工业环境与周围神经损害

周围神经大多数兼有感觉、运动和自主神经的混合神经,病变时常同时受累,临床以感觉运动型多发性周转神经病为最常见,除急性砷、铊有机磷农药中毒,周转神经的员害呈急剧进展外,大多周转神经损害呈渐进性发展,患起病隐袭,逐渐出支体远端对称感觉障碍和下运动神经元性运动障碍,伴有局部自主神经功能紊乱。     

周围神经疾病行神经活检术患者的护理

周围神经疾病（peripheral neuropathy）是指周围运动、感觉和自主神经的结构和功能障碍。周围神经疾病分类复杂,以往临床常由于对周围神经疾病的多样性认识不足及缺乏明确的诊治手段而延误疾病的治疗。近年来,第二军医大学长海医院神经内科开展神经活检术以区别神经髓鞘损害和轴索损害,用以指导临床诊治,取得了一定成效。     

神经源性膀胱

正常膀胱功能的实现依赖于躯体神经和自主神经的运动与感觉成分相互协调。控制排尿功能的中枢神经系统或周围神经受到损害而引起的膀胱功能障碍称为神经源性膀胱。     

黄芪桂枝五物汤合当归四逆汤治疗糖尿病周围神经病变26例

糖尿病周围神经病变是糖尿病常见的一种主要并发症之一,以周围对称性感觉和运动神经病变及自主神经病变为主.糖尿病神经病变的发生和发展是代谢异常和神经血液供应障碍共同参与的结果.     

分期康复护理在周围神经完全性损伤神经断端吻合术后患者中的应用

目的探讨分期康复护理在周围神经完全性损伤患者神经断端吻合术后的应用效果,为提升周围神经完全性损伤患者术后康复方案制定提供参考。方法选择我院2015年2月至2017年1月收治的周围神经完全性损伤患者80例为研究对象,所有患者均行神经断端吻合术治疗,按照手术顺序编号,采用数字随机表法将患者等分为对照组和观察组。对照组患者按照常规护理路径实施术后护理,观察组患者行分期康复护理。两组患者均随访1年,比较两组患者术后3,6周及1年受损部位感觉功能恢复情况、运动功能恢复情况、发汗试验评定自主神经功能恢复情况、病损部位活动功能问卷得分。结果两组患者术后3周感觉功能恢复情况、运动功能恢复情况、自主神经功能恢复情况、病损部位活动功能问卷评分比较差异无统计学意义(P 0. 05)。术后6周及1年观察组患者的感觉功能恢复情况、运动功能恢复情况、自主神经功能恢复(有汗率)均明显高于对照组(P 0. 05),病损部位活动功能问卷评分明显低于对照组(P 0. 05)。结论分期康复护理能明显提升周围神经完全性损伤患者神经断端吻合术后6周及1年的运动、感觉、自主神经功能恢复效果,提升患者病损部位功能活动能力,是更适合此类患者的一种康复模式,具有较高的临床价值。     

周围神经病损的康复治疗

１引言周围神经病损是指周围运动、感觉和自主神经的结构和功能的障碍。常由感染、外伤、中毒、受压、遗传、缺血和营养代谢障碍等所致。临床表现为受损神经支配范围内的感觉、运动和或自主神经功能异常,其部位及范围随受损神经的分布形式而异,但有其共同的特性。以往周围神经病损后偏重于药物、支具固定、手术等传统治疗。近年来,人们越来越认识到综合性康复治疗的重要性,并把其应用于临床。２功能评定周围神经病损后,应进行功能检查与评定,以期了解周围神经病损的程度,作出预后评估有无恢复的可能及其大致时间,为临床和康复治疗提…     

实验性糖尿病大鼠周围神经病变形成及发病机制研究进展

糖尿病周围神经病变(DPN)是糖尿病最常见的并发症之一,也是引起糖尿病患者致残的主要原因。糖尿病性神经病变可累及神经系统任何部位,中枢神经及周围神经均可累及,而糖尿病性周围性神经病变发病率最高[1]。主要表现为对称性疼痛、感觉异常、间歇性或持续性发作,呈电击样、烧灼样,静止时或夜间加剧,出现感觉麻木、迟钝或关节麻痹。糖尿病并发慢性神经病变的机制至今尚未完全阐明,近年来大量临床和实验研究证明,DPN以高血糖为始动因素外,遗传因素、代谢障碍、微循环异常、环境等诸多因素相互影响致运动、感觉、自主神经功能缺失。影响因素…     

牛痘疫苗接种家兔炎症皮肤提取物联合丹红注射液治疗糖尿病周围神经病临床研究

糖尿病周围神经病变(diabetic peripheral neuropathy,DPN)是糖尿病最常见的慢性并发症之一,可累及感觉、运动和自主神经,导致手足感觉缺失、疼痛、麻木甚至截肢、死亡,是糖尿病患者致残、致死的重要原因。目前糖尿病周围神经病变病因不明,尚无特效疗法。2011年1月至2012年1月我院应用牛痘疫苗接种家兔皮肤炎症提取物(神经妥乐平)     

糖尿病性神经病变的观察与护理

神经病变是糖尿病(Dm)最常见的并发症之一,其病变主要以周围神经和植物神经损害为主,偶见有脊髓和脑部损害。周围神经损害多因糖代谢紊乱引起糖基化导致脊髓前角细胞以下的周围神经对称性损害及下运动神经元体征和营养障碍。临床表现为:感觉障碍呈周围性分布,出现套式感觉障碍,腱反射减弱或消失,下肢肌力减低,往往伴脚的骨间肌萎缩。植物神经损害多表现有心率加快,胃肠功能紊乱及神经膀胱等症状。一、临床资料自1986年1月—1987年10月,我科共收治Dm患者70人,其中并发神经病变者20人,占住院总人数的28.6％,男性15人,女性5人,平均年龄46岁。典型病例1:患者,女,38岁,住院号18389。     

焉耆县儿童血铅情况调查

科学研究发现,铅进入人体内可损害骨髓造血系统,使血红蛋白合成障碍引起贫血,而且还损害神经系统引起末梢神经炎,干扰神经功能.能使神经传导速度减慢,造成行为、意识及神经效应改变,引起运动、感觉异常,闪电样疼痛.进而发展到感觉减退和肢体无力,甚至造成周围神经麻痹;同时还损害消化系统,引起肝肿大、食欲下降等.……     

Abstract 16: Effect of chronic occupational organophosphate exposure on peripheral nerves among filipino ricefield workers.

Objectives: To investigate whether chronic occupational exposure to organophosphates among ricefield workers in a rice institute is related to electrodiagnostically detectable measures of multiple peripheral neuropathy, that is, to investigate whether rotation in areas of work would improve the conduction velocities of those workers found to have peripheral neuropathy, after being shifted from an exposed to a nonexposed status in their work. Design: A 2-year prospective research. Setting: Academic medical center. Participants: 24 male workers with exposure to organophosphates and a well-matched control group of 64 men from the general population who were not exposed to organophosphates. Interventions: All participants in the study and control groups were tested electrodiagnostically for peripheral neuropathy work-up. Those positive for peripheral neuropathy in the study (exposed) group were rotated from their field of work to a nonexposed status for 1 year. A repeated electromyographic nerve conduction velocity test was conducted after 1 year in all participants in the study group. Main Outcome Measures: The chi-square test was used to determine the association between exposure to organophosphate and multiple peripheral neuropathy. The Wilcoxon signed-rank test was used to test for differences in the electrodiagnostic data for the years 2001 and 2002. Results: 6 of 24 participants in the study group had multiple peripheral neuropathy, while 20 of 64 participants in the control group had multiple peripheral neuropathy (P=.707). Only 4 cases of those diagnosed with peripheral neuropathy in 2001 improved in nerve conduction velocities in their repeat testing in 2002 (P=.096). Level of statistical significance was set at .05. Conclusions: The results failed to show an association between chronic occupational organophosphate exposure and multiple peripheral neuropathy. Likewise, the nerve conduction velocities of those workers with peripheral neuropathy did not improve 1 year after being shifted from an exposed status to a nonexposed status.     

重金属中毒所致周围神经损害的电生理研究

目的：探讨处于重金属环境中的作业工人急、慢性中毒性周围神经损害的电生理改变。方法：应用常规肌电图技术对30例重金属接触者进行肌电图(EMG)、神经传导速度(NCV)检测。结果：30例患者的电生理检查均呈周围神经损害．其中急性起病18例．以轴索损害为主；慢性蓄积性中毒12例，以脱髓鞘损害为主；电生理改变下肢较上肢明显．感觉神经传导异常重于运动神经传导。结论：电生理学检查对研究重金属中毒所致的周围神经损害提供了重要的客观依据。可作为临床诊断、鉴别诊断以及了解病损程度的动态随访指标。     

A Mechanistic Approach for Modulation of Arsenic Toxicity in Human Lymphocytes by Curcumin, an Active Constituent of Medicinal Herb Curcuma longa Linn

Chronic exposure of humans to high concentrations of arsenic in drinking water is associated with skin lesions, peripheral vascular disease, hypertension, blackfoot disease and a high risk of cancer. Arsenic induces single strand breaks, DNA-protein crosslinks and apurinic sites in DNA, which are prerequisites for induction of cancer. Amelioration of such damages with natural compounds could be an effective strategy to combat arsenic toxicity. Curcumin is the active ingredient of turmeric, a common household spice, which is a rich source of polyphenols and this compound has been extensively studied as a chemopreventive agent against many types of cancer. The present study investigates whether curcumin could counteract the DNA damage caused by arsenic as assessed by single cell gel electrophoresis (SCGE) using peripheral blood lymphocytes, from healthy donors. It was observed that DNA damage induced by arsenic could be efficiently reduced by curcumin and the effect was more pronounced when lymphocytes were pre-incubated with curcumin prior to arsenic insult. Arsenic caused DNA damage by generation of reactive oxygen species (ROS) and enhancement of lipid peroxidation levels. Curcumin counteracted the damage by quenching ROS, decreasing the level of lipid peroxidation and increasing the level of phase II detoxification enzymes like catalase, superoxide dismutase and glutathione peroxidase. Curcumin also enhanced the DNA repair activity against arsenic induced damage. The expression of polymerase, a repair enzyme, was found to be highly elevated when arsenite induced damaged cells were allowed to repair in presence of curcumin. Results indicate that curcumin has significant role in confronting the deleterious effect caused by arsenic, which could be an economic mode of arsenic mitigation among rural population in West Bengal, India.     

Peripheral neuropathy caused by high-dose cytosine arabinoside treatment in a patient with acute myeloid leukemia

The central nervous system toxicity of high-dose cytosine arabinoside is well recognized, but the toxicity of cytosine arabinoside in the peripheral nervous system has been infrequently reported. A 49-year-old Japanese man was diagnosed with acute myeloid leukemia. After he achieved complete remission, he received high-dose cytosine arabinoside treatment (2 g/m² twice a day for 5 days; total, 20 g/m²) as consolidation therapy. The first course of high-dose cytosine arabinoside resulted in no unusual symptoms, but on day 21 of the second course of treatment, the patient complained of numbness in his right foot. Electromyogram and nerve-conduction studies showed peripheral neuropathy in both peroneal nerves. This neuropathy was gradually resolving; however, after the patient received allogeneic bone marrow transplantation, the symptoms worsened, with the development of graft-versus-host disease, and the symptoms subsequently responded to methylprednisolone. Although the mechanisms of peripheral neuropathy are still unclear, high-dose cytosine arabinoside is a therapy that is potentially toxic to the peripheral nervous system, and auto/alloimmunity may play an important role in these mechanisms.     

Impact of caloric restriction on peripheral nerve injury‐induced neuropathic pain during ageing in mice

The incidence of peripheral neuropathy development and chronic pain is strongly associated with the arrival of senescence. The gradual physiological decline that begins after the mature stage produces myelin dysregulation and pathological changes in peripheral nervous system, attributed to reduction in myelin proteins expression and thinner myelin sheath. Moreover in elder subjects, when nerve damage occurs, the regenerative processes are seriously compromised and neuropathic pain (NeP) is maintained. We previously demonstrated that caloric restriction (CR) in adult (4 months) nerve‐lesioned mice was able to facilitate remyelination and axons regeneration, to have anti‐inflammatory action and to prevent NeP chronification. Here, we show CR therapeutic potential on nerve injury‐induced neuropathy in mice at the beginning of the senescence (12 months). Long lasting decrease in hypersensitvity induced by peripheral nerve lesion and powerful reduction in proinflammatory circulating agents have been observed. Moreover, our results evidence that CR is able to counteract the ageing‐related delay in axonal regeneration, enhancing Schwann cells proliferation and accelerating recovery processes. Differently from adults, it does not affect fibres myelination. In light of a continuous growth in elderly population and correlated health problems, including metabolic disorders, the prevalence of neuropathy is enhancing, generating a significant public cost and social concern. In this context energy depletion by dietary restriction can be a therapeutic option in NeP.     

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. This 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.     

18. Painful Diabetic Polyneuropathy

In the industrialized world, polyneuropathy induced by diabetes mellitus (DM) is one of the most prevalent forms of neuropathy. Diabetic neuropathy can result from a direct toxic effect of glucose on nerve cells. Additionally, the damage of the nerve structures (central and peripheral) is accompanied by a microvascular dysfunction, which damages the vasa nervorum. More than 80% of the patients with DM‐induced polyneuropathy have a distal and symmetric presentation. The initial symptoms are: signs of diminished sensation, burning feet, which may occur particularly during the night and worsen when touched, and tingling sensation in the feet. Attacks of shooting pain may also occur. Proper control of DM is mandatory. Based on the recently published National Institute for Health and Clinical Excellence guidelines, treatment of painful diabetic neuropathy should start with duloxetine or amitriptyline if duloxetine is contraindicated. If pain relief is inadequate, monotherapy with amitriptyline or pregabalin, or combination therapy with amitriptyline and pregabalin should be considered. If pain relief is still insufficient, tramadol instead of or in combination with a second‐line agent should be considered. In patients who are unable to take oral medication, topical lidocaine can be considered for localized pain. There are currently four studies showing that spinal cord stimulation can potentially provide pain alleviation for the longer term in patients with painful diabetic polyneuropathy. Complications are mainly implant related, though infections also occur. The available evidence (2 C+) justifies spinal cord stimulation to be considered, preferably study related.     

The Effects of Thallium Salts, with Particular Reference to the Nervous System Changes: A REPORT OF THREE CASES

Three cases of proven thallium poisoning are presented, allof whom showed peripheral neuropathy with differing grades ofseverity. Post-mortem examination was made of two who died.The more acutely affected case showed little evidence of neuronaldegeneration in the sciatic nerve and spinal cord. The lessacutely affected second case showed marked and extensive distaldegeneration of nerve fibres in all nerves examined, and earlydegenerative changes in nerve fibres in oculomotor muscles.Chromatolysis of affected motor nerve cells was prominent, butno other neuronal changes were visible in the rest of the centralnervous system. The distal ‘dying back’ type patternin sensory and motor nerves was consistent with the clinicalsymptomatology in all three cases. Thallium was detected inthe cremated remains of Case 1, in the post-mortem tissues ofCase 2, and in the urine seven weeks after poisoning in Case3. The effects of thallium on the nervous system are re-evaluatedin the light of these anatomical findings, and the general effectsof thallium poisoning are reviewed.     

Orofazialer Schmerz - Trigeminusneuralgie und posttraumatische Trigeminusneuropathie

Neuropathic pain is the result of a lesion or disease of the somatosensory system in the peripheral or central nervous system. Classical trigeminal neuralgia and posttraumatic trigeminal neuropathy are pain disorders which oral and maxillofacial surgeons and dentists are confronted with in the differential diagnostics in routine daily practice. The etiopathogenesis of classical trigeminal neuralgia is attributable to pathological blood vessel-nerve contact in the trigeminal nerve root entry zone to the brain stem. The typical pain symptoms are characterized by sudden stabbing pain attacks. The pharmaceutical prophylaxis is based on the individually titrated administration of anticonvulsant drugs. The indications for interventional treatment are dependent on the course, response to drug treatment, resilience and wishes of the patient. The neuropathic mechanism of posttraumatic trigeminal neuropathy originates from nerve damage, which leads to peripheral and central sensitization with lowering of the pain threshold and multiple somatosensory disorders. The prophylaxis consists of avoidance of excessive acute and long-lasting pain stimuli. Against the background of the biopsychosocial pain model, the treatment of posttraumatic trigeminal neuropathy necessitates a multimodal, interdisciplinary concept.     

Management of chemotherapy-induced peripheral neuropathy

Recent advances in the development and administration of chemotherapy for malignant diseases have been rewarded with prolonged survival rates. The cost of progress has come at a price and the nervous system is frequently the target of chemotherapy-induced neurotoxicity. Unlike more immediate toxicities that effect 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 toxicity is directed against the peripheral nerve, resulting in chemotherapy-induced peripheral neuropathy (CIPN). Chemotherapeutic agents used to treat hematologic and solid tumors target a variety of structures and functions in the peripheral nervous system, including the neuronal cell body, the axonal transport system, the myelin sheath, and glial support structures. Each agent exhibits a spectrum of toxic effects unique to its mechanism of toxic injury, and recent study in this field has yielded clearer ideas on how to mitigate injury. Combined with the call for a greater recognition of the potentially devastating ramifications of CIPN on quality of life, basic and clinical researchers have begun to investigate therapy to prevent neurotoxic injury. Preliminary studies have shown promise for some agents including glutamine, glutathione, vitamin E, acetyl-L-carnitine, calcium, and magnesium infusions, but final recommendations await prospective confirmatory studies.