盐酸多奈哌齐联合高压氧治疗脑卒中后血管性认知障碍的效果观察

目的观察盐酸多奈哌齐联合高压氧治疗脑卒中后血管性认知障碍的临床疗效。方法我院收治的126例脑卒中后血管性认知障碍患者,按随机数字表分为2组,对照组63例采用盐酸多奈哌齐治疗,5mg每晚口服,研究组63例在对照组治疗的基础上加用高压氧治疗(HBO),治疗前后采用蒙特利尔认知评价量表(MoCA)评价患者的认知损害程度,应用改良Barthel指数(MBI)评价患者的日常生活活动能力,观察治疗前后2组事件相关电位P300的变化。结果治疗前2组MoCA评分与MBI评分比较差异无统计学意义(P0.05);治疗8周后2组MoCA评分与MBI评分均较治疗前显著提高(P0.05),研究组MoCA评分与MBI评分的改善程度较对照组明显(P0.05)。治疗前2组P300潜伏期和波幅无显著性差异(P0.05);治疗后2组上述指标均有明显改变,治疗组优于对照组(P0.05)。结论高压氧联合盐酸多奈哌齐能促进脑卒中后血管性认知障碍患者认知功能障碍的康复,改善或延缓患者的认知损害,改善患者视空间与执行功能,改善延迟记忆,提高患者的日常生活活动能力,值得临床推广应用。     

计算机辅助认知障碍康复训练系统联合多奈哌齐治疗脑外伤认知障碍的临床研究

目的 自行研发计算机辅助认知障碍康复训练系统(CCRS)软件,并探讨CCRS 联合盐酸多奈哌齐治疗创伤性颅脑损伤认知障碍的疗效与安全性.方法 根据目前国内外认知研究结果研发出适用于TBI 认知训练的软件,用自行研制的计算机辅助认知评定系统(CCAS)筛选出270 例存在认知障碍的TBI 患者,其中轻、中、重度认知障碍患...     

盐酸多奈哌齐片联合银杏叶片治疗老年血管性认知障碍分析

目的 探讨盐酸多奈哌齐片联合银杏叶片治疗老年血管性认知障碍患者的疗效.方法 选择80例血管性认知障碍患者为研究对象,按照随机数字表随机分为2组,对照组40例采用银杏叶片治疗,观察组40例采用盐酸多奈哌齐片联合银杏叶治疗,比较2组的治疗效果.结果 治疗3～6个月,观察组MMSE评分和ADL评分均较对照组明显改善.结论 盐酸多奈哌齐片联合银杏叶片可明显改善VCI患者的认知功能障碍和日常生活能力,值得临床应用.     

盐酸多奈哌齐治疗阿尔茨海默病

阿尔茨海默病(Alzheimer，sdisease，AD)是引起老年期痴呆最常见的原因。该病属于神经系统变性疾病，患病率随着年龄的增加而升高，85岁以上的老年人群罹患率约为30％。阿尔茨海默病的临床表现主要为渐进性记忆力减退，认知功能障碍，情感行为异常，严重影响患的工作、生活能力以及生活质量。目前，阿尔茨海默病的确切发病机制尚不清楚，但以往的大量临床及病理生理研究证实，脑组织内的胆碱能系统受损，乙酰胆碱水平下降是其重要原因之一，故提高和稳定脑组织内乙酰胆碱系统的代谢功能成为主要治疗靶点。     

盐酸美金刚与盐酸多奈哌齐治疗阿尔茨海默病疗效对比

目的比较盐酸美金刚与盐酸多奈哌齐治疗阿尔茨海默病(AD)的有效性和安全性。方法将72例AD患者随机分为2组:美金刚组36例给予盐酸美金刚片20mg/d,多奈哌齐组36例给予盐酸多奈哌齐10mg/d,2组疗程均为6个月。2组患者治疗前和治疗3个月、6个月后均采用简易智能精神状态检查量表(MMSE)和AD评定量表的认知次级量表(ADAS-cog)评价患者认知功能、精神行为及痴呆严重程度。结果经治疗3个月、6个月后,2组患者MMSE、ADAS-cog评分均较治疗前明显好转(P<0.05或P<0.01);治疗3个月、6个月后,2组患者MMSE、ADAS-cog评分比较差异无统计学意义(均P>0.05);美金刚组的不良反应发生率低于多奈哌齐组(χ2=4.5714,P>0.05)。结论盐酸美金刚与盐酸多奈哌齐均能显著改善AD患者的认知功能、日常生活能力和人格情感障碍,两药疗效无明显差异,且盐酸美金刚具有良好的安全性。     

盐酸多奈哌齐治疗血管性痴呆的疗效观察

目的观察盐酸多奈哌齐治疗血管性痴呆的效果。方法我院2010-03—2012-03收治血管性痴呆患者70例,随机分为对照组与观察组,对照组常规治疗,观察组在常规治疗基础上口服5mg盐酸多奈哌齐,1次/d,治疗8周后对2组患者进行MMSE评分来判断认知能力,并通过ADL量化法评价生活活动能力。结果经过8周治疗,观察组MMSE和ADL评分与对照组相比差异有统计学意义(P<0.05);同时观察组在血浆黏度改善、血清NO含量与血浆ET-1方面均好于对照组。结论盐酸多奈哌齐治疗血管性老年痴呆有明显疗效,可缓解认知功能障碍,改善痴呆程度,提高生活能力。     

盐酸多奈哌齐治疗老年痴呆临床疗效观察

正老年痴呆又称阿尔茨海默病(Alzheimer′s disease,AD),为起病隐匿、呈进行性发展的神经系统退行性疾病,将会导致患者出现人格、行为等改变,给患者日常生活带来严重影响[1]。1资料与方法1.1一般资料选取我院2012-01—2015-10诊治的60例老年痴呆患者为研究对象,男33例,女27例;年龄65~78岁,平均(72.5±1.5)岁;病程2~5a,平均(3.5±0.5)a。临     

多奈哌齐治疗脑外伤后痴呆疗效观察

外伤性痴呆是指脑外伤引起的智能障碍综合征,包括生理、认知、行为、情感方面的障碍,其持续时间长,一般持续数周乃至数月以上.对于初中以上文化脑外伤患者,简易智能量表(mini-mental state examination,MMSE)评分≤23分者,即认为存在程度不等的腩外伤后痴呆.     

灯盏生脉胶囊联合盐酸多奈哌齐治疗阿尔茨海默病的临床研究

目的 观察灯盏生脉胶囊联合盐酸多奈哌齐对阿尔茨海默病患者认知功能、日常生活能力及安全性的影响。方法 将98例阿尔茨海默病患者随机分为治疗组与对照组各49例; 对照组给予每日口服盐酸多奈哌齐5 mg/次,1次/d,治疗组在对照组的基础上口服灯盏生脉胶囊0.36 g/次,3次/d; 比较2组患者治疗前与治疗3、6月后认知功能评分(MMSE、ADAS-cog)、日常生活能力评分(ADAS-ADL)、血清一氧化氮(NO)、内皮素(ET)水平及不良反应发生率。结果 治疗6月后治疗组MMSE评分为(21.85±2.58)分,对照组为(20.48±2.23)分(P<0.05); 治疗3、6月后治疗组ADAS-cog评分为(45.48±5.94)、(41.57±5.10)分,对照组为(48.69±6.23)、(414.24±5.53)分(P<0.05); 治疗3、6月后治疗组ADAS-ADL评分为(43.91±4.25)、(47.57±3.86),对照组为(41.77±4.44)分、(44.46±5.18)分(P<0.05); 治疗3、6月后治疗组NO水平为(41.95±7.62)、(37.89±5.93)μmol/L,对照组为(45.28±6.68)、(41.55±7.92)μmol/L(P<0.05); 治疗3、6月后治疗组ET水平为(140.48±22.94)、(132.04±10.08)ng/L,对照组为(152.08±17.39)、(143.91±17.60)ng/L(P<0.05); 2组药物不良反应主要有恶心、失眠、头痛、乏力、头晕、腹泻、皮疹,治疗组和对照组药物不良反应发生率分别为20.41%和14.28%(P>0.05)。结论 灯盏生脉胶囊联合盐酸多奈哌齐可提高阿尔茨海默病患者认知功能及日常生活能力,减少神经毒性物质NO、ET的生成,且安全性较好     

多奈哌齐治疗老年性痴呆的临床研究

目的:探讨乙酰胆碱和促炎症细胞因子在AD发病机制中的相互关系。方法:采用对照研究,对36名阿尔茨海默病(Alzheimer’sdisease,AD)患者用MMSE量表测定其治疗前后认知功能;采用Elisa方法测定乙酰胆碱酯酶抑制剂治疗前后脑脊液中白介素-1、肿瘤坏死因子、白介素-6等细胞因子的变化。结果:多奈哌齐组治疗24周后认知功能与治疗前比较明显提高,认知功能改善比脑复康组明显,同时CSF中IL-1、TNF-α、IL-6和sIL-6R的水平与治疗前相比,均明显降低且有显著意义(P<0.01)。结论:胆碱酯酶抑制剂多奈哌齐治疗AD,改善认知功能的同时,可使脑内促炎症细胞因子有所降低。提示胆碱能功能与促炎症细胞因子在AD发病中相互影响,具有密切联系。     

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     

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     

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。     

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]     

Gamma frequency entrainment rescues cognitive impairment by decreasing postsynaptic transmission after traumatic brain injury

Introduction

The relationship between oscillatory activity in hippocampus and cognitive impairment in traumatic brain injury (TBI) remains unclear. Although TBI decreases gamma oscillations and 40 Hz light flicker improves TBI prognosis, the effects and mechanism of rhythmic flicker on TBI remain unclear.

Aims

In this study, we aimed to explore whether light flicker could reverse cognitive deficits, and further explore its potential mechanisms in TBI mouse model.

Methods

The Morris water maze test (MWM), step-down test (SDT), and novel object recognition test (NOR) were applied to evaluate the cognitive ability. The local field potential (LFP) recording was applied to measure low gamma reduction of CA1 in hippocampus after TBI. And electrophysiological experiments were applied to explore effects of the gamma frequency entrainment on long-term potentiation (LTP), postsynaptic transmission, and intrinsic excitability of CA1 pyramidal cells (PCs) in TBI mice. Immunofluorescence staining and western blotting were applied to explore the effects of 40 Hz light flicker on the expression of PSD95 in hippocampus of TBI mice.

Results

We found that 40 Hz light flicker restored low gamma reduction of CA1 in hippocampus after TBI. And 40 Hz, but not random or 80 Hz light flicker, reversed cognitive impairment after TBI in behavioral tests. Moreover, 40 Hz light flicker improved N-methyl-D-aspartate (NMDA) receptor-dependent LTP (LTP_NMDAR) and L-type voltage-gated calcium channel-dependent LTP (LTP_L-VGCC) after TBI treatment. And gamma frequency entrainment decreased excitatory postsynaptic currents (EPSCs) of CA1 PCs in TBI mice. Our results have illustrated that 40 Hz light flicker could decrease intrinsic excitability of PCs after TBI treatment in mice. Furthermore, 40 Hz light flicker decreased the expression of PSD95 in hippocampus of TBI mice.

Conclusion

These results demonstrated that 40 Hz light flicker rescues cognitive impairment by decreasing postsynaptic transmission in PCs after TBI treatment in mice.     

轻中型颅脑损伤继发轻度认知功能障碍危险因素分析

目的探讨轻中型颅脑损伤患者继发轻度认知功能障碍(mild cognitive impairment,MCI)的危险因素。方法收集2014年7月1日至2015年7月1日我院收治的106例轻中型颅脑损伤患者影像资料,采用简易精神状态检查量表(MMSE)、蒙特利尔认知评估量表(Mo CA)、Addenbrooke改良认知评估量表(ACE-R)评估患者颅脑损伤后3个月的认知功能,以患者是否继发MCI为因变量、脑组织病变部位和类型为自变量,采用单因素和多因素logistic回归分析研究不同病变部位对于患者继发轻度认知功能障碍的影响性。结果共30例患者继发MCI、69例患者认知功能正常,7例患者失访。单因素logistic回归分析显示:患者的年龄及GCS评分均未见显著差异(P0.05);多发病灶、损伤半球、累及脑叶、脑白质病变、累及内囊之间存在统计学意义(P0.05)。多因素logistic回归分析显示:累及左半球(P=0.029,OR=1.637,95%CI:1.348~2.169)、累及颞叶(P0.001,OR=1.521,95%CI:1.240~2.203)、累及内囊(P=0.024,OR=1.526,95%CI:1.107~2.329)、多发病灶(P0.001,OR=1.936,95%CI:1.287~3.228)是危险因素。结论位于左半球、双侧额叶及颞叶区、内囊前肢的损伤病变及多发损伤病灶是轻、中型颅脑损伤患者继发MCI的危险因素。     

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.     

Endogenous adult neurogenesis and cognitive function recovery following traumatic brain injury in the rat hippocampus

BACKGROUND:Endogenous neural progenitor cells play a beneficial role for cognitive recovery following traumatic brain injury.However,there are few classification-control studies aimed at varying graded brain trauma.OBJECTIVE:To observe the effects of adult endogenous neurogenesis on cognitive function repair and regeneration of neural progenitor cells following varying graded traumatic hippocampal injury to determine the significance of endogenous neurogenesis in the repair of brain injury.DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment was performed at the Key Laboratory of Injuries,Variations and Regeneration of Nervous System,Tianjin Medical University General Hospital,from February to October 2009.MATERIALS:Mouse anti-rat 5-bromodeoxyuridine (BrdU) and neuronal nuclei (NeuN) monoclonal antibodies were purchased from Millipore Corporation,USA.METHODS:A total of 45 Wistar rats were randomly assigned to three groups.Mild and severe injury groups were respectively subjected to (182 ± 2) kPa and (284 ± 4) kPa lateral fluid percussion to establish models of brain injury,and the control group was subjected to surgery with no lateral fluid percussion.MAIN OUTCOME MEASURES:Cognitive function was estimated using the Morris water maze.Proliferation,survival,and differentiation of newly generated cells in the injured hippocampus were observed through the use of immunofluorescent staining.RESULTS:At 7 days post-injury,the number of BrdU+ cells in the hippocampal dentate gyrus significantly increased in the mild and severe injury groups compared with the control group (P<0.01).At 61 days post-injury,the number of BrdU7NeuN+ cells in the hippocampal dentate gyrus was significantly greater in the mild injury group compared with the severe injury and control groups (P< 0.01).In addition,the control group exhibited the greatest proportion of surviving cells that differentiated into mature neurons compared with the injury groups (P< 0.01).Moreover,at 61 days post-injury,cognitive function in rats with mild injury recovered to normal levels,whereas the severe injury group exhibited cognitive deficits (P< 0.01).CONCLUSION:Traumatic brain injury may be a stimulation factor for proliferation of neural progenitor cells in the adult hippocampus but severe brain trauma does not lead to an increased number of newly generated cells.Endogenous adult neurogenesis repairs neurological functions to an extent.However,recovery of neurological function remains limited following severe traumatic brain injury.