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)

Mechanisms producing hypertriglyceridemia during bacterial sepsis have not been well defined. In this study lipid disposal mechanisms were assessed in 76 infected and 19 control male rhesus monkeys by the ability to dispose of triglycerides after: (1) oral lipid loading; (2) intravenous lipid loading; and (3) by lipolytic enzyme activity tests as measured by postheparin lipolytic activity (PHLA). Studies were performed both before and 48 hr after intravenous inoculation with either Salmonella typhimurium or Diplococcus pneumoniae when illness was uniformly severe and fasting serum triglyceride elevations were increased maximally. S. typhimurium-infected monkeys demonstrated significant fasting hypertriglyceridemia (p is less than 0.001), reduced clearance of orally and intravenously administered lipid and markedly reduced PHLA. During this gram-negative sepsis, mild lethargy, slight diarrhea, and a 2% mortality were observed. During D. pneumoniae sepsis, average fasting triglyceride concentrations were slightly, but not significantly elevated. While oral lipid clearance was impaired, intravenous lipid clearance was unimpaired, and PHLA was slightly reduced. Marked lethargy, agitation, and a 20% mortality were present during this gram-positive infection. Results of this study support the concept that an impairment of lipid disposal mechanisms, particularly during gram-negative sepsis with S. typhimurium, may significantly contribute to the observed hypertriglyceridemia.
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PMID:Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys. 0 48

Case histories of four elderly patients with central nervous system signs of digitalis toxicity were reviewed. Evidence of toxicity included lethargy, depression which was not present previously, confusion, restlessness, emotional instability, hyperventilation, and vertigo. Vomiting developed four days after the onset of the mental changes. No cardiac arrhythmias were observed. Digoxin serum levels ranged between 4.2 and 7.0 ng/ml. Serum potassium values were within normal limits. Three of the four patients recovered with a return of their mental status to the pretoxic state. The fourth case was fatal. At autopsy long-standing myocardial ischemia was the only significant finding.
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PMID:Digitalis delirium in elderly patients. 53 71

A simple implanted device was used to occlude acutely the left middle cerebral artery (MCA) of 16 conscious cats. Eight received no treatment and 8 were given intravenous mannitol (1.2 gm/kg) at the time of occlusion. The initial neurological findings in both groups were similar, that is, agitation, forced circling, and right hemiparesis. The treated cats remained alert but the untreated cats became lethargic and drowsy. Perfusion with a mixture of colloidal carbon and buffered paraformaldehyde was carried out from 30 minutes to 6 hours following MCA occlusion. Results of morphological examination of brains from the treated and untreated groups suggested that mannitol had a protective effect upon cerebral tissue during the primary phase of acute focal ischemia. Light microscopic analysis of neuronal alterations demonstrated considerable preservation of neurons in brains of treated cats. Beneficial effect of mannitol was attributed partly to prevention of capillary narrowing and suppression of ischemic cerebral edema.
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PMID:Modification of acute focal ischemia by treatment with mannitol. 62 43

Digitalis is a ubiquitous drug in modern clinical medicine and digitoxicity is one of the more common iatrogenic disorders. Psychiatric problems are often overlooked as manifestations of digitalis excess and may range from mild disorientation, lethargy, or restlessness to full blown delirium. In this paper we discuss two patients who presented to a psychiatric inpatient unit and were later found to be digitoxic. Psychiatrists are advised to consider digitalis as a possible cause of mental abnormalities and are reminded that psychiatric signs may be the first indication of a potentially lethal drug toxicity. Psychiatric patients may also be at special risk for the development of digitoxicity because of erratic drug taking, electrolyte imbalance or increased autonomic tone.
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PMID:Digitalis delirium: psychiatric considerations. 70 Sep 28

Nineteen patients with senile brain disease (including 2 with parkinsonian symptoms) were treated with amantadine in an oral dosage of 200--300 mg daily. Seven showed definite clinical benefits such as increased alertness and decreased agitation, and 2 others showed slight benefits. However, in only one instance was the benefit maintained without complications. Toxic effects such as overactivity, anxiety and visual hallucinations were observed in 8 patients. Withdrawal effects (e.g., lethargy and staggering) occurred when amantadine was discontinued. The electroencephalograms (EEGs) of all 19 patients showed a frequency increase, chiefly of occipital alpha activity, and sometimes a return to normal, irrespective of clinical changes. Toxic side effects were associated with particularly prominent EEG acceleration. In 10 of the 19 patients, the clinical changes were further validated by by additional psychologic assessments. Although the value of amantadine is limited when given in this way to patients with senile brain disease, it seems important to observe its effects in drug combinations aimed at correction of neurotransmitter imbalances.
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PMID:Amantadine in senile dementia: electroencephalographic and clinical effects. 75 72

As a causative factor in spontaneous subarachnoid hemorrhage, vascular anomalies, especially aneurysm or arteriovenous malformation, have been generally recognized. On the other hand, subarachnoid hemorrhage from brain tumor and cryptic vascular malformation are rare. We experienced two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma as an initial symptom. Case 1: A 48-year-old woman, who complained of severe headache and vomiting on Feb. 10th, 1972, gradually became lethargic. Lumbar puncture revealed moderately hemorrhagic C.S.F.. On the fifth day after the onset, she was admitted to our hospital. On admission she showed disorientation and disturbance of resent memory. Aphasia and agnosia were slightly observed. On ophthalmologic examination right homonymous lower quadrant hemianopsia was observed. The carotid angiogram showed slight square shift of the anterior cerebral artery to the right side, elevation of the middle serebral artery and a homogeneous tumor stain in the occipital region in capillary phase. A walnut sized tumor invading the middle portion of the left lateral sinus and showing firm adhesion to the tentrium was found. There was an intracerebral hematoma behined the tumor. The tumor, the tentrium and the lateral sinus were extirpated en bloc and the intracerebral hematoma was aspirated. Histologically, the tumor was angioblastic meningioma. Case 2: A 7-year-old boy, who complained of severe abrupt headache, nuchal pain and vomiting on Sept. 17th, 1972, became gradually lethargic. Lumbar puncture revealed hemorrhagic C.S.F., On the tenth day after the onset, he was admitted to our hospital. He showed confusion and agitation. The carotid angiogram showed an unrolling of the pericallosal artery, but no findings of space taking lesions. An air study indicated a globular filling defect protruding into the anterior horn of the right lateral ventricle. The tumor located in the laterobasal wall of the anterior horn was removed picemiel by transventricular approach. Histologically, the tumor was vascular hamartoma. Furthermore, we discussed various brain tumors showing subarachnoid hemorrhage as an initial symptom, its frequency and bleeding mechanism on the literature.
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PMID:[Two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma (author's transl)]. 98 94

A new antidepressant Fluoxetine, a serotonin re-uptake inhibitor, was tried on 26 resistant depressed patients. There were four drop out due to severe side effects. Improvement was noticeable soon after the first week and was maximum within 3 weeks of medication in 14 (63.6%) patients while in 8 (36.4%) patients it was as late as 6-12 weeks. The decline in improvement after three weeks in 7(31.8%) patients, needs attention in future studies. Bradycardia in 2 patients above the age of sixty indicate that the drug should be used with caution in elderly. GIT disturbance, insomnia, anorexia, restlessness and lethargy were common side effects. A well planned double blind study is recommended before its place is assigned in our patient population.
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PMID:Early experience with fluoxetine. 176 70

Delirium, an acute confusional state, is an organic brain syndrome that manifests deficits in attention, irrelevant or rambling speech, and other cognitive deficits. Its symptoms often fluctuate over the course of the day, and patients may be hyperactive--for example, restless and screaming--or hypoactive--for example, quiet, inactive, and stuporous. Occurring in approximately 20% of hospitalized elderly patients, delirium is the most common psychiatric syndrome in acutely ill general medical and surgical patients. Fifteen to 30% of delirious patients expire, and others are prone to a variety of complications: falls, pressure ulcers, oversedation, dehydration, and others. Almost any acute illness can cause delirium in the elderly, but the most common offenders are acute infections and drugs. Many patients have a pre-existing dementia. The first step in arriving at a correct diagnosis is to distinguish delirium from other psychiatric syndromes that can cause confusion, such as dementia, depression, schizophrenia, and mania. Once delirium is established, a comprehensive general examination and a mental status examination is required. Routine laboratory and radiologic tests are directed at the common metabolic and infectious disorders that precipitate delirium. Treatment is directed at the underlying acute illness. In all patients, it is important (1) to treat the underlying acute illness, (2) to provide appropriate fluid and electrolytes, (3) to discontinue any unnecessary drugs, and (4) to allay the patient's fear and agitation through the use of simple, repetitive instructions, orientation cues, and by limiting the use of physical restraints. If psychotropic medications are needed to treat psychotic symptoms, to prevent patients from harming themselves or others, or to facilitate necessary diagnostic and therapeutic interventions, then haloperidol is the drug of choice in most instances. Drugs with anticholinergic properties should be avoided.
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PMID:Delirium in the elderly. 218 81

The sedative effect of SCH 34826, an enkephalinase inhibitor, was evaluated by studying electroencephalographic (EEG) activity, behaviour and the sleep-waking cycle in the rat. The reference opioid, morphine, was used for comparison. After administration of morphine (10 mg/kg s.c.) the rats were motionless and stuporous at first and then hyperactive. An increase of slow wave sleep, at the expense of both wakefulness and REM sleep was recorded, with high-amplitude slow wave bursts appearing in the EEG tracings during the waking, albeit stuporous, phase. Relative spectral power in the 1-4 and 12-16 Hz bands was increased and there was a shift of the dominant frequency to a lower frequency. The specific opioid antagonist, naltrexone, readily reversed most of these effects. The drug SCH 34826 (10-100 mg/kg p.o.) had no effect on the parameters examined; large doses (300 and 1000 mg/kg p.o.) induced restlessness in some animals, resulting in increased waking. This effect was antagonized by naltrexone. The data indicate that SCH 34826, at doses far greater than those proposed for clinical use, is devoid of sedative liability and does not induce any of the behavioural or EEG effects typical of morphine.
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PMID:Effects of the enkephalinase inhibitor SCH 34826 on the sleep-waking cycle and EEG activity in the rat. 232 30

102 children with acute gastroenteritis were thought by the admitting junior doctors to be 5% or more dehydrated. As judged by subsequent weight recovery in hospital, the main indicators of mild to moderate dehydration were decreased peripheral perfusion, deep breathing, decreased skin turgor, high urea, low pH, and a large base deficit; a history of increased thirst was just short of statistical significance. Dehydration was not indicated by a history of oliguria, by the presence of restlessness or lethargy, sunken eyes, dry mouth, or a sunken fontanelle or by the absence of tears. Clinical signs of dehydration became apparent at 3-4% rather than 5% dehydration. The degree of dehydration was overestimated by a mean of 3.2%; this caused unnecessary hospital admissions and overtreatment with intravenous fluid.
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PMID:Clinical signs of dehydration in children. 257 63


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