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PubMedDate not supplied

[Evaluation of the evoked potentials in various acquired polyneuropathies (Guillain-Barré syndrome and chronic recurrent polyneuropathy). Preliminary report].

In 15 patients with acquired polyneuropathy (Guillain-Barré syndrome and chronic recurrent polyneuropathy) the conduction velocity was measured in the peripheral nerves of the upper and lower extremities, the latency of the F wave was determined, and the somatosensory evoked potentials were assessed stimulating the median enerve and posterior tibial nerve. The abnormalities were assessed in the parameters of the obtained somatosensory evoked potentials comparing them with the changes of F wave and the velocity of conduction in peripheral nerves. The sensitivity and usefulness of these methods in acquired polyneuropathies are discussed.

Adolescent↗
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↗
PubMed1989

[Multifocal polyneuropathy with persistent conduction blockage. A new subset of chronic inflammatory polyneuropathies].

Recently a subset of chronic demyelinating inflammatory polyneuropathies with asymmetrical involvement limited to upper limbs, at least at the onset, resembling a multifocal mononeuropathy has been described. Electrodiagnostic testing disclosed multifocal CB outside the common entrapment sites has been described. We report a 55 years old man with a 4 years history of paresis, numbness, fasciculations, myokymia, cramps and mild amyotrophy. Electrophysiological evaluation showed proximal multifocal conduction block and abundant spontaneous activity as fasciculations, myokymia and scarce denervation activity. The importance of taking into account this entity in the differential diagnosis of patients with suspected mononeuritis multiplex or motoneuron disease is emphasized. The nosologic place of this entity is also discussed.

Arm↗
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↗
PubMed1990

[Factors affecting the incidence and severity of polyneuropathy in type I diabetes mellitus].

194 type I diabetics were subjected to neurological and electromyographic examinations. In 161 patients, i.e. in 83%, signs of polyneuropathy were detected, the severity of which was evaluated according to a 5-grade scale where grade 1 was the mildest and the 5th grade the most severe one. The authors proved a statistically significant correlation of the incidence and severity of polyneuropathy and the duration of diabetes. It was found that the decisive period of persistence of diabetes was 6-10 years. During this period the incidence of polyneuropathies increased from 30 to 87%. After 20 years duration of diabetes there was not only a 100% incidence of polyneuropathy, but severe affections--grade 3-5--predominated in 78%. In patients with severe grades of polyneuropathy diabetes was manifested at a significantly lower age than in patients without polyneuropathy and with a milder affection. The authors did not detect a significant relationship between the height of the patients and the incidence of polyneuropathy nor significant differences between men and women.

Adult↗
PubMed1990

[Relation of diabetic polyneuropathy to vascular and organ complications in type I diabetes mellitus].

The authors investigated in 194 type I diabetics the incidence and severity of diabetic polyneuropathy in relation to other organ and vascular complications, incl. autonomous neuropathy. It was revealed that the increasing severity of polyneuropathy was significantly v séru (Cr equal to or less than 130-200 mumol/l); 4--Cr greater than 200 mumol/l; associated with severe stages of nephropathy and proliferative retinopathy with amaurosis. The concurrent presence of hypertension and polyneuropathy was surprising and striking--even in patients with the mildest grade 1 polyneuropathy hypertension was present in 10% and the incidence increased significantly with the increasing severity of polyneuropathy. Ischaemic heart disease and ischaemia of the lower extremities was significantly more frequent only in patients with grade 5 polyneuropathy. In patients with grade 4 and 5 neuropathy there was a 100% incidence of autonomous neuropathy in the cardiovascular sphere. The authors did not reveal significant differences between men and women as regards the relationship between the incidence of polyneuropathy and organ and vascular complications.

Autonomic Nervous System Diseases↗
PubMed1986

[Sensorimotor and autonomous polyneuropathies in diabetic children and adolescents].

In 28 juvenile and adolescent diabetics (14 males, 14 females) ranging in age between 9 and 20 years (mean: 14.9) we investigated several electrophysiological parameters, the vibration threshold and the cardiovascular reflexes in order to determine the incidence of sensomotor and autonomic polyneuropathy. 6 patients showed evidence of sensomotor polyneuropathy, 2 more had signs of autonomic polyneuropathy. Both groups with polyneuropathy did not differ significantly from the whole group of diabetics concerning the mean onset of illness and several metabolic parameters. The mean duration of illness and the average age was clearly higher in the patients with sensomotor polyneuropathy than in the whole group. Out of 5 patients with diabetic retinopathy 3 had signs of sensomotor polyneuropathy. No patient was clinically affected by polyneuropathy. In 1 patient the distal latency and the amplitude of the compound muscle action potential of the peroneal nerve showed pathologic values, in a second patient the maximal conduction velocity of the median nerve was slowed. 4 patients had abnormally high vibration threshold. The heart rate variation during rest was reduced in 2 patients. Significant differences between the diabetics and the controls could only be found concerning the maximum conduction velocities of the peroneal and the median nerve. Our results will be compared and discussed.

Adolescent↗
PubMed1992

The relative diagnostic sensitivity of different F-wave parameters in various polyneuropathies.

We studied F-wave minimum latency, persistence, and chronodispersion in the median and ulnar nerves of 70 controls and 75 patients with various polyneuropathies. Prolonged minimum latency was the most frequent F-wave abnormality in all groups of patients with polyneuropathy. The finding of decreased persistence or absence of F-responses was comparable in sensitivity to prolonged minimum latency in Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), whereas chronodispersion had a comparable sensitivity only in CIDP. Decreased persistence of obtained F-responses, and the absence of F-responses in nerves with low compound muscle action potential amplitudes, were nonspecific findings. F-wave studies often provide useful additional information in the evaluation of patients suspected of having a polyneuropathy. In patients with axonal polyneuropathies, we found that F-wave studies are significantly more sensitive than standard motor conduction studies in identifying physiological abnormalities of motor axons. Furthermore, in a patient with an acquired polyneuropathy, the finding of markedly prolonged minimum latency, or the absence of F-responses in nerves with normal CMAP amplitude, is highly specific for the presence of demyelination.

Adult↗
PubMed1992

Plasma-cell dyscrasia with polyneuropathy. The spectrum of POEMS syndrome.

BACKGROUND: The POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) syndrome and osteosclerotic myeloma (polyneuropathy and sclerotic bone lesions) may both be manifestations of plasma-cell dyscrasia, but the interrelation of these diseases is not clear. We therefore set out to define the clinical spectrum of disease in patients with plasma-cell dyscrasia and polyneuropathy who have the complete or incomplete form of the POEMS syndrome or osteosclerotic myeloma. METHODS: Among 2714 patients with plasma-cell dyscrasia who were identified between 1973 and 1989, we reviewed the cases of those with polyneuropathy and plasma-cell dyscrasia who fulfilled the criteria for the POEMS syndrome or osteosclerotic myeloma. RESULTS: Thirty-eight patients (1.4 percent) with a median age of 51 years were identified, 22 of whom were male. By definition, all had polyneuropathy (37 combined sensorimotor, and 1 primarily motor). Other findings included osteosclerotic bone lesions (82 percent), skin abnormalities (58 percent), lymphadenopathy (42 percent), papilledema (37 percent), peripheral edema (29 percent), hepatomegaly (24 percent), splenomegaly (21 percent), and ascites (11 percent). Thirty-three patients (87 percent) had an abnormal M protein in serum or urine (17 had IgA lambda, and 12 IgG lambda). Five patients fulfilled all the criteria for the POEMS syndrome. The estimated five-year survival in the 38 patients was 60 percent, which was significantly better than the 20 percent survival in 869 patients with multiple myeloma (P < 0.05). The clinical course was similar among the patients with the complete form of the POEMS syndrome and those with the incomplete form. CONCLUSIONS: Plasma-cell dyscrasia with polyneuropathy is a rare multisystem disease that often presents with osteosclerotic bone lesions. The differentiation of the POEMS syndrome from so-called osteosclerotic myeloma with peripheral neuropathy appears to have no clinical value.

Adult↗
PubMed1992

Clinical examination versus neurophysiological examination in the diagnosis of diabetic polyneuropathy.

Several methods have been used to diagnose diabetic polyneuropathy and to quantitate the degree of affection of peripheral nerves. Using a newly developed scoring system we compared bedside clinical examination with neurophysiological examination in a group of 78 diabetic patients. Individual scores for clinical examination were significantly correlated with scores for neurophysiological examination (r = 0.7, p < 0.0005). All 78 patients had at least one clinical symptom or sign of polyneuropathy. Clinical examination indicated polyneuropathy in three patients with neuropathic complaints, while neurophysiological examination in these patients showed no abnormalities. In 12 out of 14 patients with normal neurophysiological sensory nerve function, clinical examination showed at least one abnormal sensory modality. Comparing the four different sensory modalities, light touch sense and pinprick sense indicated polyneuropathy better than vibration or position senses. An abnormal Hoffmann reflex of the soleus muscle was always associated with a decreased or absent ankle jerk. The scoring system for the clinical examination proved useful for diagnosing and quantitating the severity of diabetic polyneuropathy. Clinical sensory deficits could not be inferred from the results of neurophysiological testing of sensory nerve function. Pinprick sense, light touch sense, and ankle jerks were the most important parameters in the clinical diagnosis of diabetic polyneuropathy.

Diabetic Neuropathies↗
PubMed1987

Neurotoxic effects of n-hexane on the human central nervous system: evoked potential abnormalities in n-hexane polyneuropathy.

An outbreak of n-hexane polyneuropathy as a result of industrial exposure occurred in printing factories in Taipei area from December 1983 to February 1985. Multimodality evoked potentials study was performed on 22 of the polyneuropathy cases, five of the subclinical cases, and seven of the unaffected workers. The absolute and interpeak latencies of patterned visual evoked potential (pVEP) in both the polyneuropathy and subclinical groups were longer than in the normal controls. The pVEP interpeak amplitude was also decreased in the polyneuropathy cases. Brainstem auditory evoked potentials (BAEP), showed no difference of wave I latency between factory workers and normal controls, but prolongation of the wave I-V interpeak latencies was noted, corresponding with the severity of the polyneuropathy. In somatosensory evoked potentials (SEPs), both the absolute latencies and central conduction time (CCT) were longer in subclinical and polyneuropathy cases than in the unaffected workers and normal controls. From this evoked potentials study, chronic toxic effects of n-hexane on the central nervous system were shown.

Adolescent↗
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↗
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↗
PubMed1976

[Motor nerve conduction velocity in uraemic polyneuropathy: correlation with metabolic factors (author's transl)].

The following parameters have been examined in twenty-one patients suffering from chronic renal failure (creatinine level between 4.5 and 18.8 mg/100 ml serum): maximum motor nerve conduction of the peroneal nerve, amplitude of the compound muscle action potential of the extensor digitorum brevis muscle, serum creatiine, total protein, serum globulins, serum albumins, alkali reserve, time of increase of serum creatinine above 4 mg/100 ml up to time of determination of the maximum motor nerve conduction, daily urinary excretion, mean blood pressure, (p less than 0.01) was found between maximum motor nerve conduction, as well as amplitude of the compound muscle action potential, and the serum albumin level only. Decreased levels of serum albumin, is correlated with diminished nerve conduction and a lower amplitude. The relationship between the electrophysiological data and serum albumin levels maybe explained on the basis of progression of a pre-existing polyneuropathy due to additional dietary malnutrition. A different interpretation is the assumption of an inactivation of neurotoxin on binding by albumins. A decrease in the albumin level would, therefore, result in an increased amount of unbound toxic agent. The values of the maximum motor nerve conduction were between 16 m/sec and 51 m/sec (mean value 42.2 m/sec), pointing to a polyneuropathy of primary axonal type rather that to primary demyelinization. The amplitudes of the compound muscle action potentials were not greatly reduced and thus the uraemic polyneuropathy seems to be of mixed type. In uraemic polyneuropathy different aetiological factors have to assumed. According to the prevalent factor a polyneuropathy of predominantly axonal or predominantly demyelinizing type may result.

Action Potentials↗
PubMed1992

[Polyneuropathies associated with lymphoplasmacytic dyscrasias: the clinical and instrumental characteristics of a 38-patient case load].

A varying percentage from 40 to 60% of patients having lymphoplasmacytic dyscrasias with a monoclonal component shows a clinical or subclinical polyneuropathy. From a different viewpoint, a monoclonal gammopathy has been detected in 10% of patients effected by chronic idiopathic polyneuropathy. A case study of 38 patients with lymphoplasmacytic dyscrasia subjected to clinical, immunohematological and electrophysiological examination revealed a high prevalence of polyneuropathy (84%), mainly axonal (72%) and often subclinical. The neuropathy was evenly distributed between patients having malignant and benign lymphoplasmacytic dyscrasias. No statistically significant correlation was found between the presence of neuropathy and the main clinical and immunohematological data. This supports the concept that the pathogenesis of polyneuropathy associated with lymphoplasmacytic dyscrasias may be multifactorial. Nor can it be ruled out that the paraprotein may in fact be secondary to the polyneuropathy or sometimes a simple coincidence.

Adult↗
PubMed1991

Chlorpyrifos-induced delayed polyneuropathy.

Chlorpyrifos [0,0-diethyl 0-(3,5,6-trichloro-pyridyl) phosphorothioate] caused delayed polyneuropathy in man. Contrary to previous studies, we report here that it also causes delayed polyneuropathy in the hen, the animal model for this toxicity. The minimal neuropathic dose was 60-90 mg/kg p.o., corresponding to 4-6 times the estimated LD50. Consequently, pralidoxime (2-PAM) in conjunction with atropine was necessary to reverse acetylcholinesterase (AChE) inhibition and cholinergic toxicity in hens given high enough doses of chlorpyrifos to cause neuropathy. Chlorpyrifos was slowly absorbed after single oral doses and the threshold of inhibition (greater than 70%) of neuropathy target esterase (NTE), the putative target for delayed neuropathy, was reached within 5-6 days. High AChE inhibition (greater than 90%), however, was measured within hours after dosing because of the higher potency of chlorpyrifos to inhibit this enzyme. In vitro studies showed that chlorpyrifos-oxon, the active metabolite of chlorpyrifos, was 10-20 times more active against AChE than against NTE, confirming the clinical observation. No differences were seen between human and hen enzymes in this respect. Hen and human brain homogenates contain A-esterases which hydrolysed chlorpyrifos to about the same extent in both species. In conclusion, chlorpyrifos causes delayed polyneuropathy in the hen, as was reported in man. The reasons for previous negative data in the hen are probably due to the relatively lower doses which were used. Judging from in vitro studies with hen and human enzymes, there are no differences in the two species as far as their relative sensitivity to delayed polyneuropathy. It is likely that delayed polyneuropathy would develop in both species only after severe cholinergic toxicity requiring aggressive antidotal treatment.

Animals↗