盐酸多奈哌齐治疗轻、中型脑外伤后认知障碍的临床研究

目的探讨盐酸多奈哌齐对轻、中型脑外伤患者伤后认知障碍及临床预后的影响。方法本组轻、中型脑外伤合并认知障碍患者78例,随机分成治疗组和对照组,治疗组应用盐酸多奈哌齐,对照组应用吡拉西坦,两组的治疗周期为12周。治疗前及治疗后分别应用简明精神状态检测量表（MMSE）、国人修订成人韦氏智力量表（WAIS-RC）和格拉斯哥预后评分（GOS）评价疗效。结果两组治疗后12周MMSE和WAIS-RC评分均较治疗前提高（P〈0.05）。治疗组MMSE和WAIS-RC评分提高较对照组明显（P〈0.05）,治疗组GOS预后优良率优于对照组（P〈0.05）。结论盐酸多奈哌齐对轻、中型脑外伤后认知障碍有积极治疗作用,并能改善临床预后。     

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     

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 injury     

Consistency of traumatic brain injury reporting in older adults with and without cognitive impairment

Objective: Medical history information regarding prior traumatic brain injury (TBI) usually relies on self-report, although little is known about the reliability of this information with regard to injuries sustained years or decades earlier. Even less is known about the reliability of self-reported medical history information in older individuals with cognitive impairment. To this end, we assessed the test-retest reliability of self-reported TBI history in a large, national sample. Methods: Participants (n = 4309) were older adults with intact cognition, mild cognitive impairment (MCI) and Alzheimer’s disease (AD) from the National Alzheimer’s Coordinating Center. Subjects provided TBI history information at baseline and one annual follow-up visit. Consistency of self-reported history of TBI with <5 minutes loss of consciousness (mLOC) and TBI with ≥5 mLOC reported at time 1 and 2 was analyzed across diagnostic groups. Results: Overall, subjects provided reports of TBI history at follow-up that were highly consistent with baseline reports (97.8–99.6% agreement), and Cohen’s kappa coefficients were all larger than .80 and statistically significant, maximum p < .001. Furthermore, level of cognitive impairment was not a significant predictor of consistency in reporting. Conclusions: These data are some of the first to suggest that self-report may be a consistent method of obtaining remote TBI history in the absence of medical records for older individuals, regardless of cognitive impairment.     

Association between cognitive impairments and anxiety disorders following traumatic brain injury

This study examined the association between cognitive impairment and anxiety disorders following traumatic brain injury (TBI). Sixty-six participants recruited from a rehabilitation hospital completed the Structured Clinical Interview for the DSM–IV (Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition) and cognitive tests at one year post injury. Prevalence of anxiety disorder was 27.3%. Logistic regression analyses revealed that the attention/working memory, information processing, and executive functions models were significantly associated with anxiety disorder. The memory model was not significant. Processing speed emerged as the strongest model associated with anxiety disorder. The role of cognitive impairment in the etiology of anxiety disorders after TBI is discussed, and treatment implications are explored.     

Neurobehavioural treatment for obsessive-compulsive disorder in an adult with traumatic brain injury

Although obsessive-compulsive disorder has been reported as one of many anxiety-related sequelae of brain injury, few empirical data of its responsiveness to psychological intervention are available. In this study, a single participant changing criterion experimental design was used to evaluate a neurobehavioural intervention for compulsive behaviour of an adult with severe traumatic brain injury. The participant, a man aged 24 years, had sustained frontal-temporal lobe brain trauma 12 months earlier, and presented with compulsive counting and voiding of bladder. The neurobehavioural intervention consisted of regular in-home consultations, self-regulation procedures including self-recording of compulsive behaviour, stress-coping strategies, errorless remediation, social reinforcement, and gradual fading of intervention. Baseline showed counting occurred on average 80% of daily hourly intervals, and voiding 12 times per day. Intervention produced elimination of compulsive counting, acceptable voiding at 8 times per day, and reports of the participant's satisfaction with intervention methods and outcomes. At 6 months follow-up, counting remained at zero levels, and voiding had decreased further to 7 times per day.     

强迫症认知功能与临床症状的相关性

目的：探讨强迫症的认知功能与临床症状的相关性。方法：采用韦氏记忆量表（WMS）、数字划销测验、威斯康星卡片分类测验（WCST）评估记忆、注意、执行功能。结果：强迫思维与持续错误呈显著正相关。结论：强迫症的记忆和注意损害障碍与其临床症状严重程度无明显相关,强迫症的持续错误与其强迫思维显著相关。     

载脂蛋白E基因多态性和急性脑损伤的关联研究

背景 急性脑损伤及其预后的影响因素是多方面的,如年龄、损伤程度与患者体质情况等,但其对外伤性脑损伤的预后结局仅作部分预测.近年来,有关遗传因素对脑损伤的影响和其预后的报道开始增多,关于载脂蛋白E在颅脑外伤预后中所起作用已引起人们的关注.在国外以往的研究中,关于载脂蛋白E基因多态性和脑损伤预后的研究结果也不相同.本研究初步探讨有关我国急性脑损伤及其预后与APOE基因之间的关系.方法 采用病例对照研究,选取94名车祸脑损伤患者和正常人作为研究对象,采用聚合酶链式反应(PCR)限制性片段长度多态性(RFLP)方法鉴定载脂蛋白E(APOE)基因型,探讨其等位基因及基因型同车祸脑损伤及其预后的关系.结果 车祸脑损伤患者中其等位基因ε2频率为0.1010,其基因型ε2/ε3的频率为0.1596明显高于正常人群ε2等位基因频率0.0050,及ε2/ε3基因型的频率0.0100(P＜0.05).同时,患者中,其未愈死亡组中ε2等位基因频率为0.1970及ε2/ε3基因型的频率为0.2727,明显高于好转治愈组ε2等位基因频率0.0508及ε2/ε3基因型的频率0.1017(P＜0.05),有统计学意义.结论 APOE基因的等位基因ε2基因型ε2/ε3初步可作为预示不良的预后参数.     

大鼠脑损伤后NMDAR1表达及其认知障碍变化的关系

目的同步考量脑损伤后大鼠与认知功能较为密切的脑区N-甲基-D-天冬氨酸受体1（NMDAR1）表达与认知功能的变化。方法参照Feeney法建立大鼠创伤性脑损伤模型,伤后1d,2d,4d,7d1）．2免疫组化SABC法检测大鼠额叶皮质、海马区、基底前脑区NMDAR1表达,以行走实验、平衡实验及记忆功能测定评估大鼠认知障碍变化。结果轻、中型脑损伤组大鼠于伤后2d认知障碍最严重,分别于伤后3,7d基本恢复正常。轻型、中型脑损伤组脑额叶皮质、海马区、基底前脑区NMDAR1均于伤后1d升高,于2d降至较低水平后再呈缓慢增高趋势,与认知障碍变化趋势呈同步变化,且中型脑损伤组NMDAR1表达高于假手术组与轻型脑损伤组（P〈0．05）。结论大鼠经创伤性脑损伤后,额叶皮质、海马区、基底前脑区细胞中的NMDAR1含量和损伤后认知障碍的变化趋势有相似性;创伤性脑损伤后表达增加的NMDAR1对大鼠认知功能有加重损害作用。     

颅脑损伤后神经递质系统变化与认知障碍的研究进展

近年来,颅脑损伤(traumatic brain injury,TBI)的发生率、致残率逐渐增高,随着对脑外伤急性期治疗F段的不断提高,已能大大降低早期的死亡率.然而,它仍是慢性期致残的主要原因,其中认知功能障碍是最持久和最严重的症状之一[1].虽然大部分患者中这些功能在1年后恢复正常,但仍有10％～15％的轻型脑损伤患者存在功能障碍,在中、重型TBI患者中比例更高[2].TBI后认知障碍的确切机制至今仍不十分清楚,研究发现大脑内学习和记忆等认知活动与多种神经递质相关,包括乙酰胆碱(acetylcholine,Ach),去甲肾上腺素,多巴胺(DA),5-羟色胺(5-HT),γ-氨基丁酸,谷氨酸,神经营养因 子等[3].本文就TBI后主要神经递质系统的变化及其与认知障碍的研究进展进行简要综述.     

脑外伤后进展性出血性脑损伤的诊治体会

目的研究脑外伤后进展性出血性脑损伤的临床特点,总结其发病机制,探讨及时诊断、治疗的方法。 方法回顾性分析解放军第二五一医院神经外科自2015年1月至2017年6月收治的167例脑外伤后进展性出血性脑损伤患者的临床资料。本组患者入院时按GCS评分：3~5分11例,6~8分36例,9~12分83例,13~15分37例。临床表现均有不同程度的颅高压症状,观察治疗过程中,76例患者出现意识障碍或意识障碍加深,94例患者肢体肌力减退,81例患者频繁呕吐,43例患者躁动,5例患者脑疝。 结果手术治疗94例,保守治疗73例。所有患者依据GOS评分判断：恢复良好114例,中残32例,重残13例,死亡8例（4.8%）。 结论动态CT观察是早期发现进展性出血性脑损伤的有效方法。对外伤性颅内血肿的患者绝不能仅仅依赖首次CT结果即制定一成不变的治疗方案,应进行专科监测和动态CT观察,根据患者血肿量的变化及时调整治疗方案。     

多奈哌齐治疗颅脑创伤后记忆和智能障碍的临床观察

目的 观察多奈哌齐治疗96 例颅脑创伤后记忆和智能障碍的疗效.方法 颅脑创伤后记忆和智能障碍患者96例,治疗组给予多奈哌齐片5mg,1次/d, 晚上睡前口服;对照组给予尼莫地平片常规治疗.治疗期为1个月.结果 治疗组患者记忆功能、认知功能改善较为明显, 与对照组比较有明显差异(P ＜ 0.05).结论 多奈哌齐对颅脑创伤后记忆和智能障碍患者早期治疗效果好, 安全性高, 不良反应少, 服用方便.     

Sequelae following traumatic brain injury: The cerebrovascular perspective

Traumatic brain injury (TBI) initiates a huge repertoire of biochemical perturbations. On one hand, destructive events are set into motion while on the other hand, protective and recovery mechanisms are evoked, each with their own temporal and spatial characteristics. The brain exists as a finely tuned balance between vascular, neuronal and glial interactions and so a complex interplay between these factors will dictate the final evolution of pathogenesis. Although vascular damage is a key event, it remains a somewhat neglected component to the underlying degenerative processes that evolve following injury to the brain. The present review will act to integrate the current knowledge of the vascular events proceeding injury to the brain, with an emphasis on how this impacts the control of vascular function and thus cerebral blood flow.     

儿童脑外伤脑电图特征分析

目的探讨脑电图在儿童脑损伤中的应用价值及脑电图诊断标准与儿童伤后智力障碍的相关关系。方法对86例儿童脑外伤后行脑电图检测并给予儿童韦氏智力量表进行评分。结果中、重度异常脑电图的脑外伤患儿有显著的智力下降(P<0.05);对脑电图分级与智力评分采用Spearman秩相关分析,二者呈负相关。结论脑电图可以作为间接了解儿童脑外伤后智力水平的辅助指标。     

Chronic ibuprofen administration worsens cognitive outcome following traumatic brain injury in rats

Traumatic brain injury (TBI) can induce progressive neurodegeneration in association with chronic inflammation. Since chronic treatment with the non-steroidal anti-inflammatory drug (NSAID), ibuprofen, improves functional and histopathologic outcome in a mouse model of Alzheimer's disease (AD), we investigated whether it would also improve long-term outcome following TBI. Anesthetized adult rats were subjected to fluid percussion brain injury. Over the following 4 months the injured animals received ibuprofen per os (formulated in feed) at the approximate doses of 20 mg/kg body wt/day (n=13), 40 mg/kg body wt/day (n=13), or control (feed only, n=12). Sham animals underwent surgery without injury or ibuprofen treatment (n=9). At 4 months post-injury, a Morris water maze task revealed a profound learning dysfunction in all three injured groups compared to the sham group. Surprisingly, the learning ability of injured animals treated with either chronic ibuprofen regimen was significantly worsened compared to non-treated injured animals. However, there was no difference in the extent of progressive atrophy of the cortex or hippocampus between treated and non-treated injured animals. These data may have important implications for TBI patients who are often prescribed NSAIDs for chronic pain.     

Bipolar disorder after traumatic brain injury

Objective. We report the case of a 47-year-old man with no psychiatric antecedents who developed manic and depressive symptoms after traumatic brain injury (TBI). Methods and results. Findings on neurobehavioral examination, neuropsychological test battery, electrophysiological and imaging exams suggested the presence of a diffuse cerebral injury with a predominance of left fronto-temporal findings. Conclusions. This case demonstrates that TBI may cause vulnerability to psychiatric disorders, with long latency periods, and that its course may be independent of cognitive impairment and recovery.     

Age-dependent synuclein pathology following traumatic brain injury in mice

Synucleins (Syn), a family of synaptic proteins, includes alpha-Syn, which plays a pivotal role in Parkinson's disease and related neurodegenerative diseases (synucleinopathies) by forming distinct brain pathologies (Lewy bodies and neurites). Since traumatic brain injury (TBI) is a poorly understood risk factor for Parkinson's disease, we examined the effects of TBI in the young and aged mouse brain on alpha-, beta-, and gamma-Syn. Immunohistochemical analysis showed that brains from sham-injured young and aged mice had normal alpha- and beta-Syn immunoreactivity (IR) in neuropil of cortex, striatum, and hippocampus with little or no gamma-Syn IR. At 1 week post TBI, the aged mouse brain showed a transient increase of alpha- and beta-Syn IR in the neuropil as well as an induction of gamma-Syn IR in subcortical axons. This was associated with strong labeling of striatal axon bundles by antibodies to altered or nitrated epitopes in alpha-Syn as well as by antibodies to inducible nitric oxide synthase. However, these TBI-induced changes disappeared by 16 weeks post TBI, and altered Syn IR was not seen in young mice subjected to TBI nor in alpha-Syn knockout mice while Western blots confirmed that TBI induced transient alterations of alpha-Syn in the mouse brains. This model of age-dependent TBI-induced transient alterations in alpha-Syn provides an opportunity to examine possible links between TBI and mechanisms of disease in synucleinopathies.     

氢质子磁共振波谱成像技术在创伤性脑损伤后认知障碍中的应用

创伤性脑损伤(TBI)可引起一系列复杂的病理生理过程变化,这些变化包括脑内物质代谢异常,导致机体出现包括头痛、认知、运动和情感障碍等在内的长、短期症状,而认知障碍是阻碍TBI患者日常生活质量恢复和延缓其回归社会的重要因素。氢质子磁共振波谱成像技术(1H-MRS)可对急、慢性脑部损伤患者的脑组织代谢进行非侵入性检测,具有辅助诊断和预测长期功能预后的价值。该文将近年来1H-MRS在TBI后认知障碍中的应用进行总结和展望。[国际神经病学神经外科学杂志, 2021, 48(2):197-201]     

New-onset tic disorder following circumscribed brain injury

Adult-onset tics represent either a secondary tic disorder (“tourettism”) or a late presentation of childhood tics, which may have been previously unrecognised. Head trauma has been recognised as an infrequent cause of adult-onset tic disorder, which exhibits variable temporal relationship to the inciting injury and response to therapy. We present a patient who presented with late-onset tics seven years after a circumscribed brain injury, responding well to antidopaminergic treatment. A review of all the previously reported cases of post-traumatic tic disorder is provided. Our patient is unusual in that the injury presumed to be responsible for the development of tics was of a very focal nature, akin to previously described tic disorder following vascular insults. We discuss the rare occurrence of tourettism after such focal brain lesions and analyse the insights this provides into the anatomical substrates underlying tic disorders.     

多奈哌齐与安慰剂治疗脑外伤后记忆障碍的对照研究

目的　探讨多奈哌齐治疗脑外伤后记忆障碍的有效性和安全性。方法　对59 例脑外伤病人随机分成两组,分别给予口服多奈哌齐与安慰剂治疗6个月,采用WMS评价临床疗效,定期查体和实验室检查评价药物不良反应。结果　治疗后多奈哌齐组WMS各项评分均有显著提高(P<0.01~0.05),与安慰剂比较,WMS评分长时记忆、瞬时记忆、记忆商有统计学差异(P<0.05)。口服多奈哌齐未见严重药物不良反应。结论　多奈哌齐治疗脑外伤后记忆障碍有效,安全性好。。