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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Encephalopathy is a potentially fatal toxicity of ifosfamide. Clinical manifestations of encephalopathy range from fatigue and confusion to coma and death. Early identification of this toxicity and prompt cessation of ifosfamide are the essential elements in the management of ifosfamide encephalopathy. Accurate prediction of this toxicity is often difficult. Based on the limited available evidence, methylene blue, an electron acceptor, may have a role in the treatment and the prevention of neurotoxicity. This paper reviews the current understanding of ifosfamide encephalopathy.
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PMID:Ifosfamide encephalopathy. 1735 5

In 1892 Osler described 'rapid loss of flesh' in prolonged sepsis. Thereafter, for years, limb weakness was attributed to cachectic myopathy, and difficulty weaning from mechanical ventilation was attributed to diaphragmatic fatigue. In 1961 Mertens described 'coma-polyneuropathies', and in 1971 Henderson and colleagues described polyneuropathy in patients with burns. In 1984 Bolton and colleagues, in a series of reports, defined the clinical, electrophysiological and morphological features of septic encephalopathy and critical illness polyneuropathy. Evidence suggested that polyneuropathy was due to the 'toxic' effects of sepsis. Polyneuropathy was a common cause of difficulty in weaning when lung and cardiac cause had been excluded. Since 1984, cases of critical illness polyneuropathy have been reported from several countries. Moreover, a number of investigators reported instances of critical illness myopathy. Comprehensive studies by Latronico and colleagues indicated that polyneuropathy and myopathy often occurred together in the same patient. With successful treatment of sepsis, improvement often occurred in encephalopathy, polyneuropathy and myopathy, except in very severe cases.
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PMID:The discovery of critical illness polyneuropathy. 1828 19

Lyme disease is the most common tick-borne disease in the United States. This review details the risk factors, clinical presentation, treatment, and prophylaxis for the disease. Information was obtained from a search of the PubMed and MEDLINE databases (keyword: Lyme disease) for articles published from August 31, 1997, through September 1, 2007. Approximately 20,000 cases of Lyme disease are reported annually. Residents of the coastal Northeast, northwest California, and the Great Lakes region are at highest risk. Children and those spending extended time outdoors in wooded areas are also at increased risk. The disease is transmitted to humans through the bite of the Ixodes tick (Ixodes scapularis and Ixodes pacificus). Typically, the tick must feed for at least 36 hours for transmission of the causative bacterium, Borrelia burgdorferi, to occur. Each of the 3 stages of the disease is associated with specific clinical features: early localized infection, with erythema migrans, fever, malaise, fatigue, headache, myalgias, and arthralgias; early disseminated infection (occurring days to weeks later), with neurologic, musculoskeletal, or cardiovascular symptoms and multiple erythema migrans lesions; and late disseminated infection, with intermittent swelling and pain of 1 or more joints (especially knees). Neurologic manifestations (neuropathy or encephalopathy) may occur. Diagnosis is usually made clinically. Treatment is accomplished with doxycycline or amoxicillin; cefuroxime axetil or erythromycin can be used as an alternative. Late or severe disease requires intravenous ceftriaxone or penicillin G. Single-dose doxycycline (200 mg orally) can be used as prophylaxis in selected patients. Preventive measures should be emphasized to patients to help reduce risk.
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PMID:Diagnosis and treatment of Lyme disease. 1845 88

MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is commonly associated with the A3243G mitochondrial DNA (mtDNA) mutation encoding the transfer RNA of leucine (UUR) (tRNA (Leu(UUR))). The pathogenetic mechanisms of this mutation are not completely understood. Neuronal functions are particularly vulnerable to alterations in oxidative phosphorylation, which may affect the function of the neurotransmitter glutamate, leading to excitotoxicity. In order to investigate the possible effects of A3243G upon glutamate homeostasis, we assessed glutamate uptake in osteosarcoma-derived cytoplasmic hybrids (cybrids) expressing high levels of this mutation. High-affinity Na(+)-dependent glutamate uptake was assessed as radioactive [(3)H]-glutamate influx mediated by specific excitatory amino acid transporters (EAATs). The maximal rate (V(max)) of Na(+)-dependent glutamate uptake was significantly reduced in all the mutant clones. Although the defect did not relate to either the mutant load or magnitude of oxidative phosphorylation defect, we found an inverse relationship between A3243G mutation load and mitochondrial ATP synthesis, without any evidence of increased cellular or mitochondrial free radical production in these A3243G clones. These data suggest that a defect of glutamate transport in MELAS neurons may be due to decreased energy production and might be involved in mediating the pathogenic effects of the A3243G mtDNA mutation.
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PMID:MELAS mitochondrial DNA mutation A3243G reduces glutamate transport in cybrids cell lines. 1845 61

On 7 August 1954, the world 42 km marathon record holder, Jim Peters, collapsed repeatedly during the final 385 metres of the British Empire and Commonwealth Games marathon held in Vancouver, Canada. It has been assumed that Peters collapsed from heatstroke because he ran too fast and did not drink during the race, which was held in windless, cloudless conditions with a dry-bulb temperature of 28 degrees C. Hospital records made available to us indicate that Peters might not have suffered from exertional heatstroke, which classically produces a rectal temperature > 42 degrees C, cerebral effects and, usually, a fatal outcome without vigorous active cooling. Although Peters was unconscious on admission to hospital approximately 60 minutes after he was removed from the race, his rectal temperature was 39.4 degrees C and he recovered fully, even though he was managed conservatively and not actively cooled. We propose that Peters' collapse was more likely due to a combination of hyperthermia-induced fatigue which caused him to stop running; exercise-associated postural hypotension as a result of a low peripheral vascular resistance immediately he stopped running; and combined cerebral effects of hyperthermia, hypertonic hypernatraemia associated with dehydration, and perhaps undiagnosed hypoglycaemia. But none of these conditions should cause prolonged unconsciousness, raising the possibility that Peters might have suffered from a transient encephalopathy, the exact nature of which is not understood.
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PMID:Jim Peters' collapse in the 1954 Vancouver Empire Games marathon. 1892 34

Pellagra is associated with low levels of vitamin B3 (niacin) and/or tryptophan and often involves other other B vitamins. Since the time Gasper Casal first described the disease in 1972, it was observed that the patients with pellagra were all poor, subsisted mainly on maize, and rarely ate fresh meat. Subsequent occurrences have been in the form of epidemic outbreaks, consequent to either introduction to maize as a major food or increased consumption of other niacin-deficient diets like Jowar (Sorgum vulgare). The virtual disappearance of pellagra as an endemic health problem in recent years can be attributed to a rise in the standard of living of farmers and diversification of the diet globally. The clinical picture is a combination of multisystem alterations typically involving gastrointestinal, skin and central nervous system abnormalities. The cardinal manifestations have been popularly known as the three D's, which are dementia, dermatitis and diarrhea. Psychiatric manifestations are fairly common but are easily overlooked due to their non specific nature. These are commonly seen as irritability, poor concentration, anxiety, fatigue, restlessness, apathy and depression. The occurence of psychosis in pellagra is an uncommon finding, which is usually seen in advanced stages of pellagroid encephalopathy, commonly found in chronic alcoholics. Delusional parasitosis has been also reported in this condition, although the association is still controversial. We report a case of pellagra manifesting with delusional parasitosis in a man whose delusion resolved rapidly after he started niacin-augmentation therapy. This case may provide clues to the biological underpinnings of delusional parasitosis as well as niacin treatment as treatment option in similar cases.
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PMID:Rapid resolution of delusional parasitosis in pellagra with niacin augmentation therapy. 1906 87

A solvent can be defined as "a liquid that has the ability to dissolve, suspend or extract other materials, without chemical change to the material or solvent". Numerous chemical or technical processes rely on these specific properties of organic solvents in industry. Occupational exposure to solvents is not rare and some activities may cause substantial exposure to these substances in the workforce. Short-term or acute exposures cause a prenarcotic syndrome, and long lasting exposure conditions have been associated with various neurological and neuropsychiatric disorders, e.g., anosmia, hearing loss, colour vision dysfunctions, peripheral polyneuropathy and depression, but most significantly with the gradual development of an irreversible toxic encephalopathy. For the last 3 decades reports and epidemiological studies have been published reporting sleep disturbances among other complaints, related to long-term exposure to these compounds. In addition, the question has been posed if solvents can be the cause of a sleep apnoea syndrome in exposed workers, or on the contrary, if these workers are misdiagnosed and 'common' sleep apnoea syndromes are the cause of their chronic symptoms of fatigue and memory and attentional disturbances.
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PMID:Sleep disturbances and occupational exposure to solvents. 1920 Dec 27

Moulds are responsible for diseases in humans through the three pathogenetic mechanisms of infection, allergy, and toxicity. Fungal infection is especially a risk factor for immunodeficient patients, but it occurs in immunocompetent patients as well. Fungal allergy is manifested as bronchial asthma, hypersensitivity pneumonitis, allergic bronchopulmonary aspergillosis, or allergic fungal sinusitis. Mycotoxicosis is almost exclusively the result of ingestion of mould-contaminated foodstuffs. In each case there is specificity for the etiologic mould. There is controversy regarding the ability of indoor airborne mould spores to cause human disease through non-specific toxicity via the inhalation route. Pulmonary mycotoxicosis is an established, although rare, occupational disease of farmers who inhale enormous quantities of mycotoxins, endotoxins, and other toxic chemicals from contaminated silage. Other conditions attributed to indoor airborne mycotoxin are unproven. These include infantile pulmonary hemosiderosis, epistaxis, 'toxic encephalopathy', immune dysregulation and a variety of subjective complaints without objective signs of pathology such as fatigue, headache, dyspnea, gastrointestinal distress, neuromuscular and skeletal complaints, etc. Non-specific irritation from moulds via the inhalation route is also a controversial subject that remains unproven. Published studies alleging an epidemiologic causal relationship are unconvincing.
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PMID:Sick Building Syndrome: is mould the cause? 1925 24

Anxiety symptoms are commonly described in children with chronic fatigue syndrome or myalgic encephalopathy (CFS/ME) but to date there has been little information on the type of anxiety children experience or the relationship between anxiety and school attendance, disability or fatigue. The aim of this study was to first describe the prevalence and type of anxiety symptoms in children with CFS/ME compared with a normal European population, and secondly to investigate the association of anxiety symptoms with age, gender, school attendance, fatigue, and physical function in paediatric CFS/ME. Data were prospectively collected on children and young people with CFS/ME referred to a large specialist CFS/ME service. One hundred and sixty-four children with CFS/ME had complete data for the Spence Children's Anxiety Scale. Teenage girls had the highest rates of total anxiety symptoms with 38% (95% CI 27-49) over the cut off (top 10% of normal European population) and significantly higher rates of symptoms in each subscale. Younger girls were more likely to score over the cut off in separation anxiety (37%, 19-40) and social phobia (39%, 25-47). There was no evidence of association between total anxiety symptoms and: time at school, time to assessment, pain or age. Associations with fatigue and physical function were attenuated when adjusted for other variables. Although anxiety symptoms are high in CFS/ME, particularly in teenage girls, it does not appear to be associated with school attendance or other measures of disability. Separation anxiety and social phobia were the most clearly elevated in paediatric CFS/ME.
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PMID:Anxiety in children with CFS/ME. 1945 95

Mutations in nuclear and mitochondrial DNA impacting mitochondrial function result in disease manifestations ranging from early death to abnormalities in all major organ systems and to symptoms that can be largely confined to muscle fatigue. The definitive diagnosis of a mitochondrial disorder can be difficult to establish. When the constellation of symptoms is suggestive of mitochondrial disease, neuroimaging features may be diagnostic and suggestive, can help direct further workup, and can help to further characterize the underlying brain abnormalities. Magnetic resonance imaging changes may be nonspecific, such as atrophy (both general and involving specific structures, such as cerebellum), more suggestive of particular disorders such as focal and often bilateral lesions confined to deep brain nuclei, or clearly characteristic of a given disorder such as stroke-like lesions that do not respect vascular boundaries in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode (MELAS). White matter hyperintensities with or without associated gray matter involvement may also be observed. Across patients and discrete disease subtypes (e.g., MELAS, Leigh syndrome, etc.), patterns of these features are helpful for diagnosis. However, it is also true that marked variability in expression occurs in all mitochondrial disease subtypes, illustrative of the complexity of the disease process. The present review summarizes the role of neuroimaging in the diagnosis and characterization of patients with suspected mitochondrial disease.
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PMID:The use of neuroimaging in the diagnosis of mitochondrial disease. 2081 27


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