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)

Four children with brain tumors had marked alterations in levels of consciousness and vital signs after contrast-enhanced cranial computed tomography (CT). Each had clinical evidence of increased intracranial pressure but was alert and coherent before CT. During the procedure, 2 to 2.5 mL/kg 60% diatrizoate meglumine was administered intravenously, and within hours the patients became progressively lethargic and disoriented and bradycardia and hypertension developed; two had generalized seizures. Two children died immediately after the CT procedure. Contrast-enhanced CT may produce grave neurologic complications in children with brain tumors, and this study should be reserved for those patients in whom the probability of obtaining additional information is high. Use of low-osmolality agents or nonionic contrast agents may decrease the morbidity and mortality associated with the procedure.
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PMID:Neurotoxic complications of contrast computed tomography in children. 368 47

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

Intracarotid BCNU (100 mg/m2) and cisplatin (60 mg/m2) were administered to 36 patients with malignant brain tumors recurrent or progressive after cranial irradiation. Courses of therapy were repeated at 4-6 week intervals. Of 23 evaluable patients with recurrent glioma, 9 (39%) had tumor regression by CT scan and 3 had stable disease. The median time to tumor progression for responding patients was 37 weeks. For all patients with primary tumors it was 14 weeks. Six of 9 patients with no prior chemotherapy had a response and 1 had stable disease. Of 14 patients who had received prior chemotherapy, 3 had a response and 2 had stable disease. Survival ranged from 9 weeks to 95+ weeks (median 34 weeks) from start of therapy. Six of 23 patients with primary tumors are alive 1 year or more following therapy. Four of 11 patients with brain metastases had a response and 2 had stable disease. Major neurologic toxicity of intracarotid BCNU and cisplatin appeared cumulative and consisted of reversible hemiparesis in 3% of 118 courses, TIA in 1%, expressive aphasia in 9%, lethargy in 3%, seizures in 12%, and reversible confusion in 1%. Retinal toxicity consisted of mild blurring of vision in 4 patients and ipsilateral blindness in 5 patients. Three of 22 patients who had received supraophthalmic infusion later developed evidence of leukoencephalopathy. Intracarotid BCNU and cisplatin appears to have modest increase in activity over intracarotid cisplatin alone (Cancer 54:794, 1984), however, neurologic and retinal toxicity may also be increased.
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PMID:Phase II trial of intracarotid BCNU and cisplatin in primary malignant brain tumors. 370 37

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

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

The centrally active, alpha-2 adrenergic receptor agonist clonidine was given to 12 spinal cord injury patients with problematic spasticity not adequately controlled by recognized spasmolytic drug therapy. Five patients had an excellent reduction and 2 patients had some reduction in clinical spasticity (average dose 0.39 mg daily). Four of the 7 responders discontinued clonidine because of adverse reactions after an average of ten weeks of therapy. Three responders have continued to tolerate the drug well with excellent control of spasticity for 18 to 34 months. Five patients had no change in clinical spasticity (average dose of 0.24 mg daily). Three of the non-responders discontinued clonidine because of adverse reactions after an average of three weeks of therapy. Significant associated adverse reactions included syncopal seizures (3), cerebrovascular accident (1), deep vein thrombosis (1), autonomic hyperreflexia (3), lethargy/drowsiness (3), and nausea/vomiting (1). Possible mechanisms of action for clonidine to affect spasticity and the unstable cardiovascular system of quadriplegics is discussed. While spinal cord injured patients with severe spasticity may benefit from clonidine, great caution is recommended during its use until further study establishes safe parameters of administration and efficacy is confirmed on controlled studies.
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PMID:Early clinical experience with clonidine in spinal spasticity. 374 98

A case of interhemispheric subdural hematoma (ISH) following closed head injury is reported. Our patient had seizures and mental status changes. Cranial computed tomography (CT) demonstrated areas of increased density along the right side of the falx cerebri and over the right leaf of the tentorium cerebelli. Conservative treatment was chosen and the patient recovered. Ten other patients with ISH were compared with ours. Head injury is the leading cause of ISH. Most patients display confusion, lethargy, or a "falx syndrome," with a delayed interval of prominent neurological deficits from the time of injury until presentation. Although patients with ISH can be successfully treated by medical management, surgical intervention may be required.
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PMID:Interhemispheric subdural hematoma. 379 68

Report of a case of Maple syrup urine disease in a female neonate, with diagnosis at 26th day of life. The neurological picture consisted of alternating periods of hyper with hypotonicity, seizures, lethargy, poor feeding and respiratory arrest. Demonstration of elevation of plasma branched-chain amino-acids, was the most widely available confirmatory test, and the therapy with MSUD resulted in improvement of the patient.
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PMID:[Leucinosis: study of a case]. 383 42

We reviewed the natural history and differential diagnosis of ornithine transcarbamylase deficiency (an X-linked inborn error of urea synthesis) in 13 symptomatic female heterozygotes. The patients presented as early as the first week of life or as late as the sixth year. The most common symptoms before diagnosis were nonspecific: episodic extreme irritability (100 percent), episodic vomiting and lethargy (100 percent), protein avoidance (92 percent), ataxia (77 percent), Stage II coma (46 percent), delayed physical growth (38 percent), developmental delay (38 percent), and seizures (23 percent). Including the proband, 42 percent of the female members of the 13 families studied had symptoms. The median interval between the onset of major symptoms (vomiting and lethargy, seizures, and coma) and diagnosis was 16 months (range, 1 to 142). Five patients had IQ scores below 70 at the time of diagnosis. We suggest that careful evaluation of the family history, the dietary history, the episodic nature of the nonspecific symptoms, the response of these symptoms to the withdrawal of protein, and their frequent onset at the time of weaning from breast milk will permit early diagnosis and might thereby reduce the risk of death or neurologic impairment in female patients with partial ornithine transcarbamylase deficiency.
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PMID:Natural history of symptomatic partial ornithine transcarbamylase deficiency. 394 92


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