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

We describe conduction block as an unusual electrophysiologic manifestation in a patient with necrotizing angiopathy. The patient developed subacute symptoms over a 1-month period consisting of progressive pain, tingling, and weakness of the lower extremities. Physical examination revealed a pattern consistent with a polyneuropathy. Electrodiagnostic studies provided evidence of a conduction block in the left ulnar nerve. Pathologic studies confirmed the process to be a necrotizing angiopathy. This report establishes the role of conduction block in human nerve ischemia.
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PMID:Necrotizing angiopathy presenting with multifocal conduction blocks. 162 80

This study investigated the effect of ultrasound on nerve conduction in patients with polyneuropathy. Eight able-bodied controls (Group C) and 16 patients with clinical and physiologic evidence of polyneuropathy were tested. Eight patients (Group NP) had no aching pain symptoms; eight patients (Group P) had severe aching pain, burning sensation, unpleasant tingling, and/or hyperesthesia in the lower extremities. For two minutes, therapeutic ultrasound in doses of 0.5, 1.0, and 1.5W/cm2 were applied over the anterior surface of the leg along the pathway of the deep peroneal nerve. Peroneal nerve conduction studies were performed before, during, and after ultrasound treatment. The compound muscle action potential (CMAP) was recorded from the extensor digitorum brevis muscle. Nerve conduction studies on all eight patients in Group P revealed a significant decrease (41.4% and 44% reduced for doses of 1.0W/cm2 and 1.5W/cm2, respectively; p less than .05) in amplitude of CMAP (from baseline to the first negative peak), and an increase (6.4% and 6.7% increased for doses of 1.0W/cm2 and 1.5W/cm2, respectively; p less than .05) in proximal latency one minute after ultrasound application with a dose of 1.0 or 1.5W/cm2, but not with a dose of 0.5W/cm2 (p greater than 0.1). Changes returned to pretreatment values within five minutes of cessation of ultrasound therapy. In Groups C and NP, there were no significant changes in amplitudes of CMAP or proximal latency before, during, or after ultrasound therapy at a dose of 0.5, 1.0, or 1.5W/cm2. It was concluded that ultrasonic therapy with therapeutic dosage may cause a reversible conduction block on patients with painful polyneuropathy.
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PMID:Reversible nerve conduction block in patients with polyneuropathy after ultrasound thermotherapy at therapeutic dosage. 184 38

Questionnaires, mailed to approximately 30,000 dentists and an equal number of dental assistants requesting information regarding professional exposure to anesthetics and health problems, showed an increased incidence of neurologic complaints in dental professionals who worked with nitrous oxide. The most striking differences were noted in individuals reporting symptoms of numbness, tingling, and/or muscle weakness. For dentists heavily exposed to nitrous oxide, the rate of these complaints was 4-fold greater than for nonanesthetic-exposed dentists. For dental assistants heavily exposed to nitrous oxide, a 3-fold increase in these same complaints was noted. In view of recent evidence that nitrous oxide abuse may lead to polyneuropathy, the results suggest that occupational exposure to nitrous oxide by both dentists and dental assistants may be associated with similar neuropathy.
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PMID:Exposure to nitrous oxide and neurologic disease among dental professionals. 719 94

A patient with chronic inflammatory demyelinating polyneuropathy (CIDP) associated with type B and type C hepatitis virus infection is reported. A 54-year-old female who had a blood transfusion at the age of 31 years was diagnosed as a carrier of hepatitis B virus at the age of 43. Liver dysfunction was first noted in 1987 and gradually grew worse year by year. Beginning in early June 1992, the patients general fatigue became worse, her serum GOT and GPT levels became elevated, and she complained of a tingling sensation in her arms and legs. Neurological examination revealed moderate sensory disturbance of the glove-and-stocking type in all of her extremities. Deep tendon reflexes were all diminished. Hepatitis C antibody was detected in the serum at this time. On June 12, 1993, progression of her sensory disturbance was found to be associated with generalized muscle weakness. Cerebrospinal fluid studies showed increased protein without pleocytosis. Motor nerve conduction studies revealed marked prolongation of terminal latencies, reduction of conduction velocities, and abnormal temporal dispersion of the motor potentials. No sensory potentials could be evoked at any of the sites stimulated. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation. A diagnosis of CIDP was made. Treatment with corticosteroids was started, but there was little improvement in neurological function. The liver dysfunction progressed further and ultimately the patient died of hepatic failure. An autopsy demonstrated liver cirrhosis, but no malignant tumors were evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic inflammatory demyelinating polyneuropathy associated with chronic liver disease due to type B and type C hepatitis virus]. 766 15

To determine the value of a detailed evaluation of neuropathic sensory complaints in assessing diabetic polyneuropathy, a questionnaire listing different sensory symptoms was compared with a clinical and neurophysiological examination of the peripheral nerves. Thirty-seven insulin dependent and thirty-one non-insulin dependent diabetic patients who were consecutively referred because of suspected polyneuropathy were investigated. In all patients both clinical and neurophysiological examination confirmed the diagnosis of polyneuropathy. Only the scores of the clinical examination were significantly correlated with the scores of the sensory symptoms (r = 0.31, P < 0.01). Using a factor analysis, a dimension of complaints of sensory alteration could be distinguished from a dimension of complaints of neuropathic pain (alpha coefficients 0.88 and 0.86, respectively). Tingling sensations turned out to be an expression of the dimension of complaints of sensory alteration. The scores of clinical and neurophysiological examinations were only significantly correlated with the dimension of sensory alteration (r = 0.38, P < 0.002; r = 0.37, P < 0.02, respectively). We conclude that only symptoms of numbness and tingling sensations in hand and feet are associated with objectively assessed diabetic polyneuropathy.
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PMID:Complaints of neuropathy related to the clinical and neurophysiological assessment of nerve function in patients with diabetes mellitus. 787 47

An 82-year-old man was admitted to the hospital in the summer of 1995 due to dyspnea, peripheral edema, and a tingling sensation and muscle weakness in all extremities. Physical examination showed heart failure and polyneuropathy. Laboratory data showed a low concentration of vitamin B1 (10 ng/ml normal 23.8-45.9 ng/ml) and a low level of erythrocyte transketolase activity (0.58 IU/gHb normal 0.75-1.30 IU/gHb). A chest X-ray film revealed cardiomegaly (cardiothoracic ratio 57.1%) and ultrasonic cardiography revealed increased motion of the left ventricle. A diagnosis of beriberi was made. The disease in this case may have been caused by hard work in the summer heat. The patient was treated with thiamine and his symptoms and signs resolved within a few weeks. A search of the literature revealed no previous report of beriberi in a patient of this age, but reports of beriberi in older patients in Japan are more common now than in previous years. Beriberi should be included in the differential diagnosis of polyneuropathy in elderly patients.
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PMID:[An elderly patient with beriberi]. 926 56

A male worker who handled thallium-containing raw material for glass manufacturing over a period of four years complained of alopecia, abdominal pain, diarrhea and tingling in the four extremities. Neurological examination of this patient revealed signs of mild glove-stocking-type polyneuropathy. Lower sensory nerve conduction velocity of the median nerve in the right hand than in the left hand suggested that conduction function in the dominant hand was reduced. The thallium content of the hair, as determined by an ICP-MS method, was 20 ng/g for the patient and 576 ng/g for his successor in the time of 32 months and 13 months, respectively, after they had ceased their glass production work. Those levels of thallium exposure were considered high, compared with the control levels so far reported. The clinical course of signs and symptoms, neurophysiological findings and thallium content of hair suggested that the patient suffered from chronic poisoning due to occupational exposure to thallium-containing dust.
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PMID:A probable case of chronic occupational thallium poisoning in a glass factory. 970 11

A 62-year-old Portuguese man, with no history of familial amyloid polyneuropathy (FAP), and a 2(1/2)-year history of tingling in the toes and sexual dysfunction was found neurophysiologically to have a sensory-motor axonal polyneuropathy. Autonomic tests showed slight sympathetic and marked parasympathetic involvement. Heart, kidney, and eyes were normal. Single strand conformation polymorphism (SSCP) mutation analysis for the transthyretin (TTR) gene was performed. The SSCP pattern suggested the presence of a mutation in exon 2, but was different from the pattern observed for a control representing the most common TTR mutation associated with FAP, i.e., TTR V30M. DNA sequencing analysis revealed an A-to-G transition in the first base of codon 28 normally encoding a valine, giving rise to a methionine residue. The presence of this extra methionine was confirmed by peptide mapping and mass spectrometry analysis. Biopsy of nerve and skin of the propositus showed amyloid deposits that were immunoreactive for TTR. This is a new variant TTR related to late-onset amyloid neuropathy with autonomic dysfunction. This case confirms that TTR mutation screening should be considered in patients with a clinical disorder consistent with amyloid neuropathy even in the absence of a family history.
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PMID:New transthyretin mutation V28M in a Portuguese kindred with amyloid polyneuropathy. 1088 95

The study was conducted to estimate the prevalences of neurological disorders and mucous membrane irritation complaints among workers of shoe workshops in Hebron City, in particular to measure the associations between the occurrence of symptoms indicating polyneuropathy among workers and exposure to organic solvents in the glueing tasks. A group of 103 male workers from 30 workshops, exposed to organic solvents for more than one year were recruited to the study during the years 1996-1997. A validated Swedish neuropsychiatric questionnaire which contained questions on neurological and mucous irritation symptoms was used. Prevalence ratios were used as an indicator for relative risk. The overall prevalence of painful tingling of limbs (used as indicator of polyneuropathy) was high among the workshop workers (40%) and was significantly associated with long term exposure to organic solvents in glueing tasks (PR 2.8: 95% CI 1.0-8.3). Moderate associations were seen in other tasks. Headache and mental irritability did not show any association with organic solvent exposure in the workshop tasks. Breathing difficulty showed a moderate non-significant association with long term exposure to organic solvents (72 months) in cleaning tasks (1.9,0.7-4.8), while sore eyes also showed a moderate non-significant association with exposure to organic solvents for 25-72 months in the glueing tasks. Long term exposure to n-hexane (mainly found in the glues) could be the main cause of polyneuropathy among the workers of Hebron shoe workshops. The absence of effective ventilation systems and personal protective equipment might increase the prevalence of polyneuropathy among these workers. In conclusion, glues containing high concentrations of n-hexane are still in use in many shoe workshops in Hebron City (as well as in other developing countries), and long term exposure to n-hexane in glueing compounds could result in polyneuropathy among the workers. However, in the absence of objective measurements our results must be interpreted with caution. Well planned longitudinal studies with objective measures of exposure and disease are important for future research in developing countries.
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PMID:Prevalence of self-reported health complaints among shoe workers of small workshop exposed to organic solvents in Hebron City, West Bank: a cross-sectional survey. 1096 69

Patients with complaints of numbness, tingling, and dysesthesias in the toes and feet are frequently referred to neurologists. Often, the only objective evidence for peripheral nerve dysfunction in these patients is limited to small-caliber sensory nerve fibers. On examination these patients may have reduced distal pinprick sensation, and distal leg skin biopsies show loss of small-caliber nerve fibers. Studies focusing on small-caliber nerve fibers have led to a growing impression that neuropathy can be associated with early diabetes or impaired glucose tolerance (IGT). Often, neuropathy can be the presenting symptom of either diabetes or IGT. Furthermore, the oral glucose tolerance test appears to be a more sensitive measure of glucose dysmetabolism in these patients than levels of fasting blood glucose or glycated hemoglobin. Patients with IGT-associated neuropathy may represent an attractive target population for future regenerative studies given that their neuropathy is less severe and presumably more easily reversed than neuropathy occurring in patients with diabetes.Historically, small-caliber fibers have not been extensively evaluated due to a lack of objective measures. Several measures to evaluate these fibers are emerging, including skin biopsy with visualization of epidermal nerve fibers. The accessibility of epidermal nerve fibers makes them an attractive target for nerve injury models, which have potential for development as novel outcome measures. Such approaches may address some of the challenges of past diabetic polyneuropathy trials.
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PMID:New insights into diabetic polyneuropathy. 1296 30


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