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Encephalopathy acute, features

One of the most confusing features of Al encephalopathy is the lag phase between exposure and clinical symptoms and the subsequent rapid course of the disease. The delay can be months to years in the classical form and several weeks in the acute form. Because patients are generally symptom-free or demonstrate minor symptoms like microcytic anemia, physicians are unaware of the exposure until the development of severe symptoms. Until recently it was not known that a relatively short dialysis related exposure time to Al can be fatal. [Pg.19]

Table 5. Clinical features of acute and chronic aluminum encephalopathy... [Pg.20]

Gleeson JG, duPlessis AJ, Barnes PD, Riviello JJ Jr. Cyclosporin A acute encephalopathy and seizure syndrome in childhood clinical features and risk of seizure recurrence. J Child Neurol 1998 13(7) 336 4. [Pg.762]

The clinical features of acute and chronic encephalopathy or death in these 48 patients were classified into three groups based on the initial findings of ataxia in 6, behavioral changes in 8, and seizures in 34. The onset of neurological findings varied in severity from ataxia or behavioral changes to prolonged seizures or coma. Fever preceded the onset of acute encephalopathy by several hours to several days in 43 of 48 children. There was a measles-like rash with a post-vaccination onset from day 6 to day 15 in 13 children. [Pg.2210]

A 7-year-old boy with Duchenne muscular dystrophy and attention deficit hyperactivity disorder (ADHD) developed acute hepatic failure, with features of autoimmune hepatitis (2). The only medications he had taken were pemoline (56 mg/day) and cjrproheptadine (2 mg/day). Pemoline was withdrawn after 8 months as the presumed cause of his raised transaminases. Two weeks later he developed an altered mental state, jaundice, and encephalopathy. The histological features of the liver and his autoimmune antibody panel were consistent with autoimmune hepatitis. He was treated with corticosteroids and azathioprine and recovered. [Pg.2728]

Chang KH, Han MH, Kim HS, et al Delayed encephalopathy after acute carbon monoxide intoxication MR imaging features and distribution of cerebral white matter lesions. Radiology 184 117-122, 1992... [Pg.240]

Type A encephalopathy and type B and C encephalopathy share many clinical symptoms. However, there are also a considerable number of clinical features which are significantly different. Generally the brain s reaction to a distinct metabohc disturbance differs depending on the rate at which the metabolic alteration occurs, since there is little scope for adaptation to acute severe metabohc alterations. [Pg.181]

Greco-Roman era to ca. 200 CE Acute abdominal distress, vomiting, muscle pain, paralysis, hallucination death in extreme, untreated cases Acute lead poisoning with acute encephalopathy and peripheral neuropathic features Hippocrates Nikander Galen Vitruvius Dioscorides Pliny the Elder Major (1945), Waldron (1973), Nriagu (1983a,b 1985), Relief and Cilliers (2006)... [Pg.403]

Lead colic has long been recognized among clinicians as a symptomatic correlate of clinical-level lead exposures in infants, toddlers, and highly exposed lead workers. The earlier literature has been described in several expert consensus documents (NAS/NRC, 1972 U.S. CDC, 1978 U.S. EPA, 1977, 1986). Typically, the clinical G1 effects of Pb that are clustered under the label of lead colic include anorexia, abdominal pain, constipation, nausea, and vomiting. These may empt along with acute encephalopathy or be a persistent feature of chronic neuropathy in infants and toddlers, while Pb workers are typically plagued with chronic G1 disturbances. [Pg.710]


See other pages where Encephalopathy acute, features is mentioned: [Pg.777]    [Pg.537]    [Pg.1382]    [Pg.1755]    [Pg.2210]    [Pg.1807]    [Pg.826]    [Pg.323]    [Pg.1138]    [Pg.172]    [Pg.19]    [Pg.115]    [Pg.440]    [Pg.570]    [Pg.168]    [Pg.52]    [Pg.125]   
See also in sourсe #XX -- [ Pg.115 ]




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