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

The obstructive sleep apnea syndrome is a highly prevalent and underdiagnosed disease. Repetitive arousals due to upper airway obstruction lead to hypersomnia. Due to the insidious onset, patients often underestimate the severity of their symptoms. Relatives can give helpful additional informations and should be involved in history taking and motivation for treatment. In general, GP's are confronted with the problem of fatigue and hypersomnia in the first line. They play the most important role in selecting patients for further investigations. The patient history helps to separate hypersomnia from fatigue. Hypersomnia indicates falling asleep at daytime in unappropriate situations, especially when the subject is passive. Often, a multidisciplinary approach including respiratory physicians, ENT specialists, orthopedic dentists and neurologists is warranted. Anatomic narrowing of the upper airway must be ruled out by clinical investigation. Overnight sleep studies detect apneas/hypopneas and repetitive arousals. Continuous positive airway pressure, applied by a nose mask and a flow generator remains the mainstay of therapy. Motivation, counseling and troubleshooting especially in the beginning of this therapy are of outmost importance. Ongoing research aims to improve comfort of nose masks and optimize function of flow generators.
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PMID:[Diagnosis of sleep apnea syndrome--role of family practitioner]. 1095 50

The Fatigue Severity Scale (FSS) is a self-report instrument used to assess levels of fatigue and its effect on daily functioning. The FSS was normed on individuals with multiple sclerosis and has been used in studies examining such factors as obstructive sleep apnea and aerobic exercise. Current research has extended it to obese subjects to assess their level of fatigue in conjunction with a 16-week obesity treatment program. Participants were 118 females with an average age of 45.24 (SD = 11.44). The results yield high pre- and post-test reliability for the FSS and weight loss.
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PMID:Extending the Fatigue Severity Scale to an obese population. 1108 95

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49

Intermittent hypoxia (IH), associated with obstructive sleep apnea, initiates adaptive physiological responses in a variety of organs. Little is known about its influence on diaphragm. IH was simulated by exposing rats to alternating 15-s cycles of 5% O2 and 21% O2 for 5 min, 9 sets/h, 8 h/day, for 10 days. Controls did not experience IH. Diaphragms were excised 20-36 h after IH. Diaphragm bundles were studied in vitro or analyzed for myosin heavy chain isoform composition. No differences in maximum tetanic stress were observed between groups. However, peak twitch stress (P < 0.005), twitch half-relaxation time (P < 0.02), and tetanic stress at 20 or 30 Hz (P < 0.05) were elevated in IH. No differences in expression of myosin heavy chain isoforms or susceptibility to fatigue were seen. Contractile function after 30 min of anoxia (95% N2-5% CO2) was markedly preserved at all stimulation frequencies during IH and at low frequencies after 15 min of reoxygenation. Anoxia-induced increases in passive muscle force were eliminated in the IH animals (P < 0.01). These results demonstrate that IH induces adaptive responses in the diaphragm that preserve its function in anoxia.
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PMID:Selected Contribution: Improved anoxic tolerance in rat diaphragm following intermittent hypoxia. 1135 20

The therapeutic effect of a functional magnetic system on obstructive sleep apnea and the system's operating mechanism have not been examined. Two hypotheses are postulated: a functional magnetic system increases the size of the oral cavity airway passage, or it increases the pharyngeal space. Twenty-eight patients with mild-to-moderate obstructive sleep apnea were examined; 10 patients (9 men and 1 woman; aged, 50.5 +/- 2.6 years) met the study criteria. After baseline nocturnal polysomnography and daytime tiredness self-evaluation, a functional magnetic system was inserted. The functional magnetic system is a mandibular repositioning appliance that uses a pair of attractive magnets (Sm2Co17), placed opposite each other in the jaws, which results in an advancement-to-opening ratio of 1:2. After 8 weeks of functional magnetic system treatment, polysomnography, daytime tiredness, and nighttime snoring were evaluated, and cephalogram radiographs with and without the appliance were taken. It was found that the respiratory disturbance index decreased significantly; minimal oxygen saturation increased significantly, reaching a normal value; day time tiredness improved; snoring declined; the oral cavity anterior region increased significantly, and the pharyngeal airway passages did not change. Reduction in the respiratory disturbance index and enlargement of the anterior oral cavity area were highly and significantly correlated. In conclusion, the functional magnetic system is a reliable mandibular repositioning appliance that has no apparent adverse effects. A functional magnetic system operates by increasing the anterior region of the oral cavity, mainly vertically, with no change in the posterior oral cavity region and pharyngeal airway passages.
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PMID:Cephalometric and polysomnographic analyses of functional magnetic system therapy in patients with obstructive sleep apnea. 1150 Jun 59

A 68-year-old female referred for excessive daytime sleepiness, strong morning headaches, snoring and suspected chronic fatigue syndrome. The polyMESAM examination was performed with following results: Respiratory Disturbances Index--RDI (average number of apnoeas and hypopnoeas in one hour of registration) 26, Oxygen Desaturation Index--ODI (average number of oxygen haemoglobin saturation drops in one hour) 51, basal oxygen haemoglobin saturation 90% and average oxygen haemoglobin saturation minimas 82%. Her condition was rated as grave OSAS. CPAP therapy was, however, impeded by anxiety state caused by claustrophobia. Analysis of lateral cephalogram proved significant constriction of the retrolingual posterior airway space to 6 mm (the bottom standard limit for women is 12 mm), with a relatively good position of the hyoid bone. The genioglossus advancement surgery was therefore performed on the patient as the only causational therapy. Then the patient referred improvement of sleepiness, snoring, fatigue and morning headache. PolyMESAM recorded two months after the surgery showed a strong improvement of OSAS: RDI 11, ODI 14, basal oxygen haemoglobin saturation 93% and average oxygen haemoglobin saturation minimas 89%.
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PMID:[Genioglossal advancement in the surgical treatment of obstructive sleep apnea syndrome in adults]. 1170 82

Many facets of health-related quality of life are diminished in obstructive sleep apnea (OSA) as they are in other chronic medical conditions. We speculated that impairment in health-related quality of life (HRQoL) might result from the fatigue and daytime somnolence associated with the sleep disorder, as an indirect result from the fragmentation of night-time sleep in OSA. Our hypothesis was that sleep fragmentation measures would correlate with poorer HRQoL measured by medical outcomes study (MOS) subscales. Thirty-nine patients with polysomnographically-confirmed OSA participated in this study. Pearson's correlations were performed with the following sleep architecture variables: wake after sleep onset, the total number of brief arousals, the number of respiratory-related arousals, the rate of respiratory events per hour, and total sleep time. To our surprise, although the total number of arousals was associated with health distress (r=-0.481, P < 0.005), it did not correlate with any other subscales indicating poorer physical and mental health. The relatively insensitive measure of total sleep time (TST) correlated in the expected direction with most subscales. However, after controlling for age and gender, respiratory disturbance indices (RDI) and/or number of arousals emerged as significantly associated with mobility, cognitive functioning, social functioning, energy and fatigue, and health distress. Our findings suggest that polysomnographic indicators of sleep quality and sleep continuity may be an important influence determining many aspects of HRQoL in OSA patients.
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PMID:Association between polysomnographic sleep measures and health-related quality of life in obstructive sleep apnea. 1190 60

Mental fatigue in patients with obstructive sleep apnea syndrome (OSAS) was investigated and compared with subjects without OSAS. The study series comprised 189 habitual snoring patients and 75 controls. To measure subjective mental fatigue and somnolence, subjects were asked to complete the Maastricht Questionnaire (MQ) and the Epworth Sleepiness Scale (ESS), respectively, and patients also underwent diagnostic polysomnography. According to the apnea and hypopnea index, patients were classified into the following groups: primary snorers, or having mild, moderate, or severe OSAS. The lowest MQ and highest ESS scores were found in those patients with severe OSAS. It is proposed that the lowest MQ score is due to mental fatigue impairing awareness in patients with severe OSAS, probably because of attention loss.
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PMID:Evaluating mental fatigue in patients with obstructive sleep apnea syndrome by the Maastricht Questionnaire. 1204 11

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.
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PMID:Cardiovascular consequences of sleep-related breathing disorders. 1235 Feb 42

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39


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