Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Toxic encephalopathy

Rasmussen K, Jeppesen HJ, Sabroe S. 1993d. Solvent-induced chronic toxic encephalopathy. AmJlnd Med 23 779-792. [Pg.287]

Target serum theophylline concentrations are 5 to 15 mg/L (28 to 83 fimol/L). Adverse effects generally are not problematic at serum concentrations below 15 mg/L (83 ftmol/L), but the increased risk of adverse effects outweighs the increase in bronchodilation in most patients above 15 mg/L (83 fimol/L).36 Headache, nausea, vomiting, and irritability may occur at serum concentrations less than 20 mg/L (110 fimol/L) but are rare when the dose is started low and increased slowly. More serious adverse effects, including cardiac arrhythmias, seizures, toxic encephalopathy, and death can occur at higher concentrations.18 Arrhythmias and seizures may occur without nausea and vomiting, particularly in chronic toxicity. [Pg.223]

Callender TJ, Morrow L, Subramanian K, et al. 1993. Three-dimensional brain metabolic imaging in patients with toxic encephalopathy. Environ Res 60 259-319. [Pg.179]

Perl, T.M., et al.. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid, N. Engl. J. Med., 322, 25, 1775, 1990. [Pg.191]

Cases of toxic encephalopathy and macro-qAic anemia have been reported from industrial exposures that may have been as low as 60 ppm. Symptoms were headache, drowsiness, lethargy, and weakness. Manifestations of central nervous system instability included ataxia, dysarthria, tremor, and somnolence. These effects were usually reversible. In acute exposures, the central nervous system effects were the more pronounced, whereas prolonged exposure to lower concentrations primarily produced evidence of depression of erythrocyte formation. When exposure was reduced to 20 ppm, no further cases occurred. [Pg.445]

Jaundice is notitseifa disease but is an important diagnostic indicator of many underiying conditions, in newborns, jaundice can iead to toxic encephalopathy due to deposition of bilirubin within the lipid regions of membranes of the brain (kernicterus). [Pg.135]

Sulfonamides compete for sites on plasma proteins that are responsible for the binding of bilirubin. As a result, less bilirubin is bound, and in the newborn, the unbound bilirubin can be deposited in the basal ganglia and subthalamic nuclei, causing kernicterus, a toxic encephalopathy. For this reason, sulfonamides should not be administered to newborns or to women during the last 2 months of pregnancy. [Pg.517]

Over dose/acute salicylate poisoning is characterized by salicylism which consists of tinnitus, vertigo and deafness, hyperthermia, toxic encephalopathy (agitation, confusion and convulsions followed by coma), dehydration (due to hyperpyrexia, sweating and vomiting), disturbances of acid base balance and petechial haemorrhages. [Pg.86]

W.B. Ketel J.R. Hughes, Toxic Encephalopathy with Seizures Secondary to Ingestion of Composition C-4 , Neurology 22, 871 (1972)... [Pg.837]

The most notable toxicological effects of carbon disulfide are on the nervous system, including damage to the peripheral nervous system.18 Individuals exposed to carbon disulfide have lost consciousness. Decreased nerve conduction velocities have been observed in workers exposed to 10 to 20 ppm of carbon disulfide in the workplace over periods of 10 to 20 years. Brain abnormalities suggesting toxic encephalopathy have been observed in exposed workers. Some studies have suggested the possibility of mental performance and personality disorders in workers exposed to carbon disulfide, including heightened levels of anxiety, introversion, and depression. [Pg.265]

Measurements taken at my workplace indicated that the ventilation was barely functioning, allowing chemical substances and gases to accumulate too much. Within a year I was once again very sick with very diverse complaints pain everywhere, heart palpitations, high blood pressure, intestinal problems, skin problems, difficulty thinking, and so on. Coincidentally my internal specialist read an article in the newspaper about chronic toxic encephalopathy (CTE or psycho-organic syndrome). [Pg.112]

Ketel WEB, Hughes JR. 1972. Toxic encephalopathy with seizures secondary to ingestion of an explosive material composition C-4 A clinical and electroencephalographic study. Electroencephalogr Clin Neurophysiol 33 352-353. [Pg.97]

Metabolic/toxic encephalopathy hypoglycemia, hepatic failure, alcohol intoxication... [Pg.114]

As late as 1994 a toxic encephalopathy, relapsing but reversible, was reported in a woman who had received a large dose of bismuth when bismuth iodoform paraffin paste was inserted extradurally (24). Elsewhere neurotoxicity has been reported (SEDA-19, 446). [Pg.520]

Toxic encephalopathy has been reported in children sprayed repeatedly with diethyltoluamide 10-15% (1). [Pg.1124]

Edwards DL, Johnson CE. Insect-repeUent-induced toxic encephalopathy in a child. Clin Pharm 1987 6(6) 496-8. [Pg.1124]

Brain damage in this patient was restricted to the white matter. Although hypoxia was present at the time of admission, the authors did not believe that it was the only causative factor. By a process of elimination, they concluded that ecstasy might have caused the toxic encephalopathy, although it was not detected by toxicological... [Pg.2296]

Chronic application of 70% DEET solution caused paranoid psychosis, pressurized speech, flight of ideas, and delusions after 2 weeks of daily application for the inappropriate treatment of a skin rash. Repeated application causes erythema. Extensive daily dermal application of 10-15% DEET for 2 days to 3 months has resulted in encephalopathy in children. Toxic encephalopathy has been associated with DEET in children. Signs of toxicity included agitation, weakness, disorientation, ataxia, seizures, coma, and, in three cases, death. As part of the Reregistration Eligibility Decision on DEET released in 1998, however, the US Environmental Protection Agency reviewed all available data on the toxicity of DEET and concluded that... [Pg.729]

White RF, Feldman RG, Moss MB, et al. 1993. Magnetic resonance imaging (MRI), neurobehavioral testing, and toxic encephalopathy Two cases. Environ Res 61 117-123. [Pg.655]

ATV-dimethyTm-toluamide (DEET) is the active ingredient in numerous commercial mosquito repellants. DEET by itself or as formulated into commercial products permeates through human skin. Dermal exposures to DEET and to mixtures containing DEET have been associated with toxic encephalopathy in children. I22 It has been shown that ethanol, the solvent for DEET, significantly enhances the permeation of DEET through the skin. I23 Toxic effects attributed to DEET absorption may, therefore, be enhanced by the incorporation of ethanol into commercial product formulations. [Pg.233]

Briassoulis G, Narlioglou M, Hatzis T. Toxic encephalopathy associated with use of DEET insect repellants A case analysis of its toxicity in children. Hum Exp Toxicol2m 20(1) 8—14. [Pg.241]

A 57-year-old man who had spent 41 years as a painter was disabled and forced to retire. He was diagnosed with chronic toxic encephalopathy. The man started work as a painter at the age of 16. He started experiencing impaired short-term memory function while in his forties. His condition progressed until he retired and his exposures to the paint solvents ceased. Following his retirement, his condition stabilized and even improved in some areas. Material safety data sheets provided by his employer indicated that this man had been exposed to lead, titanium dioxide, creosote, and the following volatile solvents ... [Pg.312]

Geier DA, Geier MR. A case series of children with apparent mercury toxic encephalopathies manifesting with clinical symptoms of regressive autistic disorders. J Toxicol Environ Health A 2007 70(10) 837-51. [Pg.349]

The minimum effective therapeutic concentration of valproic acid is 5O 0,g/mL. Concentrations in excess of 100 tg/mL have been associated with hepatic toxicity and acute toxic encephalopathy. Glycine has been observed to accumulate in patients on valproic acid therapy. [Pg.1253]

Muller J, Kralovanszky J, Adleff V et al (2008) Toxic encephalopathy and delayed MTX clearance after high-dose methotrexate ther-... [Pg.683]

Gamier R, Reygagne A, Maladry-Muller P, et al. 1991. [Evolution of chronic toxic encephalopathy induced by organic solvents after the cessation of exposure Report of a case with a 5-year followup.] Arch Mai Prof 52 349-354. (French)... [Pg.208]


See other pages where Toxic encephalopathy is mentioned: [Pg.122]    [Pg.283]    [Pg.204]    [Pg.471]    [Pg.694]    [Pg.524]    [Pg.122]    [Pg.283]    [Pg.25]    [Pg.52]    [Pg.84]    [Pg.108]    [Pg.117]    [Pg.594]    [Pg.179]    [Pg.4813]    [Pg.77]    [Pg.339]    [Pg.2145]    [Pg.6]    [Pg.219]    [Pg.49]   
See also in sourсe #XX -- [ Pg.312 ]




SEARCH



Cases chronic toxic encephalopathy

Chronic toxic encephalopathy

Encephalopathies

Nervous system toxicity encephalopathy

© 2024 chempedia.info