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)

Hartnup disease is an inborn abnormality of renal and intestinal transport involving the neutral amino acids. Intermittent pellagra-like rash, attacks of cerebellar ataxia and psychiatric disturbance are characteristic symptoms of this disease. We described here a patient with adult-onset Hartnup disease who presented unique neuropsychiatric symptoms but no dermatologic symptoms, and reported features of amino acids transport in this patient and his family. The patient, a man aged 37 years, was referred to us because of lasting daytime bruxism. He is the second child of healthy parents who are first cousin; his elder brother who has been mentally retarded became bed-ridden and died at 32 years of age. His younger brother is completely healthy. Although the patient's development in infancy has been slightly retarded, he completed compulsory 9-year education. At 29 years of age, he experienced episodes of diplopia, ataxic gait and insomnia, and at 33 years of age, of transient stupor. There had been no history of photosensitivity or dermatitis. On neurological examination, there were trunkal ataxia, increased muscular tone and decreased mental activity besides bruxism. These symptoms remained unchanged despite of several medications including trihexyphenidyl, diazepam, halloperidol, tiapride and sulpiride. Two months later, the patient became stuporous; bruxism and hypertonicity became exaggerated. Myerson's sign, sucking reflex and grasp reflex in both hand appeared. There was no dermal lesion. A cranial computed tomography revealed a small calcification in the right frontal subcortical region and a single photon emission tomography indicated possible bifrontal hypoperfusion. Electroencephalograms demonstrated non-specific slowing. Somatosensory evoked potentials and nerve conduction velocities were normal. There were constant indicanuria and amino-aciduria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adult-onset Hartnup disease presenting with neuropsychiatric symptoms but without skin lesions]. 258 82

The widespread use of phenytoin results in frequent accidental and intentional toxicity. Metabolism is enzymatic and can be described by Michaelis-Menten kinetics. This results in an increased half-life in overdose situations and a protracted clinical course which may last a week or more. The primary toxicity is on the central nervous system. The most common initial finding in mild toxicity is nystagmus. As concentrations increase ataxia, decreased coordination, hyper-reflexia, slurred speech and diplopia may develop. Progressive increases result in confusion, lethargy and coma. Various methods tried to increase elimination including dialysis, haemoperfusion, diuresis and plasmaphoresis have been ineffective and are not without risk. Meticulous supportive care including ventilation if necessary should provide a good clinical outcome. Multiple-dose activated charcoal may be helpful in shortening the duration of symptoms.
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PMID:Clinical features and management of poisoning due to phenytoin. 267 94

Transient recurrent confusional and stuporous states of nonepileptic origin are clearly less frequent than epileptic ones. They are relatively common in diseases of disturbed vigilance, like narcolepsy, idiopathic hypersomnolence, and sleep apnea. These patients often suffer from attacks of hypovigilance, characterized by altered awareness, automatic behaviour and partial or complete amnesia for the attack. Because of the memory 'black outs' and the frequently associated hypnagogic hallucinations, the patients behave inappropriately and often appear confused. Confusional states also typically arise during basilar artery migraine attacks. This special form of complicated migraine predominantly affects young females and is characterized by symptoms and signs of brain stem dysfunction such as vertigo, ataxia, paresthesia, limb weakness, dysarthria; in 75% of the cases, disorders of consciousness dominate. Transient ischemic attacks are sometimes recurrent and, when involving the cranial basilar territory, may result in confusional states without significant motor dysfunction. Attacks of transient global amnesia are possibly also ischemic in nature and are assumed to arise from transient bilateral limbic failure. Affecting only memory functions, they are strictly spoken not confusional, but must nevertheless be taken into consideration when proper observation during the attack was not possible.
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PMID:[Non-epileptic impaired consciousness in neurologic diseases]. 267 60

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

T-2 toxin [3 alpha-hydroxy-4 beta, 15-diacetoxy-8 alpha-(3-methylbutyryloxy)-12,13-epoxytrichotec-9-ene] is an emetic Fusarium trichothecene mycotoxin known to cause lethargy, ataxia and feed refusal in economically important animals. Experiments were conducted to determine the effect of acute oral doses of T-2 toxin on tissue concentrations of neurotransmitters thought to play some role in regulation of feed consumption. Sixty-seven male weanling rats were intubated with a few grams of diet in a liquid slurry with or without 2.0 mg T-2 toxin per kilogram of body weight. At 1, 2, 4, 6, 8, 12, 24 and 48 h following dosing, rats were killed, and brains, spleens, hearts and adrenal glands were excised and analyzed for concentrations of neurotransmitters and metabolites using high-performance liquid chromatography with electrochemical detection. Administration of T-2 toxin caused increases in brain concentrations of tryptophan and serotonin at the early time intervals after dosing. Brain concentrations of dopamine increased, whereas concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) decreased at the later time interals following dosing. Concentrations of dopamine were increased in adrenal glands, whereas epinephrine concentrations decreased. Epinephrine was detected in spleen and heart after administration of T-2 toxin. It was concluded that the increase in brain indoleamines induced by T-2 toxin could contribute to feed refusal in animals suffering from T-2 toxicosis.
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PMID:Effect of acute oral doses of T-2 toxin on tissue concentrations of biogenic amines in the rat. 289 54

The traditional treatment of African sleeping sickness (trypanosomiasis) with central nervous system involvement is an organic arsenical compound, melarsoprol, which is associated with severe and even life-threatening side effects. A polyamine biosynthesis inhibitor, eflornithine (chemical name, DL-alpha-difluoromethylornithine, supplied as monohydrochloride monohydrate), was used to treat a 3 1/2-year-old child with newly diagnosed severe trypanosomiasis that had been acquired more than two years previously in Zaire or the Congo. Treatment consisted of 300 to 400 mg/kg/d of eflornithine by continuous intravenous infusion for 25 days followed by 300 mg/kg/d of eflornithine by mouth divided in four equal doses daily for 17 days. The child's recovery was dramatic, with eradication of blood and cerebrospinal fluid parasites in the first week. Cerebrospinal fluid pleocytosis resolved completely. Her generalized adenopathy and fever gradually resolved. Severe ataxia, inability to walk or to change posture on her own, marked language regression, and lethargy all improved during and after her therapy. The drug was well tolerated; the only noted adverse effect was transient thrombocytopenia during the fourth week of therapy. Eflornithine was a safe and effective agent for treatment of trypanosomiasis with central nervous system involvement in this child.
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PMID:African sleeping sickness in the United States. Successful treatment with eflornithine. 312 3

Chickens infected as embryos with RAV-7 developed neurological signs including ataxia, lethargy, and imbalance. Evoked spinal cord potentials for RAV-7 infected SC chickens were considerably slower (64.8 m/s) than for uninfected SC (103.4 m/s), genetically hypothyroid (OS) (93.9 m/s) or special C (95.1 m/s) chickens. Conduction velocity measurements of sciatic nerves showed normal values for all the chickens examined in this study. Histopathological studies revealed non-suppurative meningoencephalomyelitis in RAV-7 infected SC chickens. The inflammatory infiltrate consisted of lymphocytes, macrophages, and occasional plasma cells. The cells in the infiltrate reacted with mouse monoclonal antibodies directed against la and T-cell antigens. Astrocytic hypertrophy and hyperplasia, demonstrated by the use of monoclonal antibody specific for glial fibrillary acidic protein (GFAP), was associated with the CNS lesions. The results of this investigation indicate that RAV-7 causes significant central nervous system lesions and functional impairment in the infected chicken. This system may serve as a useful model for studying retrovirus-induced neurological dysfunction.
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PMID:Functional and structural alterations of the nervous system induced by avian retrovirus RAV-7. 319 74

A 41 year old male presented with headache, lethargy, and ataxia and found to have a left temporal lobe mass and a leukoerythroblastic peripheral blood smear. The latter prompted an iliac crest bone marrow biopsy on which a diagnosis of metastatic glioma was made and verified by immunohistologic characterization. The patient was treated with cranial irradiation and simultaneous systemic BCNU (bis-dichloroethylnitrosurea) with complete response. This case with diffuse bone marrow involvement demonstrates that a glioblastoma is capable of extracranial metastases without previous intervention. From a review of reported cases of gliomas of extraneural metastasis, it is concluded that untreated gliomas are capable of vascular spread although less frequently than previously manipulated tumors.
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PMID:Intracranial astrocytoma with diffuse bone marrow metastasis: a case report and review of the literature. 329 52

Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
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PMID:Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. 329

Portosystemic shunt was diagnosed in a 6-month-old Quarter Horse filly with acute onset of apparent blindness and a 3-month history of depression, lethargy, and ataxia. Clinicopathologic test results indicated slightly high gamma-glutamyl transpeptidase activity and serum total bilirubin concentration. Sulfobromophthalein half time was prolonged, and plasma ammonia and serum bile acid concentrations were high as well. Histopathologic findings of percutaneous liver biopsy included widespread hepatocyte atrophy and numerous prominent small arterioles in the area of the portal triad. On the basis of history, clinical findings, and clinicopathologic abnormalities, a presumptive diagnosis of portosystemic vascular anomaly was made. To confirm the tentative diagnosis, nuclear hepatic scintigraphy and operative mesenteric portography were performed. Medical treatment was unsuccessful, and the foal was euthanatized. Portosystemic shunts have been described in dogs and cats, but few cases have been reported in large animal species. Other, more common causes of neurologic abnormalities in foals, such as trauma, vertebral body abscesses, brain abscesses, and meningitis, must be ruled out before portosystemic shunt is considered.
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PMID:Clinical and diagnostic features of portosystemic shunt in a foal. 335 82


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