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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

80 strictly selected patients with chronic renal insufficiency with plasma creatinine values of 1.4-14.5 mg% were examined for clinical and electrophysiological signs of nephrogenic polyneuropathy. The motor symptoms complained of were cramps in 43.8% of the patients, "restless leggs" in 18.7%, muscular twitchings in 12.5%. It was emphasized that the first two symptoms do not always indicate the presence of polyneuropathy. 30% complained of paresthesias, 5% of "burning feet". The most frequent clinical finding was the impairment of vibration sense in the feet in 37.5% followed by diminshed appreciation of passive movement of the toes in 30%, weakening or absence of the ankle jerk in 23.8% and finally, weakening of the patellar reflex in 5%...
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PMID:Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention. II. Peripheral nerve disturbances. 5 92

It has recently been noted that peripheral nerve fibres are involved in the course of chronic liver disease. The existence of hepatic polyneuropathy is still a matter of debate. A series of 29 subjects (not including diabetics or alcoholics) were examined clinically and electromyographically. Signs of distal lower extremity polyneuritis (paresthesia, hypoesthesia and osteotendinous hypo-areflexia) were noted in 31%. Latent neuropathy was observed in the form of slow maximum and minimum motor conduction rates in clinically unimpaired nerves. Electromyographical alterations were more evident in subjects with frankly chronic as opposed to barely chronic liver disease.
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PMID:[Value of electromyography for the detection of peripheral neuropathies in the course of chronic hepatopathies]. 20 93

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.
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PMID:[The diabetic polyneuropathy. II. Polyneuropathy, angiopathy and nerve conduction velocity]. 53 79

Five cases of a chronic neuromuscular syndrome consisted of muscular aching and sometimes burning pain, fasciculations, cramps, fatigue, and occasional paresthesia. The disorder affected the legs and, less commonly, the girdle, trunk, and arm muscles. The symptoms were enhanced by physical activity and were usually improved by rest. Neither muscular wasting nor weakness was found, although the condition was present for an average of 4.7 years and, in one patient, as long as 10 years. Electrophysiologic studies showed motor abnormalities indicative of axonal degeneration and muscle fiber denervation, most marked in the legs. Light microscopy of skeletal muscle and spinal cord in one case disclosed evidence of mild denervation atrophy in muscle, but no loss of anterior horn cells. The findings are compatible with a benign polyneuropathy.
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PMID:The muscular pain-fasciculation syndrome. 56 28

Two cases of lead arsenate polyneuropathy are described in two farmers from the same rural area; the etiology of the neurologic al disorder was ascertained only after repeated hospital admissions. It was a neuropathy of the radial nerve associated with signs of peripheral impairment of the lower limbs with pains and paresthesias. Abdominal colies, arterial hipertension, anaemia and signs of renal impairment were also present. Specific therapy was undertaken which was soon followed by nearly full recovery. Lead and arsenic toxicology are discussed with particular focusing on the necessity emphasis on commun occupational hazards both in terms of diagnostic and therapeutic procedures. The differential diagnosis is considered between the observed clinical picture and other polyneuropathies of different etiology i.e. dysmetabolic (porphyria) or toxic (insecticides, T.O.C.P., etc).
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PMID:[Lead arsenate as an underestimated cause of polyneuropathy in rural environment: description of two cases]. 102 47

An 85-year-old man with a 2-year history of progressive lower limb weakness and paresthesia was found to have an IgG kappa monoclonal gammopathy of undetermined significance (mgus). Clinical and electrophysiological studies revealed a severe distal bilateral symmetrical polyneuropathy. A sural nerve biopsy showed extensive nerve fibre loss with the deposition of large amounts of amorphous material throughout the endoneurium. Electron microscopy showed the deposits to be composed of microtubular structures which were located diffusely throughout the endoneurium. The deposits were also located within the lumina of the vasa nervorum, some of which were undergoing disintegration and rupture with release of the proteinaceous material into the endoneurium. The regions of the nerve in which they appeared most numerous showed more severe nerve fibre damage than other areas. These microtubular structures were also observed in disintegrating vessels and adjacent endoneurium. On immunohistochemistry they stained with antibody to IgG. Identical deposits were found in the dermis in which there was a leucocytoclastic vasculitis. Located in linear arrays within the axons of myelinated and unmyelinated fibres were highly organised tubular structures resembling immunotactoids. Identification of immunotactoid-like structures within the nerve is unique and may be another mechanism by which monoclonal proteins can induce nerve fibre injury.
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PMID:Immunotactoid-like endoneurial deposits in a patient with monoclonal gammopathy of undetermined significance and neuropathy. 821 78

According to the authors' observations, the symptoms of nervous system derangement associated with legionnaires' disease rather often enter the disease structure and can virtually be characterized as a manifestation of infectious and toxic encephalopathy and polyneuropathy (encephalopolyneuropathy). In the majority of cases, the neurological disorders develop acutely or subacutely after or simultaneously with respiratory lesions. The clinical picture of encephalopathy is marked by permanent headache, mental abnormalities, memory disturbances, insomnia, pronounced astheno-vegetative and vascular manifestations. In patients with legionellosis, polyneuropathy is manifested by paresthesias, less frequently by pains in the distal parts of the limbs and myasthenia without visible atrophies. Vegetative disorders such as vegetative polyneuropathy of the hands and legs, visceral polyneuropathies are typical symptoms of the disease whatever its gravity. Vegetovascular dystonia together with long-term AP instability is an obligate sign of the disease. Electrophysiological examinations (EEG, REG, EMG) support the clinical findings and may serve the basis for an objective evaluation of the gravity of the neurological disorders. The degree of pulmonary lesions and the intensity of vegetative disorders eventually determine the torpidity and characteristics of the disease course.
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PMID:[Nervous system involvement in legionellosis (legionnaires' disease)]. 164 36

Sensory ataxia as the chief manifestation of acute neuropathy is rather rare. Of the 224 cases of acute polyneuropathy seen over 6 years (1984-1990) only 10 patients (M:F 3:7) had disabling ataxia as the presenting feature. Their ages ranged from 14-61 years. Antecedent febrile illness was present in 6 patients and the peak deficit evolved over 2-25 days. Severe ataxia, paresthesia, distal areflexia and predominant joint sense loss were common to all, motor weakness was either absent or insignificant. CSF was acellular and revealed elevated protein in 3 subjects. All patients had electrophysiological evidence of severe sensory neuropathy with mild or no motor neuropathy. Sural nerve biopsy in one patient showed loss of large, as well as small, diameter myelinated fibres, secondary demyelination, but no evidence of inflammation. At follow up marginal to moderate improvement in ataxia was noted in only 5 patients. Absence of ophthalmoplegia and motor weakness, poor prognosis and characteristic electrophysiological and histopathological observations suggest that acute ataxic neuropathy may be a distinct entity.
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PMID:Acute ataxic neuropathy: a clinical, electrophysiological and morphological study. 166 83

The influence of successful simultaneous pancreas and kidney transplantation on peripheral polyneuropathy was investigated in 53 patients for a mean observation period of 40.3 months. Seventeen patients were followed-up for more than 3 years. Symptoms and signs were assessed every 6 months using a standard questionnaire, neurological examination and measurement of sensory and motor nerve conduction velocities. While symptoms of polyneuropathy improved (pain, paraesthesia, cramps, restless-legs) and nerve conduction velocity increased, there was no change of clinical signs (sensation, muscle-force, tendon-reflexes). Following kidney-graft-rejection there was a slight decrease of nerve conduction velocity during the first year, which was not statistically significant. Following pancreas-graft rejection there was no change of nerve conduction velocity during the first year. Comparing the maximum nerve conduction velocity of the patients with pancreas-graft-rejection to the nerve conduction velocities of these patients at the end of the study, there was a statistically significant decrease of 6.5 m/s. In conclusion, we believe that strict normalization of glucose metabolism alters the progressive course of diabetic polyneuropathy. It may be stabilized or partly reversed after successful grafting even in long-term diabetic patients.
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PMID:Follow-up study of sensory-motor polyneuropathy in type 1 (insulin-dependent) diabetic subjects after simultaneous pancreas and kidney transplantation and after graft rejection. 193 73

Detailed electrophysiological studies were performed in 4 patients with myeloneuropathy induced by abuse of nitrous oxide for 1 to 4 years. All presented with paresthesias, weakness, and Lhermitte's phenomena, and exhibited signs of sensorimotor polyneuropathy, ataxia, and arreflexia. Two had subnormal serum vitamin B12 levels. Baseline electrophysiologic testing revealed reduced motor unit potentials, prolonged F wave latencies, absent H reflexes, denervation potentials, and delays in motor and sensory conduction. Three had peripheral and nuchal delay after median nerve stimulation. All were reevaluated after 3 to 12 months' abstinence and treatment with vitamin B12, and all showed substantial clinical improvement. Parallel improvement in electrophysiologic findings occurred, but residual minor conduction delays, loss of H reflexes, electromyographic evidence of denervation, or abnormalities of posterior tibial SEP were noted. These findings confirm the reversibility of myeloneuropathy of nitrous oxide abuse and describe the profile of electrophysiologic recovery in subjects who abstain from further neurotoxic exposure.
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PMID:Reversible myeloneuropathy of nitrous oxide abuse: serial electrophysiological studies. 199 94


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