Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of perhexiline (Pexide) to rats causes generalized occurrence of lamellated and crystalloid cytoplasmic inclusions which resemble those described in patients with perhexiline-induced polyneuropathy. It is concluded that perhexiline being an amphiphilic cationic compound is a potent inducer of generalized lipidosis.
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PMID:Perhexiline induces generalized lipidosis in rats. 20 4

A generalized toxic polyneuropathy was identified in a 23-year-old woman after excessive intentional inhalation of compressed N2O delivery from cartridges through a whipped-cream dispenser. The chronology of the patient's N2O abuse correlated clearly with two episodes of recurrent polyneuropathy. The toxic effects were limited to the nervous system, primarily involving the peripheral nerves, although some signs suggested a possible effect on the cerebellum or its connections. The findings on sural nerve biopsy were nonspecific, characterized principally by axonal degeneration. Gas chromatographic analysis of the N2O cartridges dispensed through the whipped-cream canister revealed an exposure to N2O and 26 other compounds. Three of these, trichloroethylene, toluene, and phenol, are known neurotoxins.
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PMID:Polyneuropathy from inhalation of N2O cartridges through a whipped-cream dispenser. 20 15

After the long-term exposure to cadmium chloride in drinking water, the Wistar rats developed peripheral polyneuropathy. The main lesion was of myelin degeneration. Ultrastructural examination of the roots and sciatic nerves revealed segmental demyelination beginning from the node of Ranvier. There was the active autophagocytosis of Schwann cells which contained a number of myelin remnants and dense bodies. There was, on the other hand, the evidence of remyelination with toxic damage, in which the thinner myelin sheaths and abnormal myelinations were observed with increase of Schwann cells containing rich ribosomes. Axoplasmic changes were minimal, but consisted of accumulation of glycogen particles which very often produced glycogenosomes in characteristic appearance with axoplasmal dysfunction.
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PMID:An ultrastructural study of chronic cadmium chloride-induced neuropathy. 20 91

An electroneurographic study performed on the peripheral nerves of 25 patients with severe cirrhosis following viral hepatitis showed slight slowing (P greater than 0.05) of motor conduction velocity (CV) and significant diminution (P less than 0.001) of sensory CV and mixed sensorimotor-evoked potentials, associated with a significant decrease in the amplitude of sensory evoked potentials. The slowing was about equal in the distal (digital) and in the proximal segments of the same nerve. A mixed axonal degeneration and segmental demyelination is presumed to explain these findings. The CV measurements proved helpful for an early diagnosis of hepatic polyneuropathy showing subjective symptoms in the subclinical stage.
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PMID:Electroneurographic evidence of polyneuropathy in chronic liver disease. 20 28

Five patients developed a mild to severe polyneuropathy while under treatment with perhexiline maleate, a drug used in long-term treatment of angina pectoris. Recovery took place within a few months after drug withdrawal. We performed qualitative and quantitative light and electron microscopical studies, including teased fiber preparations, in different patients; 16 to 90% of the fibers showed segmental demyelination, an unusual feature in drug-induced neuropathies, and 3 to 20% were undergoing wallerian degeneration. Severe loss of myelinated axons was noted in all 5 patients. In these patients clinical symptoms occurred only when a great number of fibers had already been lost and most of the surviving fibers showed demyelination.
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PMID:Perhexiline neuropathy: a clinicopathological study. 20 53

A diagnosis of adult-onset metachromatic leukodystrophy (MLD) was established in a living 63-year-old man with progressive dementia and peripheral neuropathy. Decreased nerve conduction velocities and elevated spinal fluid protein concentration led to more specific diagnostic studies required to confirm the diagnosis. This case expands the spectrum of adult-onset MLD to patients with dementia and polyneuropathy past the sixth decade of life. Measurement of nerve conduction velocities may help to uncover cases of adult-onset MLD and should be included in the evaluation of dementia.
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PMID:Late adult-onset metachromatic leukodystrophy. Dementia and polyneuropathy in a 63-year-old man. 20 95

Since April 1976 we have performed clinical investigations with multiple doses of the hypoxic cell radiosensitizer misonidazole in 21 patients. A significant side effect of the drug was the development of peripheral sensory neuropathies in 13 patients (8 mild, 5 severe) and of a transient acute organic psychosyndrome in 2 of the 5 patients with a severe polyneuropathy. The severity of the polyneuropathies is related to the total dose of misonidazole and the overall time of drug administration. Treatment schedules designed to obtain the desired sensitizing effect without neurological side effects are under investigation.
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PMID:Further clinical experiences of a phase I study with the hypoxic cell radiosensitizer misonidazole. 20 10

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.
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PMID:Polyneuropathy and folate deficiency. 21 Jul 47

Pharmacological studies of the pupils of 7 patients with familial amyloid polyneuropathy (FAP) were performed in order to demonstrate the site of the lesion. Supersensitivity to 1.25% epinephrine was observed frequently, but not to 2.5% methacholine. The lesions of the sympathetic nervous system, judging from the epinephrine and tyramine tests, were regarded as preganglionic in 2 patients and postganglionic in 4. Among 3 patients reexamined six months later, 1 had developed signs of sympathetic postganglionic disturbance and another showed a peripheral parasympathetic disturbance associated with progress of a sympathetic preganglionic disturbance. From these results it was suggested that in FAP, sympathetic abnormalities involve the pupils more often than parasympathetic disturbances, and pharmacological studies can detect the autonomic dysfunction before it becomes clinically apparent.
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PMID:Pharmacological studies of the pupils in familial amyloid polyneuropathy. 21 32

A 35-year-old man developed a distal sensorimotor polyneuropathy after taking disulfiram, 500 mg daily for five months. His symptoms improved after the drug therapy was discontinued. Clinical, electrophysiological, and pathological observations during the acute stage and during recovery suggest that disulfiram produces a distal axonopathy.
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PMID:Disulfiram neuropathy. 21 96


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