老年人周围神经疾病的特点

周围神经疾病是神经系统常见的疾病,目前尚无统一的分类,临床上常见的分类包括:按病理分为轴索变性周围神经病和脱髓鞘性周围神经病;按病因分为感染性多发性周围神经病、中毒性周围神经病、营养缺乏和代谢性周围神经病、遗传性周围神经病、副肿瘤综合征、免疫介导的周围神经病及结缔组织病所致的周围神经病等;按受损神经的功能分为感觉性周围神经病、运动性周围神经病和自主神经病;按受累神经分布形式或范围分为单神经病和多发单神经病.各种分类之间有明显的重叠.周围神经疾病的诊断除了依靠临床表现以外,主要的客观检查手段是肌电图和神经传导测定以及周围神经病理检查.     

糖尿病周围神经病理与电生理的研究进展

目的针对糖尿病周围神经病临床诊断的研究进展进行分析研究,以初步探讨各种诊断方法之间的差异。方法对糖尿病周围神经病临床诊断方法分别在病理和神经电生理方面进行比较分析。结果对早期糖尿病性周围神经病变进行临床准确诊断的一种比较重要的方法就是病理和神经电生理诊断。结论对糖尿病周围神经病临床诊断研究进展的初步探讨,对于提高糖尿病周围神经病的疗效具有重要一定的借鉴意义。     

糖尿病周围神经病分型及神经电生理检查研究进展

糖尿病是累及全身多系统和器官的最常见的慢性疾病之一，近年来有年轻化和多发的趋势。糖尿病神经病（DPN）通常指伴有糖尿病的各种周围神经病，其中远端对称性感觉运动性多发性周围神经病最常见。胰岛索依赖型糖尿病（IDM）DPN的主要临床特征为自主神经障碍和疼痛；而非胰岛索依赖型糖尿病（NIDM）DPN为远端感觉障碍和无力。病理改变主要表现为周围神经脱髓鞘和（或）轴索变性，IDM以小纤维为主，而NIDM以大纤维型损害多见。神经电生理检查有助于糖尿病周围神经病的早期诊断和鉴别诊断，现将近年来相关研究进展综述如下。     

老年人糖耐量受损相关痛性周围神经病的临床特征及危险因素

目的分析老年人糖耐量受损(IGF)相关痛性周围神经病的临床特征与危险因素,以利于早期诊断和治疗。方法选取年龄60岁,Leeds神经病理性疼痛评分12分,IGT相关痛性周围神经病患者60例(IGT组),2型糖尿病痛性周围神经病患者70例(DM组),正常对照组60例,分别比较三组的临床特征与相关危险因素。结果 IGT相关痛性周围神经病多数表现为烧灼样、针刺样、电击样或麻木样疼痛,部分为自发性痛或触摸痛;疼痛部位以双侧对称性肢体远端常见,其次为单神经分布区。与正常对照组比较,IGT组患者双侧跟腱反射消失、大足趾振动觉减退、腓肠神经传导异常、皮肤交感反应异常的比例较高(P0.05),在其他方面差异无统计学意义(P0.05);与DM组比较,IGT组的患者双侧跟腱反射消失、大足趾振动觉减退、腓肠神经传导异常的比例较低(P0.05),在其他方面差异无统计学意义(P0.05)。经Logistic多因素回归分析,结果显示肥胖、血清甘油三酯、总胆固醇、低密度脂蛋白胆固醇水平升高是IGT相关痛性周围神经病的危险因素。结论老年人IGT相关痛性周围神经病的重要特点是符合周围神经分布的异常疼痛,以远端对称性感觉或运动性多神经病变常见,其次是单神经病变,常有跟腱反射消失与大足趾振动觉减退等神经系统体征,腓肠神经传导速度减慢、皮肤交感反应异常是早期电生理指标。肥胖、血清甘油三酯、总胆固醇与低密度脂蛋白胆固醇水平升高是影响IGT相关痛性周围神经病的危险因素。     

周围神经病的治疗进展

临床神经疾病类型中,周围神经病占有较高发生几率,随着医疗科技取得的巨大进步,近年来其治疗取得飞跃发展,但与其它神经疾病比较,发展呈缓慢显示。病因包括肿瘤、代谢、外伤、中毒、遗传、感染等。近几年各种周围神经疾病治疗为研究重点,基础研究取得巨大进展,但相对滞后,还需系统综述,综合分析研究结果,以改善预后。     

多发性周围神经病的腹直肌肌电图检测

目的 探讨腹直肌肌电图在多发性周围神经病诊断中的作用.方法 对109例多发性周围神经病患者进行神经传导研究和肌电图检测,检查肌肉包括腹直肌、第一骨间肌、胫前肌.同时进行正常对照组和肌萎缩侧索硬化组相关研究.比较三组腹直肌肌电图的异同.结果 周围神经病组腹直肌肌电图出现神经源性改变,其运动单位电位波幅(451.67±75.01)μV高于正常组[(373.78±56.46)μV,t=2.01,P<0.04],低于肌萎缩侧索硬化组[(537.19±159.04)μV,t=2.32,P<0.03].结论 腹直肌肌电图可用于多发性周围神经病中肋间神经损害的检测.     

腓肠神经活检对周围神经病的诊断意义

周围神经病常由多种原因造成,如感染、外伤、肿瘤、血管炎、代谢中毒性疾病。遗传性疾病等等。当周围神经病的临床表现伴随全身性疾病出现时,例如糖尿病、尿毒症性神经病等,诊断常不困难。有些周围神经病常在全身疾病出现前作为首发症状出现,如非转移性癌性神经病;或者某些周围神经病以多发性单     

职业性慢性砷化物中毒周围神经病患者的临床研究

周围神经病（PN）主要是指周围神经系统功能障碍现象。周围神经病的发生对患者的正常生活带来极大的不便,当前对于该疾病的评价体系研究的很多。砷是一种有名的有毒物质,且能对神经系统尤其是末梢神经构成严重伤害,是一种常见的神经致毒物质。近年来随着工业的发展,砷中毒引起神经系统损害案例逐渐增多。     

药物中毒性周围神经病

临床上治疗的新药在不断增多。而对人类的神经毒性不可能预先在动物试验中都得到确定,需要在临床使用中发现和证实;很多药物已知有神经毒性,使用时需仔细观察。为了避免严重的神经损害,因此掌握药物中毒性周围神经病是重要的。药物对周围神经的毒性作用,可在局部,如细胞毒性药剂肌肉注射或动脉内滴注可有周围神经或神经丛的局部损害;青霉素肌肉注射后偶可发生臂丛神经病(推测由于过敏)。临床上常见的有以下两种。     

糖尿病周围神经病128例临床与神经电生理分析

目的探究糖尿病周围神经病患者临床病症特点以及神经电生理特点。方法选择2017年1月—2018年12月于该院收治的128例糖尿病周围神经病患者作为研究对象,测定所有患者的运动神经与感觉神经传导水平,共计有32例患者接受常规针极肌电图检测。结果 128例患者共计有93例患者检测出存在神经电生理异常,有72例患者被诊断为多发性周围神经疾病。发现患者神功传导功能正常情况下正极肌电图有异常。结论糖尿病周围神经患者中临床病症和神经电生理变化均已感觉神经功能异常为主,并非所有周围神经疾病都能检测出电生理异常,不建议单独使用针极肌电图作为筛查糖尿病周围神经症疾病手段。     

强化治疗对糖尿病周围神经病变疗效的观察

目的评价胰岛素泵强化治疗对糖尿病周围神经病变的疗效。方法对22例明确诊断存在糖尿病周围神经病变的初诊断2型糖尿病患者进行胰岛素泵强化治疗14天,强化治疗后复查神经电生理,评价神经病变的改善程度。结果强化治疗后,空腹血糖及餐后两小时血糖均得到较大程度的改善,尺神经感觉波幅、正中神经感觉波幅、腓肠神经感觉传导速度及波幅,腓总神经波幅均有明显改善。结论强化治疗能部分改善糖尿病周围神经病变。     

2型糖尿病患者高血压与糖尿病性神经病变的关系

目的 探讨2型糖尿病患者高血压与糖尿病性神经病变的关系。方法 利用心自主神经功能检测系统和神经电生理检测仪对107例（高血压组52例,非高血压组55例）2型糖尿病患者的心自主神经功能和肢体的末梢神经传导速度、皮肤痛温觉、振动沉进行测定,以判断心自主神经病变和末梢神经病变。结果 两组间末梢神经功能和心自主神经功能各指标除心的是距频谱分析的高频值外差异均无显著性（P＜0.05）。Logistic回归分析显示高血压与心自主神经病变显著相关（P＜0.01）,而与末梢神经病变无显著相关。结论 2型糖尿病患者高血压是心自主神经病变发病的危险因素,而与末梢神经病变无明显关系。     

刺五加离子导入治疗糖尿病周围神经病变30例疗效观察

为观察刺五加离子导入治疗糖尿病周围神经病变的临床疗效，用该法对31例糖尿病周围神经病变患者(治疗组)进行治疗，并与29例经常规糖尿病治疗者(对照组)进行对比。结果显示，治疗组各临床症状好转率，特别是肢体疼痛、足背动脉波动减弱、肢体皮肤色泽变浅及体位性低血压好转率明显高于对照组，两组比较有显著性差异(P＜0．01)；治疗组正中神经、尺神经和腓总神经的感觉神经传导速度(SCV)、运动末端潜伏期(MLP)较同组治疗前和对照组治疗后均明显改善，组间比较有显著性差异(P均＜0．01)。提示刺五加离子导入疗法可在一定程度上促进受损神经组织的修复和再生，改善神经髓鞘功能，降低糖尿病周围神经病变的致残率．     

Diagnosis and treatment of primary Sjögren syndrome-associated peripheral neuropathy: a six-case series

Objectives

The clinical and therapeutic aspects of primary Sjögren syndrome (PSS) in patients with peripheral neuropathy were analyzed and the specifics of individual case studies are discussed.

Methods

We retrospectively studied six patients (four women, two men; mean age 64.5 years) presenting with PSS with peripheral neurological involvement over a five-year period (2008–2012). All patients had neurological examinations, including nerve conduction studies, somatosensory evoked potentials, and sural nerve biopsies. Treatment regimens included corticosteroids, intravenous gammaglobulin, or immunosuppressive treatment.

Results

Peripheral neuropathy was observed in six (7.9 %) of 76 patients with SS as the underlying disease; three were cases of multiple mononeuropathy, two cases had sensory ataxic neuropathy, one of which was autonomic neuropathy, and one case was diagnosed as painful sensory neuropathy without sensory ataxia. Four of the six patients were diagnosed with SS after the onset of neurological symptoms. Individual peripheral neuropathies had distinct neurological, electrophysiological, and pathological characteristics. The effect of steroids and intravenous gammaglobulin differed depending on the case.

Conclusions

In PSS patients, a precise diagnosis is important, because the therapeutic strategy and response varies depending on the type of neuropathy. In clinical practice, it is important to consider a diagnosis of SS when patients present with peripheral neuropathy.     

Neuropathies périphériques au cours des maladies de système : partie I (connectivites et granulomatoses)

Systemic diseases (connective disease, granulomatosis) may be associated with peripheral neuropathies. The diagnosis can be complex when the neuropathy is the presenting manifestation of the disease, requiring close collaboration between neurologists and internists. Conversely, when the systemic disease is already known, the main question remaining is its imputability in the neuropathy. Regardless of the situation, the positive diagnosis of neuropathy is based on a systematic and rigorous electro-clinical investigation, specifying the topography, the evolution and the mechanism of the nerve damage. Certain imaging examinations, such as nerve and/or plexus MRI, or other more invasive examinations (skin biopsy, neuromuscular biopsy) enable to specify the topography and the mechanism of the injury. The imputability of the neuropathy in the course of a known systemic disease is based mainly on its electro-clinical pattern, on which the alternatives diagnoses depend. In the case of an inaugural neuropathy, a set of arguments orients the diagnosis, including the underlying terrain (young subject), possible associated systemic manifestations (inflammatory arthralgias, polyadenopathy), results of first-line laboratory tests (lymphopenia, hyper-gammaglobulinemia, hypocomplementemia), autoantibodies (antinuclear, anti-native DNA, anti-SSA/B) and sometimes invasive examinations (neuromuscular biopsy).     

Neuropathies périphériques associées aux syndromes lymphoprolifératifs : spectre clinique et démarche diagnostique

Lymphoproliferative syndromes (multiple myeloma, Waldenström's disease, chronic lymphocytic leukemia, lymphomas) may be associated with peripheral neuropathies. The mechanism can be dysimmune, associated or not with monoclonal gammopathies; paraneoplastic; infiltrative; or more commonly, iatrogenic or due to vitamin deficiency. The diagnosis can be complex, especially when the neuropathy is the presenting manifestation, requiring a close cooperation between internists and neurologists. The positive diagnosis of the neuropathy is based on a systematic electro-clinical investigation, which specifies the topography and the mechanism of the nerve damage, sometimes reinforced by imaging examinations, in particular, nerve and/or plexus MRI. The imputability of the neuropathy to a lymphoproliferative syndrome is based on a set of arguments including the clinical context (B signs, tumour syndrome), first-line laboratory tests (hemogram, protein electrophoresis, viral serologies, complement), auto-antibodies discussed according to the neuropathy (anti-MAG, anti-gangliosides) and sometimes more invasive examinations (bone marrow or neuro-muscular biopsies).     

Neuropathies périphériques au cours des maladies de système : partie II (vascularites)

Primary systemic vasculitides, mainly of the small and medium-sized vessels, are frequently associated with peripheral neuropathies. When the disease is already known, the appearance of a neuropathy should suggest a specific injury, especially when associated with other systemic manifestations. Conversely, when neuropathy is inaugural, close collaboration between neurologists and internists is necessary to reach a diagnosis. A standardized electro-clinical investigation specifying the topography, the evolution and the mechanism of the nerve damage enables the positive diagnosis of the neuropathy. Several elements orient the etiological diagnosis and allow to eliminate the main differential diagnosis: non systemic vasculitic neuropathy. The existence of associated systemic manifestations (glomerular or vascular nephropathy, interstitial lung disease, intra-alveolar hemorrhage, ENT involvement…), biological markers (ANCA, cryoglobulinemia, rheumatoid factor), and invasive examinations allowing histological analysis (neuromuscular biopsy) are all useful tools for.     

Correlation between serum vitamin B12 level and peripheral neuropathy in atrophic gastritis

AIM To explore the correlation between serum vitamin B12 level and peripheral neuropathy in patients with chronic atrophic gastritis(CAG). METHODS A total of 593 patients diagnosed with chronic gastritis by gastroscopy and pathological examination fromSeptember 2013 to September 2016 were selected for this study. The age of these patients ranged within 18-to 75-years-old. Blood pressure, height and weight were measured in each patient, and the body mass index value was calculated. Furthermore, gastric acid, serum gastrin, serum vitamin and serum creatinine tests were performed, and peripheral nerve conduction velocity and Helicobacter pylori(H. pylori) were detected. In addition, the type of gastritis was determined by gastroscopy. The above factors were used as independent variables to analyze chronic gastritis with peripheral neuropathy and vitamin B12 deficiency risk factors, and to analyze the relationship between vitamin B12 levels and peripheral nerve conduction velocity. In addition, in the treatment of CAG on the basis of vitamin B12, patients with peripheral neuropathy were observed. RESULTS Age, H. pylori infection, CAG, vitamin B9 and vitamin B12 were risk factors for the occurrence of peripheral nerve degeneration.Furthermore,CAG and H. pylori infection were risk factors for chronic gastritis associated with vitamin B12 deficiency. Serum vitamin B12 level was positively correlated with sensory nerve conduction velocity in the tibial nerve(R = 0.463). After vitamin B12 supplementation, patients with peripheral neuropathy improved. CONCLUSION Serum vitamin B12 levels in patients with chronic gastritis significantly decreased, and the occurrence of peripheral neuropathy had a certain correlation. CAG and H. pylori infection are risk factors for vitamin B12 deficiency and peripheral neuropathy. When treating CAG, vitamin B12 supplementation can significantly reduce peripheral nervous system lesions. Therefore, the occurrence of peripheral neuropathy associated with vitamin B12 deficiency may be considered in patients with CAG. Furthermore, the timely supplementation of vitamin B12 during the clinical treatment of CAG can reduce or prevent peripheral nervous system lesions.     

Peripheral Neuropathy as a Presenting Feature of Type 2 Diabetes: A Case-Controlled Study

The characteristics and outcome of 68 newly diagnosed Type 2 diabetic patients who presented with clinically evident peripheral neuropathy were compared with matched controls who had no neuropathy at diagnosis. All subjects (34 male) whose median age was 68 (range 47–89) yr were identified from a computerized diabetes register and presented in 1982–1990. The groups were compared at diagnosis for haemoglobin A₁, body mass index, blood pressure, smoking, and alcohol consumption, and for co-existent coronary and peripheral vascular disease. Mortality and morbidity were recorded to March 1991. Significantly more patients with neuropathy had co-existent peripheral vascular disease: 24(35%) compared to 6(9%) controls (p = 0.0021). Twenty (30%) of those with neuropathy and no controls had retinopathy at diagnosis, which was sight-threatening in 10. Seven (10%) with neuropathy but no controls presented with foot ulcers, one requiring limited amputation. Two more patients with neuropathy and one control subsequently developed foot ulcers resulting in one or more amputation in each group. Twenty-one (31%) of those with neuropathy and 14 (21%) controls died (p = 0.2109). In conclusion more diabetic patients with clinically evident peripheral neuropathy at diagnosis have peripheral vascular disease than matched patients without neuropathy. It is likely that macrovascular disease either exacerbates or causes the neuropathy in this group of patients. They are at high risk of developing foot ulceration and high priority should be given to foot care in planning their management.     

Peripheral nerve damage associated with administration of taxanes in patients with cancer

Peripheral neuropathy is a well recognized toxicity of taxanes, usually resulting to dose modification and changes in the treatment plan. Taxanes produce a symmetric, axonal predominantly sensory distal neuropathy with less prominent motor involvement. A “dying back” process starting from distal nerve endings followed by effects on Schwann cells, neuronal body or axonal transport changes and a disturbed cytoplasmatic flow in the affected neurons is the most widely accepted mechanism of taxanes neurotoxicity. The incidence of taxanes-induced peripheral neuropathy is related to causal factors, such as single dose per course and cumulative dose and risk factors including treatment schedule, prior or concomitant administration of platinum compounds or vinca alcaloids, age and pre-existing peripheral neuropathy of other causes. The most reliable method to assess taxanes neurotoxicity is by clinical examination combined with electrophysiological evaluation. There is currently no effective symptomatic treatment for paclitaxel-associated pain, myalgias and arthralgias. Tricyclic antidepressants and anticonvulsants have been used as symptomatic treatment of neurotoxicity with some measure of success. Therefore, new approaches for prophylaxis against taxanes-induced peripheral neuropathy are needed. Several neuroprotective agents including, thiols, neurotrophic factors, and antioxidants hold promise for their ability to prevent neurotoxicity resulting from taxanes exposure. However, further confirmatory trials are warranted on this important clinical topic. This review critically looks at the pathogenesis, incidence, risk factors, diagnosis, characteristics and management of taxanes-induced peripheral neuropathy. We also highlight areas of future research.