Peripheral neuropathy in the hands of diabetic patients with lower extremity amputations

One hundred unilateral ambulatory lower extremity amputees underwent sensibility testing of their remaining foot and right hands to determine if the magnitude of peripheral neuropathy present in the feet of patients with diabetes was of greater magnitude than that in their hands. Testing was performed with a series of Semmes-Weinstein monofilaments. Ninety-one of the subjects were male, and 9 were female. Sixty-five were diabetic, 40 required insulin. The magnitude of peripheral neuropathy was compared between the hands and feet of patients with and without diabetes, and between insulin-dependent and non-insulin-dependent diabetics. There was a slight trend to a more severe degree of insensitivity in the feet as compared with the hands in each of the individual groups. There was no statistically significant difference when comparing hand and foot sensibility in any of the comparison groupings. The quantitative amount of peripheral neuropathy appears to affect the hands and feet of diabetics in a similar "stocking-glove" fashion. The results of this screening gives further support to the concept of prophylactic foot care programs in diabetics with peripheral neuropathy to decrease the risk for the development of foot ulcers, which are often the precursor of eventual lower extremity amputation.     

Peripheral neuropathy in burn patients

Neuropathy in burn patients is frequently overlooked. This study aimed at looking for neuropathies among burn patients. It included 55 burn patients, whether symptomatic or asymptomatic, with variable depths of burn at different stages. Their ages ranged from 8 to 55 years with a mean age of 23.6 ± 11.1 years. All patients were submitted to clinical examination, electromyographic and motor conduction velocities of burned and unburned limbs. Serum electrolyte, blood urea and creatinine were measured for all patients. Sixteen patients (29 per cent) had peripheral neuropathy. Only six had symptoms and signs of peripheral neuropathy. The most frequently diagnosed neuropathy in this study was mononeuritis multiplex in nine patients (56 per cent), then generalized distal axonal neuropathy in five patients (31 per cent) and entrapment neuropathy in two patients (13 per cent). In patients with mononcuritis, 29 nerves were affected, 24 nerves related to the site of the burn and five nerves were away from the site of the burn. All the entrapment neuropathy developed after wound healing. Age above 20 years, electric burns, burns involving full thickness of the skin and a surface area of more than 20 per cent were associated with a significantly higher prevalence of neuropathy. Other parameters were not found to be significant in the development of neuropathy.     

Painful diabetic neuropathy

The podiatric physician often encounters complex painful neuropathies in daily practice. Diabetic neuropathy is one form of chronic neuropathic pain dealt with on a regular basis. The goal of this article is to review the pathophysiology, diagnosis, and treatment options of this complaint. Medical and surgical interventions are discussed, with a clinical emphasis on patient selection and prevention.     

Peripheral neuropathy and celiac disease

Opinion statement Peripheral neuropathy (PN) is one of the most frequently reported neurologic manifestations associated with celiac disease (CD), a multigenetic, T-cell-mediated autoimmune disorder that results from a loss of tolerance to gluten. Sensory axonal and small fiber sensory polyneuropathies are the most frequently reported PN subtypes. Multifocal motor or sensorimotor neuropathies and a more fulminant neuropathy, associated with ataxia and other neurologic manifestations, also have been reported. The effect of a gluten-free diet on CD-associated PN has not been studied systematically or prospectively; nevertheless, a gluten-free diet currently is the cornerstone of therapy. Although idiopathic ataxia associated with anti-gliadin antibodies and other neurologic complications have been reported to respond to this diet; there is data that indicate that neurologic manifestations may develop or persist, independent of gluten exposure. There is evidence to suggest that inflammatory processes may be involved. Immunomodulatory agents (such as intravenous immunoglobulin or infliximab), described to be beneficial in the treatment of refractory CD or CD-associated ataxia, may have a role in the management of CD-associated PN     

Peripheral neuropathy due to leprosy

Opinion statement Leprosy, also known as Hansen’s disease, remains a significant cause of disability worldwide. After the introduction of treatment regimens using a combination of dapsone, rifampin, and clofazimine, the prevalence of the disease declined from 5.4 million registered cases in 1985 to less than a million in 1999. However, the incidence of new cases has remained stable due at least in part to a population of asymptomatic carriers. Immune-mediated nerve damage can occur during treatment or after treatment is completed and mandates continued careful follow-up of patients. Patient education and rehabilitation are crucial aspects of disease management and prevention of disability. In the US, patient care and medications are available through regional clinics sponsored by the Department of Health and Human Services. Patients should contact the National Hansen’s Disease Program at 1770 Physician’s Park Drive, Baton Rouge, Louisiana 70816; 1-800-642-2477.     

Peripheral neuropathy due to cobalamin deficiency

Opinion statement  

Peripheral neuropathy during treatment with ornidazole

The case is reported of an 18 year old patient who developed a peripheral neuropathy after being given 1.5 g ornidazole daily for 6 days and 2 g daily for 16 days (total dose: 41 g). Bilateral radial paralysis was noted clinically, whilst electrical investigations showed diffuse motor and sensitive anomalies. Three months after the drug had been stopped, all symptoms and signs had disappeared. The pathogenesis of this complication is discussed. The part played by ornidazole is suggested but cannot be proved because of the multiple disorders presented by the patient.     

Cutaneous thermal sensitivity in diabetic neuropathy

BACKGROUND: The goal of this investigation was to determine if cutaneous thermal sensitivity could be used as a discriminator of peripheral neuropathy in diabetic subjects who were sensate to the Semmes-Weinstein 5.07 monofilament. METHODS: Sixty adult subjects were separated into two groups. The control group (A) was composed of 30 young healthy individuals without a history of diabetes. The focus group (B) was composed of 26 individuals with adult onset diabetes and four with juvenile onset. All of the subjects underwent thermal sensitivity testing in peripheral nerve root dermatomes of their hands and feet. Testing was performed with custom devices fabricated from materials with different thermal conduction capacities (copper, steel, glass, and plastic). Similar tests were performed with glass tubes containing heated or cooled water to develop a range of thermal sensitivity for the subjects. RESULTS: There was a strong relationship between cold perception and stimulation with the copper probe in dermatomes of the radial nerve of the upper limb and the superficial peroneal dermatome of the lower limb. CONCLUSIONS: Thermal sensitivity to copper and cold stimulation may be more discriminative and have a higher threshold than sensitivity to the Semmes-Weinstein monofilament. This simple method may have a role in the early detection of peripheral neuropathy in adult-onset diabetes mellitus.     

糖尿病周围神经病变在糖尿病骨病中的发病机制研究进展

糖尿病骨病是指糖尿病患者出现骨质减少、关节病变、骨皮质变薄、骨骼脆性增加甚至骨折的一种全身性、代谢性骨病,是糖尿病的重要并发症之一。随着糖尿病患者生活质量的提高以及病程的延长,患者的肌肉骨骼病变发生率在逐年提高,严重者可导致残疾或死亡。其发病机制目前尚未完全阐明,近年来,随着对糖尿病骨病的深入研究,发现糖尿病周围神经病变在骨骼疾病的发病和进展中起着重要作用。本文就糖尿病骨病、神经病变之间的关系加以综述,旨在探索神经病变导致骨代谢失调、骨密度下降、骨折风险的可能机制,为糖尿病骨病的诊断、预防、治疗提供新思路。     

Peripheral neuropathy in rats induced by insulin treatment

The effect of sustained insulin-induced hypoglycemia on peripheral nerve function and structure was examined in rats. After a period of hypoglycemia (less than 2.5 mmol/L) of at least 72 h, axonal degeneration and reduction of the maximal amplitude of the evoked muscle action potential occurred, the two abnormalities being correlated negatively (r = -0.99, 2P = 0.00097). One of five rats developed paresis of both hindlegs as well as nerve damage and perikaryal alterations of lower motor neurons.     

Local sympathetic denervation in painful diabetic neuropathy

This study assessed whether painful diabetic neuropathy is associated with abnormal sympathetic nervous function in the affected limbs. Nine patients with diabetes (four men, five women; age 61 +/- 7 years) and painful peripheral neuropathy of the feet, but without evidence of generalized autonomic neuropathy, underwent intravenous infusion of tritiated norepinephrine (NE) and sampling of arterial and venous blood in both feet and in one arm to quantify the rate of entry of NE into the local venous plasma (NE spillover). In the same patients, positron emission tomography (PET) scanning after intravenous injection of the sympathoneural imaging agent 6-[(18)F]fluorodopamine was used to visualize sympathetic innervation and after intravenous [(13)N]ammonia to visualize local perfusion. The results were compared with those in the feet of normal volunteers and in an unaffected foot of patients with unilateral complex regional pain syndrome (CRPS). In addition, neurochemical results obtained in painful diabetic neuropathy were compared with those obtained in diabetic control patients with painless neuropathy and diabetic control patients without neuropathy. Local arteriovenous difference in plasma NE levels (DeltaNE(AV)) and NE spillover in the arms did not differ across the groups. However, DeltaNE(AV) in the feet was significantly less in the group with painful diabetic neuropathy than in the control groups. Also NE spillover in the feet tended to be lower in painful neuropathy. DeltaNE(AV) of diabetic control patients without neuropathy (n = 6) resembled values in the control groups without diabetes, whereas patients with painless diabetic neuropathy (n = 6) had evidence suggesting partial loss of sympathetic innervation. PET scanning revealed decreased flow-corrected 6-[(18)F]fluorodopamine-derived radioactivity in patients with painful diabetic neuropathy, compared with values in normal volunteers and patients with CRPS. The results provide neurochemical and neuroimaging evidence for regionally selective sympathetic denervation in the painful feet of patients with diabetic neuropathy.     

Peripheral neuropathy in cystic fibrosis: A prevalence study

BackgroundInformation on peripheral neuropathy in children with cystic fibrosis is scanty. The etiology can be multifactorial (micronutrient deficiency, chronic hypoxia, impaired glucose tolerance, immunological, vasculopathic, critical illness).MethodsForty five cystic fibrosis children aged 1–18 years on vitamin E supplementation for at least 6 months underwent detailed neurological examination, serum vitamin E, vitamin B12, folate, copper levels and detailed nerve conduction studies.ResultsThe mean age of the study population was 8.35 years (± 4.9 years) with 62.2% being males. Overall 22 out of 45 (48.88%,CI: 33.7–64.2) had electrophysiological evidence of peripheral neuropathy which was predominantly axonal (86.4%), sensory (50%), and polyneuropathy (95.45%). There was no significant association between status of serum micronutrients and electrophysiological evidence of peripheral neuropathy.ConclusionPatients with cystic fibrosis have electrophysiological evidence of peripheral neuropathy (predominantly axonal, sensory and polyneuropathy). There is significant association of higher chronological age with occurrence of peripheral neuropathy.     

糖尿病性周围神经病变与糖尿病足

糖尿病性周围神经病变是引起糖尿病足最重要的原因之一.糖尿病患者肢体局部血供及代谢变化可导致神经节段性脱髓鞘、许旺细胞丢失以及不同程度的轴突变性,使肢体感觉、运动等重要功能丧失,加之物理或机械性刺激等启动因素,最终导致下肢感染、溃疡形成和(或)深部组织破坏.随着近年患者人数不断升高,糖尿病足发病神经机制研究逐渐成为热点....     

Renal transplantation and diabetic autonomic neuropathy

This report describes six episodes of cardiovascular collapse in the perioperative period of a young diabetic woman undergoing general anaesthesia for renal transplantation and a similar episode after a second anaesthetic. She was subsequently found to have an autonomic neuropathy. Recommendations for the management of similar patients are made.