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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central nervous system (CNS) involvement is very frequently observed in pediatric AIDS. Clinical manifestations include encephalopathy, cognitive deficits, acquired microcephaly, neurological signs, myelopathy, and peripheral neuropathy. Neurological complications can be related to opportunistic viral infections such as encephalitis, atypical aseptic meningitis, progressive multifocal leukoencephalopathy, and myelitis. Nonviral syndromes include: toxoplasmosis, cryptococcal meningitis, candidiasis, Mycobacterium tuberculosis meningitis, and Mycobacterium avium subacute encephalitis. Bacterial infections, tumors, cerebrovascular complications, and peripheral neuropathies are not frequently observed in pediatric AIDS. The most severe complications of HIV infection is encephalopathy resulting from HIV infection of brain tissue. Direct HIV invasion of the CNS has been demonstrated. Clinical features of HIV encephalopathy are classified into three categories: (1) normal neurological findings; (2) static encephalopathy; and (3) progressive encephalopathy. AIDS dementia complex can be differentiated from the predominance of behavioral and cognitive disabilities.
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PMID:Acquired immune deficiency syndrome in childhood. Neurological aspects. 268 79

Objective measures of neurologic function were used to assess response to treatment in patients with late Lyme borreliosis. Neurophysiologic evidence of peripheral neuropathy was present in 64 of 137 patients tested. Measures of distal axon function (sensory amplitude and conduction velocity, motor terminal latency) were most affected. Repeat studies following 60 patients receiving antimicrobial therapy demonstrated significant improvement in these values. Before and after therapy 17 patients with late Lyme borreliosis and prominent subjective cognitive dysfunction underwent neuropsychologic tests of memory, conceptual ability, concentration, psychomotor function, overlearned intellectual abilities, and mood. Significant abnormalities were evident before treatment; all reversed with antimicrobial therapy. Many patients with this encephalopathy had specific abnormalities revealed by magnetic resonance imaging of the brain and had evidence of intrathecal synthesis of antibody to Borrelia. These findings indicate that late Lyme borreliosis commonly causes nervous system abnormalities that are reversible with appropriate antibiotic therapy.
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PMID:Abnormalities of the nervous system in Lyme disease: response to antimicrobial therapy. 268 62

Infection with the AIDS virus itself (HIV, HTLV-III, LAV, ARV) is associated with a full spectrum of neurological disorders. The application of diagnostic studies for HTLV-III infection has demonstrated that these neurologic disorders can be the first manifestation of AIDS or occur in the absence of AIDS. The most common conditions associated with HTLV-III infection alone are a subacute encephalopathy (AIDS dementia) and peripheral neuropathy; however, vacuolar myelopathy and both acute and chronic aseptic meningitis are also common. Congenital (or neonatal) transmission of the virus can result in a mental retardation syndrome of delayed onset. The AIDS virus is neurotropic as well as targeting T-helper lymphocytes. The virus has been readily identified in neural tissues and cerebrospinal fluid, including instances in which other central nervous system infections, such as toxoplasmosis, coexist. Hence, recognition of an appropriate syndrome, neurodiagnostic studies, and exclusion (or treatment) of other infections, as well as evidence for HTLV-III infection are required for diagnosis. The development of successful therapy will require agents which cross the blood-brain barrier.
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PMID:Neurology of AIDS virus infection: a clinical classification. 282 50

Clinical and biochemical findings in a male subject with progressive encephalopathy and peripheral neuropathy are presented. Early development was normal. At age 3.5 years, he had seizures associated with fever. Subsequently, there was progressive neurologic deterioration. A CT brain scan at age 4 years, 2 months demonstrated multiple areas of variable density in the white matter. There was mild slowing of nerve conduction velocities and a sural nerve biopsy revealed segmental demyelinative neuropathy. Metachromatic leukodystrophy was suspected, but arylsulfatase A activity in leukocytes and fibroblasts was in the normal range. The cerebroside sulfate loading test on intact cultured fibroblasts showed attenuated hydrolysis leading to a tentative diagnosis of cerebroside sulfatase activator deficiency. However, the attenuated response of proband fibroblasts was not normalized by supplementation with activator in a reproducible manner, and urine showed hyperexcretion rather than deficiency of activator. Ultimately, an assay for galactosylceramide beta-galactosidase activity established a deficiency of this enzyme leading to the diagnosis of late-onset Krabbe disease.
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PMID:Late-onset Krabbe disease initially diagnosed as cerebroside sulfatase activator deficiency. 290 3

Three specific patterns of neurologic deficit were seen in a group of 52 patients with the idiopathic hypereosinophilic syndrome. Central nervous system dysfunction was seen in 7 patients (15%), 4 of whom had a distinctive encephalopathy characterized by behavioral disturbances and upper motor neuron signs. Peripheral neuropathy was found in 27 patients (52%), with a sensory polyneuropathy the commonest form (in 23 patients), although mononeuritis multiplex and radiculopathy were also seen. Central nervous system abnormalities from embolic disorders were seen in 6 patients (12%). Thus, a total of 65% of these patients had some neurologic dysfunction. Although the spectrum of neurologic disease is broad and includes very different manifestations, we conclude that distinct patterns of neurologic involvement are characteristic of this syndrome.
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PMID:Neurologic dysfunction in the idiopathic hypereosinophilic syndrome. 298 93

Disulfiram toxicity is a well-recognized cause of peripheral neuropathy and encephalopathy, usually developing within a few months of the start of therapy. We describe a patient who insidiously developed a peripheral neuropathy and encephalopathy after thirty years of disulfiram ingestion. Both complications partially resolved after the medication was stopped.
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PMID:Reversible, late-onset disulfiram-induced neuropathy and encephalopathy. 298 11

A 63-year-old female developed unexplained hyperglycemia and glycosuria during administration of a total parenteral nutrition regimen on which she had been stable for several months. Because the patient had no history of diabetes or evidence of an infection, chromium deficiency was considered. Plasma chromium level was 0.1 microgram/dl (laboratory reference interval: 1.8-3.8 micrograms/dl). Fourteen days of supplemental intravenous chromium chloride (200 micrograms/day) allowed complete withdrawal of exogenous insulin with no further hyperglycemia or glycosuria. Correction of unexplained glucose intolerance following vigorous chromium supplementation indicates that the patient had chromium deficiency. Subsequent plasma chromium levels remained unchanged, possibly reflecting the sensitivity limits of the assay that was used, the uncertainty that exists regarding appropriate reference intervals for this element, and the fact that plasma levels do not always correlate with total body stores. The patient did not manifest peripheral neuropathy, which was present in one of the two previously reported cases, nor encephalopathy, which was reported in the other. We conclude that this patient developed chromium deficiency as a result of inadequate administration of chromium in the parenteral formula (6 micrograms/day) plus excessive enteric losses, and she presented with glucose intolerance as the only clinical manifestation of the deficiency. Caution should be exercised when interpreting plasma chromium in patients with suspected deficiency.
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PMID:Chromium deficiency after long-term total parenteral nutrition. 308 63

A study was conducted to determine if there were any health effects among the polythene printers who were exposed to toluene and to evaluate the use of urinary hippuric acid in biological monitoring. The study covered 54 printers from 6 plants out of the universe population of 32 polythene printing plants who used toluene as ink dilutants. They were matched with 54 controls for age, sex, race and similar occupational status. All were interviewed and examined clinically. 23 patients were selected for neurobehavioural tests. 26% of the printers had more than 10 years of exposure to toluene. No case of clinical encephalopathy or peripheral neuropathy was detected. 38.9% of the printers had hand dermatitis compared with 1.9% among the controls. Results of the neurobehavioural tests for the 23 printers were not statistically different from the controls. The results of the liver function test were within normal limits. The mean toluene-in-air level was 246 +/- 25 mg/m. Mean blood toluene was 0.63 +/- 0.14 microgram/ml. The mean urinary hippuric acid was 2.83 +/- 0.48 mg/ml as compared to 0.35 +/- 0.08 mg/ml in the controls. Urine hippuric acid corrected to SG of 1.016 was well correlated to air toluene level (r = 0.81). Toluene appears not to have any significant nervous system or liver effects in these printers. Urinary hippuric acid is a useful indicator for biological monitoring of atmospheric exposure to toluene.
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PMID:A study on the health hazard of toluene in the polythene printing industry in Singapore. 368 3

A 20-year-old man survived acute massive arsenic ingestion. The resultant severe encephalopathy and peripheral neuropathy showed limited long-term recovery over the following two years. The patient's clinical course was followed using visual and auditory evoked potentials, computed tomography, electroencephalography, and electromyography.
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PMID:Long-term survival in acute arsenic encephalopathy. Follow-up using newer measures of electrophysiologic parameters. 382 8

The essentiality of chromium (Cr) in animal and human nutrition is now well accepted. In animals, Cr deficiency can cause a diabetic-like state, impaired growth, elevated blood lipids, increased aortic plaque formation, and decreased fertility and longevity. The ability of Cr to potentiate insulin sensitivity has considerable experimental support. In the human, Cr deficiency has been demonstrated unequivocally in only one clinical situation, patients on total parenteral nutrition without added Cr. In such patients, impaired glucose tolerance, hyperglycemia, relative insulin resistance, peripheral neuropathy, and a metabolic encephalopathy have been noted with reversal of the clinical phenomena by Cr repletion. Many studies have been performed to determine whether Cr deficiency may be important in other clinical conditions, namely, diabetes mellitus, pregnant and parous women, and the aged population. Available data indicate that Cr supplementation can improve glucose metabolism in glucose intolerant individuals and decrease the total/HDL cholesterol ratio regardless of the status of glucose tolerance. However, whether Cr supplementation has long-term health benefits is unknown. Further, despite many tantalizing observations, it is still unclear whether Cr deficiency, latent or overt, is common in any human situation other than generalized malnutrition and total parenteral nutrition without added Cr. Technical uncertainties in the analysis of Cr, Cr contamination of food by the use of stainless steel processing equipment and eating utensils, and the lack of a clinically feasible test for Cr deficiency continue to impede progress in Cr research. Nevertheless, there is considerably more clarity as to plasma and urine Cr levels, food and tissue Cr content, and metabolic pathways of Cr metabolism than existed a decade ago. It is expected that progress will accelerate, since critical questions can now be addressed regarding the role of Cr in human nutrition.
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PMID:Clinical and biochemical aspects of chromium deficiency. 388 57


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