糖尿病周围神经病变的临床观察分析

目的对糖尿病周围神经患者病变的临床治疗方法进行观察分析。方法从我院在2009-06～2010-12进行的糖尿病周围神经松解术治疗的神经病变患者28例中进行随机抽取,对28例患者进行临床治疗方法及结果的综合分析与观察。结果 28例患者经松解术治疗后均有明显好转或完全好转。结论鉴于周围神经松解术对糖尿病性周围神经病变的治疗效果,在临床上当引起重视。     

糖尿病性周围神经病的外科治疗进展

糖尿病性周围神经病（DPN）是最常见的糖尿病性神经病变,由于糖代谢异常而受损的周围神经在肢体生理解剖狭窄处受卡压在DPN发生、发展过程中起重要作用。周围神经减压术通过对神经进行松解减压,使肢体末端感觉和运动功能障碍得到缓解,为DPN治疗提供了新的有效途径。本文就DPN的外科治疗相关进展进行综述。     

周围神经松解术治疗糖尿病性周围神经病变的临床应用

目的 探讨周围神经松解术治疗糖尿病性周围神经病变的临床疗效.方法 选择我院收治的42例糖尿病性周围神经病变患者,均行周围神经松解术治疗,观察治疗后患者的肢体麻木及疼痛缓解情况,同时比较治疗前后患者的胫神经和腓神经变传导速度.结果 本组42例经治疗后肢体麻木及疼痛症状明显缓解率分别为81.0％和76.2％,缓解率分别为14.3％和21.4％,恶化率分别为4.8％和2.4％.患者治疗后的胫神经和腓总神经平均传导速度较治疗前有明显提高,差异有统计学意义(P＜0.05).结论 周围神经松解术治疗糖尿病周围神经病变能够显著改善患者的肢体麻木和疼痛症状,改善神经缺血、缺氧,增加神经传导功能,值得临床推广应用.     

糖尿病病程对糖尿病下肢周围神经病变的影响

目的探讨糖尿病（DM）病程对糖尿病周围神经病变（DPN）严重程度及下肢周围神经显微减压术疗效的影响,以及糖尿病周围神经病变早期诊断、早期手术的意义。方法以5年糖尿病痛程作为标准,将我科近年收治的1526例糖尿痛周围神经病患者分为短DM病程组和长DM病程组,按Dellon术式对卡压的神经进行下肢周围神经显微减压术。所有患者术前、术后1.5年进行神经高频超声、定量感觉检查（QST）、神经感觉传导速度（NCV）检测,并选取50例正常人群作为对照组检测相同指标。结果与对照组相比,DPN患者的NCV、冷感觉阈值较低,热感觉阈值、振动觉阈值及神经横断面积（CSA）较高,差异有统计学意义（P〈0．05）。患者术后各项指标明显改善,与术前相比,差异有统计学意义（P〈0．05）。短DM病程DPN患者术前和术后各指标均优于长DM病程DPN患者,两组比较差异有统计学意义（P〈0．05）。短DM病程DPN患者NCV阳性检测率为71．5％,QST阳性检测率为93．7％;长DM病程DPN患者NCV阳性检测率为90．3％,QST阳性检测率为95．3％。结论糖尿病痛程对DPN患者发病时的严重程度至关重要,同时也对DPN患者的手术疗效和预后产生影响。DPN的早期诊断、早期手术具有重要临床价值。     

糖尿病性周围神经病的神经外科治疗

糖尿病性周围神经病（diabetic peripheral neuropathy，DPN）是最为常见的糖尿病性神经病变，其中又以双侧肢体末端对称性多发感觉运动神经病变（distal symmetric sensorimotor polyneuropathy，DSSP）最多见。进展性DSSP常给患者带来巨大痛苦，防治极为困难。应用周围神经减压术可有效缓解DSSP症状，并有可能逆转DPN的自然病程，为DPN的治疗提供了一种新途径。     

61例糖尿病患者周围神经传导速度临床分析

目的 探讨周围神经传导速度（NCV）在糖尿病性周围神经病（DPN）诊断中的价值。方法 对61例糖尿病（DM）患者行正中神经、尺神经和腓总神经运动传导速度（MCV）及正中神经、尺神经和腓浅神经感觉传导速度（SCV）进行检测。结果 61例糖尿病患者NCV异常率为81．97％（50／61）。共检测732条神经,MCV366条．SCV366条,异常率分别为27．05％（99／366）、49．45％（181／366）,差异有非常显著性意义（P〈0．01）。上肢检测488条神经,异常率为30．94％（151／488）;下肢检测244条神经,异常率为48．77％（119／244）,差异有非常显著性意义（P〈0．01）。结论 检测周围神经传导速度不但可以早期诊断糖尿病性周围神经病,而且有助于发现亚临床患者,是DPN的重要辅助检查手段。     

糖尿病周围神经病的手术治疗

目的探讨Dellon三联周围神经减压术（腓总神经、腓深神经及胫后神经减压术）治疗糖尿病周围神经病（DPN）下肢病变的手术疗效。方法分析2006年7月～2011年11月采用Dellon三联周围神经减压手术治疗的40例（DPN）患者的资料,观察他们的临床特点、手术方法、手术效果和随访结果。结果临床表现以渐进性小腿和足底、足背部麻木起病者35例,以渐进性疼痛起病者5例。术后下肢麻木症状缓解率90％,术后下肢疼痛症状缓解率92％。术后平均随访12个月临床症状缓解的所有患者病情稳定,1例患者术后1个月出现足底部分区域疼痛缓解后再次出现疼痛,其余病人症状无复发或加重。结论Dellon三联周围神经减压术对于（DPN）缓解疼痛、恢复感觉有较好疗效,是一种安全、有效、微创治疗新技术和新方法。     

2型糖尿病患者合并周围神经病变相关危险因素分析

目的 探讨2型糖尿病周围神经病变的相关危险因素.方法 选取2型糖尿病（DM）患者114例为研究对象,根据有无合并周围神经病变将其分为糖尿病周围神经病变组（DPN组）和非糖尿病周围神经病变组（NDPN组）.分析患者临床资料,探讨2型糖尿病周围神经病变相关因素.结果 （1） DPN组与NDPN组病患年龄、病程、FPG、2hPG、HbA1C、尿 A/C 差异均有统计学意义（P〈0.05）.（2）Logistic分析显示糖尿病病程、年龄、糖化血红蛋白（HbA1C）是糖尿病周围神经病变的独立危险因素.结论 糖尿病病程、年龄、空腹血糖、餐后 2 h血糖、糖化血红蛋白等是 2 型糖尿病并周围神经病变的相关危险因素.其中年龄大、病程长、高HbA1C的糖尿病患者发生 DPN 的风险增加.提示临床医生应在糖尿病早期对DPN和相关危险因素进行预防和干预.     

依帕司他与甲钴胺联合治疗糖尿病周围神经病变疗效观察

目的探讨依帕司他联合甲钴胺治疗糖尿病周围神经病变（DPN）的疗效。方法对96例DPN患者随机分为治疗组48例和对照组48例。在控制血糖血脂等治疗的基础上,治疗组采用依帕司他联合应用甲钴胺,对照组单用甲钴胺,8周后比较2组治疗前后症状、体征变化及神经传导速度（包括腓总神经和正中神经运动神经传导速度（MNCV）和感觉神经传导速度（SNCV）。结果治疗组总有效率87.50%,明显优于对照组64.58%（P〈0.01）;正中、腓总神经传导速度（MNCV和SNCV）2组间和组内进行比较,差异均有统计学性意义（P〈0.05）。结论采用依帕司他联合甲钴胺治疗DPN能明显改善患者症状、体征、传导功能,从而达到良好的治疗效果。     

糖尿病性周围神经病患者的神经电图改变

目的 观察糖尿病性周围神经病（DPN）患者神经电图的改变。方法 对78例DPN患者进行神经电图检查,包括运动神经传叶速发（MCV）、感觉神经传导速度（SCV）和F波检查。结果 共检查78例患者的468条神经,其中MCV减慢166条,MCV减慢合并远端潜伏期延长39条,异常率43．8％;SCV减慢175条,末引出电位75条,SCV减慢兼远端潜伏期延长26条,异常率58．9％．检查102条神经的F波,其中异常66条,异常率为64．7％,12条神经（11．8％）F波时间离散度增加。结论 神经电图是诊断DPN的敏感及特异性的检查,多个参数相结合有助于提高阳性检出率。     

Axonal regeneration from the spinal cord to peripheral nerve induced by end-to-side neurorrhaphy Evidence from acetylcholinesterase staining and Fluorogold retrograde tracing

BACKGROUND： In recent years, surgeons have advocated root or trunk repair of avulsed nerve roots for overall recovery. However, donor nerves pose a major problem, because they do not contain adequate numbers of axons. Moreover, the procedures lead to nerve deficits in the donor nerve following transplantation. OBJECTIVE： To observe whether axonal regeneration occurs by end-to-side neurorrhaphy in the peripheral nerve and spinal cord. DESIGN, TIME AND SETTING： A neuroanatomical, randomized, controlled, animal study was performed at Functional Anatomy Lab in Nagoya University School of Medicine from May 2002 to July 2003. MATERIALS： Fluorogold was purchased from Fluorochrome, LLC, USA. BX50 light microscope and fluorescent microscope were purchased from Olympus, Japan. METHODS： A total of 21 rats were randomly divided into three groups, and the posterior avulsion injury model （C6-8） of the brachial plexus was performed. In the ventral root graft group, the avulsed C7 ventral roots were reanastomosed to the small anterior lateral aspect window of the spinal cord via nerve grafts. In the dorsal root graft group, the C7 dorsal roots were reanastomosed at the small pia mater window of the posterior lateral aspect of the spinal cord via nerve grafts. In the control group, the avulsed nerve roots were not repaired. MAIN OUTCOME MEASURES： The nerve grafts were collected from the ventral and dorsal root graft groups, and the C7 proximal nerve end was collected from the control group. Acetylcholinesterase staining was performed on the tissue. Fluorogold retrograde tracing technique was applied to determine the origin of the regenerating axons. RESULTS： Results showed that acetylcholine-positive axons existed in nerve grafts of the ventral and dorsal root graft groups. However, axons were not found in the avulsed nerve roots of the control group. Fluorogold retrograde tracing confirmed the presence of fluorogold-containing neurons in the ventral and dorsal horn of the ventral and dorsal root graft groups. Fluorogold-positive neurons were not observed in the control group. CONCLUSION： End-to-side neurorrhaphy induced axonal regeneration from the spinal cord to the peripheral nervous system.     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

马来酸桂哌齐特联合甲钴胺治疗糖尿病周围神经病变的临床观察

目的观察马来酸桂哌齐特联合甲钴胺治疗糖尿痛周围神经病变（DPN）的临床疗效。方法将120例DPN患者随机分为两组,联合治疗组60例,对照组60例。两组在积极控制血糖的基础上,联合治疗组予马来酸桂哌齐特注射液（克林澳,北京四环制药有限公司）160mg加入生理盐水250ml静脉滴注,1次／d,连用2周;同时予治疗组用甲钴胺粉针剂1mg加入生理盐水100ml中静脉滴注,1次／d,连用2周后改口服甲钴胺片1mg,3次／d×2周;对照组予维生素B1100mg和维生素B12250μg肌内注射,1次／d,连用2周后改口服维生素B1片20mg,3次／d＋维生素B12片50μg,3次／d×2周。比较两组治疗前后症状、体征、神经传导速度变化及不良反应。结果治疗组患者症状体征明显改善、感觉及运动神经传导速度有显著提高,与对照组比较差异具有统计学意义（P均〈0．01）。结论马来酸桂哌齐特与甲钴胺联合应用可明显提高对糖尿病周围神经病变（DPN）的治疗疗效。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

糖尿病周围神经病的外科手术治疗

糖尿病周围神经病变（DiabeticNeuropathy,DNP）是糖尿病一种常见的并发症。2007～2008年中华医学会糖尿病学分调查估计我国20岁以上成年人糖尿病患病率为9．7％,我国糖尿病患者将达到9240万人;中华医学会糖尿病学分会分析了1991年1月～2000年12月的24496例糖尿病患者资料,     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.