SEARCH · PubMed Health

Results for “Polyneuropathies”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 55 records · Page 3Linked to original sources

PubMed2006

Electrodiagnostic pattern approach for childhood polyneuropathies.

Electrophysiologic studies play a key role in the detection and characterization of the pattern in childhood polyneuropathies. In this study, the etiologic profile of 74 children with polyneuropathy was prospectively evaluated based on the electrophysiologic studies. Five electrodiagnostic patterns were identified in the cohort: (1) acute axonal polyneuropathy (n: 32, 43%); (2) chronic axonal polyneuropathy (n: 16, 22%); (3) demyelinating motor and sensory polyneuropathy (n: 13, 17%); (4) pure sensory polyneuropathy (n: 11, 15%); (5) high-low syndrome (n: 2, 3%). Etiologic factors were identified in all of the patients with three electrodiagnostic patterns of polyneuropathy: acute axonal, pure sensory, and high-low syndrome. However, etiologic factors could not be determined in 5 (31%) children with chronic axonal polyneuropathy and in 3 (23%) children with demyelinating sensory and motor polyneuropathy. Among children with the acute axonal pattern, toxic causes were evident in 18 (56%), acute motor axonal neuropathy in 11 (35%), and acute motor sensory axonal polyneuropathy in 3 (9%). Nine (82%) patients with pure sensory polyneuropathy had diabetes mellitus. In conclusion, a thorough history and physical examination in conjunction with specific electrodiagnostic patterns might provide a cost-effective and rational differential diagnosis of childhood polyneuropathies.

Adolescent↗

PubMed2002

Low prevalence of ataxic polyneuropathy in a community with high exposure to cyanide from cassava foods.

INTRODUCTION: Ataxic polyneuropathy, which occurs in endemic form in an area in southwest Nigeria, is attributed to exposure to cyanide from cassava foods. Exposure to cyanide from cassava is, however, not exclusive to this endemic area. In this study, the occurrence of ataxic polyneuropathy was compared in two communities in Nigeria, one located in the endemic area and the other located outside the endemic area. Both communities have been shown to have high exposure to cyanide from cassava foods. METHOD: The prevalence of ataxic polyneuropathy in Jobele, Nigeria, a community located outside the endemic area, was compared with the prevalence of ataxic polyneuropathy in Ososa, Nigeria, a reference community located in the endemic area. Subjects aged 10 years and above in both communities were screened for ataxic polyneuropathy. Ataxic polyneuropathy was diagnosed if sensory gait ataxia and sensory polyneuropathy were present. The intake of cassava foods, biomarkers of exposure to cyanide, and intake of protein and sulphur were measured. RESULTS: Prevalence of ataxic polyneuropathy were 490 per 10,000 in Ososa, and 17 per 10,000 in Jobele. The age-adjusted prevalence ratio is 4 (95% CI 0-9). The mean intake of all cassava foods in Jobele was 7 meals/person/week (95% CI 6-8), while the mean intake of all cassava foods in Ososa was 10 meals/person/week (95 % CI 9-11). The concentration of thiocyanate in the plasma was above the reference limit in 65% (95% CI 57-73) in Jobele, and 40 % (95% CI 27-52) in Ososa. The intake of protein was significantly lower in Ososa than in Jobele, but the concentrations of glutathione, cysteine and gamma-glutamylcysteine in the plasma were within the same range in Jobele and Ososa. CONCLUSION: This study shows that the occurrence of ataxic polyneuropathy is low in a community where exposure to cyanide is high. This suggests that exposure to cyanide is not a direct cause of ataxic polyneuropathy.

Adolescent↗

PubMed2003

Polyneuropathy associated with IgG/IgA monoclonal gammopathy: a clinical and electrophysiological study of 15 cases.

Peripheral neuropathy has been widely reported in patients with monoclonal gammopathy (MG), more frequently immunoglobulin M (IgM) or IgG than IgA. Nevertheless, it remains unclear whether this association has clinical or pathogenic relevance. In order to clarify the possible role of IgG/IgA MG in neuropathy, we studied the clinical and electrophysiological features of 15 consecutive patients with polyneuropathy and IgG/IgA-MG, and compared them to those of 40 patients with polyneuropathy associated with IgM-MG, previously reported. Nine middle-aged patients (60%) had a chronic progressive or relapsing demyelinating polyneuropathy (DP) that was clinically and electrophysiologically indistinguishable from classic chronic inflammatory demyelinating polyneuropathy (CIDP) and frequently responded to immunosuppressive treatments, both characteristics supporting a dysimmune process. Six older patients (40%) had a chronic axonal distal polyneuropathy similar to the so-called chronic cryptogenic sensory polyneuropathy: there was no clear relationship with the MG in these patients and the response to immunosuppressive treatments was poor. Several features allowed us to distinguish between polyneuropathies associated with IgG/IgA-MG (IgG/IgA-PN) considered together and polyneuropathies associated with IgM-MG (IgM-PN). In the first group, the proportion of patients with a predominantly sensory clinical picture (27%) was less than that in the second group (75%), and there were fewer changes in nerve conduction studies. In addition, we found that the nine patients with DP associated with IgG/IgA-MG (IgG/IgA-DP) differed from the 31 with DP associated with IgM-MG (IgM-DP): clinical and electrophysiological studies clearly showed that the demyelinating pattern was more heterogeneous in IgG/IgA-DP than in IgM-DP. The spectrum of polyneuropathies associated with IgG/IgA-MG is heterogeneous, including DP, which is similar to classic CIDP, and axonal polyneuropathy, in which the pathogenic role of the MG remains elusive. In addition, IgG/IgA-DP differ from IgM-DP on clinical and electrophysiological grounds, suggesting probable different physiopathological mechanisms.

Adrenal Cortex Hormones↗

PubMed1999

Hyperhomocysteinaemia is not related to risk of distal somatic polyneuropathy: the Hoorn Study.

OBJECTIVE: Distal somatic polyneuropathy is a major contributing factor in the pathogenesis of chronic foot infections and ulcers, and may lead to lower limb amputations. Both metabolic and vascular abnormalities may contribute to the development of impaired nerve function. We therefore assessed the association between hyperhomocysteinaemia, a risk factor for cardiovascular disease, and polyneuropathy. DESIGN, SETTING AND SUBJECTS: We studied an age-, sex- and glucose-tolerance-stratified random sample of a 50- to 75-year-old general Caucasian population in the Hoorn Study (N = 629). Any polyneuropathy (N = 95) was defined as the absence of at least two of the three following sensory modalities or reflexes of either foot: light touch sense, ankle reflex and vibration sensation. Definite polyneuropathy (N = 25) was present if, in addition, the vibration perception threshold of the right big toe was abnormal. RESULTS: The prevalence of any polyneuropathy was 12.4% (33 of 266) in subjects with normal glucose tolerance (NGT), 12.6% (21 of 167) in those with impaired glucose tolerance (IGT), and 25.3% (41 of 162) in those with type 2 diabetes. The prevalence of definite polyneuropathy was 2.6% (7 of 266) in subjects with NGT, 2.4% (4 of 167) in those with IGT and 8.7% (14 of 161) in type 2 diabetic subjects. Polyneuropathy was associated with known risk factors such as diabetes, hyperglycaemia and body height. After adjustment for age, sex, HbA1c and hypertension, the odds ratio (95% CI) for any polyneuropathy per 5 micromol L-1 (about 1 SD) serum total homocysteine increment was 1.00 (0.72-1.39). After adjustment for age and sex, it was 0.62 (0.21-1.89) for definite polyneuropathy. CONCLUSION: Although a weak relation (as judged from the confidence intervals) cannot be excluded, we conclude that hyperhomocysteinaemia is probably not related to risk of distal somatic polyneuropathy.

Aged↗

PubMed2004

Drug therapy for chronic idiopathic axonal polyneuropathy.

BACKGROUND: Chronic idiopathic axonal polyneuropathy is an insidiously progressive sensory or sensorimotor polyneuropathy that affects elderly people. Although severe disability or handicap does not occur, it reduces quality of life. OBJECTIVES: To assess whether drug therapy for chronic idiopathic axonal polyneuropathy reduces disability, ameliorates neurological symptoms and associated impairments, and whether treatment is safe. SEARCH STRATEGY: We searched Cochrane Library (Cochrane Neuromuscular Disease Review Group Register, Cochrane Database of Systematic Reviews, Cochrane Database of Abstracts of Reviews of Effectiveness, and the Cochrane Central Register of Controlled Trials), MEDLINE, EMBASE, ISI, and ACP Journal Club's Best Evidence, from 1981 until December 2002. We also hand searched the reference lists of relevant articles, reviews and textbooks identified electronically, and contacted authors and other experts in the field to identify additional studies. SELECTION CRITERIA: We sought all randomised or quasi-randomised (alternate or other systematic treatment allocation), unconfounded trials that examined the effects of any drug therapy in patients with chronic idiopathic axonal polyneuropathy at least one year after the onset of treatment. Patients with chronic idiopathic axonal polyneuropathy had to fulfil the following criteria: age 40 years or older, distal sensory or sensorimotor polyneuropathy, absence of systemic or other neurological disease, chronic clinical course not reaching a nadir in less than two months, exclusion of any recognised cause of the polyneuropathy by medical history taking, clinical or laboratory investigations, electrophysiological studies in agreement with axonal polyneuropathy without evidence of demyelinating features. The primary outcome was the proportion of patients with a significant improvement in disability. Secondary outcomes were change in the mean disability score, change in the proportion of patients who make use of walking aids, change in the mean Medical Research Council sum score, degree of pain relief and/or reduction of other positive sensory symptoms, change in the proportion of patients with pain or other positive sensory symptoms, and frequency of adverse effects. DATA COLLECTION AND ANALYSIS: Two reviewers independently reviewed and extracted details of trial methodology and outcome data of all potentially relevant trials. MAIN RESULTS: Eighteen studies were identified and assessed for possible inclusion in the review, but all were excluded because of insufficient quality or lack of relevance. REVIEWERS' CONCLUSIONS: Even though chronic idiopathic axonal polyneuropathy has been clearly described and delineated, no adequate randomised or quasi-randomised controlled clinical treatment trials have been performed. In their absence there is no proven efficacious drug therapy.

Aged↗

PubMed2005

Distal symmetrical polyneuropathy: definition for clinical research.

The objective of this report was to develop a case definition of "distal symmetrical polyneuropathy" to standardize and facilitate clinical research and epidemiological studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetrical polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiological studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach for defining distal symmetrical polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiological research studies will ensure greater consistency of case selection.

Electrodiagnosis↗

PubMed2005

Distal symmetrical polyneuropathy: a definition for clinical research. A report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

The objective of this report was to develop a case definition of "distal symmetrical polyneuropathy" to standardize and facilitate clinical research and epidemiologic studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetrical polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiologic studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach to defining distal symmetrical polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiologic research studies will ensure greater consistency of case selection.

Electrodiagnosis↗

PubMed2005

Effect of critical illness polyneuropathy on the withdrawal from mechanical ventilation and the length of stay in septic patients.

OBJECTIVES: No previous study has demonstrated whether critical illness polyneuropathy itself lengthens mechanical ventilation or whether this prolonged duration of ventilatory support is explained by concomitant risk factors for weaning failure. Our objectives were to evaluate the impact of critical illness polyneuropathy on the length of mechanical ventilation after controlling for coexisting risk factors for weaning failure and to assess the impact of critical illness polyneuropathy on the length of the stay in a cohort of septic patients. DESIGN: Prospective cohort study. SETTING: Intensive care unit of a tertiary hospital. PATIENTS: All patients with severe sepsis or septic shock who required mechanical ventilation for > or =7 days who were considered ready to discontinue mechanical ventilation. INTERVENTIONS: Patients underwent a neurophysiologic evaluation at onset of weaning from mechanical ventilation. MEASUREMENTS AND MAIN RESULTS: Sixty-four critically ill septic patients were enrolled, and 34 developed critical illness polyneuropathy (53.1%; 95% confidence interval, 40.2-65.7%). Length of mechanical ventilation was significantly higher in patients who had developed critical illness polyneuropathy (median 34 days vs. 14 days, p < .001). The duration of the weaning period was also significantly greater in patients with critical illness polyneuropathy (median 15 days vs. 2 days, p < .001) even though factors suspected to influence the weaning process did not differ between these two groups. Multiple logistic regression analysis indicated that critical illness polyneuropathy was the only risk factor independently associated with weaning failure (odds ratio, 15.4; 95% confidence interval, 4.55, 52.3; p < .001). Lengths of intensive care unit and hospital stays were significantly higher in patients with critical illness polyneuropathy. CONCLUSIONS: In critically ill septic patients, critical illness polyneuropathy significantly increases the duration of mechanical ventilation and prolongs the lengths of intensive care unit and hospital stays.

Critical Illness↗

PubMed2005

Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

The objective of this report was to develop a case definition of distal symmetric polyneuropathy to standardize and facilitate clinical research and epidemiologic studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetric polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiologic studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach to defining distal symmetric polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiologic research studies will ensure greater consistency of case selection.

Clinical Protocols↗

PubMed2002

N(epsilon)-Carboxymethyllysine in diabetic and non-diabetic polyneuropathies.

Increased oxidative stress and advanced glycosylation are important factors in the development of diabetic neuropathy. In non-diabetic neuropathies their influence has not been investigated in detail so far. We studied the localisation of N(epsilon)-carboxymethyllysine (CML) - a biomarker for oxidative stress - by immunohistochemistry in sural nerve biopsies of 31 patients with different polyneuropathies [diabetic polyneuropathy (n=5), alcohol-associated polyneuropathy (n=4), vitamin B12-deficient polyneuropathy (n=6), chronic inflammatory demyelinating polyneuropathy (CIDP) (n=6), vasculitic neuropathy (n=6), Charcot-Marie-Tooth disease type I (CMT I) (n=4)] and 4 normal controls. CML was detected in the perineurium of patients with diabetic, alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathies. Epineurial, perineurial and endoneurial vessels were CML positive in diabetic, vitamin B12-deficient and vasculitic polyneuropathies. CML was also found in mononuclear inflammatory cells in vasculitic neuropathy. In CIDP and normal controls there was only marginal perineurial CML deposition in 2/6 and 1/4 cases. In CMT I no CML was detected. Immunohistochemical results were confirmed by immunoblot. Our data suggest a role of oxidative stress in the pathogenesis not only of diabetic but also of alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathies. It may be a minor pathogenetic factor in CIDP and may not be involved in CMT I. Underlying causes for increased oxidative stress may be an elevated production of reactive oxygen species and an impairment of antioxidative defences. Therefore, an antioxidative treatment should be considered in alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathy.

Adult↗

PubMed1995

Polyneuropathy induced by carbon disulphide in viscose rayon workers.

OBJECTIVES: To understand the prevalence of polyneuropathy and correlations among the clinical manifestations, electrophysiological findings, and degree of exposure to carbon disulphide (CS2) in workers who were exposed to variable concentrations of CS2 in a viscose rayon factory. METHODS: All the 163 workers received a detailed physical and neurological evaluation. Fixed point air samples were analysed for CS2. Nerve conduction velocity was studied in 26 workers with symptoms similar to neuropathy. RESULTS: Nine workers (53%) with overt polyneuropathy from the fibre cutting department and 19 workers (13%) with oligosymptoms similar to polyneuropathy from various jobs were noted. The fixed point air concentrations of CS2 were 150-300 ppm in the cutting areas and 15 to 100 ppm in the spinning areas. The estimated eight hour time weighted averages in the fibre cutting areas were 40-67 ppm. The occurrence of polyneuropathy was generally correlated with the degree of exposure to CS2. Nerve conduction velocities (NCVs) were significantly different in the overt polyneuropathy and subclinical polyneuropathy groups from the normal controls. The sensitive indicators for CS2 polyneuropathy were distal latency, motor NCV, and amplitude of sensory nerve action potentials in sensory NCVs. CONCLUSION: The outbreak of polyneuropathy was attributed to higher concentrations of CS2 in fibre cutting areas. Even in other jobs with relatively lower concentrations of CS2, the hazard of subclinical polyneuropathy cannot be overlooked.

Adult↗

PubMed1995

The role of polyneuropathy in motor convalescence after prolonged mechanical ventilation.

OBJECTIVE: To test the hypothesis that prolonged motor recovery after long-term ventilation may be due to polyneuropathy and can be foreseen at an early stage by electromyography (EMG). DESIGN: Cohort study with an entry period of 18 months. Polyneuropathy was identified by EMG studies in the intensive care unit (ICU). During a 1-year follow-up, amount of time was recorded to reach a rehabilitation end point. SETTING: The general ICU of a community hospital. PATIENTS: Fifty patients younger than 75 years who were receiving mechanical ventilation for more than 7 days. MAIN OUTCOME MEASURES: A rehabilitation end point was defined as return of normal muscle strength and ability to walk 50 m independently. RESULTS: In 29 of 50 patients, an EMG diagnosis of polyneuropathy was made in the ICU. Patients with polyneuropathy had a higher mortality in the ICU (14 vs 4; P = .03), probably related to multiple organ failure (22 vs 11; P = .08) or aminoglycoside treatment of suspected gram-negative sepsis (17 vs 4; P = .05). Rehabilitation was more prolonged in 12 patients with polyneuropathy than in 12 without polyneuropathy (P = .001). Of nine patients with delays beyond 4 weeks, eight had polyneuropathy, five of whom had persistent motor handicap after 1 year. In particular, axonal polyneuropathy with conduction slowing on EMG indicated a poor prognosis. CONCLUSIONS: Polyneuropathy in the critically ill is related to multiple organ failure and gram-negative sepsis, is associated with higher mortality, and causes important rehabilitation problems. EMG recordings in the ICU can identify patients at risk.

APACHE↗

PubMed2001

[Pain therapy in HIV-associated polyneuropathy].

Only some patients with HIV-infection receive an adequate pain therapy. In later stages of HIV-infection up to 50% 6 of patients perform extraordinary doctor visits because of pain. Principally primary and secondary neuromanifestations of HIV-infection have to be differentiated. Rare forms of HIV-associated polyneuropathies represent mononeuropathy or mononeuritis multiple acute and chronic inflammatory demyelinating polyneuropathy and polyneuropathy caused by opportunistic infections. HIV-associated distal-symmetric polyneuropathy represents the most common form during HIV-infection with a prevalence up to 50%. Typical clinical symptoms and signs are pain, hyp- and dysaesthesia, diminuted deep tendon reflexes, motor deficits and autonomic disturbances. Always neurological examination and neurophysiologic investigation on the sural and peronaeal nerve are necessary for monitoring progression of polyneuropathy and as basics before starting antiretroviral therapy with neurotoxic substances. According to momentary opinion, HIV-associated distal-symmetric polyneuropathy represents no indication for antiretroviral therapy. Symptomatic therapy includes antiepileptic medication as gabapentine, antidepressive drugs as amitiptyline and additionally retarded opiates. Depressive disorders ma y accentuate pain problems a n d need psychotherapeutic and thymoleptic therapy. Special problems occur when neurotoxic substances evoke or deteriorate polyneuropathy. In these cases an individual therapeutic proceeding about continuation or discontinuation of neurotoxic medication is necessary. Symptoms of myopathy during HIV-infection are muscle pain, elevation of CK and typical changes of motor units detected by electromyography. In most cases biopsy is necessary for diagnosis of specific forms of HN-associated myopathy. HIV-associated polymyositis is treated by non-steroid analgetics, corticoids, immunoglobulines and plasmapheresis, myopathy induced by neurotoxic medication analogous to polyneuropathy.

Acute Disease↗

PubMed2003

Incidence of endemic ataxic polyneuropathy and its relation to exposure to cyanide in a Nigerian community.

BACKGROUND: The occurrence of ataxic polyneuropathy in an endemic area in south west Nigeria has been attributed to exposure to cyanide from cassava foods. However, it has been shown that the prevalence of ataxic polyneuropathy is not high in several communities in the tropics where exposure to cyanide from cassava foods is high. OBJECTIVES: To determine the incidence of ataxic polyneuropathy in an endemic community, and to compare the intake of cassava foods, exposure to cyanide, and levels of thiols in cases and controls. METHODS: A cohort of 3167 healthy subjects aged 10 years and over in Ososa, Nigeria, was followed for two years, screened, and examined neurologically. Ataxic polyneuropathy was diagnosed if sensory polyneuropathy and sensory gait ataxia were both present. Controls were selected randomly within 10 year age groups of subjects who screened negative. Intake of cassava foods, exposure to cyanide, concentrations of thiols (glutathione, cysteine, and gamma glutamylcysteine) in plasma, and visual evoked potentials were measured. RESULTS: Person-years of follow up were 6246 for 1469 male and 1698 female subjects in the cohort. The incidence of ataxic polyneuropathy was 64 per 10,000 person-years (31 for male and 93 for female subjects). Multivariate odd ratios were 0.78 (95% CI 0.23 to 2.61) for intake of the commonest cassava food, and 1.64 (0.56 to 5.09) for concentration of thiocyanate in plasma. The concentration of thiols was less than the reference limits in two controls, but in none of the cases. The latency of P100 was prolonged in 20 cases (69%) compared with 14 controls (42%) (p<0.05). CONCLUSIONS: The incidence of ataxic polyneuropathy is high in Ososa, Nigeria, but the intake of cassava foods, exposure to cyanide, and levels of thiols, are not related to the occurrence. These findings do not suggest that cyanide is the cause of endemic ataxic polyneuropathy.

Adolescent↗

PubMed1997

[Referral of patients with polyneuropathy by the family physician: influence of type of symptoms but not of age].

OBJECTIVE: To investigate the influence of the age of the patient and the nature of a polyneuropathy on the referral behaviour of general practitioners (GPs). DESIGN: Written questionnaire sent to GPs regarding paper case records of polyneuropathy. SETTING: University Hospital Utrecht, the Netherlands. METHODS: 1590 GPs were asked about their differential diagnosis regarding a paper case record of a patient with polyneuropathy. There were six case records, differing in age (53, 64 and 73 years) and nature of the disease (sensory or sensorimotor polyneuropathy). The GPs were divided into six groups with similar demographic characteristics and type of practice. To avoid focus on polyneuropathy, all GPs also received questions about three other neurological cases (amaurosis fugax, radicular syndrome and vasovagal collapse). RESULTS: The mean response of the questionnaire was 54% (n = 844). Most GPs diagnosed the polyneuropathy (analysis of variance; p < 0.0001). The age of the patient did not influence the diagnosis nor the referral behaviour. At least 73% of the patients with a sensory and 81% of the patients with a sensorimotor polyneuropathy were referred to neurologists for further investigations (chi(2)-test; p < 0.05). CONCLUSION: At least 73% of the GPs referred a patient with polyneuropathy to a neurologist; patients with muscle weakness were referred more often than patients with only sensory disturbances. Referral was not influenced by the age of the patient.

Age Factors↗

PubMed1992

Salivary hypofunction in patients with familial amyloidotic polyneuropathy.

Patients who suffer from familial amyloidotic polyneuropathy frequently complain of mouth dryness and an increased need for dental treatment. The aim of the present investigation was to study saliva secretion rate and composition and other factors related to the risk of dental caries in patients with familial amyloidotic polyneuropathy. Thirty patients with familial amyloidotic polyneuropathy volunteered for the study and were compared with a matched control group. Samples of unstimulated and stimulated whole saliva were collected in a standardized manner. The secretion rates were calculated, and the concentrations of electrolytes, glycoprotein markers, and proteins with antibacterial properties were analyzed. Dental caries and variables related to the risk of dental caries were also scored. The results show that familial amyloidotic polyneuropathy patients frequently have a decreased rate of saliva secretion and that the degree of salivary hypofunction is positively correlated to the progress of familial amyloidotic polyneuropathy. Forty-three percent of the familial amyloidotic polyneuropathy patients in this study had no detectable secretion of unstimulated saliva. A low secretion rate of stimulated saliva (< 0.7 ml/min) was found in 33% of the patients. The concentrations of salivary protein, amylase, lysozyme, salivary peroxidase, secretory IgA, hexosamines, sialic acid, fucose, phosphate, potassium, and the degree of protein glycosylation were higher in the familial amyloidotic polyneuropathy patients than in the control patients. We conclude that patients with familial amyloidotic polyneuropathy have a reduced saliva secretion and are subsequently at risk for increased development of dental caries.

Adult↗

PubMed1994

Distal accentuation of conduction slowing in polyneuropathy associated with antibodies to myelin-associated glycoprotein and sulphated glucuronyl paragloboside.

In four patients with a chronic, demyelinating polyneuropathy associated with monoclonal IgM antibodies to myelin-associated glycoprotein (MAG) and sulphated glucuronyl paragloboside (SGPG), we have observed a marked prolongation of distal motor latencies disproportionate to proximal segment-conduction velocities, in nearly all nerves studied. Distal accentuation of conduction slowing distinguished these patients from those with Charcot-Marie-Tooth polyneuropathy type 1A, chronic inflammatory polyneuropathy, and from controls, as demonstrated by regression of distal motor latency on proximal conduction velocity. Sixteen of 21 nerves (76%) studied in the patients with anti-MAG/SGPG polyneuropathy had a terminal latency index of < or = 0.25 versus 11 of 195 nerves (6%) of Charcot-Marie-Tooth polyneuropathy type 1A patients, three of 49 nerves (6%) of patients with chronic inflammatory polyneuropathy and none of the controls (P = 0.0001). Recognition of this unique pattern of generalized, distally predominant conduction slowing in anti-MAG/SGPG polyneuropathy may be useful in clinically distinguishing this from other chronic demyelinating polyneuropathies, and in possibly providing insights into the pathophysiology of this disorder.

Aged↗

PubMed1997

Local human sural nerve blood flow in diabetic and other polyneuropathies.

Microangiopathy is considered relevant to the pathogenesis of several forms of peripheral nerve disease, particularly diabetic polyneuropathy. In diabetes, however, it is uncertain whether reductions in mixed nerve trunk blood flow account for early features of polyneuropathy in contrast to later disease, where microvascular changes have been described. To address this issue, we measured local sural nerve blood flow in patients with mild diabetic polyneuropathy who were enrolled in a clinical trial (n = 26), patients with other polyneuropathies being studied by diagnostic sural nerve biopsy (n = 17), patients with vasculitic polyneuropathy (n = 3) and one patient with rapidly progressive severe diabetic polyneuropathy and lumbosacral plexopathies. Standardized measurements were made at 10 sites along the sural nerve of each patient prior to sural nerve resection for biopsy. We used a laser Doppler flowmetry probe sensitive to red blood cell flux to measure sural nerve blood flow. This was slightly higher in patients with mild diabetes compared with those with other polyneuropathies, but was reduced in patients with vasculitis. In patients with mild diabetes, there was no relationship between sural nerve blood flow and prebiopsy sural nerve action-potential amplitude, sural myelinated fibre density, haemoglobin A1C, duration of diabetes or age of the patient. Ten diabetic patients entered in the clinical trial had sural nerve blood flow recorded in one sural nerve, followed 1 year later by a second sural nerve blood flow measurement prior to biopsy of the contralateral sural nerve. Despite a mild trend toward decline in fibre density between the nerves over this period of time, sural nerve blood flow was similar. The patient with severe diabetic polyneuropathy and lumbosacral plexopathies had reduced sural nerve blood flow. Our findings do not provide evidence that reductions in sural nerve blood flow are associated with early peripheral neuropathy in diabetes, unlike vasculitis. The early trend toward slight rises in sural nerve blood flow may be a result of early functional microangiopathy that accompanies nerve dysfunction but does not cause it.

Aged↗