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)

Standardized individual psychoeducational school-readiness tests were completed by 127 nondisabled survivors of moderate (lethargy, hypotonia, and suppressed primitive reflexes) or mild (hyperalertness, hyperexcitibility) neonatal encephalopathy associated with term birth asphyxia. Application of the readiness test battery to the children with moderate or mild encephalopathy and a peer population, revealed that children with moderate encephalopathy had significantly lower scores for many tests than those in the other groups. Children with mild encephalopathy performed well. We found no significant differences due to social variables. For the moderate group, we found an increased number of types of anticonvulsants and abnormal findings on the neurologic examination at neonatal intensive care unit (NICU) discharge to be predictors of low achievement on school-readiness tests. Also for the nondisabled moderate group, multiple regression analysis of the independent variables with the 5.5-year scores added variables suggestive of intrauterine growth retardation to the prediction of lower scores on many school-readiness tests. We conclude that clinical categorizing of moderate neonatal encephalopathy associated with birth asphyxia in term infants selects a group of children with an increased percentage of school-readiness delay, and could be a useful indicator for clinicians and educators in defining those neonates who may need special preschool evaluation and benefit from a modified early school program.
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PMID:Educational readiness of survivors of neonatal encephalopathy associated with birth asphyxia at term. 297 68

Isolated cerebral angiitis was confirmed by brain parenchyma biopsy in a 31-year-old man with a rapidly progressive encephalopathy and normal cerebral angiography and magnetic resonance imaging. Presenting features of aphasia, hemiparesis, and lethargy resembled herpes simplex encephalitis. Severe neurologic deficits rapidly resolved with steroids plus cyclophosphamide, and he remains in remission after two years. This case illustrates potentially misleading early manifestations of isolated cerebral angiitis, diagnostic limitations of angiography, the value of biopsy that includes both brain parenchyma and leptomeninges, and the potential efficacy of steroid and cyclophosphamide therapy in small-vessel disease. Clinical features and response to treatment vary widely in reported cases, suggesting that isolated cerebral angiitis may have diverse etiologies.
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PMID:Isolated small-vessel angiitis of the central nervous system. 336 77

The effects of phenytoin (PHT) on the modifications of ammonia (NH+4) metabolism caused by sodium valproate (VPA) are here studied in order to identify the drug combinations susceptible of evoking stuporous states in epileptics, a rare condition attributed to a hyperammonemic encephalopathy induced by VPA. During chronic treatment with PHT or VPA-PHT, the acute injection of VPA increases the kidney's output of NH+4. During chronic PHT treatments, the acute injection of VPA modifies the liver's NH+4 metabolism and the arterial hyperammonemia is high (mean = 90 mumol/l). During chronic VPA-PHT treatments, the acute injection of VPA does not affect the hepatic NH+4 metabolism, suggesting that adaptation occurs, and the arterial hyperammonemia is moderate (mean = 60 numol/l). Disturbances of the hepatic adaptive mechanisms may explain certain complications observed during multiple-drug regimens.
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PMID:Adaptation of hepatic ammonia metabolism after chronic valproate administration in epileptics treated with phenytoin. 392 65

Two patients had clinical findings of encephalopathy that progressed in 4 to 5 months. One patient had headache, fatigue, lethargy, hemiparesis, and a seizure. The second patient had only forgetfulness, confusion, and lethargy without focal signs. Herpes simplex virus was grown from brain biopsy in the first patient and from CSF in the second patient. These cases suggest that herpes simplex virus caused the encephalitis and that it should be considered in the differential diagnosis of chronic encephalopathy.
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PMID:Chronic encephalitis possibly due to herpes simplex virus: two cases. 403 28

A 69-year-old woman suddenly became comatose. Within 24 hours, she became lethargic, with a diffuse encephalopathy and no focal neurologic abnormalities. CT revealed a large, nondominant thalamic infarct.
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PMID:Syndrome of diffuse encephalopathy due to nondominant thalamic infarction. 403 38

A transient cerebral disturbance characterized by somnolence of varying degree is described in children after cranial irradiation given as part of central nervous system (C.N.S.) prophylaxis for acute lymphoblastic leukaemia in remission.Out of 28 such children receiving cranial irradiation as part of the Medical Research Council protocol for C.N.S. prophylaxis 11 (39%) developed pronounced symptoms of somnolence, anorexia, and lethargy some six weeks after the completion of cranial irradiation, and a further 11 (39%) developed these features in mild form. In all cases the symptoms were transient, no focal neurological abnormality was detected, and all children made a spontaneous and complete recovery. E.E.G. studies on five somnolent children showed similar abnormal activity of diffuse and patchy distribution over both hemispheres. Indirect evidence is presented to support the concept that this syndrome represents a transient radiation encephalopathy, analogous to acute transient radiation myelopathy, caused by temporary disturbance of myelin synthesis.
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PMID:Somnolence after prophylactic cranial irradiation in children with acute lymphoblastic leukaemia. 451 11

Toxic irreversible encephalopathic syndromes developed in 2 patients treated with lithium carbonate and haloperidol. Symptoms consisted of lethargy, fever, tremulousness, confusion, and extrapyramidal and cerebellar dysfunction, accompanied by leucocytosis and elevated serum enzyme, blood urea nitrogen, creatinine and fasting blood glucose levels. One patient suffered widespread irreversible brain damage; the other was left with persistent dyskinesias. Although causal factors have not been identified, this report and others in the literature suggest that diffuse irreversible encephalopathy may occasionally develop in individuals with abnormal brain sensitivity to the lithium carbonate/haloperidol combination. Evidence for this is based on the fact that in our patients and others mentioned in the literature the dosage and blood levels of lithium were not high.
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PMID:Toxic irreversible encephalopathy induced by lithium carbonate and haloperidol. A report of 2 cases. 641 23

A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However, in either case hyperammonemic episodes should be treated aggressively to prevent coma, subsequent brain damage, or death. This involves restricting protein intake, providing adequate calories, and giving agents that remove accumulated nitrogen. Long-term therapy relies on diagnosing the specific disease rate. This rarely requires invasive procedures such as liver biopsy. In most cases measurement of plasma amino acids and urinary organic acids will identify the defect. Treatment involving restriction of nitrogen intake, vitamin supplementation, or stimulation of alternative pathways of waste nitrogen excretion can then be instituted. Early therapy, especially in patients with neonatal-onset hyperammonemia, is imperative to avoid severe brain damage. On this basis, the plasma ammonium level should be determined in virtually every newborn with lethargy, hypotonia, poor feeding, seizures, and/or respiratory distress of unclear origin (Table 12).
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PMID:Hyperammonemia. 651 17

The D(-) isomer of lactic acid appears to cause a form of metabolic encephalopathy experienced by patients who have had jejunoileal bypass for morbid obesity. However, analysis for D(-)-lactate is not routinely available in clinical or reference laboratories. We describe an enzymic centrifugal-analyzer assay for D(-)-lactate in plasma or serum, with use of D(-)-lactate dehydrogenase. The method involves two-point kinetic calibration and preincubation of specimen and NAD+, thus eliminating the need for specimen-blanking or protein-precipitating pretreatment. This rapid, accurate, and precise assay should be helpful in evaluating patients with "short-bowel syndrome" who display confusion, lethargy, ataxia, or other central nervous-system disturbances that may be ascribable to D(-)-lactic acidosis.
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PMID:Kinetic enzymic assay for D(-)-lactate, with use of a centrifugal analyzer. 661 31

Three elderly men being evaluated for cerebrovascular disease developed acute confusional states following arteriography with approximately 50 ml of meglumine iothalamate. Two patients became stuporous. All recovered in several days, and no specific cause was found for the disorder. In the absence of other demonstrated abnormalities, we suggest that in each patient the encephalopathy may have been a toxic reaction to the contrast agent.
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PMID:Encephalopathy following arteriography: a possible toxic effect of contrast agents. 671 82


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