反常栓塞致双侧丘脑旁正中区域梗死一例

临床资料 患者,女,24岁,主因"7 d前突发视物模糊、头晕、意识丧失1次,视物成双6 d"于2009年5月22日入院.患者7 d前晚间上网时无明显诱因突感视物模糊、变形,伴头晕及视物旋转,几分钟后意识不清,12 h后意识渐好转,视物成双,问话回答反应慢,不切题.既往史、个人史无特殊.体检:血压95/65 mm Hg(1 mm Hg=0.133 kPa),心率70次/min,律齐,各瓣膜区可闻及3/6级收缩期吹风样杂音.意识清楚,语言流利.高级皮质功能粗测正常.左侧眼球位置高于右侧,双眼球垂直运动欠灵活,有复视.     

迟发性面神经麻痹的Miller-Fisher综合征1例报告

<正>1临床资料患者,男,28岁,主因"视物成双,行走不稳4 d"于2019年3月18日入院。患者于入院前8 d出现上呼吸道感染症状,未予以特殊治疗。入院前4 d出现视物成双、行走不稳、双手麻木,无明显肢体活动障碍。1 d后患者症状加重,出现双脚麻木、言语不清、吞咽费力。于当地医院行头部核磁共振(Magnetic Resonance Imaging,MRI)检查,颅内未见明显责任病灶。2 d后患者肢体麻木范围较前扩大,双上肢、双下肢     

以可逆性后部白质脑病综合征为首发表现的结节性多动脉炎一例

临床资料 患者,男性,18岁,主因“双眼视力下降2周”于2011年10月19日入院.入院前2周晨起时自觉双眼视物不清,左眼视野中间及右眼视野外侧隔一层雾,左眼明显,但无视物成双、头痛、肢体无力麻木.上述症状持续无缓解,约2d后无明显诱因又出现恶心,伴呕吐,为非喷射性胃内容物,仍无头痛,持续约2d后自行好转.10 d前患者就诊于当地医院,颅脑MRI检查示“脑干及小脑多发异常信号,无明显强化”,予激素、消炎药(具体不详)治疗4d后,自觉视物不清较前稍好转,但仍未完全恢复正常,为进一步诊治收入我科.患者近3年余常有发作性后枕部头痛,为胀痛或跳痛,不伴心慌、视物不清等,每次持续半天至1d自行好转,未诊治;3d前就诊于我院门诊,测血压210/160 mm Hg(1 mm Hg =0.133 kPa),无头痛、心慌等不适;病前无上呼吸道感染、腹泻、疫苗接种病史;母亲有高血压病史.     

大动脉炎致脑梗死一例

1病历摘要患者女性,27岁。入院前2年出现头晕,多于劳累、情绪激动后发作,伴视物旋转、四肢无力,偶有恶心、呕吐,无意识障碍,无视物成双,无言语不清,无肢体抽搐,无二便障碍。每次症状持续数十分钟,休息后可缓解,未行系统     

复发性急性眼肌麻痹的抗GQ1b抗体综合征一例

临床资料 患者女性,39岁,主因"发作性视物成双17年"于2009年4月1日入院.患者2009年3月13日受凉后出现发热、上呼吸道感染,治疗1周后好转.3月23日患者出现看远处物体视物成双,同时伴有双眼皮沉重感,症状逐渐加重,第3天看远、近物体均有视物成双,双手指尖麻木,颈、腰部肌肉僵硬不适.患者曾分别在1992年、2007年2次出现上呼吸道感染后视物成双,不伴视力减退,当时均未作特殊检查及治疗,20～30 d左右复视症状自行恢复.     

复发性急性眼肌麻痹的抗GQ1b抗体综合征一例

临床资料 患者女性,39岁,主因"发作性视物成双17年"于2009年4月1日入院.患者2009年3月13日受凉后出现发热、上呼吸道感染,治疗1周后好转.3月23日患者出现看远处物体视物成双,同时伴有双眼皮沉重感,症状逐渐加重,第3天看远、近物体均有视物成双,双手指尖麻木,颈、腰部肌肉僵硬不适.患者曾分别在1992年、2007年2次出现上呼吸道感染后视物成双,不伴视力减退,当时均未作特殊检查及治疗,20～30 d左右复视症状自行恢复.     

复发性急性眼肌麻痹的抗GQ1b抗体综合征一例

临床资料 患者女性,39岁,主因"发作性视物成双17年"于2009年4月1日入院.患者2009年3月13日受凉后出现发热、上呼吸道感染,治疗1周后好转.3月23日患者出现看远处物体视物成双,同时伴有双眼皮沉重感,症状逐渐加重,第3天看远、近物体均有视物成双,双手指尖麻木,颈、腰部肌肉僵硬不适.患者曾分别在1992年、2007年2次出现上呼吸道感染后视物成双,不伴视力减退,当时均未作特殊检查及治疗,20～30 d左右复视症状自行恢复.     

表现为八个半综合征的脑桥梗死一例

正1病例报告患者女,78岁。主因"视物成双1d"于2017-03-01入院。1d前无明显诱因出现视物成双,向左侧注视时为著,伴头晕、恶心、呕吐,无耳鸣,头晕为持续性,与视物成双相关,闭眼后头晕可缓解。无肢体麻木及感觉异常,无肢体活动障碍,无言语不利、声音嘶哑、饮水呛咳等,无耳聋耳鸣,无出汗异常,无意识障碍及大小便障碍。既往2型糖尿病史9年余,平素口服二甲双胍0.5g,2次/d,血     

基底动脉型偏头痛合并基底动脉近端成窗畸形1例报道

1病例 患者,男性,12岁。因发作性头痛伴头晕、视物晃动、恶心1d于2010年2月24日入院。患者2010年2月23日晚上21：00左右无明显诱因出现头痛,以双颞侧为著,性质呈搏动性闷痛,伴头晕、视物晃动、恶心、四肢乏力、无呕吐,无视物不清、视物成双,无耳鸣、听力减退,     

疼痛性眼肌麻痹综合征1例报告

疼痛性眼肌麻痹综合征１例报告新疆医学院一附院神经内科丁兴国林峰报道患者，女性，１０岁，哈萨克族，以双眼眶周持续胀痛伴视物不清１５天入院。起病时双眼眶周持续胀痛，伴恶心呕吐，次日出现双眼球活动不灵，视物不清，当地医院给予抗生素及镇痛对症治疗无效。病前无...     

以双侧丘脑受累为主要表现的脑深静脉血栓形成的临床及影像分析

目的 探讨大脑深静脉血栓形成（DCVST）的临床及影像学特点.方法 回顾性分析3例经MR或DSA证实为大脑深静脉血栓形成的临床资料并复习有关文献.结果 DCVST临床特征以颅高压症状和认知、行为异常、意识障碍为突出表现;其影像学表现以双侧丘脑受累,尤其是伴有出血为主要特征.结论 当出现双侧丘脑受累为主要的临床及影像表现时,要及时想到脑深静脉血栓形成的可能,并尽快行MRV和DSA进行确诊.     

人参皂甙Rg1对去卵巢大鼠面神经核脑源性神经营养因子表达的影响：半定量分析

BACKGROUND： Estrogen is neuroprotective effects such as breast carcinoma, endometria but long-term estrogen treatment can induce side cancer, and stroke. However, phytoestrogen is neuroprotective without these side effects. OBJECTIVE： To study the effects of Ginsenoside Rgl on facial neurons and brain-derived neurotrophic factor （BDNF） expression in the facial nucleus in ovariectomized rats. DESIGN, TIME AND SETTING： The randomized, controlled animal experiments were performed at the Ultrasonic Institute, Second Affiliated Hospital, Chongqing Medical University, China, from September 2007 to September 2008. MATERIALS： Ginsenoside Rgl （Sigma, USA）, rabbit anti-rat BDNF, Bcl-2, Bax antibodies, biotin-labeled goat anti-rabbit IgG （Boster, China）, and a TUNEL kit （Roche, Germany） were used in this study. METHODS： A total of 48 adult Sprague Dawley rats undergoing ovariectomy were randomly assigned into sham operation （n = 8）, model （n = 20）, and Ginsenoside Rgl （n = 20） groups. Facial nerve damage was induced by bilateral clamping of the facial nerve trunk. The bilateral facial nerve trunk was exposed in the sham operation group, with no clamping. Rats in the Ginsenoside Rgl group were intraperitoneally injected with 10 mg/kg per day Ginsenoside Rgl; other groups received 2 mL saline, once a day, for 14 days. MAIN OUTCOME MEASURES： Morphologic changes in neurons of the facial nucleus were observed following hematoxylin-eosin staining. Neuronal apoptosis was detected by TUNEL. Changes in ultrastructure of the facial nerve fibers were observed with a transmission electron microscope. Expression of BDNF, Bcl-2, and Bax protein was quantified by semiquantitative immunohistochemistry. RESULTS： At 3-14 days following facial nerve damage, Ginsenoside Rgl increased BDNF expression and the number of regenerated nerve fibers, and produced thicker myelin sheaths （P 〈 0.05）. Ginsenoside Rgl also gradually increased Bcl-2 protein expression and decreased Bax protein expression （P 〈 0.05）. By day 7, apoptosis was observed in facial neurons, but Ginsenoside Rgl reduced the number of apoptotic neurons. Sham animals did not show any changes in BDNF, Bcl-2, or Bax expression or facial neuron morphology. CONCLUSION： Ginsenoside Rgl can substantially inhibit facial neuronal apoptosis by increasing endogenous BDNF and Bcl-2 expression and by decreasing Bax expression in ovariectomized rats after facial nerve damage.     

Hippocampal CA1 pyramidal cells and neurotrophic factors in a rat model of vascular dementia following Xiongma drop pill versus Ginkgo leaf tablets

BACKGROUND： Previous studies have demonstrated the neuroprotective effects of Xiongma drop pill （XMDP） in a mouse model of vascular dementia. Neurotrophic factors play an important role in repair and regeneration of injured neurons. OBJECTIVE： To compare the effects of XMDP and Ginkgo leaf tablets on the appearance and number of hippocampal CA1 pyramidal neurons, as well as neurotrophic factor content in brain tissues, during vascular dementia formation to explore the neuroprotective mechanisms of XMDP. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Pharmacology, College of Pharmacy, Harbin University of Commerce between April 2007 and December 2008. MATERIALS： XMDP was prepared by the College of Pharmacy, Harbin University of Commerce, with each 40 mg pill containing ferulic acid （≥ 0.149 mg） and gastrodin （≥ 0.171 mg）. Ginkgo leaf tablets were purchased from Taiyuan Qianyuan Pharmacy, China. METHODS： Healthy, adult, male, Wistar rats were randomly assigned to 6 groups： sham-operation, model, XMDP （high-, middle-, and low- dose）, and Ginkgo leaf tablets. The 6 groups were subdivided into two subgroups according to administration days, i.e., 30 and 60 days, with 8 animals in each subgroup. Rats in the model, XMDP, and Ginkgo leaf tablets groups were subjected to permanent bilateral ligation of the common carotid artery to establish a vascular dementia model. At 8 days after model establishment, all groups received intragastric administration once daily of the following： 10 mL/kg normal saline in the sham-operation and model groups; 0.4, 0.2, and 0.1 g/kg XMDP in the high-, middle-, and low-dose XMDP groups, respectively; and 50 mg/kg Ginkgo leaf tablets in the Ginkgo leaf tablets group. MAIN OUTCOME MEASURES： Hematoxylin-eosin staining was used to observe appearance and to quantify the number of hippocampal CA1 pyramidal neurons. Brain-derived neurotrophic factor and nerve growth factor concentrations in brain tissues were detected by enzyme-linked immunosorbent assay. RESULTS： Following model establishment, hippocampal CA1 neurons exhibited pathological changes. Compared with the sham-operation group, the number of pyramidal neurons significantly decreased （P 〈 0.05 or P 〈 0.01）, and neurotrophic factor concentration increased in the model rats （P 〈 0.05 or P 〈 0.01）. XMDP attenuated neuronal injury in a dose-dependent manner： the number of pyramidal neurons and neurotrophic factor concentrations were significantly increased compared with the model group （P〈 0.05 or P〈 0.01）. High- and middle-dose XMDP resulted in equivalent effects to Ginkgo leaf tablets. In addition, neurotrophic factor concentrations in all XMDP groups, after 60 days of administration, were remarkably greater than corresponding concentrations at 30 days （P 〈 0.05 or P 〈 0.01 ）. CONCLUSION： Hippocampal CA1 pyramidal cells exhibited pathological injury following establishment of the vascular dementia model. Middle- and high-dose XMDP increased neurotrophic factor expression in the brain of vascular dementia rats, which suggested neuroprotection equivalent to Ginkgo leaf tablets.     

Express,on of estrogen receptor alpha,nerve growth factor,interleukin-2, and androgen receptor in the cerebellum of ovariectomized rats following soybean isoflavone treatment

BACKGROUND： Studies have shown that estrogen receptor alpha （ERα）, nerve growth factor （NGF）, interleukin-2 （IL-2）, and androgen receptor （AR） expression in the cerebellum decreases when estrogen levels decrease in vivo. Soybean isoflavone, a type of non-steroid estrogen with similar molecular structure and function to estradiol, exhibits estrogen-like characteristics. OBJECTIVE： To investigate the effects of various doses of soybean isoflavone on expression of ERa, NGF, IL-2, and AR in the cerebellum of ovariectomized rat, and to determine whether there is a dose-dependent effect.DESIGN, TIME AND SETTING： Controlled trial at the cellular and molecular level. The study was performed at the Experimental Animal Engineering Center, College of Veterinary Medicine, Sichuan Agricultural University from July 2006 to May 2008. MATERIALS： Soybean isoflavone, comprised of daidzin, genistein and isoflavone, was provided by Taiyuan Yuantai Biochemical Industry, China. The ERα, NGF, IL-2, and AR in situ hybridization kit, rabbit anti-rat ERa, NGF, IL-2, and AR monoclonal antibodies, and SABC kit were purchased from Wuhan Boster Biological Technology, China. METHODS： A total of 50 female, Sprague Dawley rats, aged 3 months, were randomly assigned to 5 groups, with 10 animals in each group. With the exception of the sham-operation group （abdominal cavity opening alone）, all rats underwent bilateral ovariectomy. At 14 days after surgery, rats in the high-, middle-, and low-dose soybean isoflavone groups were subcutaneously injected with 1.5, 1.0, and 0.5 mg/kg soybean isoflavone, respectively, every 2 days for 6 consecutive weeks. Rats in the sham-operation and ovariectomized groups were subcutaneously injected with absolute alcohol （0.5 mL/kg）. MAIN OUTCOME MEASURES： Expression levels and distribution of ERα, NGF, IL-2, and AR in the cerebellum were detected by immunohistochemistry and in situ hybridization. RESULTS： Compared with the sham-operation group, immunoreactive products and hybridization signals of ERa, NGF, IL-2, and AR were significantly decreased in the cerebellar cortex and nuclei of ovariectomized rats （P 〈 0.05 or P 〈 0.01）, but increased following soybean isoflavone treatment. In particular, levels of the high-dose soybean isoflavone group were almost restored to levels of the sham-operation group （P 〉 0.05）. The immunoreactive products were primarily located in the cytoplasm and neurites, and rarely in the cell membrane and nuclei. However, the hybridization signals were predominantly located in the nuclei, but rarely in the cytoplasm, cell membrane, or neurites. CONCLUSION： Soybean isoflavone upregulated ERα, NGF, IL-2, and AR protein and gene expression in a dose-dependent manner, and played an important role in sustaining and protecting structure and function of cerebellar neurons. Moreover, the similarity of expression patterns of these molecules indicated that they were mutually interactive during the regulation of soybean isoflavone to the cerebellum.     

头颈部动脉夹层研究进展

头颈部动脉夹层,是指各种原因造成的头颈部动脉壁各层之间分离,血肿在动脉壁间积聚或血液在动脉壁间流通.按其发生的部位分为颅外段动脉夹层和颅内段动脉夹层,包括颈内动脉、椎动脉、基底动脉及其分支动脉的夹层形成,其中以颅外段颈内动脉夹层最为常见.     

神经生长因子促再生坐骨神经血管生成的作用

BACKGROUND： It remains to be determined whether nerve growth factor （NGF） can promote angiogenesis in regenerating peripheral nerves during repairing peripheral nerve injury.
OBJECTIVE： To evaluate the effects of NGF on angiogenesis, and to analyze the influencing mechanisms of NGF, according to the expression patterns of CD34, von Willebrand factor （vWF）, vascular endothelial cell growth factor （VEGF）, and the NGF receptor TrkA in proliferating vascular endothelial cells from a rat model of sciatic nerve injury.
DESIGN, TIME AND SETTING： Randomized, controlled study performed at the Research Institute of Field Surgery, Daping Hospital affiliated to the Third Military Medical University of Chinese PLA, between October 2003 and July 2005.
MATERIALS： Forty-five healthy, adult, Wistar rats underwent sciatic nerve injury. The rats were randomly divided into four groups： NGF ＋ chitosan （n = 15）, NGF ＋ chitosan ＋ anti-VEGF （n = 10）, chitosan （n = 10）, and physiological saline （n = 10）. METHODS： A 1 -cm defected sciatic nerve was bridged with a silica gel conduit. NGF ＋ chitosan group： 100 μ L chitosan and 5 μ L NGF （20 mg/L） were injected into the silica gel conduit; NGF ＋ chitosan ＋ anti-VEGF group： an additional 5μ L anti-VEGF monoclonal antibody （1 g/L） was injected into the silica gel conduit; chitosan group： 100μL chitosan and 5 μL physiological saline were injected into the silica gel conduit; physiological saline group： only 5μL physiological saline was injected into the silica gel conduit.
MAIN OUTCOME MEASURES： CD34 and vWf were used to label blood capillaries and large-diameter blood vessels in the regenerating peripheral nerves, respectively. At day 14 following surgery, immunohistochemistry was used to detect and semi-quantitatively analyze expressions of CD34, vWf, VEGF, and TrkA in proliferating vascular endothelial cells in the regenerating sciatic nerve. A confocal laser microscope was used to determine co-expression. RESULTS： Expressions of TrkA, CD34, vWf, and VEGF in the NGF ＋ chitosan group were significantly greater than the physiological saline and chitosan groups （P 〈 0.05-0.01）. Expressions of CD34 and VEGF in the NGF ＋ chitosan ＋ anti-VEGF group were completely inhibited, while expressions of vWf and TrkA gradually decreased, compared with the NGF ＋ chitosan group （P 〈 0.01）. Confocal microscopy revealed strong co-expression of VEGF and CD34 in the regenerating sciatic nerve, and CD34 expression positively correlated with VEGF expression. In addition, VEGF expression was greater than CD34 expression, and coexpression of VEGF and vWf was also strong.
CONCLUSION： VEGF was expressed in blood capillaries and large-diameter blood vessels, while exogenous NGF promoted VEGF expression in regenerating sciatic nerves, thereby increasing angiogenesis.     

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.     

Xenon-enhanced CT assessment of cerebral blood flow in stroke-in-progress patients with unilateral internal carotid artery or middle cerebral artery stenosis

Carotid or cerebral artery stenosis resulting in low perfusion is a major cause of ischemic stroke.Understanding the unique hemodynamic features in each patient undergoing a stroke-in-progress（SIP） and the correlation between progression and cerebral blood flow（CBF） status would help in the diagnosis and treatment of individual patients.We used xenonenhanced CT（Xe-CT） to examine cerebral perfusion in patients with or without SIP（30 patients/group）,recruited from October 2009 to October 2010.Only SIP patients with unilateral stenosis in the internal or middle cerebral artery were recruited.The occurrence of watershed infarction was higher in the SIP group than in the non-SIP group（P ＆lt;0.05）.In the SIP group,larger hypoperfused areas were found around the lesions than in the non-SIP group.In the SIP group,the CBF values in the ipsilateral areas were significantly lower than those in corresponding regions on the contralateral side.CBF values in the contralateral hemisphere were significantly lower in the SIP group than in the non-SIP group.In SIP patients,infarctions were surrounded by larger hypoperfused areas than in non-SIP patients.These larger hypoperfused areas may result in pathological damage to the brain that is responsible for the progression of stroke.     

应用生长激素释放肽心力衰竭大鼠心肌胆碱能神经纤维密度分布的变化

BACKGROUND： Changes in the cardiac autonomic nerve are considered to be important factors in the mechanisms of heart failure. It is possible to reduce or slow down nerve degeneration and necrosis, provided that patients take effective neuroprotectants during the early stages of heart failure. Moreover, it is possible to relieve the pathological process and reduce the risk of death. OBJECTIVE： To study the effect of growth hormone releasing peptide （GHRP） on cardiac cholinergic nerve fiber density distribution in a rat model of heart failure, and verify whether GHRP can ameliorate denervation. DESIGN, TIME AND SETTING： A randomized controlled study was performed at the Key Laboratory of Anatomy, Harbin Medical University, between June and October 2009. MATERIALS： Fifty adult, healthy, female, Wistar rats, weighing （200± 20） g, were randomly divided into GHRP （n = 30）, model （n = 10）, and sham operation （n = 10） groups. GHRP-2 was made in Shanghai, China （batch No. z071212-03）. METHODS： Acute myocardial infarction was established by ligating the left anterior descending coronary artery in the GHRP and model groups. Five weeks later, myocardial function was detected using color ultrasound electrocardiograph a successful marker of chronic heart failure models Ejection fraction 〈 60% was considered to be However, the left anterior descending coronary artery was not ligated in the sham operation group. The GHRP group was injected with 100 μ g/kg GHRP-2, and the other two groups were injected with the same volume of physiological saline, once per day. MAIN OUTCOME MEASURES： After 4 weeks, pathological changes in cardiac cholinergic nerve fibers were detected under optic microscopy following hematoxylin/eosin staining. In addition, density distribution was measured using a multi-function color pathological image system. RESULTS： In the sham operation group, myocardial cells were regular, uniformly stained, and no inflammatory cells were present. In the model group, myocardial cells were unevenly stained, exhibited nuclear atrophy, degeneration, dissolution, or disappearance. In the GHRP group, myocardial damage was less than in the model group; cardiac muscle fibers exhibited slight degeneration. The myocardium in the sham operation group was serried, spreading the cholinergic innervations along the cardiac fiber. In the model group, there was a decreased number of cholinergic nerve fibers decreased, which also became shorter and smaller, compared with the sham operation group （P 〈 0.01）. In the GHRP group, cholinergic positive nerve fibers were significantly increased compared with the model group （P 〈 0.01）, but still less than the sham surgery group （P 〈 0.05）. CONCLUSION： GHRP delayed denervation and reduced nerve reconstitution following heart failure in rats.     

骨髓神经组织定向干细胞化组织工程神经桥接坐骨神经缺损

BACKGROUND： Schwann cells are the most commonly used cells for tissue-engineered nerves. However, autologous Schwann cells are of limited use in a clinical context, and allogeneic Schwann cells induce immunological rejections. Cells that do not induce immunological rejections and that are relatively easy to acquire are urgently needed for transplantation. OBJECTIVE： To bridge sciatic nerve defects using tissue engineered nerves constructed with neural tissue-committed stem cells （NTCSCs） derived from bone marrow; to observe morphology and function of rat nerves following bridging; to determine the effect of autologous nerve transplantation, which serves as the gold standard for evaluating efficacy of tissue-engineered nerves. DESIGN, TIME AND SETTING： This randomized, controlled, animal experiment was performed in the Anatomical Laboratory and Biomedical Institute of the Second Military Medical University of Chinese PLA between September 2004 and April 2006. MATERIALS： Five Sprague Dawley rats, aged 1 month and weighing 100-150 g, were used for cell culture. Sixty Sprague Dawley rats aged 3 months and weighing 220-250 g, were used to establish neurological defect models. Nestin, neuron-specific enolase （NSE）, glial fibrillary acidic protein （GFAP）, and S-100 antibodies were provided by Santa Cruz Biotechnology, Inc., USA. Acellular nerve grafts were derived from dogs. METHODS： All rats, each with 1-cm gap created in the right sciatic nerve, were randomly assigned to three groups. Each group comprised 20 rats. Autograft nerve transplantation group： the severed 1-cm length nerve segment was reverted, but with the two ends exchanged; the proximal segment was sutured to the distal sciatic nerve stump and the distal segment to the proximal stump. Blank nerve scaffold transplantation group： a 1-cm length acellular nerve graft was used to bridge the sciatic nerve gap. NTCSC engineered nerve transplantation group： a 1-cm length acellular nerve graft, in which NTCSCs were inoculated, was used to bridge the sciatic nerve gap. MAIN OUTCOME MEASURES： Following surgery, sciatic nerve functional index and electrophysiology functions were evaluated for nerve conduction function, including conduction latency, conduction velocity, and action potential peak. Horseradish peroxidase （HRP, 20%） was injected into the gastrocnemius muscle to retrogradely label the 1-4 and L5 nerve ganglions, as well as neurons in the anterior horn of the spinal cord, in the three groups. Positive expression of nestin, NSE, GFAP, and S-100 were determined using an immunofluorescence double-labeling method. RESULTS： NTCSCs differentiated into neuronal-like cells and glial-like cells within 12 weeks after NTCSC engineered nerve transplantation. HRP retrograde tracing displayed a large amount of HRP-labeled neurons in I-45 nerve ganglions, as well as the anterior horn of the spinal cord, in both the autograft nerve transplantation and the NTCSC engineered nerve transplantation groups. However, few HRP-labeled neurons were detected in the blank nerve scaffold transplantation group. Nerve bridges in the autograft nerve transplantation and NTCSC engineered nerve transplantation groups exhibited similar morphology to normal nerves. Neither fractures or broken nerve bridges nor neuromas were found after bridging the sciatic nerve gap with NTCSCs-inoculated acellular nerve graft, indicating repair. Conduction latency, action potential, and conduction velocity in the NTCSC engineered nerve transplantation group were identical to the autograft nerve transplantation group （P 〉 0.05）, but significantly different from the blank nerve scaffold transplantation group （P 〈 0.05）. CONCLUSION＂ NTCSC tissue-engineered nerves were able to repair injured nerves and facilitated restoration of nerve conduction function, similar to autograft nerve transplantation. ＂