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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the comparatively short history of human evolution man's lifespan has doubled, posing the question, by what means was this prolongation of life achieved. One line of thought correlates lifespan with oxygen consumption and energy generation, pointing out that small homeothersms which expend energy at a very high rate, are invariable short lived, while animals living more economically in terms of energy expenditure, like some heterotherms and large homeotherms, can attain greatly increased lifespan potentials. The correlation between lifespan and energy expenditure is generally valid, but some animals with low energy needs, notably tropical animals and some lethargic, inactive animals, do not live as long as expected on the basis of the theory. The present paper suggest that the aging process could be accelerated by hyperthermia and the longevity of some homeotherms, beside its connection with energy needs, could also be correlated with the evolution of temperature regulating mechanisms, resulting in more accurate thermal homeostasis. Man's uniquely capacious sweating mechanism, for example, may play a part in the attainment of his long life.
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PMID:The evolution of human longevity. 744 91

Dietary cells and the vitamins B12 and folate are necessary for the production of the red blood cells (erythrocytes), which carry oxygen from the lungs to the tissues and carbon dioxide from tissues to lungs. Deficiency of either one results in anaemia, which is characterised by low haemoglobin concentration. Symptoms result from reduced tissue oxygenation and include weakness, lethargy, palpitation, headache and shortness of breath. The first-time laboratory test of all patients suspected of being anaemic is the full blood count. Results of a full blood count may suggest the anaemia is caused by a nutritional deficiency of B12 folate or iron. Laboratory measurement of the concentration in blood of iron and vitamin B12 and folate, along with several other tests described here, are useful in the differential diagnosis of the anaemic patients.
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PMID:Deficiency testing for iron, vitamin B12 and folate. 760 52

Pharyngeal flaps are often used to correct velopharyngeal insufficiency. They produce a permanent partial obstruction of the velopharyngeal space. Respiratory obstruction and obstructive sleep apnea have been reported following this surgery. We undertook a study to find out the incidence of sleep apnea associated with pharyngeal flap surgery. Forty-one children (aged 2 to 22 years) admitted for a pharyngeal flap underwent a polysomnographic recording prior to their surgery. One child with Steinert's disease showed some episodes of obstructive apnea, and the surgery was canceled. Forty children underwent pharyngeal flap surgery, and polysomnography with continuous arterial saturation was repeated following surgery. Postoperative polysomnograms were normal in 26 patients (65 percent) and abnormal in 14 patients (35 percent). Among the 14 abnormal patients, we found 6 with obstructive apneas, 6 with central apneas, and 2 with both central and obstructive apneas. Ten of the 14 abnormal patients were restudied in the following months. Eight children had normal recordings, while 2 had central apneas. The 4 patients who declined a follow-up recording had no clinical symptoms of respiratory difficulty when sleeping. Of the 2 children with abnormal recordings on long-term follow-up, 1 is asymptomatic, while the second has persistent snoring, nocturnal awakening, sweating, and daytime lethargy. A section of his flap has been recommended. Independent analysis of arterial oxygen saturation revealed that the percentage of time with a saturation of less than 90 percent identifies patients with clinically significant apneas. Our data show that significant sleep apneas following pharyngeal flaps may not be as frequent or permanent as previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnea following a pharyngeal flap: a feared complication. 813 86

We reported here 19-year-old man suffering from circadian sleep-wake (S-W) rhythm disturbance after total tumor resection and whole brain irradiation. This 19-year-old man was diagnosed as having astrocytoma in the right temporal lobe by CT scan and angiography at the age of 6 months. After total tumor resection and whole brain irradiation (60Co 60 Gy), he showed profound psychomotor retardation, endocrinologic dysfunction including hypothyroidism and growth hormone deficiency, and sleep-wake rhythm disturbance. At the age of 19, brain MRI revealed asymmetrical low intensity in the hypothalamic region. On endocrinological examination panhypopituitarism due to primary hypothalamic lesion was evident. His S-W rhythm was disturbed showing a dispersed type sleep, i.e., sleep periods were dispersedly distributed throughout the 24 hours. So he showed a lethargic tendency in the daytime. All-day polysomnography revealed abnormal sleep structure such as the absence of sleep spindle and hump, peripheral apnea, snoring and low oxygen saturation. After L-thyroxine supplementation his daily activity improved gradually. The decrease in short time sleep and tendency of a free-running rhythm were observed and oxygen saturation improved remarkably. Peripheral apnea and snoring disappeared. The wakening effect of L-thyroxine administration may be due to improvement of hypothyroidism symptom such as myxoedematous pharynx. In addition, it seems related to the alteration of the central S-W rhythm regulation, because free-running rhythm appeared after L-thyroxine administration. Vitamin B12 (VB12), which has been reported to be effective for sleep-wake rhythm disorders, was not effective for our patient's free-running rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Circadian rhythm disturbance after radiotherapy for brain tumor in infantile period--clinical effect of L-thyroxine and vitamin B12]. 821 1

Fatigue and lethargy, common symptoms in uraemia, have been attributed to many factors. To assess possible bioenergetic contributions to this, we examined the forearm muscle of five patients in end-stage renal failure using 31P-magnetic resonance spectroscopy. There was a small increase in the ratio of intracellular inorganic phosphate to ATP in resting muscle, suggesting an increased cytosolic phosphate concentration. During exercise, increased phosphocreatine breakdown was accompanied by rapid intracellular acidification and an increase in calculated lactic acid accumulation in the muscle of the uraemic subjects, suggesting glycolysis dominating over oxidative phosphorylation as a source of ATP. After exercise, the half-time of phosphocreatine (PCr) recovery was longer in the uraemic subjects, suggesting diminished mitochondrial function. The initial rate of PCr resynthesis was not significantly decreased, but when account was taken of the high cytosolic ADP concentration (which drives mitochondrial oxidative ATP synthesis) the calculated maximum oxidative capacity was significantly reduced in the uraemic subjects. Thus there was evidence of mitochondrial dysfunction in uraemia due either to limitation of oxygen supply, reduced mitochondrial content, or an intrinsic mitochondrial defect. This resulted in increased phosphocreatine depletion and increased glycolytic ATP production during exercise and there was partial compensation of the mitochondrial abnormality by increased ADP concentration. In three of these patients studied after elevation of haemoglobin with erythropoeitin (from 8 to 12 g/dl), initial phosphocreatine breakdown and lactic acid accumulation during exercise were normalized, while exercise duration and calculated maximum oxidative capacity remained significantly abnormal. This suggests that anaemia contributes to these metabolic abnormalities but does not fully explain them.
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PMID:Effect of chronic uraemia on skeletal muscle metabolism in man. 838 87

In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. Methaemoglobinaemias are usually the result of xenobiotics, either those that may directly oxidise haemoglobin or those that require metabolic activation to an oxidising species. The most clinically relevant direct methaemoglobin formers include local anaesthetics (such as benzocaine and, to a much lesser extent, prilocaine) as well as amyl nitrite and isobutyl nitrite, which have become drugs of abuse. Indirect, or metabolically activated, methaemoglobin formation by dapsone and primaquine may cause adverse reactions. The clinical consequences of methaemoglobinaemia are related to the blood level of methaemoglobin; dyspnoea, nausea and tachycardia occur at methaemoglobin levels of > or = 30%, while lethargy, stupor and deteriorating consciousness occur as methaemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% are usually fatal. Cyanosis accompanied by a lack of responsiveness to 100% oxygen indicates a diagnosis of methaemoglobinaemia, which should be confirmed using a CO-oximeter. Pulse oximeters do not detect methaemoglobin and may give a misleading impression of patient oxygenation. Methaemoglobinaemia is treated with intravenous methylene blue (methyl-thioninium chloride; ;1 to 2 mg/kg of a 1% solution). If the patient does not respond, perhaps because of glucose-6-phosphate dehydrogenase (G6PD) deficiency or continued presence of toxin, admission to an intensive care unit and exchange transfusion may be required. Dapsone-mediated chronic methaemoglobin formation can be reduced by coadministration of cimetidine to aid patient tolerance. Increasing knowledge and awareness of drug-mediated acute methaemoglobinaemia among physicians should lead to prompt diagnosis and treatment of this potentially life-threatening condition.
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PMID:Drug-induced methaemoglobinaemia. Treatment issues. 882 17

The thermal and metabolic physiology of Chalinolobus gouldii, an Australian vespertilionid bat, was studied in the laboratory using flow-through respirometry. Chalinolobus gouldii exhibits a clear pattern of euthermic thermoregulation, typical of endotherms with respect to body temperature and rate of oxygen consumption. The basal metabolic rate of euthermic Chalinolobus gouldii is approximately 86% of that predicted for a 17.5-g mammal and falls into the range of mass-specific basal metabolic rates ascribed to vespertilionid bats. However, like most vespertilionid bats, Chalinolobus gouldii displays extreme thermolability. It is able to enter into torpor and spontaneously arouse at ambient temperatures as low as 5 degrees C. Torpid bats thermoconform at moderate ambient temperature, with body temperature approximately ambient temperature, and have a low rate of oxygen consumption determined primarily by Q10 effects. At low ambient temperature (< 10 degrees C), torpid C. gouldii begin to regulate their body temperature by increased metabolic heat production; they tend to maintain a higher body temperature at low ambient temperature than do many northern hemisphere hibernating bats. Use of torpor leads to significant energy savings. The evaporative water loss of euthermic bats is relatively high, which seems unusual for a bat whose range includes extremely arid areas of Australia, and is reduced during torpor. The thermal conductance of euthermic C. gouldii is less than that predicted for a mammal of its size. The thermal conductance is considerably lower for torpid bats at intermediate body temperature and ambient temperature, but increases to euthermic values for torpid bats when thermoregulating at low ambient temperature.
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PMID:Temperature regulation and metabolism of an Australian bat, Chalinolobus gouldii (Chiroptera:Vespertilionidae) when euthermic and torpid. 905 7

Noninvasive positive pressure ventilation (NPPV) via nasal mask is well known to be effective in the treatment of acute respiratory failure (ARF) secondary to chronic obstructive pulmonary disease (COPD). A case of ARF with hypercapnic coma due to exacerbation of COPD is described. Six hours of conservative therapy with oxygen and medical treatment did not show any result. As endotracheal intubation (ET) was avoided on the basis of advanced age, poor life expectancy of the patient and family wish, NPPV was set up using a pressure triggered ventilator. After 61 hours of uninterrupted NPPV, the acid-base alteration and the lethargic status was fully reversed. The conclusions is drawn that NPPV may be useful also in the treatment of patients affected by severe decompensated hypercapnic respiratory failure in whom ET is not indicated.
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PMID:[Non-invasive nasal ventilation in a a case of hypercapnic coma]. 948 10

This 3-month study evaluated the effects of hyperbaric oxygen on drug-induced neuropathies in 22 patients with human immunodeficiency virus. All patients included in the study had been taking an antiretroviral medication for at least 12 months and had subjective symptoms of numbness or tingling, lethargy, and a decrease in deep tendon reflex. Patients with an active substance abuse history or Kaposi's sarcoma were excluded. Of the 20 patients who completed the series, 17 had significant improvement, 2 had a demyelinating disorder that may have affected the outcome, and 1 had no change.
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PMID:The effectiveness of intermittent hyperbaric oxygen in relieving drug-induced HIV-associated neuropathy. 964 Sep 6

The patient was born by emergency cesarean section for fetal distress at 35 weeks gestation with a weight of 2740 g. The early neonatal course was complicated by transient tachypnea and renal failure. He was receiving oxygen and diureticus in incubator for 5 days and his condition was very improved on day 5. On day 7 he became lethargy and there was inability to tolerate feeding. Investigation of the cerebrospinal fluid revealed 8,000 leukocytes/microliter. S. marcescens was grown from cultures of both blood and cerebrospinal fluid. Treatment was started with cefotaxime and ampicillin every 6 hour. On day 14 the CT showed a brain abscess located parietooccipitally on the left side and diffuse infarction on the right side. On day 14 and 23 recurrence of increased leukocytes in the cerebrospinal fluid, high values of serum CRP and deterioration of clinical symptoms were observed. It is thought that the episodes show rupture of the abscess into the lateral ventricle. On day 55 surgical drainage was performed for the hydrocephalus. On day 110 the abscess was not found in the brain CT scan. His psychomotor development 3 years later was equivalent to two years old and he had secondary epilepsy.
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PMID:[Serratia marcescens brain abscess in a newborn]. 978 May 89


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