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)

In the summer of 1999/2000, an epizootic occurred in cultured juvenile redclaw crayfish Cherax quadricarinatus on one commercial crayfish farm in northern Queensland, Australia. Mortalities occurred over 4 wk, with up to 96% cumulative mortalities in 2 earthen ponds stocked with juveniles. The crayfish were weak, anorexic and lethargic. A transmission trial was conducted, using filtered, cell-free extract prepared from infected crayfish as inoculum. The disease was reproduced, with on-going mortalities occurring in inoculated crayfish over 55 d. Experimentally inoculated crayfish showed gross signs of malaise, anorexia and disorientation before dying. Two types of intranuclear inclusion bodies (INIBs) were seen in tissues of endodermal, ectodermal and mesodermal origin by light microscopy with haematoxylin and eosin (H&E) stained sections. 'Early'-stage INIBs were eosinophilic, rounded and located centrally within slightly enlarged nuclei while 'late'-stage INIBs were well-rounded and deeply basophilic. The gills, cuticular epithelium and epithelial cells of the foregut, midgut and hindgut were the most heavily infected tissues. By transmission electron microscopy, virions with an average diameter of 19.5 nm were seen within electron-dense granular inclusion bodies within enlarged nuclei of both naturally and experimentally infected crayfish. The size of the virions and cytopathology are consistent with characteristics of viruses in the Family Parvoviridae. This is the first reported case of mass mortality caused by a parvo-like virus infection in C. quadricarinatus.
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PMID:A parvo-like virus in cultured redclaw crayfish Cherax quadricarinatus from Queensland, Australia. 1218 Jul 8

A 56 year old man was admitted cause he had increasing symptoms as weakness, lethargy, disorientation. The total eosinophil count was 3000/mm3, the serum sodium concentration was 120 mmol per litre. In spite of severe hyponatriemia, urinary sodium excretion was not suppressed and serum osmolality (240 mOsm/Kg was lower than urine osmolality (488 mOsm/Kg). SIADH and Idiopathic Hypereosinophilic Syndrome was diagnosed because we found systemic failure signs due to hypereosinophilia (hepatitis, gastritis, pulmonary hypertension, and encefalopathy). Cortisonic treatment was started with symptoms improving, natriemia, eosynophil count and hepatitis signs normalization. After treatment stopping, reappeared asymptomatic hypereosinophilia, than we choosed Idrossiurea but, non-standing hypereosinophilia disappeared, appeared signs of preexisting adrenal insufficiency, emphasized by stopping cortisone therapy. A RMN showed an hypofiseal adenoma. Many cases of SIADH and Hypereosinophilia hiding adrenocortical insufficiency are reported with severe and unusual hypereosinophilia.
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PMID:[Association of hyponatremia and eosinophilia: correlated idiopathic hypereosinophilic syndrome and SIADH or adrenal insufficiency with secondary eosinophilia]. 1285 64

A 3-year-old spayed female Siberian Husky was presented due to acute vision loss. Examination revealed bilateral optic neuritis and lymphocytic meningoencephalitis. The serum (1:800) and cerebrospinal fluid (CSF; 1:200) immunoglobulin (Ig)G titers for tick-borne encephalitis virus (TBEV) were elevated as were the serum IgG titer for Anaplasma phagocytophilum (1:640) and serum IgM titer for Toxoplasma gondii (1:20). Intracytoplasmic inclusion bodies such as ehrlichial or anaplasmal morulae were not observed in the CSF or blood smear. The dog was treated with methylprednisone and doxycycline. The left eye regained vision; the right eye remained blind. Anti-inflammatory therapy was stopped on day 18 after diagnosis. Four days later the dog showed evidence of hyperesthesia in the cervical region. Analysis of CSF showed no abnormalities and CSF IgG titers for TBEV and A. phagocytophilum were negative. Funduscopic evidence of active papillitis was absent on day 22 in the left eye and on day 86 in the right eye. On day 243, the dog was presented again with lethargy, ataxia, disorientation and temporary head tilt. The IgG titer for TBEV was again elevated in the CSF (1:800) and in serum (1:400). After interpretation of all findings, we assume that meningoencephalitis and optic neuritis in this patient was caused by TBEV and associated immune-mediated inflammation. In endemic areas, TBEV should be considered as cause of optic neuritis in dogs.
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PMID:Tick-borne encephalitis virus as a possible cause of optic neuritis in a dog. 1520 Jun 24

Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the rate of free ammonia production by protein catabolism under normal circumstances, such that any increase in free blood ammonia concentration is a reflection of either biochemical or pharmacologic impairment of urea cycle function or fairly extensive hepatic damage. Clinical signs of hyperammonemia occur at concentrations > 60 micromol/L and include anorexia, irritability, lethargy, vomiting, somnolence, disorientation, asterixis, cerebral edema, coma, and death; appearance of these findings is generally proportional to free ammonia concentration, is progressive, and is independent of the primary etiology. Causes of hyperammonemia include genetic defects in the urea cycle ("primary") or organic acidemias ("secondary"), as well as genetic or acquired disorders resulting in significant hepatic dysfunction. Thus, because of the neurotoxic implications of hyperammonemia and the typical absence of other specific laboratory abnormalities, appearance of the clinical signs should trigger an emergent search for elevated blood ammonia concentration.
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PMID:Hyperammonemia, bane of the brain. 1549 74

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.
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PMID:Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma. 1555 3

Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.
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PMID:Neuropsychiatric adverse effects of interferon-alpha: recognition and management. 1569 25

Medium chain acyl-coenzyme A dehydrogenase (MCAD) deficiency is an inherited disorder of fatty acid metabolism that usually presents in early childhood. This case report describes a 19-year-old woman who presented with lethargy, disorientation, and vomiting. She had a cardiopulmonary arrest from which she could not be resuscitated 24h after the onset of the illness. Pre-mortem blood studies confirmed MCAD deficiency. An MCAD deficiency and other metabolic disorders lie within the differential diagnosis of a patient presenting with acutely altered mental status. The inheritance of MCAD deficiency and its clinical presentation, pathophysiology, treatment, and prevention are discussed.
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PMID:Sudden death in a young woman from medium chain acyl-coenzyme A dehydrogenase (MCAD) deficiency. 1667 80

Toxicological effects of the widely used flame retardant, tetrabromobisphenol A (TBBPA) were assessed in a partial life-cycle test with zebrafish (Danio rerio). Exposure of adult fish during 30 days to water-borne TBBPA in nominal concentrations ranging from 0 (control) to 1.5 microM was followed by exposure of the offspring in early life stages up to 47 days posthatching (dph) to the same concentrations. Adults exposed to 3 and 6 microM showed severe disorientation and lethargy shortly after beginning of exposure and were euthanized. Because semistatic exposure resulted in fluctuating water concentrations, pooled fish samples were chemically analyzed for internal dose assessment. Egg production was decreased in fish exposed to TBBPA concentrations of 0.047 microM and higher, and a critical effect level of 7.2 microg/g lipid with a lower 5% confidence limit of 3.9 microg/g lipid for 50% decreased egg production was calculated. Histology of adult ovaries indicated a relative increase of premature oocytes in two surviving females exposed to 1.5 microM. Hatching of TBBPA-exposed larvae was decreased except in animals exposed to 0.375 microM. In the highest exposure concentration, early posthatching mortality was high (81%) in larvae and the surviving juveniles showed a significant predominance of the female phenotype. Exposure of eggs from control parents up to 6 microM TBBPA resulted in increasing malformation and pericardial fluid accumulation from 1.5 microM; at higher concentrations, all embryos failed to hatch. The presented results indicate decreased reproductive success in zebrafish at environmentally relevant TBBPA concentrations.
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PMID:Toxicity of tetrabromobisphenol A (TBBPA) in zebrafish (Danio rerio) in a partial life-cycle test. 1673 95

A 6-day-old, female roan antelope (Hippotragus equinus cottoni) was diagnosed with a single intrahepatic portosystemic venous shunt at necropsy. Clinical signs had included weakness, lethargy, hypothermia, diarrhea, and a weak suckle response. Multiple seizure episodes were associated with hypoglycemia and characterized by vocalization, muscle fasciculations, and disorientation. Hematologic abnormalities included anemia with hypochromasia, anisocytosis, poikilocytosis, and leukopenia with neutropenia and lymphopenia. Serum biochemical abnormalities included elevations in blood urea nitrogen and total serum bile acid concentration. A portosystemic vascular anomaly should be a differential diagnosis for nonthriving, exotic ruminant calves with overt or subtle neurologic signs, persistent hypoglycemia, and/or elevated bile acids. In very young calves, total bile acid concentration may be more useful in establishing a diagnosis than blood ammonia concentration.
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PMID:Intrahepatic portosystemic venous shunt in a neonatal roan antelope (Hippotragus equinus cottoni). 1731 83

Since the late 1990 s, monitoring efforts evaluating the effectiveness of urban stream restoration projects in the greater metropolitan area of Seattle, Washington, USA, have detected high rates of premature mortality among adult coho salmon (Oncorhynchus kisutch) in restored spawning habitats. Affected animals display a consistent suite of symptoms (e.g., disorientation, lethargy, loss of equilibrium, gaping, fin splaying) that ultimately progresses to death on a timescale of a few hours. Annual rates of prespawn mortality observed over multiple years, across several drainages, have ranged from approximately 20% to 90% of the total fall run within a given watershed. Current weight-of-evidence suggests that coho prespawn mortality is caused by toxic urban stormwater runoff. To evaluate the potential consequences of current and future urbanization on wild coho salmon, we constructed life-history models to estimate the impacts of prespawn mortality on coho populations and metapopulations. At the low (20%) and high (90%) ends of the range of observed mortality, model results indicated the mean time to extinction of localized coho populations in 115 and 8 y, respectively. The presence of productive source populations (i.e., unaffected by prespawn mortality) within a metapopulation reduced local extinction risk. However, as more populations within a metapopulation become affected by spawner die-offs prior to spawning, the source population's productivity declined. These simple models demonstrate the potential for rapid losses from coho populations in urbanizing watersheds. Because the models do not account for possible impacts of toxic runoff to other coho life stages, they likely underestimate the cumulative impacts of nonpoint source pollution on wild populations.
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PMID:Estimating the future decline of wild coho salmon populations resulting from early spawner die-offs in urbanizing watersheds of the Pacific Northwest, USA. 2178 16


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