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PubMed2000

[Sensory nerve action potentials in the evaluation of diabetic polyneuropathy].

In order to clarify the suitability of sensory nerve action potential(SNAP) in the evaluation of diabetic polyneuropathy, we studied measurements of SNAPs in the median, ulnar and sural nerves. Subjects were 253 patients with non-insulin dependent diabetes mellitus; 167 men and 86 women, aged 58.2 +/- 12.8(mean +/- SD) years old. Their diabetic history was 10.2 +/- 8.6 years. SNAPs were recorded antidromically from index finger, little finger and lateral to the Achilles tendon, respectively. Twenty-eight patients, in whom any one of the SNAPs couldn't be obtained, were already excluded from this study. The polyneuropathy index (PNI) was calculated from 12 indices concerning to the velocity or long distance latency in motor nerve conduction studies of 4 nerves. The PNI is known to be an excellent index to express the degree of diabetic polyneuropathy. Amplitude and conduction velocity in each nerve was 28.6 +/- 15.6 microV and 46.2 +/- 7.4 m/sec in the median nerve, 26.7 +/- 15.8 microV and 47.0 +/- 6.5 m/sec in the ulnar nerve, 13.1 +/- 6.5 microV and 43.1 +/- 6.0 m/sec in the sural nerve, respectively. The coefficient of correlation of the measurements between median and ulnar nerves was larger than other assortment of nerves. The coefficient of correlation of each measurement with PNI was around 0.40 in the amplitude and around 0.55 in the conduction velocity. Nevertheless, the mean value of the 3 nerves had a higher coefficient of correlation with PNI; 0.48 in the amplitude and 0.60 in the conduction velocity. SNAP measurements of a single nerve are often largely affected by the inter-individual differences, inter-nerve differences or measuring errors. But the mean value of the 3 nerves will be better in exploring the degree of diabetic polyneuropathy. Evaluation of diabetic polyneuropathy by SNAPs will be best achieved by using the mean value of these 3 nerves.

Action Potentials↗
PubMed1991

Carpal tunnel syndrome, subclinical median mononeuropathy, and peripheral polyneuropathy: common early complications of chronic peritoneal dialysis and hemodialysis.

Nerve conduction velocity studies were done in median, ulnar, and peroneal nerves, one time each in 46 patients who had been on chronic peritoneal dialysis or hemodialysis for varying lengths of time. Only six patients had normal findings; 37 had peripheral polyneuropathy (15 had isolated polyneuropathy; 22 had median nerve dysfunction in addition); 16 had subclinical median mononeuropathy (14 with polyneuropathy, two without); and nine had overt carpal tunnel syndrome (eight with polyneuropathy, one without). Abnormalities were present in seven of the 11 patients studied after one year of dialysis and in 19 of the 24 patients studied after two years of dialysis. Seventeen patients studied after five years of dialysis all had polyneuropathy. Nine patients studied after seven years of dialysis all had median nerve dysfunction. Abnormalities were as common with peritoneal dialysis as with hemodialysis. Nerve dysfunction was independent of the disease underlying renal failure, the side of the dialysis access shunt, and the presence or absence of osteodystrophy. Dialysis patients need frequent nerve conduction studies from the onset of dialysis to identify carpal tunnel syndrome early and to avoid irreversible nerve damage.

Carpal Tunnel Syndrome↗
PubMedDate not supplied

[Serum lipids in various polyneuropathies].

Serum lipids were determined in 40 cases of polyneuropathy including 17 cases of Charcot-Marie-Tooth peroneal muscular atrophy, 7 cases of Dejerine-Sot-tas polyneuropathy, 7 cases of Guillain-Barré syndrome, 2 cases of diabetic polyneuropathy, 2 cases of toxic polyneuropathy and 5 cases of polyneuropathy of unclear aetiology. In the studied material shifts were observed in the composition of serum lipids, in particular, sphingomyelin and cholesterol esters. No correlation was found beteen the type of lipid pattern changes and the clinical syndrome, type of histological changes in the sural nerve, the age at onset, as well as the duration of the disease. The probable mechanism of development of changes is discussed.

Adolescent↗
PubMed2000

Three families with polyneuropathy associated with monoclonal gammopathy.

OBJECTIVE: To report familial occurrence of polyneuropathy associated with monoclonal gammopathy. DESIGN: Case reports. PATIENTS: We describe 6 patients (3 pairs) with a polyneuropathy associated with IgM monoclonal gammopathy. Four of the 6 patients had a demyelinating polyneuropathy on neurophysiological examination. Three patients had elevated antibodies against myelin-associated glycoprotein. No duplication on chromosome 17 or a mutation on chromosome 1 was found in any family. CONCLUSION: Familial occurrence of polyneuropathy without the presence of hereditary motor and sensory neuropathy type I is a reason to search for the presence of monoclonal gammopathy.

Aged↗
PubMed2006

Axonal polyneuropathy after acute dimethylamine borane intoxication.

OBJECTIVE: To study a patient with axonal polyneuropathy due to acute dimethylamine borane (DMAB) intoxication. PATIENT: Confusion and drowsiness in the acute stage, followed by cognitive impairments and polyneuropathy, are reported in a chemical factory worker after acute exposure to DMAB. RESULTS: Nerve conduction studies indicated axonal polyneuropathy, particularly in the motor nerves. Sural nerve biopsy studies 3 months later revealed an axonal degeneration with a mild decrease of fiber density in the large myelinated fibers. Quantitative sensory testing also disclosed an impairment of pinprick, temperature, and touch sensations. Cutaneous nerve biopsy studies 9 months later demonstrated a moderate loss of epidermal nerves. During the follow-up period of 1.5 years, the clinical features and serial nerve conduction studies showed a steady improvement. CONCLUSIONS: Since DMAB is a new product and has been widely used recently in the manufacturing of semiconductors and electronics, we conclude that DMAB intoxication may produce motor-predominant axonal polyneuropathy and that the establishment of a threshold limit value is warranted.

Acute Disease↗
PubMed2001

Risk factors for hematological malignancy in polyneuropathy associated with monoclonal gammopathy.

Polyneuropathy associated with monoclonal gammopathy of undetermined significance (MGUS) is a well-known disease entity. Of the patients with monoclonal gammopathy without neuropathy, 25% develop a hematological malignancy during long-term follow-up. Whether the frequency of hematological malignancy is similar in patients with polyneuropathy associated with monoclonal gammopathy and whether hematological screening is necessary in these patients is unknown. To determine the frequency of and risk factors for a hematological malignancy, we investigated 104 patients with polyneuropathy and monoclonal gammopathy. Potential diagnostic variables were obtained from medical history, physical and neurological examination, and laboratory analysis. The associations between potential diagnostic variables and outcome, hematological malignancy, were evaluated by univariable and multivariable logistic-regression analysis. Among our patients, 23 had a hematological malignancy (8 multiple myeloma, 10 low-grade lymphoma, 3 plasmacytoma, 1 Castleman's disease and 1 POEMS syndrome [polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes]). Weight loss, progression of the neuropathy, and an M-protein level > 1 g/L were independent risk factors for malignancy. Extensive screening is indicated in patients with these features.

Adult↗
PubMed2001

Solitary osteosclerotic plasmacytoma: association with demyelinating polyneuropathy and amyloid deposition.

A 51-year-old man presented with a 1-year history of polyneuropathy necessitating the use of a wheelchair. Initial diagnosis was idiopathic chronic inflammatory demyelinating polyneuropathy (CIDP) and associated monoclonal gammopathy. Investigations for multiple myeloma, including bone marrow aspiration and biopsy, were negative. What was initially felt to be an incidental osteosclerotic focus noted on the radiographic bone survey was eventually shown to be a solitary osteosclereotic plasmacytoma with associated amyloid. This dramatically altered treatment. This case emphasizes the importance of including osteosclerotic plasmacytoma in the differential diagnosis of a focal sclerotic bone lesion in the clinical setting of polyneuropathy. These lesions are less likely to progress to multiple myeloma than lytic plasma cell neoplasms, and the presence of polyneuropathy often results in earlier diagnosis and treatment with enhanced prospect of cure. The finding of amyloid deposition within the osteosclerotic lesion may be of prognostic importance.

Amyloid↗
PubMed1996

Chronic inflammatory demyelinating polyneuropathy (CIDP) in diabetics.

Seven diabetic patients developed a progressive, moderately severe, motor rather than sensory neuropathy predominantly affecting the legs. This met clinical and electrophysiological criteria for chronic inflammatory demyelinating polyneuropathy (CIDP). Nerve biopsies showed a variety of abnormalities, none of which clearly distinguished between diabetic polyneuropathy and CIDP. The patients were treated with combinations of corticosteroids, azathioprine, plasmapheresis and intravenous immune globulin; all improved substantially. We believe that CIDP may masquerade as unusually severe and progressive diabetic distal symmetric polyneuropathy. It is important to recognize CIDP in diabetics because, unlike diabetic polyneuropathy, CIDP is treatable.

Adult↗
PubMed2006

Health-related quality of life and its predictive role for analgesic effect in patients with painful polyneuropathy.

Painful polyneuropathy is a common neuropathic pain condition. The present study describes health-related quality of life (HRQL) in a sample of patients with painful polyneuropathy of different origin and the possible predictive role of HRQL for analgesic effect. Ninety-three patients with a diagnosis of painful polyneuropathy were included in the analysis. Data were obtained from three randomised, placebo-controlled cross-over studies testing the effect of different drugs on polyneuropathic pain (St. John's wort, venlafaxine/imipramine and valproic acid). Patients completed a HRQL questionnaire (SF-36) after a drug-free baseline period and at the end of each treatment period. At baseline, all eight SF-36 scores were lower than in the normal population. No significant differences were found between SF-36 scales during placebo and treatment with valproic acid and St. John's wort. Those two drugs had not shown a pain relieving effect in former analysis. The SF-36 scale of bodily pain (BP) was improved by venlafaxine treatment (p=0.023). General health (GH) and vitality (VT) were improved under treatment with imipramine (GH: p=0.006, VT: p=0.015). In a multivariate logistic regression analysis, baseline SF-36 scores predicted subsequent response to pharmacological treatment. Results show an impaired HRQL in painful polyneuropathy and suggest that HRQL may predict response to analgesic treatment.

Adult↗
PubMed2006

Polyneuropathies in teenagers: a clinicopathological study of 45 cases.

The aim of the present study was to investigate the causes of polyneuropathy in teenagers and to describe some characteristic clinical, laboratory, electrophysiological and pathological features. Forty-five patients with peripheral nervous disorders aged 13-19 were studied. Hereditary polyneuropathy of different types was diagnosed in 28 patients (62%); nine showed chronic inflammatory demyelinating polyneuropathy (CIDP) and two showed vasculitic neuropathy. In two more cases polyneuropathy was attributed to toxic agents, while among the rest, one was diagnosed as metachromatic leucodystrophy (juvenile type), one as adrenoleucodystrophy, one as porphyric neuropathy and one as Fabry disease. The high incidence of hereditary neuropathies in teenagers differs from that in adults, but is similar to that encountered in children. In our study, CIDP appears to be a frequent cause of neuropathy in teenagers, while the other causes are broadly similar to those found in studies concerning children rather than adults.

Adolescent↗
PubMedDate not supplied

Postgastrectomy polyneuropathy with thiamine deficiency is identical to beriberi neuropathy.

OBJECTIVE: We assessed whether postgastrectomy polyneuropathy associated with thiamine deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of thiamine status. METHODS: Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with thiamine deficiency were compared with those of 11 patients who had thiamine-deficiency neuropathy caused by dietary imbalance. RESULTS: The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. CONCLUSION: This study showed that thiamine-deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that thiamine deficiency can be a major cause of postgastrectomy polyneuropathy.

Beriberi↗
PubMed2004

[Recent acquisitions in the treatment of chronic immune-mediated polyneuropathies].

Chronic immune-mediated polyneuropathies encompass chronic inflammatory demyelinating polyneuropathies, polyneuropathies associated with monoclonal gammopathy and multifocal motor neuropathy with persistent conduction blocks. Their diagnosis is made on clinical, electrophysiological and sometimes immunochemical and pathological criteria. The efficacy of intravenous immunoglobulins has been reported in the short-term treatment of these neuropathies in the same way than corticosteroids and plasma exchanges, depending on the type of the polyneuropathy. The efficacy of long-term treatments needs further evaluation.

Autoimmune Diseases of the Nervous System↗
PubMed2003

Pain phenomena and possible mechanisms in patients with painful polyneuropathy.

Painful polyneuropathy is a common neuropathic pain condition characterized by different typical pain phenomena and symptoms. The present study determined the frequency of pain phenomena and signs in painful polyneuropathy, and compared the symptomatology in patients with signs of increased small fiber response with that in patients with signs of deafferentation. Eighty-one consecutive patients with painful polyneuropathy were studied. The most common pain phenomena were deep aching pain (88%) and pain on pressure (69%), followed by pain paroxysms (59%) and less frequently pain on light touch (31%). Patients with increased cold and heat detection thresholds were more likely to have pain paroxysms (odds ratio (OR) 2.5 and 5.2) and patients with pain summation on repetitive mechanical stimulation more often had touch-evoked pain (OR=4.0) than patients without these phenomena. Findings compatible with increased small fiber response were found in six patients (7.4%), in 41 (50.6%) unequivocal signs of deafferentation were found, and 34 patients (42%) could not be classified. There was no significant difference in presenting symptoms between these groups. In conclusion, in painful polyneuropathy, (1). deep aching pain is the most frequently reported pain symptom; (2). the association between pain paroxysms with decreased small fiber function and touch-evoked pain with abnormal pain summation on mechanical stimulation indicate that central nervous system mechanisms are responsible for these symptoms; (3). sensitized small fibers as the single mechanism of pain is rare; and (4). pain symptomatology cannot predict pain mechanisms as being mainly deafferentation or sensitized small fibers.

Adult↗
PubMed2000

Polyneuropathy in late Lyme borreliosis - a clinical, neurophysiological and morphological description.

In a prospective study, detailed clinical and neurophysiological examinations were performed in 17 patients with polyneuropathy associated with the late borrelial manifestation acrodermatitis chronica atrophicans (ACA). Similar clinical and neurophysiological signs were found in most of the patients. The findings were those of a sensory polyneuropathy, mainly affecting large nerve fibres. Marked abnormality of vibration threshold was a common finding and in 4 patients this raised a suspicion of spinal cord engagement, in addition to a polyneuropathy. Sural nerve biopsy, performed in 3 of the patients, showed a mainly axonal neuropathy. Biopsy findings did not confirm earlier reports of vasculitis of epineural vessels in ACA-associated polyneuropathy.

Acrodermatitis↗
PubMed1999

Alpha-lipoic acid in the treatment of diabetic polyneuropathy in Germany: current evidence from clinical trials.

Diabetic neuropathy represents a major health problem, as it is responsible for substantial morbidity, increased mortality, and impaired quality of life. Near-normoglycaemia is now generally accepted as the primary approach to prevention of diabetic neuropathy, but is not achievable in a considerable number of patients. In the past two decades several medical treatments that exert their effects despite hyperglycaemia have been derived from the experimental pathogenetic concepts of diabetic neuropathy. Such compounds have been designed to improve or slow the progression of the neuropathic process and are being evaluated in clinical trials, but with the exception of alpha-lipoic acid (thioctic acid) which is available in Germany, none of these drugs is currently available in clinical practice. Here we review the current evidence from the clinical trials that assessed the therapeutic efficacy and safety of thioctic acid in diabetic polyneuropathy. Thus far, 15 clinical trials have been completed using different study designs, durations of treatment, doses, sample sizes, and patient populations. Within this variety of clinical trials, those with beneficial effects of thioctic acid on either neuropathic symptoms and deficits due to polyneuropathy or reduced heart rate variability resulting from cardiac autonomic neuropathy used doses of at least 600 mg per day. The following conclusions can be drawn from the recent controlled clinical trials. 1.) Short-term treatment for 3 weeks using 600 mg of thioctic acid i.v. per day appears to reduce the chief symptoms of diabetic polyneuropathy. A 3-week pilot study of 1800 mg per day given orally indicates that the therapeutic effect may be independent of the route of administration, but this needs to be confirmed in a larger sample size. 2.) The effect on symptoms is accompanied by an improvement of neuropathic deficits. 3.) Oral treatment for 4-7 months tends to reduce neuropathic deficits and improves cardiac autonomic neuropathy. 4.) Preliminary data over 2 years indicate possible long-term improvement in motor and sensory nerve conduction in the lower limbs. 5.) Clinical and postmarketing surveillance studies have revealed a highly favourable safety profile of the drug. Based on these findings, a pivotal long-term multicenter trial of oral treatment with thioctic acid (NATHAN I Study) is being conducted in North America and Europe aimed at slowing the progression of diabetic polyneuropathy using a clinically meaningful and reliable primary outcome measure that combines clinical and neurophysiological assessment.

Clinical Trials as Topic↗
PubMed1986

[Differential diagnosis, pathogenesis and therapy of alcoholic polyneuropathy].

The most common forms of polyneuropathies are the alcoholic and diabetic polyneuropathies. They each constitute 1/3 of all polyneuropathies. The first symptoms shown by the alcoholic polyneuropathy are symmetric sensory disturbances with loss of tendon reflexes and of vibration sense in the peripheral segments of the lower extremities. At the beginning one almost always finds pressure pain in the calves. Important differential clues in diagnosis compared to the diabetic neuropathy, are the age at which the disease begins, the degree to which the autonomic nerve fibres and the cranial nerves are affected, as well as the form of manifestation. Pathogenetically, a direct toxic alcohol effect can above all be suspected in accordance with the typical electrodiagnostic findings with a neurogenic pattern in the EMG in the case of normal or slightly diminished conduction velocity, and in agreement with the morphological finding of an axonal degeneration in most of the biopsies. Possibly, in a small number of cases a vitamin deficiency or a malabsorption can play a causal role. The prognosis is good by complete abstinence from alcohol.

Alcoholism↗
PubMed2001

Arterial hypertension as a risk factor for chronic symmetric polyneuropathy.

OBJECTIVE: To assess whether arterial hypertension (AH) is an independent risk factor for chronic symmetric polyneuropathy (CSP) in the elderly. BACKGROUND: A strong relationship has been detected between AH and distal symmetric polyneuropathy in insulin-dependent and non-insulin-dependent diabetes. However, the correlation between AH and polyneuropathy caused by other clinical conditions has not yet been studied. METHODS: Four thousand one hundred and ninety-one subjects aged > or = 55 years seen in office consultations by 25 general practitioners (GPs) from two separate areas in Italy were interviewed, using a pretested semistructured questionnaire covering conditions commonly associated with neuropathy and symptoms of peripheral nerve disease. A neurologist later visited individuals with > or = 2 symptoms of polyneuropathy and a diagnosis of CSP was made in the presence of bilateral, fairly symmetric impairment of at least two among strength, sensation and tendon reflexes. AH was ascertained when known to the GP and/or if the patient was being treated with antihypertensive drugs. RESULTS: One hundred and fifty one subjects had CSP (3.6%). Diabetes was the commonest associated condition (18%). AH was present in 47 patients with CSP (31%). The odds ratio (OR) of AH in patients with CSP was 4.5 [95% confidence interval (CI) 3.1-6.6]. The OR of AH was 3.2 (95% CI 1.5-6.9) in patients with diabetes, and 5.7 (95% CI 3.6-9.3) in those without diabetes. The OR of AH was 4.8 (95% CI 4.4-5.2) after adjusting for the commonest risk factors for CSP. CONCLUSION: AH may be an independent risk factor for CSP in the elderly.

Aged↗
PubMed2004

High mortality of subjects with endemic ataxic polyneuropathy in Nigeria.

BACKGROUND: Endemic ataxic polyneuropathy, a neurological syndrome that was thought to be benign, has been shown to persist in some communities in south-western Nigeria, where it was first described in the 1950s. OBJECTIVES: This study was conducted to compare mortality of cases and controls, and to determine if mortality is related to exposure to cyanide from cassava foods. MATERIAL AND METHODS: Cases of endemic ataxic polyneuropathy and two groups of controls, one group living in an endemic community and the other group living in a non-endemic community, were followed for 25 months. The outcome was death from medical causes. RESULTS: A total of 5970 subjects, 204 cases and 5766 controls - 4000 controls in the endemic community and 1766 controls in the non-endemic community, were followed. A total of 153 subjects died, 24 cases, 115 controls in the endemic community, and 14 controls in the non-endemic community. Relative risks of death (95% CI), adjusted for age and gender, were 4.5 (2.3-8.9) for cases (P < 0.0001), but 2.6 (1.5-4.6) for controls living in the endemic community (P = 0.001). CONCLUSION: This study shows that endemic ataxic polyneuropathy decreases survival. The finding of lower risk of death in the community with higher exposure to cyanide from cassava foods indicates that mortality of endemic ataxic polyneuropathy is not associated with exposure to cyanide from cassava foods.

Adolescent↗