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)

Six patients were admitted after erroneous massive intake of levothyroxine (70-1200 mg over an interval of 2-12 days). All patients developed classical symptoms of thyrotoxicosis within 3 days of the first dose; five patients presented grade II-III coma and one became stuporous (days 7-10). Two patients developed left ventricular failure and three had arrhythmias (days 8-11). Total thyroid hormone levels in serum on admission ranged 935-7728 nmol/l for T4 (TT4) and 23-399 nmol/l for T3 (TT3). All patients received treatment with hydrocortisone and Propranolol. Propylthiouracil was also given in 3 cases. Extractive techniques (charcoal haemoperfusion and/or plasmapheresis) were initiated 8-14 days after the first dose of L-T4. The plasma disappearance rate (K) of TT4 with plasmapheresis was 30 times higher, on average, than under standard medical treatment (M). Also, K of TT4 under haemoperfusion was about five times higher than K under M. K changes for TT3 were higher under haemoperfusion than under plasmapheresis. Furthermore, extractive procedures shortened the average half life of TT4, (from 106.5 +/- 44.6 to 59.7 +/- 20.2 h, p less than 0.05).
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PMID:Massive thyroxine intoxication: evaluation of plasma extraction. 355 34

The role of changes in blood-brain barrier permeability in the pathogenesis of hepatic encephalopathy remains uncertain. To test the hypothesis that brain microvessel permeability is nonselectively increased in hepatic encephalopathy we measured the blood-brain barrier permeability-surface area product in rats with acute liver failure induced by intraperitoneal injection of galactosamine. The permeability-surface area products to the diffusion-limited tracers, sucrose and methylaminoisobutyric acid, were determined as a measure of blood-brain barrier permeability. Animals were examined 24, 36 and 42 hr after injection, at times when they were stuporous, but not comatose. No significant elevations of the permeability-surface area products for either compound were detected in clinically affected experimental animals when compared to controls. Our results indicate there is no generalized increase in brain vascular permeability during hepatic insufficiency in precomatose animals.
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PMID:The effects of galactosamine-induced hepatic failure upon blood-brain barrier permeability. 357 Jan 56

This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.
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PMID:Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome. 370 9

We have presented a case of thiazide-induced hyponatremia that followed an unusual course after the patient, suffering from extreme lethargy, was admitted with a serum sodium concentration of 104 mEq/L. Although the electrolyte imbalance was essentially corrected within 20 hours and there was clinical improvement, three days later the patient suddenly lost consciousness. She was comatose for more than a month, apparently from extrapontine myelinolysis. After a dramatic improvement, the patient was discharged with almost no neurologic deficit.
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PMID:Thiazide-induced hyponatremia: an unusual neurologic course. 370 34

Central nervous system symptoms due to hyponatremia is highly dependent on its acuteness and cause. Severe acute hyponatremia (serum sodium less than 125 mEq/l) often causes confusion, lethargy, seizures or frank coma due to brain oedema. If therapy is delayed, hyponatremia carries a high mortality rate, and risk of irreversible brain damage. Hyponatremia should probably be corrected to 125-130 mEq/l at a rate of 1.5-2.0 mEq/l/h. Malnourished alcoholic patients with hyponatremia may represent a special case with possible dangers of central pontine myelinolysis if a very low serum sodium is corrected acutely to normonatremic or hypernatremic levels. Mortality in this subgroup is high whatever the therapy.
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PMID:Hyponatremia: cerebral symptoms and role in central pontine myelinolysis. 370 29

A 38-year-old man was admitted to our hospital because of severe headache following reduced level of consciousness on February 13, 1979. He was lethargic and showed neck stiffness. A lumbar puncture revealed bloody cerebrospinal fluid. Left carotid angiography showed a berry aneurysm of 11 mm in diameter at the bifurcation of the middle cerebral artery (MCA). Rebleeding occurred on February 21, and he fell into semicoma. But, his consciousness recovered to lethargy on the next day. On February 26, a direct intracranial operation was performed and a Sugita clip was placed to the aneurysmal neck. The postoperative course was uneventful. But, left carotid angiography on 8th day after operation showed a newly originated aneurysm proximal to the operated aneurysm. On the 12th postoperative day, he suddenly fell into coma. CT showed subarachnoid blood in the basal cisterns and intraparenchymal hematoma in the left temporal lobe. On the same day, left carotid angiography was performed and it showed the enlarged aneurysm. He died on the 19th day after operation. Autopsy was not performed. Three factors have been considered dealing with the recurrence of the operated aneurysm in the previous reports: first, local fragility of the vascular wall due to the clip edge. Secondly, macro- or microscopic residual aneurysmal neck, thirdly, broken or slipped clip. Our case had the following characteristics from the angiographical and operative findings: the orifice of the operated aneurysm was situated on the superior side of the parent artery and the aneurysm protruded posterosuperiorly at an angle of approximately 90 degrees to the long axis of M1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Rapid growth and rupture of a newly originated aneurysm near the clipped middle cerebral artery aneurysm]. 371 83

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

The results of treatment for 182 patients with hypertensive putaminal hemorrhage are described. The patients are graded according to the level of consciousness on admission; grade 1, fully conscious; grade 2, somnolent; grade 3, stuporous; grade 4, semicomatose; and grade 5, deeply comatose. Removal of hemorrhage was performed in 44 patients (24%), and conservative treatment was given in 138 patients (76%). One-month mortality in the surgical group was 27%; it was 22% in the conservative group. At 6 months after surgical treatment, the percentages of patients who returned to full-time work or independent life without disability or with minimal disability (good recovery) were 40% in grade 1, 30% in grade 2, 22% in grade 3, 11% in grade 4, and 0% in grade 5; after conservative treatment, percentages with good recovery were 77% in grade 1, 56% in grade 2, 29% in grade 3, 7% in grade 4, and 0% in grade 5. This study shows that surgical treatment does not give better results in the management of hypertensive putaminal hemorrhage.
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PMID:Hypertensive putaminal hemorrhage: analysis of 182 patients. 372 42

Organic acidurias are congenital errors of the intermediate metabolism caused by a specific metabolic defect which gives rise to an anomalous excretion of carboxilic acids. The majority of these disease appear in the first weeks of life with few specific symptoms as hypotonia, lethargy, coma, seizures, vomits and dehydration. From biochemical point of view the findings of metabolic acidosis, ketosis, and hyperamoniemia are common. Frequently clinical symptoms are precipitated by infectious disease, traumatism or stress situations. The treatment applied in the initial phases may be efficient; for this reason diagnostic and early treatment are necessary for avoid irreversible sequelae. The diagnosis is also important for posterior genetic counseling. Organic acidurias are an interesting field of work for the pediatrician, neuropediatrician, biochemist and dietician to offer new perspectives in the diagnosis and treatment of many congenital errors of the metabolism.
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PMID:[Organic aciduria. Forms of presentation and treatment]. 372 91

A 2 1/2-year-old child being treated with carbamazepine (CBZ) for a seizure disorder on two separate occasions experienced elevated CBZ serum concentrations (28 and 23.2 mg/L), severe liver damage (SGOT greater than 6000 IU, SGPT greater than 5000 IU), and central nervous system manifestations (coma, lethargy, seizures). During the first episode, the time course of CBZ concentrations exhibited a nonlinear decline and was accompanied by CBZ-10,11-epoxide concentrations that were elevated 4-fold compared to normal values. Cerebrospinal fluid concentrations of CBZ and CBZ-10,11-epoxide were also elevated, although their ratios to serum concentrations did not suggest enhanced permeability of the central nervous system to these substances. The concentrations of CBZ-10,11-epoxide but not CBZ were elevated for the duration of time that the patient was comatose, suggesting that this metabolite may contribute to the neurotoxic side effects observed with CBZ therapy.
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PMID:Acute hepatotoxicity after excessively high doses of carbamazepine on two occasions. 373 41


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