Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article describes the metabolic investigations to be applied in any clinical situation consistent with a late acute form of inborn error of metabolism: unexplained coma with or without focal neurological manifestations, recurrent vomiting with lethargy, episodes of ataxia with or without behaviour disorder, fits of psychiatric troubles. In each of these situations, careful medical history is of major importance searching for previous clinical manifestations such as episodes of coma, ataxia or vomiting, anorexia, failure to thrive, developmental delay, all very suggestive of metabolic disorder. The association of neurological symptoms and abnormal hepatic tests is also of great value and must not lead to the diagnosis of Reye's syndrome without considering a metabolic defect of fatty acid oxidation, urea cycle, respiratory chain, or Wilson's disease. When looking for an etiological origin, it is mandatory to collect all the biological information at the same time, also knowing that metabolic abnormalities may be mild and transitory, and that many of them are non specific (metabolic acidosis, hyperlactacidemia, hyperammonemia, hepatic tests disturbances) being encountered in collapsus, shock and multiple organ failure syndrome.
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PMID:[Diagnosis of metabolic coma in children]. 784 29

Thirty pediatric cases of carbamazepine overdoses were reviewed retrospectively for the frequency of toxic effects. Patients were divided into three groups, depending on the type of overdose: acute, acute-on-chronic, and chronic. Effects included lethargy in 93%, ataxia in 50%, nystagmus in 13%, and minor arrhythmias in 10%. Major effects included seizures in 20%, coma in 27%, and need for intubation in 20%. Higher serum carbamazepine levels were associated with these major effects in the acute and acute-on-chronic groups but not in the chronic group. Serum levels greater than 35 mg/L (147 mumol/L), were significantly associated with major toxicities.
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PMID:Pediatric carbamazepine overdoses. 784 50

An epizootic of encephalomyelitis attributable to western equine encephalitis virus was identified in emus (Dromaius novaehollandiae) from several flocks in western Texas in July 1992. Affected emus ranged from 3 months to 3 years old. Morbidity of emus in 8 flocks ranged from 15 to 50%, and 17 of 193 (8.8%) emus died. The diagnosis was confirmed by isolation and characterization of the causative virus and detection of antibody to the virus in emus that were currently ill and emus that had been ill but recovered. Clinical signs varied from mild to severe and included anorexia, lethargy with sternal recumbency, ataxia, muscle tremors, head tilt, unnatural positioning of the head on the back, acute onset of paralysis, and lateral recumbency with paddling. A few emus died without prior evidence of clinical disease. Post-mortem examination revealed 3 to 5 ml of clear pale-yellow pericardial fluid that contained a fibrin clot. Volume of the contents of the proventriculus and ventriculus were less than anticipated. Microscopic examination of numerous tissues revealed multifocal vasculitis with infiltration of plasmacytes, lymphocytes, and a few heterophilic leukocytes. The epizootic developed during a period of unseasonably heavy rainfall that resulted in higher numbers of mosquitoes than was typical for that season of year. A concurrent increase in the number of horses with encephalomyelitis attributable to western equine encephalities virus was not reported.
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PMID:An epizootic attributable to western equine encephalitis virus infection in emus in Texas. 796 Oct 99

The authors' primary purpose was to identify home healthcare needs of adults (N = 244) living with HIV disease/AIDS. The study followed a retrospective chart review of a stratified random sample of cases discharged during 1991 from a certified home health agency (CHHA) in New York City. Frequently observed signs and symptoms included dyspnea, weakness, fatigue/lethargy, pain, ataxia, cough, skin lesions, and memory deficit. Additional problems identified included inadequate nutrition, issues related to compliance with prescribed medications, inadequate in-home support systems, inadequate facilities/utilities in the home, financial concerns and lifestyles that included drug/alcohol abuse and tobacco use. The results suggest that the health care needs of people living with HIV disease/AIDS in the home care setting are multifaceted and extend beyond the clinical manifestations of HIV disease.
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PMID:Home healthcare needs of adults living with HIV disease/AIDS in New York City. 803 11

To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME). Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.
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PMID:Experimental infection of mink with bovine spongiform encephalopathy. 807 14

One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analysis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls matched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical signs typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move. The major clinical-pathologic findings were a marked increase in serum osmolality and total protein, urea nitrogen, creatinine, phosphorus, glucose, and potassium concentrations and a decrease in sodium and chloride concentration. In addition, the animals were acidotic, there was a reduction in the urine specific gravity, and the hemogram was consistent with a stress response. Emaciation and dehydration were the only pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni was cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of the affected mink. Lipid vacuoles in hepatocytes and renal tubular epithelium, hypertrophy of cells in the adrenal cortex, and pulmonary congestion and atelectasis were present in both diseased females and controls, as were various sporadic inflammatory lesions. Nursing disease may result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.
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PMID:Nursing disease in mink: clinical and postmortem findings. 811 44

A 4-year-old female German Shepherd Dog was examined to determine the cause of ataxia, progressive head tilt, anorexia, lethargy, and weight loss of 3 weeks' duration. A vestibular syndrome, generalized lymphadenopathy, bilateral uveitis, and chorioretinitis with complete detachment of the left retina were detected. Abnormal clinicopathologic findings were isosthenuria and hyperglobulinemia. The non-functional left eye was enucleated and fungal organisms resembling Aspergillus spp were identified on histologic examination. Microbial culture of a urine sample yielded Acremonium sp, which was initially considered a contaminant. The dog was considered to have systemic aspergillosis and was treated with itraconazole for 7 months, until it was euthanatized because of persistent vomiting and anorexia. Postmortem examination revealed multisystemic pyogranulomatous and necrotizing inflammation of the myocardium, pericardium, liver, and kidneys; and granulomatous splenitis, lymphadenitis, retinitis, endometritis, and meningoencephalitis. Fungal culture of affected organs yielded Acremonium sp. These findings indicated that Acremonium spp can be pathogenic and should not be ignored when cultured.
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PMID:Systemic mycosis caused by Acremonium sp in a dog. 825 22

We investigated the effects of a turf application of the insecticide diazinon AG500 on Canada geese (Branta canadensis) on a golf course in coastal Washington (USA). On both 19 and 26 March 1987, 1 ha of turf on a golf course located in Birch Bay, Washington was treated with diazinon AG500 at a target application rate of 2.2 kg active ingredient per hectare (AI/ha). Treated areas were then irrigated with 6 mm water. Grass and water samples were collected from three different sites one day before and 1, 3, 7 and 14 days after each application. Diazinon residues > or = 20 ppm were found in golf course grasses for one week after each application. Diazinon residues in study area ponds and creeks were > or = 17 ppb. Samples from two irrigation puddles one day post-application had 1.00 and 0.20 ppm of diazinon, respectively. Numbers of geese present declined following diazinon application; however, no goose mortality was observed. Geese spent 422 and 538 min feeding on the treated areas after the first and second diazinon applications, respectively. One goose feeding in treated areas demonstrated signs of poisoning (lethargy, ataxia) for several hours. Two other geese feeding in the treated areas may have been slightly intoxicated. During carcass searches, three American wigeon (Anas americana) carcasses were found. Based on brain cholinesterase (ChE) levels and gastrointestinal (GI) tract residues of diazinon present, we concluded that these wigeon died from diazinon poisoning. Numerous songbirds (Passeriformes) also fed on the treated turf but no apparent response to the insecticide was observed.
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PMID:Response of Canada geese to a turf application of diazinon AG500. 835 49

Tumor-associated hypoglycemia has been reported in dogs with pancreatic beta-cell tumors, hepatic tumors, and, rarely, with other neoplasms. This article describes 4 dogs with marked hypoglycemia associated with smooth muscle tumors (jejunal leiomyoma, gastric leiomyoma and leiomyosarcoma, and splenic leiomyosarcoma). Presenting clinical signs included grand mal seizures, lethargy, weakness, ataxia, and, in 1 dog, polyuria/polydipsia. The serum insulin concentration was low in 1 dog and normal in the other dog evaluated. Immunohistochemical staining for insulin was negative in the 4 tumors; the 3 tumors arising from the stomach and jejunum stained diffusely positive for glucagon. Blood glucose concentrations rapidly returned to normal after complete surgical resection of the tumors, and clinical signs associated with hypoglycemia resolved. Long-term follow-up available in 3 of the 4 dogs found no recurrence of clinical signs related to hypoglycemia at 15, 31, and 38 months after surgery, respectively.
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PMID:Hypoglycemia in four dogs with smooth muscle tumors. 855 89

We report 2 girls, aged 10 and 13 years, with juvenile myoclonic epilepsy (JME) who had episodes of nonconvulsive status epilepticus (NCSE). Symptoms included only mild lethargy, slow responses, and trembling of the eyelids. There was no ataxia or myoclonus of the limbs or body, and they were always able to respond. Electroencephalograms during these episodes showed almost continuous generalized polyspike-waves in both patients. Patients with JME can develop NCSE, which may be overlooked because of the subtle clinical symptoms.
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PMID:Two patients with juvenile myoclonic epilepsy and nonconvulsive status epilepticus. 859 87


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