138例糖尿病患者神经电图分析

目的探讨2型糖尿病患者周围神经病变(DPN)的神经电生理特点及其与病程的关系。方法连续记录138例血糖控制良好的糖尿病患者神经电图(包括感觉神经传导速度SCV和运动神经传导速度MCV)的检测结果,并根据糖尿病病程将其分组进行比较。结果共检测周围神经1669条,异常神经313条(18.75%),下肢异常率(132/530,24.9%)明显高于上肢(59/517,11.4%)(P<0.0001),感觉神经(122/622,19.6%)与运动神经(191/1047,18.2%)受累无差异(P=0.5665);糖尿病病程10年以上者运动、感觉神经异常率(24.3%,33%)明显高于病程小于10年组(14.2%,14%)(P<0.001)。病程大于10年组神经传导速度均较病程小于10年组减慢,正中神经、胫后神经运动传导速度和尺神经、腓肠神经感觉传导速度有统计学意义(P<0.05);除尺神经外所查运动神经近远端复合肌肉动作电位波幅(CAMP)病程≥10年组均明显低于病程<10年组。结论尽管受检时血糖控制良好,但依然有周围神经电生理异常变化。2型糖尿病患者下肢神经传导异常率高于上肢,尤以运动神经明显。病程是糖尿病周围神经损害的危险因素,随着病程增加神经传导异常率和损伤严重程度增高。     

桡神经超声结合神经传导检查在糖尿病周围神经病变患者中的应用

目的:探讨2型糖尿病伴周围神经病变患者桡神经的超声特征及电生理表现,企为临床诊治及预后评估提供参考依据.方法:选取西宁市第一人民医院70例2型糖尿病患者,分为合并周围神经病变组35例及未合并周围神经病变组35例,同时选择健康体检者35例作对照,所有受检者行桡神经超声检查及神经传导检测.结果:糖尿病合并周围神经病变者桡神经超声表现为神经束回声减低,平行线状低回声结构消失,神经外膜增厚分界不清;神经传导检测提示桡神经运动传导速度(MCV)及感觉传导速度(SCV)均有异常,且SCV更为敏感,异常率更高;糖尿病未合并周围神经病变组与正常对照组超声及神经传导检查比较,差异无统计学意义.结论:超声与神经传导检查两者结合,可以从功能及形态学两方面更明确地为临床提供糖尿病患者是否合并周围神经病的依据和判断病变程度,有助于临床诊治及预后评估.     

糖尿病神经病变研究进展

糖尿病神经病变是多因素共同作用的结果。越来越多的证据把多元醇通路异常和糖尿病神经病变的发病机制联系起来。此外似乎还有神经再生和钠钙通道异常 ,转运金属等在发病中起作用。在动物模型中 ,早期并且足疗程地使用醛糖还原酶显示了逆转神经病变的希望 ,然而迄今为止在人体实验中这些被使用的药物似乎没有足够的效力。神经营养因子和血管内皮生长因子也显示了可能的逆转作用。对神经病性疼痛的治疗将会有更多选择。本综述将关注在糖尿病神经病领域的最新进展。在西方国家 ,糖尿病神经病变可能是导致老年糖尿病患者残废的重要原因。一项研…     

轴突转运和糖尿病神经病变

本文复习了近二十年来有关轴突转运与糖尿病神经病变的研究,重点介绍了糖尿病神经病变时轴突慢转运和快转运损伤的表现以及药物对轴突转运的干预作用。     

艾塞那肽对糖尿病周围神经损伤大鼠的神经保护作用

目的 探讨艾塞那肽(EX)对糖尿病周围神经损害大鼠的神经保护作用.方法 将34只健康雄性Wistar大鼠随机分为正常对照(NC)组、糖尿病组、EX小剂量治疗(EXmin)组及大剂量治疗(EXmax)组.后3组大鼠给予脂肪乳灌胃,14 d后进行口服葡萄糖耐量试验并测算胰岛素抵抗指数;通过腹腔注射链脲佐菌素建立糖尿病模型....     

Ⅱ型糖尿病合并神经病变的多因素分析

目的 了解Ⅱ型糖尿病合并神经病变的患病率，并进一步分析影响糖尿病神经病变相关的危险因素。方法 收集在本院住院治疗的150例Ⅱ型糖尿病患者及60例正常体检者的病史和临床生化资料，Ⅱ型糖尿病患者根据有无合并神经病变分成两组。比较各组间的临床资料，使用单因素及多因素相关分析方法，分析Ⅱ型糖尿病合并神经病变相关的危险因素。结果 Ⅱ型糖尿病神经病变患病率46．7％。糖尿病神经病变组和糖尿病无神经病变组比较，SBP、糖尿病病史、吸烟史、FPG、HbAlc与空腹C肽在两组之间有明显差别，具有统计学意义（P〈0．05）。且SBP、糖尿病病史、吸烟史、FPG，PBG，和HbAlc为Ⅱ型糖尿病患者合并神经病变的独立因素。结论 神经病变在Ⅱ型糖尿病人群中有较高的患病率，其发病与众多的因素有关。     

82例糖尿病所致神经精神障碍分析

本文对82例糖尿病所致神经精神障碍作了分析。发现精神障碍主要包括神经衰弱症状群、焦虑、抑郁状态和情绪不稳;神经系统有中枢神经损害、周围神经损害及植物神经功能障碍。     

糖尿病痛性神经病变的研究进展

糖尿病神经病变是常见的糖尿病并发症之一,其中有肢体疼痛、感觉异常等多种表现,其中以疼痛最痛苦、最显著,临床多见于血糖控制不佳的患者,常表现为远端肢体自发性疼痛、痛觉过敏、异常性疼痛（如烧灼感、蚁走感或针刺感）等,夜间明显,同时患者常合并抑郁、失眠,且治疗困难。     

Ultrasonography of peripheral nerves

During sonographic examination of the extremities using high frequency "small-parts" equipment, peripheral nerves may be identified in virtually all patients. Peripheral nerves have a typical ultrasonographic pattern that correlates well with histologic structure and facilitates differentiation between nerves and tendons. The ability of this technique to depict peripheral nerves makes it possible, in many instances, to study nerve abnormalities in trauma, entrapment syndromes and tumors. Ultrasound can enable differentiation of an endoneural from an extraneural space-occupying lesion and evaluation of the extent and consistency of the lesion, as well as the integrity and dynamic behavior of the nerve involved at follow-up study. The purpose of this review article is to describe the normal ultrasonographic appearance of peripheral nerves and to discuss the potential role of this technique to image nerve lesions noninvasively. A series of paradigmatic ultrasound images of diverse pathologic processes involving peripheral nerves is presented. Although the ultrasound study of peripheral nerves remains in its infancy, with further refinement of ultrasound technology and a more precise knowledge of the ultrasound appearance of the extremities we may be optimistic to the future impact of this technique on diagnosis, treatment and prognosis in patients clinically suspected to have a nerve lesion.     

Electrodiagnosis of peripheral neuropathy

Electrodiagnostic studies are an important component of the evaluation of patients with suspected peripheral nerve disorders. The pattern of findings and the features that are seen on the motor and sensory nerve conduction studies and needle electromyography can help to identify the type of neuropathy, define the underlying pathophysiology (axonal or demyelinating), and ultimately help to narrow the list of possible causes. This article reviews the electrodiagnostic approach to and interpretation of findings in patients with peripheral neuropathies.     

Chemotherapy-induced peripheral neuropathy

Recent advances in the development and administration of chemotherapy for malignant diseases have led to prolonged survival of patients and the promise of a return to normal lives. The cost of progress comes with a price, however, and the nervous system is frequently the target of therapy-induced toxicity. Unlike more immediate toxicities that affect the gastrointestinal tract and bone marrow, chemotherapy-induced neurotoxicity is frequently delayed in onset and may progress over time. In the peripheral nervous system, the major brunt of the toxic attack is directed against the peripheral nerve, targeting the neuronal cell body, the axonal transport system, the myelin sheath, and glial support structures, resulting in chemotherapy-induced peripheral neuropathy.     

Thalidomide-induced peripheral neuropathy

Summary Prospective clinical and electrophysiological follow-up was performed on nine patients under thalidomide treatment in order to detect the very beginning of possible drug-induced peripheral neuropathy. For neurophysiological assessment, nerve conduction measurements of the median, peroneal and sural nerves (7 conduction parameters) and needle EMG examination of the anterior tibial muscle were performed. The results of a first control after about 3 months of treatment were compared with the starting point examination, and the patients were then classified as affected or not affected according to clinical and neurophysiological criteria. At this point, three patients showed clinical and electrophysiological, and another two only electrophysiological alterations suggesting early neuropathy. This classification did not change after further clinical and electrophysiological controls. Without starting-point values, the early detection of neuropathy would not have been possible in all patients. No single reliable neurophysiological parameter for detection of thalidomide-induced neuropathy could be found. Pharmacogenetic classification with regard to hydroxylation and acetylation phenotypes was then performed in some patients and interpreted with relation to thalidomide neurotoxicity. A possible relationship between slow acetylators and development of thalidomide-induced neuropathy was found.     

Inherited peripheral neuropathy

Hereditary disorders of the peripheral nerves constitute a group of frequently encountered neurological diseases. Charcot-Marie-Tooth neuropathy type 1 (CMT1) is genetically heterogeneous and characterized by demyelination with moderately to severely reduced nerve conduction velocities, absent muscle stretch reflexes and onion bulb formation. Genetic loci for CMT1 map to chromosome 17 (CMT1A), chromosome 1 (CMT1B), and another unknown autosome (CMT1C). CMT1A is most often associated with a tandem 1.5-megabase (Mb) duplication in chromosome 17p11.2-12, or in rare patients may result from a point mutation in the peripheral myelin protein-22 (PMP22) gene. CMT1 B result from point mutations in the myelin protein zero (Po or MPZ) gene. The molecular defect in CMT1 C is unknown. Mutations in the early growth response 2 gene (EGR2) are also associated with demyelinating neuropathy. Other rare forms of demyelinating peripheral neuropathies map to chromosome 8q, 10q, and 11q. X-linked Charcot-Marie-Tooth neuropathy (CMTX), which has clinical features similar to CMT1, is associated with mutations in the connexin32 gene. Charcot-Marie-Tooth neuropathy type 2 (CMT2) is characterized by normal or mildly reduced nerve conduction velocity with decreased amplitude and axonal loss without hypertrophic features. One form of CMT2 maps to chromosome 1 p36 (CMT2A), another to chromosome 3p (CMT2B) and another to 7p (CMT2D). Dejerine-Sottas disease (DSD), also called hereditary motor and sensory neuropathy type III (HMSNIII), is a severe, infantile-onset demyelinating polyneuropathy that may be associated with point mutations in either the PMP22 gene or the Po gene and shares considerable clinical and pathological features with CMT1. Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder that results in a recurrent, episodic demyelinating neuropathy. HNPP is associated with a 1.5-Mb deletion in chromosome 17p11.2-12 and results from reduced expression of the PMP22 gene. CMT1A and HNPP are reciprocal duplication/deletion syndromes originating from unequal crossover during germ cell meiosis.     

痛性周围神经病

痛性周围神经病以神经病理性疼痛为突出表现,可伴运动、感觉及自主神经功能异常,主要累及小纤维(Aδ和C纤维),根据病因可以分为遗传性和获得性.可为独立性疾病亦可为其他疾病表现的一部分,前者指特发性小纤维神经病.疼痛包括自发性和诱发性疼痛,表现为长度依赖性,呈现“手套-袜套”样分布.痛性周围神经病的主要辅助检查包括定量感觉检测、表皮内神经纤维密度、皮肤交感反应等.治疗原发病和控制疼痛是主要治疗手段,常用药物包括卡马西平、普瑞巴林、阿米替林等.     

周围神经显微减压术治疗糖尿病性下肢周围神经病

目的 探讨周围神经显微减压术治疗糖尿病性下肢周围神经病的疗效.方法 应用腓总神经、腓深神经、胫后神经主干及其分支显微减压术治疗42例糖尿病性下肢周围神经病患者(54侧下肢).结果 平均随访40个月.42例糖尿病性下肢周围神经病患者54侧下肢膝下麻木、疼痛症状术后89％ (48/54)缓解,肢体平衡问题术后70％ (21/30)缓解,随访期间54侧下肢无一侧发生顽固性溃疡或截肢.术后拇指两点辨别觉好转40侧(74％,40/54),腓总神经、胫后神经感觉、运动神经传导速度及动作电位波幅改善38侧(70％,38/54).并发症:踝部切口愈合不良3侧(6％,3/54).结论 周围神经显微减压术是治疗糖尿病性下肢周围神经病的有效方法,严格把握手术指征及术中神经彻底减压是保证疗效的关键.