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Results for “Polyneuropathies”

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PubMedDate not supplied

Angiotensin-converting enzyme insertion/deletion polymorphism and polyneuropathy in type 2 diabetes without macroalbuminuria.

Angiotensin-converting enzyme (ACE) gene polymorphism is thought to be a potent risk factor for nephropathy and retinopathy in diabetes. We investigated the association between polyneuropathy and gene polymorphisms of both the ACE insertion/deletion (I/D) and angiotensinogen (AGT) M235T genes in 84 type 2 diabetic patients without macroalbuminuria (21 with polyneuropathy and 63 without). ACE genotype distribution did not differ significantly between patients with and without polyneuropathy, but the frequency of the I allele was significantly higher in those with polyneuropathy than in those without. In contrast, neither the genotype distribution nor the allele frequencies of the AGT gene differed between the two groups. In logistic regression analysis using a D-additive model, the D allele had a protective effect on polyneuropathy (odds ratio [OR], 0.34; 95% confidence interval [CI], 0.13-0.88). A D-dominant model hypothesis also gave a significant OR (0.28; 95% CI, 0.09-0.90). ACE I/D polymorphism, but not AGT M235T polymorphism, may affect polyneuropathy development in type 2 diabetes without macroalbuminuria.

Aged↗

PubMed1999

Cadmium: a possible etiological factor in peripheral polyneuropathy.

Uncovering the exact cause of polyneuropathies seems to be impossible in up to 24% of the cases. Experimental studies have shown that cadmium (Cd), which is a well-known occupational and environmental hazard, can be a potent neurotoxicant for the peripheral nervous system. Moreover, Cd has a half-life of more than 15 years in humans. We hypothesize that older workers may be more susceptible to an increased Cd body burden, and may develop a peripheral polyneuropathy (PNP) over time. A blinded epidemiological survey was performed in 13 retired, long-term Cd-exposed workers and 19 age-matched controls. Historical Cd biomonitoring data were available over the last two decades. A neurological clinical examination, nerve conduction studies, and needle EMG were performed, and a standardized questionnaire was given to evaluate polyneuropathy complaints. If two of the following four criteria, i.e. complaints of polyneuropathy, neurophysiological changes compatible with polyneuropathy, distal symmetrical areflexia, or distal symmetrical anesthesia for vibration sense, temperature or blunt-sharp discrimination were present, the diagnosis of PNP was made. Two (11%) of the control and seven (54%) of the retired Cd workers met the PNP criteria OR: 9.92 (95%CI 1.60-61.6), Fisher exact test p=0.015. The existence of a polyneuropathy was related to the level of the Cd body burden as reflected by urinary Cd multiple logistic regression p=0.016, OR=1.26, (95%CI, 1.04-1.51), but not to blood lead (p=0.352). Our findings favour the hypothesis of a promoting role of increased cadmium body burden in the development of PNP at older age.

Aged↗

PubMedDate not supplied

Diabetic polyneuropathy. Axonal or demyelinating?

Diabetic polyneuropathy is the most common subgroup of diabetic neuropathy, but its nature is controversial as it might be demyelinating and/or axonal. We have tried to determine whether diabetic polyneuropathy is electrophysiologically axonal, demyelinating, or both. We have studied the sural and peroneal nerves and the electromyographies of leg muscles in 50 healthy subjects (average age 67.2 years, range 45 to 84 years), in 50 diabetic patients (average age 66.34 years, range 44 to 82 years) showing no symptoms and/or signs of polyneuropathy (DP1), and in 50 diabetic patients (average age 67.10 years, range 49 to 87 years) showing symptoms and/or signs of polyneuropathy (DP2). The amplitude (AMP) of sural and peroneal nerves in healthy and DP1 subjects was similar. Conduction velocity (CV) of sural and peroneal nerves was slower in DP1 subjects than in healthy subjects. DP2 subjects showed AMP and CV values significantly lower than those in DP1 subjects, and signs of acute and chronic denervation/reinervation were found in the leg muscles. We believe that this result indicates that diabetic patients have two types of polyneuropathies: a demyelinating disease that could appear in diabetic patients with and without symptoms of polyneuropathy, and an axonal loss that is responsible for most of the symptoms.

Aged↗

PubMed2002

Neurologic complications of critical illness: part II. Polyneuropathies and myopathies.

OBJECTIVE: To review the metabolic encephalopathies and neuromuscular abnormalities commonly found in the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported from 1980 to 2002 and identified through a MEDLINE search on metabolic encephalopathy, polyneuropathy and myopathy in critical illness. SUMMARY OF REVIEW: Severe weaknes in the critically ill patient may have many causes, although Guillain-Barré syndrome, critical illness polyneuropathy and critical illness myopathy are the motor disorders commonly found in the critically ill patient. Guillain-Barré syndrome is characterised by an acute ascending weakness 1-3 weeks after a gastrointestinal or upper respiratory tract infection. Intravenous immune globulin (or plasmapheresis) should be initiated as soon as possible to shorten the duration of ventilation, time to walk unaided and halt the progression of the disease. Critical illness polyneuropathy and critical illness myopathy often coexist in the critically ill patient and are probably caused by a small number of activated leucocytes that infiltrate skeletal muscle and produce pro and anti-inflammatory cytokines. Axonal degeneration of both motor and sensory fibres with preservation of the myelin sheath cause the neuropathy, and muscle fibre necrosis and atrophy causes the myopathy. Apart from treatment of the underlying cause (e.g sepsis), there is no specific treatment, although a 44% reduction in the incidence of critical illness polyneuropathy has been described in mechanically ventilated critically ill patients who received intensive insulin therapy to maintain the blood glucose level between 4.4-6.1 mmol/L. Recovery usually occurs over weeks to months depending on the severity of the disease. CONCLUSIONS: An acute motor weaknesses in the critically ill patient may be caused by Guillain-Barré syndrome, critical illness polyneuropathy or critical illness myopathy. Patients with severe Guillain-Barré syndrome should be managed in an intensive care unit and given intravenous immune globulin. Treatment of critical illness polyneuropathy or myopathy requires largely management of the underlying disorder.

Journal Article↗

PubMed1990

The improbable association between the herbicide 2,4-D and polyneuropathy.

Isolated case reports have circumstantially linked the use of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) to polyneuropathy. However, a critical review of the literature reveals numerous reasons for doubting a relationship of 2,4-D to polyneuropathy: (1) too few cases given the wide use of the chemical; (2) no valid toxicologic or epidemiologic evidence; (3) the diversity of antecedent illness; (4) an unlikely time sequence of antecedent illness to exposure (pharmacokinetics); (5) the lack of polyneuropathy in medical patients given repetitive doses of 2,4-D; (6) the lack of polyneuropathy in heavily exposed military personnel involved in operation Ranch Hand; (7) the biological properties of 2,4-D which minimize penetration of 2,4-D into the nervous system under normal exposure conditions; and (8) the lack of polyneuropathy in a variety of experimental animal species given 2,4-D by several routes of exposure and at dose levels and durations of exposure many times greater than human applicator exposure. Thus, the weight of evidence indicates that 2,4-D is an unlikely cause of polyneuropathy.

2,4-Dichlorophenoxyacetic Acid↗

PubMed1990

Middle molecular weight substances and uremic polyneuropathy.

A group of 25 uremic patients on regular hemodialysis was examined during 12 months after six-hour dialyses twice a week were changed to five-hour dialyses thrice a week. Twelve of the patients suffered from polyneuropathy, while 13 did not show signs of this uremic complication. The effect was studied of the increase of the amount of dialyses on the severity of polyneuropathy, checked by neurological and electromyographic methods, as well as on the serum levels of uremic middle molecular weight substances (MMS). Sera of the patients were subjected to gel filtration on Sephadex G-15 columns. This analysis resolved MMS into five distinct fractions in the range of middle molecular weight. Sera of the patients with polyneuropathy contained more of MMS in the 2nd and 4th fractions than those without signs of polyneuropathy. During 12 months of treatment with three hemodialyses a week, a significant improvement of polyneuropathy, together with a pronounced decrease of the serum levels of the 2nd and 4th MMS fractions were evidenced. A statistically significant negative linear relationship of polyneuropathy signs and the serum levels of MMS in these two fractions was registered.

Adult↗

PubMed1994

[Course of chronic idiopathic polyneuropathy during middle age and older: 2-year follow-up study].

OBJECTIVE: To study the clinical features and natural course of idiopathic polyneuropathy. DESIGN: Prognostic and descriptive cohort study. SETTING: University Hospital, Utrecht, the Netherlands. METHOD: 75 patients (46 men, 29 women) with a mean age of 56.5 years at onset of symptoms were clinically investigated during two years. RESULTS: The features of chronic idiopathic polyneuropathy were heterogeneous. Clinically, 44 patients had a sensorimotor, 29 patients a sensory and 2 patients a motor polyneuropathy. Electrophysiological and nerve biopsy studies were compatible with an axonal polyneuropathy. The overall clinical course was slowly progressive. None of the patients became severely disabled. After one year of follow up one patient proved to have a hereditary neuropathy. In the other 74 patients no cause for the polyneuropathy was found even after 2 years of follow-up. CONCLUSION: Chronic idiopathic polyneuropathy is a heterogeneous entity, leading to only slight disability. The neuropathy is due to axonal degeneration.

Age Factors↗

PubMed2026

Metformin Adherence and Risk of Polyneuropathy in Type 2 Diabetes Mellitus: An International Matched Cohort Study with Independent Validation.

BACKGROUND: Metformin is a popular first-line glucose-lowering medication for type 2 diabetes mellitus (T2DM). Although metformin reduces the risks of various complications of diabetes, its potential to cause polyneuropathy by depleting vitamin B12 levels is concerning. This study investigated whether the adherence or discontinuation of metformin after adding-on a second-line antiglycemic agent increases the risk of polyneuropathy in patients with T2DM. METHODS: Data from TriNetX were obtained, and patients with T2DM who were receiving second-line antiglycemic agents were divided into metformin-adherent and metformin-nonadherent groups based on prescription claims data. Neuropathy incidence was evaluated using diagnostic claims and nerve conduction examinations. For independent confirmation and external validation of the primary findings, we used data from the National Health Insurance Research Database (NHIRD) of Taiwan. RESULTS: After matching, 58,027 patients were included in each group. Compared with metformin adherent patients, metformin nonadherent patients had a higher risk of polyneuropathy (adjusted hazard ratios [aHR] 1.26; 95% confidence interval [CI] 1.23-1.29; P < 0.001). Risks of diabetic foot ulcer, amputation, neuropathy-related medication use, and bone fracture were also higher among nonadherent patients. Sensitivity analyses confirmed the robustness of findings. In the validation NHIRD cohort (31,384 matched pairs), metformin nonadherence remained associated with increased polyneuropathy risk (aHR 1.25; 95% CI 1.10-1.42; P < 0.001). CONCLUSIONS: Metformin adherence in patients with T2DM who require second-line treatment may reduce the risk of polyneuropathy; vitamin B supplementation may enhance this benefit.

Humans↗

PubMed2000

Assessing grip strength in healthy individuals and patients with immune-mediated polyneuropathies.

Grip strength reference values for a portable dynamometer, the hand-held Vigorimeter, were calculated, and its validity, reliability, and responsiveness were examined in patients with immune-mediated polyneuropathies. We studied 530 healthy controls (age 5-93 years), 113 patients with stable polyneuropathy (83 with Guillain-Barré syndrome [GBS], 22 with chronic inflammatory demyelinating polyneuropathy [CIDP], and 8 with a gammopathy-associated polyneuropathy), and 20 patients with GBS or CIDP and changing clinical conditions (longitudinal group). An arm-disability scale was also assessed. Grip-strength reference values were calculated depending primarily on age and gender. Significant association was obtained between the Vigorimeter and the arm scale (in stable group, Spearman rank: r = -0.52 to -0.62; P </= 0.0005; in longitudinal group, linear regressions: r = 0.62-0.64, P < 0.0001). Good interobserver and intra-observer agreements (analysis of variance, r = 0.95-0.97) and high responsiveness (standardized response mean scores > or = 0.8) were demonstrated for the Vigorimeter. These results emphasize the clinical usefulness of the Vigorimeter, particularly in patients with immune-mediated polyneuropathies.

Adolescent↗

PubMed1995

Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy: immune mechanisms and update on current therapies.

The relation between Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy is discussed. Most likely they represent parts of a continuum, arbitrarily separated by their time course. Within the concept of chronic inflammatory demyelinating polyneuropathy the presence of a monoclonal gammopathy of undetermined significance is discussed. The pathogenesis of inflammatory demyelinating polyneuropathies has not been elucidated yet, but involvement of the immune system has been firmly established. Preceding infections, especially with Campylobacter jejuni, and the analysis of antiganglioside antibodies lend new support to the hypothesis of molecular mimicry between epitopes on infectious agents and peripheral nerve constituents as one of the mechanisms in Guillain-Barré syndrome. In the future, a further classification of individual patients based on clinical, epidemiological, electrophysiological, pathological, microbiological, and immunological criteria may give a basis for more individualized treatment strategies. In Guillain-Barré syndrome the efficacy of high-dose intravenous immune globulin treatment was established after earlier positive findings with plasma exchange; immune globulins are easier to administer and may be superior. Even with these treatments it should be anticipated that one fourth of patients after immune globulin treatment and one third of patients after plasma exchange will show further deterioration in the first 2 weeks after onset of treatment. Despite this, just one treatment course usually is indicated in the individual patient, and no valid arguments were found to switch to the other treatment modality. In chronic inflammatory demyelinating polyneuropathy, prednisone, plasma exchange, and immune globulins are effective in a proportion of patients. The last two are equally effective. Patients may respond to one of these if a previous treatment failed, and here switching therapy may be effective due to the chronic course of the disease. Complexity and costs make plasma exchange the last choice. Whether prednisone or immune globulin is the first choice depends on the speed of recovery and the estimation of long-term loss of quality of life due to side effects of prednisone versus the costs of immune globulins. The mechanism of immune globulins in inflammatory polyneuropathies is discussed. There is evidence that idiotypic-antiidiotypic interaction may play a role, but several other mechanisms also may be involved.

Adult↗

PubMed2003

Ambulatory foot temperature measurement: a new technique in polyneuropathy evaluation.

Complaints of abnormal foot temperature are common among patients with polyneuropathy. However, there is no published method of ambulatory foot temperature measurement to identify possible thermoregulatory disturbances in these patients. We configured a digital electronic thermometer and thermocouple to measure and record distal foot and ambient temperatures simultaneously every minute for 24 to 48 h. Sixteen patients with polyneuropathy and 5 normal subjects were studied; 12 patients with polyneuropathy and 4 normal subjects had at least 24 h of successful recording. The data obtained from these patients were consistent and easily summarized by standard statistical methods. In the others, technical difficulties produced nonphysiological readings. In the patients with polyneuropathy, changes in foot temperature mirrored ambient temperature fluctuations more closely than in normal subjects. This technique shows promise in studying temperature regulation in the feet and may provide new insights into neuropathy-associated pain and the pathogenesis of polyneuropathy.

Adult↗

PubMed2004

Collagen synthesis and degradation in polyneuropathy and myopathies.

To determine the mechanisms underlying the changes in collagen metabolism responsible for muscle fibrosis in patients with neuromuscular diseases, the synthesis and degradation of collagens was studied in muscles of patients with polyneuropathy and noninflammatory myopathies. The mRNA levels for type I, III, and IV collagens and immunohistochemical staining intensities for collagen propeptides and telopeptides were increased in polyneuropathy, suggesting enhanced synthesis of collagens. In myopathy, the mRNA levels were at the control level. Matrix metalloproteinase (MMP)-2 mRNA level was increased in polyneuropathy, although the quantity of proMMP-2 was not changed. An increase in type IV collagen concentration and proMMP-9 expression was observed in polyneuropathy but not in myopathies. Our results suggest that intramuscular accumulation of type IV collagen occurs in polyneuropathy, possibly leading to thickening of the capillary and muscle fiber basement membranes. This may complicate the transportation of nutrients and cellular excreta between blood and muscle cells.

Adolescent↗

PubMedDate not supplied

Alcoholic polyneuropathy.

Alcoholic polyneuropathy is a common disorder, characterized by nonspecific clinical, electromyographic, and pathologic features. Nerve conduction studies and needle electromyography disclose findings consistent with a generalized, sensorimotor, axonal degenerative, polyneuropathy. Alcoholic polyneuropathy may be suspected when such findings occur in the setting of long-standing alcoholism and malnutrition. The lack of specific diagnostic criteria for alcoholic polyneuropathy requires that other potential etiologies be excluded before that diagnosis is made. The institution of a nutritionally-balanced diet constitutes the principal therapy for alcoholic polyneuropathy, however, significant improvement following such therapy is not frequently seen.

Alcoholism↗

PubMed2000

Quality of life in patients with axonal polyneuropathy.

"Quality of life" (QOL) measurement reflects the impact of a disease on the daily life of a patient, and this can be used as an outcome measure in clinical trials. QOL measurements are rarely used in patients with neuromuscular disease. The aim of this study was to determine whether QOL is reduced in chronic polyneuropathy, whether there is a relationship between QOL and objective measures of disease severity, and whether measuring QOL is a useful addition to the assessment of severity of polyneuropathy. We measured QOL in 90 patients with chronic axonal polyneuropathy (33 with hereditary motor and sensory neuropathy type II and 57 with chronic idiopathic axonal polyneuropathy) using the RAND 36-item Health Survey questionnaire (RAND-36). We compared the results with the QOL of a reference population, with summed motor and sensory scores, and with the Rankin scale for handicap. Patients had worse scores than the reference population on seven of eight areas of the RAND-36. Patients with both low motor and low sensory scores rated lower in physical and emotional areas than less impaired patients. A low Rankin score was related only to physical domains. We conclude that in patients with chronic axonal polyneuropathy the severity of disease can be assessed with a general QOL instrument, and that this provides additional information, particularly on areas related to emotional and social functioning.

Aged↗

PubMed2003

Plasmapheresis in immunologically mediated polyneuropathies.

One of the most common uses of therapeutic plasmapheresis is for the treatment of immunologically mediated polyneuropathies. This paper discusses the use of plasmapheresis in Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, polyneuropathies associated with paraproteins, lower motor neuron syndromes, and polyneuropathies associated with HIV. As the pathogenesis of immunologically mediated polyneuropathies becomes better understood, newer therapies for these syndromes will evolve: however, therapeutic plasmapheresis is likely to continue to play a central role in the treatment of many of these diseases.

HIV Infections↗

PubMed2001

Diagnostic yield by testing small fiber function in patients examined for polyneuropathy.

We assessed the diagnostic yield of adding quantitative sensory testing to the standard work-up for polyneuropathy in unselected patients. All patients aged 18 to 70 years referred to our department for electrodiagnosis with a tentative diagnosis of polyneuropathy and symptoms complying with predefined criteria were included in the study. We performed near nerve conduction studies in 4 nerves and determined heat and cold detection thresholds on hand and foot with a Thermotest (Somedic AB, Sweden). In order to uncover CNS diseases, somatosensory-evoked potentials were recorded in patients with abnormal quantitative sensory testing and normal nerve conduction studies. A total of 198 patients completed the study and 149 were considered to have polyneuropathy. Twenty-five patients remained undiagnosed and in 24 patients, other diseases were responsible for the symptoms. Of the patients with either polyneuropathy or no other diagnosis, 76% (n = 174) had abnormal nerve conduction. Abnormal cold sensation, heat sensation or abnormality in at least 1 of these and normal nerve conduction were found in 14, 12 and 17 patients. Of the 174 patients, 86% (95% CI 80-90%) had an abnormality in at least 1 of the tests (i.e. abnormal nerve conduction and/or abnormal quantitative testing of temperature sensation). In conclusion, quantitative testing of temperature sensation improves the diagnostic yield in patients examined for chronic polyneuropathy.

Adult↗

PubMed2005

Clinicopathological and virological analyses of familial human T-lymphotropic virus type I--associated polyneuropathy.

Human T-lymphotropic virus type I (HTLV-I) is known to be the causative agent of the chronic myelopathy, HTLV-I--associated myelopathy (HAM), and on rare occasions infection is also associated with the development of polyneuropathy. Here the authors present an HTLV-I--positive family of whom four members developed a chronic demyelinating polyneuropathy without HAM. Four female patients in a family from Hokkaido in Japan developed distal dominant paresthesia and muscle weakness in the second and third decades of their life. Neurological findings at ages ranging from 50 to 65 years included mild painful sensorimotor disturbances with atrophy of the distal parts of the extremities but without pyramidal signs or hyperactive tendon reflexes. Magnetic resonance imaging (MRI) findings of brain and spinal cord were unremarkable. Serum HTLV-I antibody levels were elevated at 1:8192 to 1:32,768, whereas those in cerebrospinal fluid were low at 1:4 to 1:8. Electrophysiological studies revealed polyphasic compound muscle action potentials with denervation potentials on nerve conduction studies and neurogenic patterns by electromyography, which were consistent with signs of chronic motor dominant demyelinating polyneuropathy. Sural nerve biopsy showed decreased myelinated fibers, occurrence of globule formation, myelin ovoid and remyelinated fibers, and an infiltration of CD68-positive macrophages with occasional CD4-positive T cells in the nerve fascicles. The polyneuropathy was responsive to steroid therapy. Analyses of serological human leukocyte antigen (HLA) types indicated that none of the patients possessed a high-risk HLA type known to be associated with adult T-cell leukemia (ATL), whereas they did have high responsive alleles to HTLV-I env similar to that observed in HAM. Nucleotide sequence analysis of the HTLV-I tax region demonstrated the B subgroup in all patients. This study suggests that HTLV-I infection can result in the development of a familial form of polyneuropathy that is associated with distinct HLA class I alleles, which might possibly involve a distinct virus subtype.

Antibodies, Viral↗

PubMed2005

Cryptogenic polyneuropathy: clinical and neurophysiological findings.

The purpose of this study was to describe the clinical and neurophysiological features of cryptogenic polyneuropathy in 168 patients in the neurological departments at three Swedish hospitals. The medical records of all patients aged 40-79 years with the diagnosis of cryptogenic polyneuropathy from 1993 to 2000 were analysed. One hundred and fourteen patients (68%) were men. The mean age at first symptom was 61 years and at diagnosis it was 64 years. Distal numbness (n = 115, 68%) was the most common symptom, but some patients complained of pain, pedal paresthesiae, and impairment of balance. The most common clinical findings were decreased or lost proprioception or sense of vibration (n = 135, 80%) and loss of ankle jerks (n = 131, 78%). Neurography in 139 patients showed mixed sensorimotor polyneuropathy of axonal or mixed axonal and demyelinating type in 97 (70%). Cryptogenic polyneuropathy is a slowly progressive sensorimotor nerve lesion of mainly axonal type. Men are more often affected than women. Most patients have a minor or moderate severe polyneuropathy.

Adult↗