率2.67%.结论婴幼儿颅脑损伤以坠落伤和跌伤较多见,加强监护是避免损伤的重要途径;婴幼儿颅脑损伤的主要临床特点是:生命体征紊乱明显;临床症状与病情不符;颅骨凹陷骨折和颅缝分离多见;外伤后脑缺血多见,且损害较重;组织修复能力强,预后较好.     

原发性脑干损伤

本文报告76例原发性脑干损伤,占同期收治的急性颅脑损伤的3.0％,占重型颅脑损伤的5.1％。总死亡率为71.1％(54例),其中59.3％(32例)死于伤情过重,33.3％(18例)死于各种并发症,7.4％(4例)死于合并伤。 本文对原发性脑干损伤的受伤原因和机制,临床表现,合并伤和并发症及诊断和治疗进行了分析和讨论。     

重症颅脑损伤患者脑氧利用率的变化及其意义

对于重症颅脑损伤过去多从患者的意识状态、生命体征、眼部征象、运动功能以及颅内压等方面进行伤情评价,而对于脑氧代谢的改变及重要性尚未引起人们足够的重视.本文对40例重症颅脑损伤患者的脑氧利用率变化进行了研究,进一步分析了其在评估病情、指导治疗中的意义.     

Intravenous multipotent adult progenitor cell therapy for traumatic brain injury: Preserving the blood brain barrier via an interaction with splenocytes

Recent investigation has shown an interaction between transplanted progenitor cells and resident splenocytes leading to the modulation of the immunologic response in neurological injury. We hypothesize that the intravenous injection of multipotent adult progenitor cells (MAPC) confers neurovascular protection after traumatic brain injury through an interaction with resident splenocytes, subsequently leading to preservation of the blood brain barrier.Four groups of rats underwent controlled cortical impact injury (3 groups) or sham injury (1 group). MAPC were injected via the tail vein at two doses (2 * 10⁶ MAPC/kg or 10 * 10⁶ MAPC/kg) 2 and 24 h after injury. Blood brain barrier permeability was assessed by measuring Evans blue dye extravasation (n = 6/group). Additionally, splenic mass was measured (n = 12/group) followed by splenocyte characterization (n = 9/group) including: cell cycle analysis (n = 6/group), apoptosis index (n = 6/group), cell proliferation (n = 6/group), and inflammatory cytokine measurements (n = 6/group). Vascular architecture was determined by immunohistochemistry (n = 3/group).Traumatic brain injury results in a decrease in splenic mass and increased blood brain barrier permeability. Intravenous infusion of MAPC preserved splenic mass and returned blood brain barrier permeability towards control sham injured levels. Splenocyte characterization indicated an increase in the number and proliferative rate of CD4+ T cells as well as an increase in IL-4 and IL-10 production in stimulated splenocytes isolated from the MAPC treatment groups. Immunohistochemistry demonstrated stabilization of the vascular architecture in the peri-lesion area.Traumatic brain injury causes a reduction in splenic mass that correlates with an increase in circulating immune cells leading to increased blood brain barrier permeability. The intravenous injection of MAPC preserves splenic mass and the integrity of the blood brain barrier. Furthermore, the co-localization of transplanted MAPC and resident CD4+ splenocytes is associated with a global increase in IL-4 and IL-10 production and stabilization of the cerebral microvasculature tight junction proteins.     

钙离子在创伤性脑损伤中的致病机制研究

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。     

Genetic polymorphisms and traumatic brain injury: the contribution of individual differences to recovery

Recovery after Traumatic Brain Injury (TBI) is variable, even for patients with similar severity of brain injury. Recent research has highlighted the contribution that genetic predisposition plays in determining TBI outcome. This review considers the potential for genetic polymorphisms to influence recovery of cognitive and social processes following TBI. Limitations and considerations that researchers should make when assessing the potential impact of polymorphisms on TBI outcome are also discussed. Understanding the genetic factors that support neuroplasticity will contribute to an understanding of the variation in outcome following injury and help to identify potential targets for rehabilitation.     

Altered seizure susceptibility and vesicular glutamate transporter subtype 1 immunoreactivity in a rat model of hypoxic brain injury☆

BACKGROUND：To the best of our knowledge, few studies have analyzed the effects of hypoxic brain injury on seizure susceptibility and pathophysiological mechanisms underlying seizure susceptibility following hypoxic brain injury. OBJECTIVE： To investigate changes in seizure susceptibility and neuronal loss, as well as expression of vesicular glutamate transporter subtype 1（VGluT1）, following hypoxic cerebral insult. DESIGN, TIME AND SETTING： A randomized controlled animal experiment was performed in the Department of Neurology, The Second Affiliated Hospital, Chongqing Medical University, between May 2006 and September 2007. MATERIALS： Seventy, male, Sprague Dawley rats, weighing 230–270 g, were used in the present study. Pentylenetetrazol （PTZ） was purchased from Sigma. Mouse NeuN monoclonal antibody and rabbit VGluT-1 polyclonal antibody were purchased from Chemicon and Gene Tex, respectively. METHODS： Rats were randomly assigned to control and hypoxia groups （n = 35 for each group）. Hypoxia was induced in rats using 8% oxygen-nitrogen gas mixture. Control rats were subjected to the same procedures, but with exposure to room air. MAIN OUTCOME MEASURES： Rats （n = 15 for each group） received intraperitoneal injections of PTZ, a sub-convulsive dose of 35 mg/kg/2 d for 20 days. The success of model establishment, as well as seizure scales, was measured. Rats from both groups, which were successfully kindled with PTZ, were divided into simple kindling and post-hypoxic kindling, respectively. A separate group, including rats from simple kindling and post-hypoxic kindling, was studied for neuronal loss and VGluT1 expression in the temporal cortex, midbrain, and hippocampal CA1 subfield using immunohistochemistry and western blot techniques, respectively. RESULTS： Seventy rats were included in the final analysis. （1）Compared with control animals （n = 7）, seizure scales were greater in hypoxic rats （n = 11）, which indicates that post-hypoxic rats reacted more sensitive to kindl     

Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats**☆

BACKGROUND： In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor （BDNF） can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE： To explore changes in BDNF expression and cognitive function in rats after brain injury. DESIGN, TIME AND SETTING： The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University （China） from July 2007 to July 2008. MATERIALS： A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS： Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney＇s method （n = 24, each group）. A bone window was made in rats from the sham operation group （n = 24）, but no attack was conducted. MAIN OUTCOME MEASURES： At days 1, 2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry （streptavidin-biotin-peroxidase complex method）. Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS： Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups （P 〈 0.05）. CONCLUSION： BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats following i     

Altered protein markers related to neural plasticity and motor function following electro-acupuncture treatment in a rat model of ischemic-hypoxic brain injury *☆

BACKGROUND：Previous studies have demonstrated that acupuncture treatment could ameliorate impaired motor function,and these positive effects might be due to neural plasticity.OBJECTIVE：Myelin basic protein（MBP）,microtubule-associated protein 2（MAP2）,growth-associated protein-43（GAP-43）,and synaptophysin（SYN） were selected as markers of neural remodeling,and expression of these markers was evaluated with regard to altered motor function following brain injury and acupuncture treatment.DESIGN,TIME AND SETTING：A completely randomized experiment was performed at the Central Laboratory of Peking University First Hospital from November 2006 to May 2007.MATERIALS：Twenty-four Sprague Dawley rat pups,aged 7 days,were selected for the present experiment.The left common carotid artery was ligated to establish a rat model of ischemic-hypoxic brain injury.METHODS：All animals were randomly divided into three groups：sham operation,model,and electro-acupuncture treatment,with 8 rats in each group.Rats in the model and electro-acupuncture treatment group underwent establishment of ischemic-hypoxic brain injury.Upon model established,rats underwent hypobaric oxygen intervention for 24 hours.Only the left common carotid artery was exposed in rats of the sham operation group,without model establishment or oxygen intervention.The rats in the electro-acupuncture treatment group were treated with electro-acupuncture.One acupuncture needle electrode was inserted into the subcutaneous layer at the Baihui and Dazhui acupoint.The stimulation condition of the electro-acupuncture simulator was set to an amplitude-modulated wave of 0-100% and alternative frequency of 100 cycles/second,as well as frequency-modulated wave of 2-100 Hz and an alternative frequency of 3 cycles/second.Maximal current through the two electrodes was limited to 3-5 mA.The stimulation lasted for 30 minutes per day for 2 weeks.Rats in the sham operation and model groups were not treated with electro-acupuncture,but only fixed to the table for     

Matrix metalloproteinase-9 expression and blood brain barrier permeability in the rat brain after cerebral ischemia/reperfusion injury**☆

BACKGROUND： The integrity of the blood brain barrier （BBB） plays an important role in the patho-physiological process of cerebral ischemia/reperfusion injury. It has been recently observed that metalloproteinase-9 （MMP-9） is closely related to cerebral ischemia/reperfusion injury OBJECTIVE： This study was designed to observe MMP-9 expression in the rat brain after cerebral ischemia/reperfusion injury and to investigate its correlation to BBB permeability. DESIGN, TIME AND SETTING： This study, a randomized controlled animal experiment, was performed at the Institute of Neurobiology, Central South University between September 2005 and March 2006. MATERIALS： Ninety healthy male SD rats, aged 3-4 months, weighing 200-280 g, were used in the present study. Rabbit anti-rat MMP-9 polyclonal antibody （Boster, Wuhan, China） and Evans blue （Sigma, USA） were also used. METHODS： All rats were randomly divided into 9 groups with 10 rats in each group： normal control group, sham-operated group, and ischemia for 2 hours followed by reperfusion for 3, 6, 12 hours, 1, 2, 4 and 7 days groups. In the ischemia/reperfusion groups, rats were subjected to ischemia/reperfusion injury by suture occlusion of the right middle cerebral artery. In the sham-operated group, rats were merely subjected to vessel dissociation. In the normal control group, rats were not modeled. MAIN OUTCOME MEASURES： BBB permeability was assessed by determining the level of effusion of Evans blue. MMP-9 expression was detected by an immunohistochemical method. RESULTS： All 90 rats were included in the final analysis. BBB permeability alteration was closely correlated to ischemia/reperfusion time. BBB permeability began to increase at ischemia/reperfusion for 3 hours, then it gradually reached a peak level at ischemia/reperfusion for 1 day, and thereafter it gradually decreased. MMP-9 expression began to increase at ischemia/reperfusion for 3 hours, then gradually reached its peak level 2 days after perfusion, and thereafter it grad     

门冬氨酸钾减轻大鼠可控性皮质打击伤引起的脑损伤

目的 门冬氨酸钾（potassium aspartate,PA）作为一种电解质补充剂,在临床上广泛使用。以往的研 究发现门冬氨酸钾在脑缺血/再灌注大鼠中对细胞凋亡有神经保护的作用。本研究将探讨门冬氨酸 钾对创伤性脑损伤（traumatic brain injury,TBI）是否有保护作用。 方法 T BI通过大鼠可控性皮质打击伤（controlled c ortical i mpact,CCI）产生。门冬氨酸钾组或溶剂对 照组在CCI发生后30 min以腹腔注射给予生理盐水或62.5 mg/kg剂量的PA,观察脑血流灌注量,改良 神经功能缺损评分（modified Neurological Severity Score,mNSS）和皮质损伤体积,并检测脑水肿以及 脑组织三磷腺苷（adenosine triphosphate,ATP）、乳酸含量和钠钾ATP酶活性。 结果 在CCI引起的大鼠皮质损伤中,与溶剂对照组相比,急性给予62.5 mg/kg剂量的PA治疗可以明 显改善神经功能缺损（P＜0.05),降低皮质损伤体积（P＜0.01）,减轻脑水肿（P＜0.05）。此外,与溶 剂对照组相比,门冬氨酸钾治疗组显著减少ATP缺失（P＜0.01）,降低乳酸含量（P＜0.05）,并增加 钠钾ATP酶的活性（P＜0.05）。 结论 PA能通过增加ATP含量和钠钾ATP酶的活性并降低脑水肿,对TBI具有神经保护作用。这为PA 在临床脑损伤时的应用提供了实验证据。     

膨体聚四氟乙烯软组织补片在鼻外伤一期整复术中的应用

BACKGROUND： Several studies have reported the use of zolpidem for induced arousal after permanent vegetative states. However, changes in brain function and EMG after zolpidem treatment requires further investigation. OBJECTIVE： To investigate the effect of zolpidem, an unconventional drug, on inducing arousal in patients in a permanent vegetative state after brain injury using visual single photon emission computerized tomography and digitized cerebral state monitor. DESIGN： A self-controlled observation. SETTING： Shenzhen People＇s Hospital. PARTICIPANTS： Seven patients in a permanent vegetative state were selected from the Department of Neurosurgery, Shenzhen People＇s Hospital from March 2005 to May 2007. The group included 5 males and 2 females, 24-55 years of age, with a mean age of 38.5 years. All seven patients had been in a permanent vegetative statement for at least six months. The patient group included three comatose patients, who had sustained injuries to the cerebral cortex, basal ganglia, or thalamus in motor vehicle accidents, and four patients, who had suffered primary/secondary brain stem injury. Informed consents were obtained from the patients＇ relatives. METHODS： The patients brains were imaged by ^99Tc^m ECD single photon emission computerized tomography prior to treatment with zolpidem [Sanofi Winthrop Industrie, France, code number approved by the State Food ＆ Drug Administration （SFDA） J20040033, specification 10 mg per tablet. At 8：00 p.m., 10 mg zolpidem was dissolved with distilled water and administered through a nasogastric tube at 1 hour before and after treatment and 1 week following treatment, respectively. Visual analysis of cerebral perfusion changes in the injured brain regions before and after treatment was performed. Simultaneously, three monitoring parameters were obtained though a cerebral state monitor, which included cerebral state index, electromyographic index, and burst suppression index. MAIN OUTCOME MEASURES： Comparison of the three brain fun     

The potential of neural transplantation for brain repair and regeneration following traumatic brain injury

Traumatic brain injury is a major health problem worldwide. Currently, there is no effective treatment to improve neural structural repair and functional recovery of patients in the clinic. Cell transplantation is a potential strategy to repair and regenerate the injured brain. This review article summarized recent de-velopment in cell transplantation studies for post-traumatic brain injury brain repair with varying types of cell sources. It also discussed the potential of neural transplantation to repair/promote recovery of the injured brain following traumatic brain injury.