Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with active rheumatoid disease may develop encephalopathy, myelopathy, peripheral neuropathy, and myopathy through a variety of tissue mechanisms. Brain involvement is usually characterized by the formation of rheumatoid nodules or by the development of vasculitis or its complications, and there is evidence to suggest that the trapping of immune complexes within the choroid plexus may be important in pathogenesis. Structural damage to the spinal cord and lower brain stem, on the other hand, most commonly results from narrowing of the bony canal, leading either to direct compression of neural tissue or to compromise of its vascular supply. The appearance of peripheral neuropathy generally signifies the presence either of inflammatory epineurial arterial disease or entrapment by neighboring anatomical structures. Skeletal muscle dysfunction may be due to vasculitis, myositis, or denervation atrophy. Both systemic and local anatomical factors, therefore, are of importance in determining the manner in which different parts of the nervous system may be affected in rheumatoid disease.
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PMID:The neuropathology of rheumatoid disease. 625 49

103 consecutive childhood cases of genetic peripheral neuropathies of heredodegenerative background were collected from Gothenburg from 1973 to 1980. From this series, 63 hereditary motor and sensory neuropathies (HMSN) were distinguished: 31 cases of demyelinating and remyelinating HMSN (HMSN I), 21 (18 families) with an autosomal dominant and 10 with sporadic mode of inheritance and unaffected parents; and 32 cases of neuronal-axonal types (HMSN II), 27 of whom (25 families) had at least one affected, if asymptomatic, parent. In one family, both parents were neurologically and neurophysiologically completely normal. Three cases of uncharacteristic HSN were diagnosed. Among 37 cases with a combined degenerative encephalopathy/myelopathy and a peripheral neuropathy, nine had hereditary spastic paraplegia, six had heredoataxias (three of the Friedreich type), nine had lysosomal storage diseases (five of the Krabbe type), seven had other known inborn metabolic errors and six had biochemically undefined disorders. Progressive neuropathies are important manifestations of a large variety of genetically determined heredodegenerative neurological disorders of infancy and childhood. For classification of HMSN, clinical and neurophysiological examinations are necessary for the index case and for both parents as well.
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PMID:The nosology of genetic peripheral neuropathies in Swedish children. 629 69

In 9 patients undergoing chronic hemodialysis for 2-10 years and suffering from encephalopathy (dialysis dementia) and peripheral neuropathy, 10 mg of biotin was given daily in three doses for 1-4 years. Within 3 months there was a marked improvement in all patients in respect to disorientation, speech disorders, memory failure, myoclonic jerks, flapping tremor, restless legs, paresthesia and difficulties in walking. It is recommended to start giving biotin regularly in any patient with advanced renal failure before severe neural or muscular lesions become manifest. The correlation of biotin with uremic neurologic disorders and the possible mechanism of its therapeutic action are discussed.
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PMID:Biotin in the management of uremic neurologic disorders. 632 32

Ninety-eight workers, 65 exposed to organic solvents and 33 unexposed, were examined in order to assess possible neurotoxic signs and symptoms related to solvent exposure. The study group, who were selected according to the type of exposure in a given work process, had been exposed to various types of solvents. The groups were comparable in regard to age, the history of brain traumas and other neurological diseases, and alcohol consumption. The exposed workers had more symptoms of intellectual impairment, poorer performances in psychological tests, and more often signs of cerebral asthenopia. Symptoms and signs of peripheral neuropathy were not significantly increased. Solvent exposure and neurotoxic signs and symptoms were mildly correlated in the study group. Such dose-effect correlations have previously been proved only in a few epidemiological studies. This warrants reevaluation of the risk of developing toxic encephalopathy during prolonged occupational exposure to solvents.
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PMID:Neurotoxic effects of organic solvents in exposed workers: an occupational, neuropsychological, and neurological investigation. 632 81

We describe a case with neurologic disease manifested as encephalopathy, generalized muscle fasciculations, and peripheral neuropathy occurring in a patient treated with therapeutic doses of gold for presumed rheumatoid arthritis. The illness remitted promptly during chelation therapy with dimercaprol (BAL). A review of the limited experience in the literature with the central nervous system toxicity of gold is given.
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PMID:Gold induced encephalopathy: case report. 632 82

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Increasingly vigorous chemotherapy of cancer including primary and metastatic central nervous system disease has resulted in prolonged good-quality survival. However, there has been an associated increase in neurotoxicity from both radiation therapy and chemotherapy. All classes of chemotherapeutic agents contain drugs that are potentially neurotoxic, often only at high doses. Mechlorethamine, the first nitrogen mustard, is not neurotoxic at conventional dosage, but at high doses, it may produce both an acute and a delayed encephalopathy. Methotrexate administered intrathecally often induces reversible aseptic meningitis, but chronic administration, either intrathecally or high-dose intravenously, may produce fatal leukoencephalopathy. 5-Fluorouracil at high dosage may cause cerebellar ataxia, but may also do so at low dosage when combined with thymidine infusions. Cytosine arabinoside at high dosage may also produce cerebellar ataxia. Vincristine produces a peripheral neuropathy, and less commonly causes both autonomic and cranial neuropathy. The enzyme L-asparaginase can produce a dose-related reversible encephalopathy. BCNU, now the mainstay of glioma chemotherapy, may combine with radiation to produce long-term cerebral atrophy. Both intracarotid and high-dose intravenous BCNU administration may cause encephalopathy. Several other chemotherapeutic agents have also been reported to cause neurotoxicity under certain circumstances.
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PMID:Neurological complications of antineoplastic therapy. 638 4

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
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PMID:Frequent neurologic toxicity associated with amiodarone therapy. 653 58

Idiopathic hemochromatosis (IHC) is a genetically determined impairment in control of iron absorption that results in excessive parenchymal iron deposition, particularly in the liver. Of patients with IHC, 50% have little or no chemical evidence of liver dysfunction. Cirrhosis may be clinically occult, but still cause a syndrome of chronic hepatocerebral degeneration. Two patients are reported with IHC and a syndrome of ataxia, rigidity, myoclonic jerks, and dementia. Other associated symptoms may include diminished libido, decreased hearing, peripheral neuropathy, and large joint disease. Because symptoms of IHC can be reversed by phlebotomy, appropriate laboratory studies should be considered to exclude IHC in any patient with unexplained dementia, encephalopathy, and gait ataxia.
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PMID:Idiopathic hemochromatosis (IHC): dementia and ataxia as presenting signs. 668 41

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30


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