Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuropathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMedDate not supplied

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 mononeuritis, 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.

Adolescent↗
PubMed2006

Performing only one cardiovascular reflex test has a high positive predictive value for diagnosing autonomic neuropathy in patients with chronic renal failure on hemodialysis.

BACKGROUND: Autonomic neuropathy is an important cause of morbidity and mortality in patients with chronic renal failure (CRF) on hemodialysis. Generally, cardiovascular reflex tests are used to determine autonomic neuropathy. Our purpose in this study was to determine the frequency of autonomic neuropathy in patients with CRF on hemodialysis by using cardiovascular reflex tests and compare the sensitivity of each test. METHODS: The authors performed five tests: heart rate response to the Valsalva maneuver, heart rate variation during deep breathing, heart rate response to standing up, blood pressure response to standing up, and blood pressure response to hand grip exercise in order to determine autonomic neuropathy. Each test subject was evaluated as normal, borderline, and abnormal and scored as 0, 1, and 2, respectively. Subjects with a total score > or = 5 were considered to have autonomic neuropathy. Forty subjects with CRF on hemodialysis were included in this study. None of the subjects had diabetes mellitus or any other etiology that could cause autonomic neuropathy. RESULTS: Thirty-five of 40 subjects (87.5%) had abnormal autonomic tests. In 35 subjects, the relationship between autonomic neuropathy and biochemical parameters, effects of treatment with vitamin D and erythropoietin, and urea reduction rate were studied. No relationship was found between autonomic neuropathy and age, time on hemodialysis, urea reduction rate, albumin, ferritin, calcium, inorganic phosphorus, intact parathyroid hormone, hemoglobin levels, and treatment with vitamin D and erythropoietin. The abnormal test results were as follows: 20 subjects (50%) in the heart rate response to the Valsalva Maneuver, 31 (77.5%) in the heart rate variation during deep breathing, 28 (70%) in the heart rate response to standing up, 6 (15%) in the blood pressure response to standing up, and 31 subjects (77.5%) in the blood pressure response to hand grip exercise tests. Among these five tests, the two most abnormal tests were the heart rate variation during deep breathing and the blood pressure response to hand grip exercise. CONCLUSION: Patients with CRF on hemodialysis frequently have autonomic neuropathy. For the diagnosis and follow-up of patients, five cardiovascular autonomic reflex tests are generally used. In this study, it was determined that performing only one test instead of all five tests has a high sensitivity and is more practicable in terms of determining autonomic neuropathy.

Adult↗
PubMed1995

Non-Hodgkin malignant lymphomas and peripheral neuropathies--13 cases.

Non-Hodgkin's malignant lymphomas (NHML) are malignant lymphoid proliferations which may be of B or T cell type. Thirteen observations of an association between peripheral neuropathy and B type NHML are reported. None of the cases had evidence of meningeal propagation or neurotoxicity from chemotherapy. The NHML were classified according to the Working Formulation and Kiel classifications. The various mechanisms of peripheral neuropathy in these cases were split into four broad groups. Group I consisted of four cases in which the peripheral nerve lesions were directly linked to a propagation of malignant cells into the peripheral nervous system; this was revealed by autopsy and/or nerve biopsy. Malignant B cell proliferation was demonstrated in three out of four of these cases by immunolabelling of the infiltrates. Group II included three patients whose serum contained a monoclonal immunoglobulin (IgM) with antimyelin activity, and two who had pathological IgM deposits in endoneurial connective tissue. Group III comprised two cases. The immune dysfunction of the NHML was responsible for a Guillain-Barré syndrome in one, and for a chronic inflammatory demyelinating polyneuropathy in the other. Group IV included two patients in whom the mechanism of the peripheral neuropathy, although almost certainly directly related to the NHML, could not be determined beyond doubt. The peripheral neuropathy might have been a result of a paraneoplasic process or, possibly, an undetected lymphomatous invasion of nervous tissue. All these cases of clinically diverse peripheral neuropathy, which either occurred before the discovery of the haemopathy or arose as complications of it, are discussed along with similar observations reported in the literature. Immunolabelling of lymphomatous proliferations and nerves is now of considerable value for classifying and indicating the exact aetiology of the peripheral neuropathy. It can also detect pathogenic consequences of any associated monoclonal dysglobulinemia. In any event, a direct link between the peripheral neuropathy and NHML represents an indication for intensification of specific chemotherapy, which in some of our patients led to significant regression of the peripheral neuropathy. Nonetheless, in some cases, the link between peripheral neuropathy and NHML could not be established with certainty. Long-term follow-up is essential in such cases. The present results show the importance of a case by case study of patients with NHML and peripheral neuropathy.

Aged↗
PubMed2000

Long-term prognosis of neuropathy associated with anti-MAG IgM M-proteins and its relationship to immune therapies.

Many data point to a pathogenetic role for IgM antibodies to the myelin-associated glycoprotein (MAG) in the neuropathy associated with IgM monoclonal gammopathy, supporting the use of immune therapies in affected patients. Almost 50% of patients have been reported to improve with these therapies, but the effect of treatment on the long-term prognosis of the neuropathy remains unclear. We analysed the outcome of 25 of the 26 patients (mean age at entry 65 years, range 45-85 years) with neuropathy and high anti-MAG IgM, first examined by us between 1984 and 1994. By January 1999, after a mean follow-up of 8.5 years (range 2-13 years) and a mean duration of neuropathy symptoms of 11.8 years (range 3-18, >10 years in 16), 17 patients (68%) (aged 58-84 years, mean 73.4) were alive, while eight (32%) (aged 69-78 years, mean 73.1) had died 3-15 years (mean 10.6) after neuropathy onset; in none of them was death caused by the neuropathy, although in three it was possibly related to the therapy for the neuropathy. By the time of last follow-up or patients' death, 11 patients (44%) were disabled by severe hand tremor, gait ataxia or both. The disability rates at 5, 10 and 15 years from neuropathy onset were 16, 24 and 50%, respectively. Of the 19 patients treated during the follow-up for 0.5-11 years (mean 4 years) with various immune therapies, five reported a consistent and four a slight improvement in the neuropathy (total 47%) after one treatment or more, but in only one patient was improvement persistent throughout, to the end of follow-up. In 10 patients (53%), severe adverse events, possibly related to therapy, occurred during treatment and were considered responsible for the patient's death in three. The neurological impairment did not differ between treated and untreated patients at the end of a similar follow-up. Our findings indicate that (i) the majority of patients with neuropathy and anti-MAG IgM have a favourable prognosis even after several years, and (ii) current immune therapies, though temporarily effective in half of the patients, are associated with considerable side effects which limit their prolonged use and efficacy, suggesting that until more effective or safer therapies become available, they should probably be reserved for patients impaired in their daily life or in a progressive phase of the disease.

Aged↗
PubMed2004

Neurofibromatosis 1-associated neuropathies: a reappraisal.

Neurofibromatosis 1 (NF1) is a common disease which is a source of various multisystemic manifestations related either to the accumulation of neurofibromas or to specific developmental abnormalities. The neurofibroma is the hallmark lesion of NF1 and develops from peripheral nerves. However, to date, the description of peripheral neuropathies of NF1 has not been investigated. To examine this question, we have evaluated 688 NF1 patients for the presentation, prognosis and associated morbidity of peripheral neuropathies in two hospital-based series. We collected 18 patients (four women and 14 men) with diffuse peripheral neuropathy (2.3%). Eight patients had a paucisymptomatic or an asymptomatic neuropathy detected only on electrophysiological study, two had minor sensory manifestations, five had moderate motor and sensory manifestations and three had severe motor and sensory manifestations. Superimposed radicular changes were observed in seven cases. Two patients had a subacute and 16 a chronic polyneuropathy. Fourteen patients had a demyelinating neuropathy with either severe axonal changes (three), moderate or minor axonal changes (four) or no axonal changes (seven). Four patients had axonal neuropathies. There was a strong association between the presence of a peripheral neuropathy and large root diffuse neurofibromas (P < 0.03) and subcutaneous neurofibromas (P < 0.0001). Severe morbidity and mortality of patients with NF1 and peripheral neuropathies was 50%, much higher than what is observed in the general population of patients with NF1, and 100% in patients with the most severe symptoms and electrophysiological changes (demyelination with severe axonal features). Four patients out of 18 (22%) developed a malignant peripheral nerve sheath tumour (MPNST), a much higher proportion than in the whole population of NF1. Two patients died. Peripheral neuropathy constitutes a potentially severe complication in patients with NF1 associated with a frequent morbidity related to spinal complications and MPNSTs. Association of proximal large neurofibromas, peripheral neuropathies and subcutaneous neurofibromas may constitute a phenotype of NF1 with a severe prognosis.

Adolescent↗
PubMed2002

Recent advances in drug-induced neuropathies.

PURPOSE OF REVIEW: Peripheral neuropathy is a common neurotoxic effect of medications. When medications are used to treat life-threatening illnesses, balancing the toxic effects of peripheral neuropathy with the therapeutic benefits of the drug can be difficult. This article examines recent research into the cellular mechanisms associated with neuropathy after treatment with medications to treat cancer, and HIV, and to prevent transplant rejection. RECENT FINDINGS: Cisplatin and suramin induce a length, dose, and time-dependent axonal sensorimotor polyneuropathy. Cisplatin and suramin both result in apoptosis in dorsal root ganglion neurons that may partially explain the neuropathy that develops with treatment. In contrast, nerve growth factor prevents initiation of the programmed cell death associated with cisplatin neurotoxicity. Suramin causes accumulation of lamellar inclusion bodies in dorsal root ganglion neurons related to dose of administration and severity of the neuropathy. Nucleoside reverse transcriptase inhibitors affect mitochondrial function and lead to depletion of the nerve's mitochondrial DNA and inhibition of DNA polymerase. These effects on the mitochondrion may be related to the polyneuropathy that develops in these patients. In contrast to the axonal neuropathies, tacrolimus and rarely suramin can result in a demyelinating neuropathy that may mimic Guillain-Barré syndrome or chronic inflammatory demyelinating polyneuropathy. Many of these neuropathies can be reversed by early recognition of the symptoms or by using sensitive electrophysiological testing. In certain instances, specific therapies may ameliorate the neuropathy. Glutamine may reduce paclitaxel-induced toxicity, while some patients with tacrolimus or suramin-induced demyelinating neuropathy may respond to intravenous immunoglobulin or plasmapheresis. SUMMARY: Improved understanding of neurotoxic mechanisms in the peripheral nervous system associated with chemotherapeutic and anti-HIV medications, coupled with early improved diagnosis, promises to help limit neurotoxicity associated with these medications.

Animals↗
PubMed2002

Review: small-fiber neuropathy.

BACKGROUND: Most peripheral neuropathies involve large as well as small-fiber dysfunction. A small subset of neuropathies present with restricted or predominant small-fiber involvement. REVIEW SUMMARY: In this review, we discuss the differential diagnosis, clinical presentation, evaluation, and treatment of small-fiber neuropathies. Although these neuropathies are rare, their differential diagnosis is broad, and includes many disorders, including metabolic, toxic, inflammatory, infectious, and genetic etiologies. As small fibers subserve pain and autonomic functions, these neuropathies usually present with pain and temperature loss, painful dysesthesias, autonomic dysfunction, or a combination. These neuropathies are especially challenging as nerve conductions and EMG, which help guide the evaluation of most peripheral neuropathies, may have normal findings in patients with small-fiber neuropathies. Other specialized studies, including tests of autonomic function, intraepidermal nerve fiber analysis, and quantitative sensory testing, are often required to confirm the presence of a small-fiber neuropathy. In some cases, the underlying etiology can be directly treated. In most, management is limited to symptomatic treatment of sensory and autonomic dysfunction. CONCLUSION: Small-fiber neuropathies are a heterogeneous group of disorders. They vary in etiologies and require special attention, as many disorders are rare and the differential diagnosis is broad. Evaluation is often extensive and may need pathologic specimen. Many patients respond to symptomatic therapy, but some are difficult to treat.

Journal Article↗
PubMed2005

Toxic neuropathy.

PURPOSE OF REVIEW: This paper examines recent research on toxic neuropathy and potential therapeutic developments. It also summarizes reports of new agents reported to cause peripheral neuropathy. RECENT FINDINGS: Gene therapy with vasoactive endothelial growth factor, neurotrophic substances such as nerve growth factor and neurotrophin-3 are reported to reverse or protect against neurotoxicity in animal models. The neuroprotective effects of more established therapeutic agents like vitamin E, tacrolimus (FK 506) and erythropoietin hold promise for the immediate future. Cisplatin and high-dose pyridoxine are used more frequently to produce robust models of peripheral neuropathy in animals. Statins do appear to cause peripheral neuropathy. The incidence is low, however, and compared to its benefits in terms of cardiovascular protection, relatively innocuous. The profile of thalidomide neuropathy is becoming clearer as the indications for this drug increases. The incidence of thalidomide neuropathy is high, up to three quarters in some series, and although the information on dose dependency is variable, lower cumulative doses appear to be less toxic. Like thalidomide bortezomib, a novel proteosome inhibitor, is reportedly effective in the treatment of multiple myeloma and is associated with peripheral neuropathy. Oxaliplatin and epothilone are emerging anticancer drugs with neurotoxic potential. Similarly, leflunomide, a new disease modifying-agent approved for the treatment of rheumatoid arthritis, is reported to cause neuropathy. SUMMARY: The study of toxic neuropathy is not only enhancing our knowledge of the mechanisms of neurotoxicity but also the neurobiology of peripheral neuropathy in general; and is likely to reveal avenues for therapeutics.

Animals↗
PubMed2005

Antiangiogenesis mediates cisplatin-induced peripheral neuropathy: attenuation or reversal by local vascular endothelial growth factor gene therapy without augmenting tumor growth.

BACKGROUND: Toxic neuropathies induced by cisplatin and other chemotherapeutic agents are important clinical problems because of their high incidence, their lack of effective treatment, and the fact that neuropathy represents a dose-limiting factor for these therapies. The pathogenic basis for toxic neuropathies induced by chemotherapeutic agents has not been completely elucidated. METHODS AND RESULTS: We investigated the hypothesis that experimental toxic neuropathy results from an antiangiogenic effect of these drugs, resulting in destruction of the vasa nervorum, and accordingly that the neuropathy could be prevented or reversed by locally administered VEGF gene transfer without augmenting tumor growth. In an animal model of cisplatin-induced neuropathy, nerve blood flow was markedly attenuated, and there was a profound reduction in the number of vasa nervorum associated with marked endothelial cell apoptosis, resulting in a severe peripheral neuropathy with focal axonal degeneration characteristic of ischemic neuropathy. After intramuscular gene transfer of naked plasmid DNA encoding VEGF-1 in animals with an established neuropathy, vascularity and blood flow returned to levels similar to those of control rats, peripheral nerve function was restored, and histological nerve architecture was normalized. Gene therapy administered in parallel with cisplatin chemotherapy completely attenuated endothelial cell apoptosis and inhibited destruction of nerve vasculature, deterioration of nerve function, and axonal degeneration. In a rat tumor model, VEGF gene transfer administered locally did not alter tumor growth or vascularity. CONCLUSIONS: These findings implicate microvascular damage as the basis for toxic neuropathy induced by cisplatin and suggest that local angiogenic gene therapy may constitute a novel prevention or treatment for this disorder without augmenting tumor growth or vascularization.

Angiogenesis Inhibitors↗
PubMed2004

Psychometric evaluation of two scales assessing functional status and peripheral neuropathy associated with chemotherapy for ovarian cancer: a gynecologic oncology group study.

PURPOSE/OBJECTIVES: To evaluate the psychometric properties of two adapted scales, one for functional status and one for peripheral neuropathy secondary to neurotoxic chemotherapy. DESIGN: Repeated measures methodologic design conducted within a Gynecologic Oncology Group (GOG) phase III clinical trial that randomly assigned patients with advanced epithelial ovarian cancer to cisplatin and cyclophosphamide or cisplatin and paclitaxel. SETTING: 8 GOG institutions participating in the GOG clinical trial. SAMPLE: 88 evaluable outpatients enrolled in the GOG clinical trial. Sample size at time 1 (T1) was 88 patients and at time 2 (T2) was 67 patients. METHODS: All scales were administered at T1 (prior to initiation of chemotherapy) and T2 (after six cycles of chemotherapy but prior to second-look laparotomy). Internal consistency reliability, criterion validity, and construct validity were evaluated, and clinical application was explored. MAIN RESEARCH VARIABLES: Self-reported peripheral neuropathy and functional status (comprised of physical function and role function subscales), the GOG performance status scale, and the GOG toxicity criteria. FINDINGS: Reliability coefficients at T1 were physical function = 0.83, role function = 0.96, and peripheral neuropathy = 0.91; at T2, they were physical function = 0.83, role function = 0.92, and peripheral neuropathy = 0.89. At T1, physical function and role function correlated positively with performance status. Peripheral neuropathy correlated positively with GOG toxicity criteria used at T2. Principal component factor analysis suggested that the functional status scale had a two-factor structure with factors representing general and specific mobility and that the peripheral neuropathy scale also had a two-factor structure with factors representing foot and hand neuropathy. CONCLUSIONS: The physical function, role function, and peripheral neuropathy scales have internal consistency, reliability, criterion validity, and construct validity. However, revision of the scales should address modification of specific questions and consider increasing the Likert scale from a four-point to a five- or seven-point scale to enhance clinical sensitivity and application. IMPLICATIONS FOR NURSING: With minor modifications, these scales should be useful in assessing physical function, role function, and peripheral neuropathy in patients who receive agents that may cause peripheral neuropathy.

Adult↗
PubMed1996

Low-dose zalcitabine-related toxic neuropathy: frequency, natural history, and risk factors.

We studied the features and frequency of sensory neuropathy among 79 HIV-1-infected individuals participating in a multicenter clinical trial of zalcitabine (2'3'-dideoxycytidine, or ddC) antiretroviral therapy. The trial compared zalcitabine monotherapy (2.25 mg/day) versus combination therapy (2.25 mg/day ddC) with zidovudine (ZDV, formerly AZT) versus monotherapy with ZDV alone. Neuropathy developed in 34% of ddC recipients but in only 4% of comparable patients treated with ZDV alone--a 7.9-fold increase in the attack rate of neuropathy. Using risk factor analysis, we found that diabetes mellitus was significantly associated with the development of toxic neuropathy (p = 0.02), and weight loss may contribute to its appearance. Like HIV-associated sensory neuropathy, ddC-related toxic neuropathy is a predominantly sensory, length-dependent, symmetric, painful neuropathy. Dose reduction lessened the severity of symptoms, although objective signs of neuropathy persisted. Patients with subclinical neuropathies or significant neuropathy risks such as diabetes may be poor candidates for ddC therapy.

Adult↗
PubMedDate not supplied

[Aspects of neuropathy in mitochondrial diseases].

INTRODUCTION: The existence of neuropathy has been described in mitochondrial disorders such as MELAS, MERRF, Leigh's syndrome, the Kearns-Saye syndrome, myoneurogastro-intestinal encephalopathy and progressive external ophthalmoplegia and constitutes a basic component of the NARP (neuropathy, ataxia and retinosis pigmentosa). However, the general prevalence of the neuropathy and its characteristics within the mitochondrial encephalopathies is not well understood. OBJECTIVES: To characterize the neuropathy and try to establish a genotype-phenotype correlation. PATIENTS AND METHODS: Within study guidelines, we made a retrospective study of 27 patients, diagnosed as having mitochondrial disease, who had had neurophysiological studies (EMG-ENG). In those in whom neuropathy had been found we analysed the clinical, neurophysiological and genetic characteristics. RESULTS: Neuropathy was present in 37% of the patients who had an average age of 13 years, ranging from 1 to 25 years. Syndromic diagnoses were: 7 encephalomyopathies, one MELAS, one MERRF and one NARP. Four of the patients were classified genetically. In all but two of the patients the neuropathy was asymptomatic. The biochemical alterations seen were: deficit of Complex 1 in 3 patients, of complex III in 3 patients, of complex IV in 2 and of pyruvate dehydrogenase in one patient. The type of neuropathy found was varied, with predominance of axonal-type motor neuropathy but no correlation with either biochemical defects or genetic diagnosis. CONCLUSIONS: Neuropathy is a common finding in mitochondrial disorders and probably is under-diagnosed. The axonal form predominates. We have not been able to establish correlations between phenotypes and genotypes.

Adolescent↗
PubMed1998

Changes in sympathetic and parasympathetic function in alcoholic neuropathy.

We examined sympathetic and parasympathetic function in 17 chronic alcoholics. The subjects were divided into 4 groups; (1) alcoholics without neurologic deficits, (2) alcoholics with mild neuropathy, (3) alcoholics with prominent neuropathy, (4) patients with alcoholic neuropathy but long abstinence. We measured pulsatile arterial pressure (AP) noninvasively and heart rate (HR) was calculated from the AP signals. The sweat response on the palm and sole were measured by ventilated capsular method, while the cutaneous blood flow response by laser Doppler flowmetry. The AP, HR, sweating and cutaneous blood flow response to the Valsalva maneuver were evaluated. In alcoholics with minimal and prominent neuropathy, a pressor (overshooting) in phase IV of the Valsalva maneuver were decreased significantly. The HR response (reflex bradycardia) in phase IV of the Valsalva maneuver was significantly decreased only in alcoholics with prominent neuropathy. The alcoholics with no or minimal neuropathy showed exaggerated sweat responses on the palm and sole. In prominent alcoholic neuropathy, the sweat response was greater on the palm, but diminished on the sole. In no or minimal neuropathy, magnitude of the blood flow response was markedly reduced on both sites. The low resting blood flow levels may contribute to the diminished response. We also evaluated pupillary light reflex and response to methacholine in 7 alcoholics with neuropathy by a portable infrared pupillometer system that can be used with personal computers. Maximum constriction velocity of the pupillary light reflex in patients with alcoholic neuropathy was slower than that in the controls. Reflex amplitude was smaller in the alcoholics than that in the control. However, local administration of methacholine did not change pupillary size and light reflex in the alcoholics same as the controls. The data suggest that preceding sympathetic hyperfunction related with distressed autonomic center is existing with sympathetic hypofunction involved from the sympathetic fibers, target organs and higher center.

Adult↗
PubMed1998

Outcome of peroneal neuropathies in patients with systemic malignant disease.

BACKGROUND: Peroneal neuropathies in patients with systemic cancer previously have been attributed to weight loss, but to the authors' knowledge other associated conditions have not been assessed, and the outcome of peroneal neuropathies in cancer patients has not been studied. METHODS: A retrospective chart review of patients evaluated at the Mayo Clinic between 1984 and 1993 with systemic malignant disease and a clinical diagnosis of peroneal neuropathy was performed to define factors associated with peroneal neuropathies and to assess outcome. All patients underwent neurologic examination and electromyography. RESULTS: Fifty-eight patients with systemic malignant disease were found to have a peroneal neuropathy. Peroneal neuropathies occurred more often in men (45 patients) than in women (13 patients). The median age of the patients was 70 years. The most common cancers were hematologic (12 patients) and pulmonary (11 patients), followed by tumors of the prostate (8 patients), gastrointestinal tract (7 patients), transitional cell (5 patients), breast (5 patients), and colon (5 patients), as well as sarcomas and melanoma (5 patients). The median time to the diagnosis of peroneal neuropathy after the diagnosis of cancer was 5 months. At the time of diagnosis, 34 patients had severe deficits, 19 had moderate deficits, and 5 had mild deficits. Associated factors included weight loss (occurring in 60% of patients), leg crossing (35% of patients), recent chemotherapy (16% of patients), cutaneous vasculitis (5% of patients), and local metastatic lesions (3% of patients). In nearly 50% of patients, peroneal neuropathy improved (25.9%) or resolved (22.4%). In 39.7% of patients, follow-up was inadequate because death occurred soon after diagnosis. Of the patients with adequate follow-up before death, 80% had either improvement (42.9%) or resolution (37.1%). CONCLUSIONS: For those patients with systemic malignant disease in whom peroneal neuropathy develops, the outcome of the neuropathy is good, with the majority of patients achieving partial or complete resolution.

Adult↗
PubMed1991

Class II antigen expression in peripheral neuropathies.

The expression of class II antigen was studied in sural nerve biopsies from patients with peripheral neuropathies. These included patients with chronic demyelinating polyradiculoneuropathy (CIDP), non-immune mediated neuropathies of diverse etiologies and controls without evidence of neuropathy. The major finding in CIDP was a marked increase in class II expression on Schwann cells. Endoneurial Schwann cell staining to the same degree as in CIDP was seen in diabetic symmetric proximal motor neuropathy, neuropathies associated with monoclonal gammopathies and hereditary sensory and autonomic neuropathy type 1. In the control nerves and the other non-immune mediated neuropathies class II expression was mainly restricted to endothelial and perineurial cells. Increased endoneurial expression of class II antigen was found to correlate with elevated cerebrospinal fluid (CSF) protein levels but not with other clinical variables or demyelination as defined by electrophysiologic criteria or teased fiber analysis. The increased expression of class II antigen on Schwann cells may be indicative of a breakdown in immunological tolerance but should not be used as a diagnostic marker for dysimmune neuropathies due to overlap with non-immune mediated neuropathies.

Adult↗
PubMed2005

Prevalence of ulnar neuropathy in patients receiving hemodialysis.

BACKGROUND: Ulnar neuropathy can cause pain, weakness, and sensory changes in the hand and can result in functional impairment. Patients with end-stage renal disease receiving hemodialysis may be predisposed to ulnar neuropathy by factors such as arm positioning during hemodialysis, underlying polyneuropathy, and upper extremity vascular access. OBJECTIVE: To determine the prevalence of clinically evident ulnar neuropathy in a cohort of 102 patients with end-stage renal disease receiving hemodialysis. DESIGN: All eligible patients in a single dialysis unit were screened for symptoms and signs of ulnar neuropathy. Those with at least 1 symptom or sign underwent nerve conduction studies to confirm the presence of ulnar neuropathy. RESULTS: Clinically evident, electrophysiologically confirmed ulnar neuropathy was present in 37 (51%) of the 73 subjects with both screening and nerve conduction study data available. The true prevalence of ulnar neuropathy in this cohort was estimated between 41% and 60%. CONCLUSIONS: There is a high prevalence of ulnar neuropathy in patients with end-stage renal disease receiving hemodialysis, which has not been previously recognized. The high prevalence of ulnar neuropathy in this population suggests that preventative efforts are indicated to prevent this functionally limiting complication.

Adult↗
PubMed1982

Plasma adrenaline and noradrenaline concentrations in diabetic patients with and without autonomic neuropathy at rest and during sympathetic stimulation.

Plasma concentrations of adrenaline and noradrenaline were measured radio-enzymatically in nine patients with diabetic autonomic neuropathy, seven diabetic patients without autonomic neuropathy and nine normal subjects, in the recumbent position and after standing. Furthermore, in six patients with autonomic neuropathy and in the normal subjects, plasma noradrenaline and adrenaline concentrations were determined during and after cyclo-ergometer exercise. No differences in plasma adrenaline concentrations were found at any time in the study. Basal plasma noradrenaline levels were significantly lower in diabetic patients with autonomic neuropathy than in the non-neuropathic diabetics or healthy control subjects. After standing, plasma noradrenaline rose to significantly higher levels in both control and diabetic subjects without neuropathy than in the patients with autonomic neuropathy. During exercise (up to 100 W load), plasma noradrenaline rose to similar levels in healthy controls and in patients with diabetic neuropathy. These data indicate that in diabetic autonomic neuropathy there is reduced peripheral neurosympathetic tone at rest but a normal response to moderate exercise. Blunted neurosympathetic responses to standing seem to be a consistent feature of diabetic autonomic neuropathy, particularly in those patients with severe postural hypotension.

Adult↗
PubMed1997

Divergent development of autonomic and peripheral somatic neuropathies in NIDDM.

There is no information on the mutual occurrence and the development of autonomic and peripheral somatic neuropathies based on long-term follow-up of patients with non-insulin-dependent diabetes mellitus (NIDDM). We investigated the relation between the changes in autonomic function values and electrodiagnostic values, and the relation between the occurrence of autonomic neuropathy and peripheral somatic polyneuropathy in a group of patients with newly diagnosed NIDDM (n = 133, aged 45-65 years) at baseline and 5 and 10 years later. Parasympathetic autonomic neuropathy was diagnosed on the basis of heart rate variability during deep-breathing and sympathetic autonomic neuropathy on the basis of fall in systolic blood pressure while changing from supine to standing. Polyneuropathy was diagnosed on the basis of both clinical criteria and electrodiagnostic studies (nerve conduction velocity and response-amplitude values). In 10 years 36 patients died, mainly from cardiovascular causes. Altogether 78 patients completed the study. At 10 years, parasympathetic autonomic neuropathy was diagnosed in 61.3% of those with polyneuropathy and 66.7% of those without. Likewise, the frequency of sympathetic autonomic neuropathy was similar in those with polyneuropathy (21.9%) and those without (26.5%). The respective figures for combined (both parasympathetic and sympathetic) autonomic neuropathy were 10.0% and 18.8%. The worsening of parasympathetic and sympathetic autonomic function values was not related to the worsening in electrodiagnostic results with time. In conclusion, the development of autonomic and peripheral somatic neuropathies was divergent in patients with NIDDM suggesting different pathophysiological processes for these neuropathies.

Autonomic Nervous System Diseases↗