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At least 19 recordsLinked to original sources
PubMed1979

[The diabetic polyneuropathy. II. Polyneuropathy, angiopathy and nerve conduction velocity].

789 patients with diabetes mellitus were studied by clinical and electroneurographical examination. Motor conduction velocity of the median and the tibial nerve and sensory conduction of the median nerve were determined. 81.1% of the patients we suffering from diabetes which began in childhood or adolescence, 13.9% were suffering from maturity onset diabetes. Average duration of the disease was 9.5 years, average age was 26.7 years. Clinical signs of polyneuropathy were found in 19.1%. Typical findings were pain and paraesthesia, lack or abolition of triceps surae reflexes, impaired pallaesthesia on lower extremities. 48.3% of 151 patients with clinical signs of polyneuropathy were suffering from combined angiopathy, 32.5% from microangiopathy, 7.9% from macroangiopathy. Severity of complicating retinopathy and macroangio,athy were found to be correlated with polyneuropathy. 58.2% of 323 diabetics with at least one delayed nerve conduction velocity exhibited signs of angiopathy. In nearly 30% of children and adolescents after comparatively short duration of the disease at least one conduction velocity was delayed. In diabetic children and adolescents metabolic disturbances are assumed to cause peripheral nerve dysfunction.

Adolescent↗
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↗
PubMed1977

Toxic polyneuropathies after sniffing a glue thinner.

In West Berlin in the autumn of 1975 through the following 5 months we observed 18 juvenile patients who had a toxic polyneuropathy and had sniffed a glue thinner. The neurological picture consisted of a symmetrical, progressive, ascending, mainly motor, polyneuropathy with pronounced muscle atrophy and characteristic vegetative alterations. The height of the disease was reached after 1 1/2-2 1/2 months and was characterized by tetraplegia in 7 patients. After 8 months all patients still had a motor deficit. Nerve biopsy showed paranodal axon swelling, dense masses of neurofilaments and secondary myelin retraction. The neurological and morphological data correspond to the "glue sniffer's neuropathy" and the n-hexane and MBK polyneuropathy after industrial exposure, as described in 10 cases to date. However, there was no MBK in the glue thinner. The polyneuropathies occurred in close time relation with the denaturation of the thinner with MEK (2-butanone). It is concluded from the data n-hexane and MBK have a common toxic mechanism with primary axonal changes and that there is an additional synergistic effect of MEK.

Adolescent↗
PubMed1975

[Uremic polyneuropathies].

The report is concerned with the results of a study of polyneuropathy in 75 patients with acute and chronic renal insufficiency. The authors described the clinical characteristics of the different forms of neuropathy. In acute renal insufficiency the first signs of polyneuropathy appear during the stage of polyuria and are reversible. In chronic renal insufficiency and hemodialysis treatment of subclinical an sensory forms of neuropathy are mainly seen (2/3 of the patients). It was demonstrated that there was a retardation in the velocity of excitative conductivity through the nerves depending upon the severity of polyneuropathy. A longterm adequate hemodialysis may prevent the further development of polyneuropathy.

Acute Kidney Injury↗
PubMed1976

[Decompression of individual nerves in anatomical strictures in polyneuropathies].

During clinical and electromyographical examination of one patient with diabetic and one with alcoholic polyneuropathy we found an especially severe lesion of the ulnar nerve at the elbow on one side. As the polyneuropathy generally affects the nerves symmetrically we presumed in addition some other most probably ulnar nerve compression syndrome at the elbow. Both patients were operated and the nerves were transposed (Prof. NIGST). The local finding during the operation, the improvement of the paresis of ulnar nerve and the worsening of the polyneuropathy--found simultaneously at control after 2 and 4 years--confirmed our supposition. Should in cases of polyneuropathy an especially severely damaged nerve be found, one ought to think of the possibility of an additional mechanical lesion and treat the patient accordingly.

Alcoholism↗
PubMed1979

[The diabetic polyneuropathy. I. Relation between impaired function in peripheral nerves and clinical findings].

789 patients with diabetes mellitus were studied by clinical and electroneurographical investigation. Motor and sensory conduction velocities of the median nerve and motor conduction velocity of the tibial nerve were determined. 86.1% of the patients suffered from juvenile diabetes, and 13.9% from maturity onset diabetes. Average duration of the disease was 9.5 years, average age of the patients was 26.7 years. Clinical signs of polyneuropathy were found in 19.1%. In 40.9% of the patients at least one of 3 conduction velocities was found to be delayed. Patients with clinical signs of polyneuropathy exhibited delayed nerve conduction velocities and delayed distal latencies. Diagnosis of polyneuropathy almost with certainty is possible by determining the three nerve conduction velocities and the three corresponding distal latencies. 22% of patients without clinical signs of polyneuropathy exhibited electroneurographical signs of impaired peripheral nerve function. Heredity, body weight, lipid metabolism, actual metabolic balance, and treatment were found to be without any significant influence on nerve conduction velocity.

Adult↗
PubMed1977

Polyneuropathy, skin hyperpigmentation, edema, and hypertrichosis in localized osteosclerotic myeloma.

1 61-year-old man had osteosclerotic myeloma that was localized in the eleventh thoracic vertebral body and associated with sensorimotor polyneuropathy, skin hyperipigmentation, edema, hypertrichosis, gynecomastia, and white nails. Cases of osteosclerotic myeloma with and without polyneuropathy in the literature were reviewed with special reference to accompanying dermatologic and endocrinologic signs and synmptoms. We assume that the polyneuropathy, cutaneous hyperpigmentation, edema, hypertrichosis, gynecomastia, and white nails are causally related to each other and are a remote effect of osteosclerotic myeloma. Quantitative histologic analysis of two sural nerves biopsied within 2 years of each other during the course of the disease indicated that both large and small myelinated fibers degenerated progressively, with relative preservation of unmyelinated fibers.

Edema↗
PubMed1978

Polyneuropathy and folate deficiency.

We studied five patients (two men and three women, age between 58 and 76 years) with clinical and electrophysiological signs of polyneuropathy. Routine neurological, hematological, and gastroenterological studies as well as procedures to test fat malabsorption were performed. Folate determinations were done using both radioactive and Lactobacillus casei methods. Two patients displayed the signs of subacute combined degeneration of the spinal cord with polyneuropathy, while three had only signs of neuropathy. All had low serum folate concentration, long-standing gastrointestinal disease, and deficient folate intake. The D-xylose absorption test gave values in all patients, while none displayed the classical malabsorption syndrome. The patients had substantial improvement or recovered (according to clinical and electrophysiological measurements) after periods ranging from 9 to 39 months of folate therapy. Such acquired folate-responsive polyneuropathy has two principal characteristics: mixed sensorimotor with mainly sensory deficits, and involvement of one or both of the lower extremities much more extensively than the upper extremities.

Aged↗
PubMed1979

Does a defect of energy metabolism in the nerve fiber underlie axonal degeneration in polyneuropathies?

A number of chemically unrelated neurotoxic compounds and several types of metabolic abnormalities cause strikingly similar patterns of distal symmetrical polyneuropathy in humans and animals. Experimental studies with laboratory species have demonstrated that many toxic polyneuropathies are associated with distal and retrograde axonal degeneration occurring in vulnerable nerve fiber tracts in the central as well as the peripheral nervous system. This has been termed central-peripheral distal axonopathy. Recent observations from the authors' laboratories regarding (1) the spatial-temporal evolution of nerve fiber degeneration in experimental toxic neuropathies and (2) the inhibition of glycolytic enzymes by chemically unrelated neurotoxic compounds point to a common metabolic basis for many distal axonopathies. It is postulated that neurotoxic compounds deplete energy supplies in the axon by inhibiting nerve fiber enzymes required for the maintenance of energy synthesis. Resupply of enzymes from the neuronal soma fails to meet the increased demand for enzyme replacement in the axon, causing the concentration of enzymes to drop in distal regions. This leads to a local blockade of energy-dependent axonal transport, which produces a series of pathological changes culminating in distal nerve fiber degeneration. The idea provides a working hypothesis with which to study the cause of inherited and acquired human and animal polyneuropathies.

Axonal Transport↗
PubMedDate not supplied

[Immunoglobulin G level in the serum of patients with polyneuropathies].

In the serum of patients with polyneuropathies of various aetiology the immunoglobulin G level was determined quantitatively using the so-called disc precipitation test. Fifty serum samples were investigated. The IgG level was higher (p less than 0.05) in the group of patients with polyneuropathy as compared with the control group. No differences were observed in the IgG level between different types of polyneuropathy which may be due to small number of cases in various groups.

Adolescent↗
PubMed1979

[Diabetic polyneuropathy. 4. Synopsis of electroneurographic findings in diabetics].

Sensory conduction velocity of the median nerve, motor conduction velocity of both median and tibial nerves, and corresponding distal laterncies are sufficient parameters to establish the diagnosis of polyneuropathy almost with certainty. Considering these six parameters yielded in detection of peripheral nerve dysfunction in 22% of diabetic patients who were free from clinical signs of polyneuropathy. Electroneurographical findings in 340 out of 677 patients with diabetes mellitus were interpreted as evidence of segmental demyelination. Within this group there was the majority of patients with clinical signs of polyneuropathy and with subclinical signs of peripheral nerve dysfunction. There existed a positive correlation between signs of nerve dysfunction with angiopathy, age and duration of the disease. A second group consisting of 243 diabetics with signs of incipient segmental demyelination with or without signs of axonaal degeneration mainly included juvenile patients with a short duration of the disease and with a low frequency of angiopathy.

Adolescent↗
PubMed2026

RFC1 Repeat Expansions in Chronic Idiopathic Axonal Polyneuropathy: Prevalence, Phenotype, and Diagnostic Implications.

BACKGROUND AND AIMS: Chronic idiopathic axonal polyneuropathy (CIAP) accounts for approximately 20%-30% of adult-onset axonal polyneuropathies. Pathogenic RFC1 repeat expansions have emerged as a frequent cause of idiopathic sensory neuropathy, but their recognition in routine clinical practice may be challenging, particularly in the presence of potentially confounding comorbidities. We aimed to determine the prevalence of pathogenic RFC1 repeat expansions in a well-defined CIAP cohort, characterize the associated clinical and electrophysiological phenotype, and evaluate whether coexisting well-controlled diabetes mellitus (DM) or monoclonal gammopathy of undetermined significance (MGUS) may hinder recognition of RFC1-related neuropathy. METHODS: We performed a retrospective observational study of adult patients with CIAP followed at a tertiary neuromuscular unit. All patients underwent RFC1 genetic testing. Clinical and electrophysiological features were compared between RFC1+ and RFC1- patients in the full cohort and after exclusion of patients with DM or MGUS. RESULTS: Ninety patients met CIAP criteria and were analyzed. Twenty-four (27%) carried biallelic pathogenic AAGGG repeat expansions in RFC1, of whom 6 (25%) had coexisting DM or MGUS. Compared with RFC1- patients, RFC1+ individuals more frequently exhibited dysautonomic symptoms, unsteadiness, history of falls, need for walking support, chronic cough, impaired vibration sense in the upper limbs and up to the knees in the lower limbs, brisk upper-limb reflexes, mild cerebellar signs, an abnormal head-impulse test, and a positive Romberg's test. Most of these differences persisted after exclusion of DM or MGUS. Electrophysiological studies in RFC1+ patients showed widespread sensory nerve involvement, including the upper limbs, with relative motor sparing, whereas RFC1- patients exhibited a more typical length-dependent pattern. INTERPRETATION: Biallelic AAGGG repeat expansions in RFC1 were identified in 27% of patients with CIAP. Specific clinical and electrophysiological features may help distinguish RFC1-related disease from other forms of CIAP and identify candidates for genetic testing, even in the presence of potentially confounding comorbidities such as well-controlled DM or MGUS.

Humans↗
PubMed2026

Impact of Baseline Polyneuropathy Severity on Eplontersen Efficacy in the NEURO-TTRansform Clinical Trial.

BACKGROUND AND AIMS: In the NEURO-TTRansform clinical trial (NCT04136184), eplontersen improved neuropathy impairment and quality of life (QoL) through Week 66 versus the NEURO-TTR historical placebo in patients with hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN). This analysis assessed the impact of baseline ATTRv-PN severity on eplontersen response in patients from NEURO-TTRansform. METHODS: This post hoc analysis grouped patients into tertiles by baseline Neuropathy Impairment Score (NIS): T1 (least baseline impairment: 3.5 to <&#x2009;27.5; n&#x2009;=&#x2009;67), T2 (27.5 to <&#x2009;55.0; n&#x2009;=&#x2009;67), and T3 (55.0 to <&#x2009;127.8; n&#x2009;=&#x2009;66). Outcomes assessed were neuropathy impairment (modified NIS+7 [mNIS+7] and NIS, Neuropathy Symptom and Change, Polyneuropathy Disability), QoL (Norfolk QoL-Diabetic Neuropathy), physical functioning (36-Item Short-Form Health Survey Physical Component Summary), nutritional status (modified body mass index), and serum transthyretin levels; these were compared with NEURO-TTR historical placebo. Autonomic dysfunction (Composite Autonomic Symptom Score-31), disability (Rasch-built Overall Disability Scale), and walking speed (10-Meter Walk Test) were also assessed. Final assessments were carried out following 65/66 or 81/85&#x2009;weeks of treatment. RESULTS: Mean mNIS+7 composite scores were maintained over 85&#x2009;weeks with eplontersen (changes from baseline of -4.5 [T1], -1.3 [T2], and -2.6 [T3] points). Other disease parameter scores were similarly maintained or improved with eplontersen. Patients receiving placebo experienced disease worsening across outcomes. T1 mean disease scores were typically better than in T2 and T3. INTERPRETATION: Consistent, sustained benefits of eplontersen were observed regardless of baseline ATTRv-PN severity. These findings strengthen the importance of early treatment initiation for patients with ATTRv-PN across the disease spectrum.

Humans↗
PubMed1975

[Correlation between sensory action potentials and vibratory perception in uremic polyneuropathy (author's transl)].

1. The sensory action potentials of the tibial nerve at the medial malleolus were studied by averaging in 51 patients with chronic renal failure treated by hemodialysis. Vibratory sense was also tested quantitatively on the dorsum of the foot with a pallesthesiometer. 2. Good correlation was found between sensory tibial nerve potentials and vibration sense in subclinical as well as in clinical uremic polyneuropathy. A biphasic potential correlated with unaffected vibration sense in 18 out of 23 patients, and impaired vibratory sense with a polyphasic response in 20 of 28 patients. Maximal nerve conduction of sensory fibres was faster (mean 37.4 m/sec) in cases with normal vibratory sense, but slower (mean 31.3 m/sec), when vibratory sense was impaired. Furthermore there was a correlation between the threshold of vibratory perception and sensory nerve conduction. 3. Sensory function, tested with conventional methods, was impaired only 5 times in 28 patients with altered vibratory perception. 4. The earlier impairment, especially of the vibratory sense, may be explained by the following neurophysiological mechanisms: a) Because of the polyphasic prolonged response of the sensory potentials, no rhythmical groups of impulses reach the central nervous system, but only a continual stream of small peaks arrives, so that vibration perception does not develop. b) A multiplication of the frequency of discharges caused by alternating firing of different sensory fibres is impossible due to the reduction of the number of axons. c) The prolongation of the relatively refractory period due to demyelinization of the surviving fibres prevents the transmission of frequent impulses. 5. Alterations of the sensory action potentials of the tibial nerve, as well as of vibratory perception tested quantitatively, are earlier signs of uremic polyneuropathy than the prolonged motor nerve conduction velocity. Since not all patients give accurate information when tests of vibratory sense are performed both methods should be applied. Physiological polyphasia of sensory action potentials and diminishing vibration perception in advanced age must be taken into account.

Action Potentials↗
PubMed1975

[Landry-type motor polyneuropathy and spinal transection syndrome with flaccid paraplegia. Rare neurological syndromes in panarteritis nodosa].

In a 59-year-old man in complete health a pure motor polyneuropathic syndrome with quadruplegia, swallowing and respiratory paralysis developed over a few hours. A few days later he died with the clinical picture of septicaemia. In a 59-year-old woman who had been investigated and treated for a suspected carcinoma for several months a predominantly distal sensomotoric polyneuropathy syndrome developed. The further course of disease was completely misleading as regards the diagnosis due to an acutely occurring transection syndrome with flaccid paraplegia, loss of reflexes, and bladder and rectal paralysis. Due to the very unusual neurological symptoms panarteritis nodosa was only diagnosed at autopsy and by histology in both cases. Panarteritis nodosa must be considered as a differential diagnosis in Landry-type polyneuropathy as well as in an acute spinal transection syndrome. The first patient demonstrates toxic damages, the second vascular damages of the nervous system which in general determine the neurological symptomatology of this vascular disease.

Acute Disease↗
PubMed1975

Infantile polyneuropathy with defective myelination: an autopsy study.

A case is reported of a boy who developed a severe polyneuropathy in early infancy and died of respiratory failure at the age of 18 months. Autopsy revealed almost total lack of myelin sheaths in the cranial, spinal and peripheral nerves. The defect involved the entire peripheral nervous system and was confined to it, central myelination being normal. It is suggested that this case is another example of the condition described by Lyon (1969) and by Kennedy et al. (1971) in which pathological observations were confined to biopsy material. In spite of some similarities between these cases and those of hypertrophic neuropathy reported by Déjerine and Sottas in 1893, they seem to form a distinct sub-group, possibly even a separate entity: infantile polyneuropathy with defective myelination.

Autopsy↗
PubMed1979

Cross-idiotypic antigens among monoclonal immunoglobulin M from patients with Waldenström's macroglobulinemia and polyneuropathy.

The monoclonal immunoglobulin (Ig)M from 5 to 16 patients with Waldenström's macroglobulinemia and a polyneuropathy shared cross-idiotypic antigenic determinants as demonstrated by hemagglutination and hemagglutination inhibition experiments as well as by precipitin reactions. This reactivity was located to the Fab (and not Fc) fragment of the protein. The IgM from 73 patients with macroglobulinemia but without neuropathy all gave negative reactions. In contrast, the monoclonal IgG from a patient with polyneuropathy also possessed similar idiotypic determinants. Since cross-idiotypic determinants are usually related to the combining site of a monoclonal Ig, this finding suggests that the monoclonal Ig of these patients may mediate the nerve injury via their antibody activity, which could be directed either to a nerve antigen or to some component involved in the pathogenesis of the neuropathy.

Animals↗