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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep physiology, viral serology and symptoms of 14 patients with chronic fatigue syndrome (CFS) were compared with 12 healthy controls. All patients described unrefreshing sleep and showed a prominent alpha electroencephalographic nonrapid eye movement (7.5-11.0 Hz) sleep anomaly (p less than or equal to 0.001), but had no physiologic daytime sleepiness. There were no group differences in Epstein-Barr virus (EBV) antibody titers. The patient group had more fibrositis tender points (p less than 0.0001), described more somatic complaints (p less than 0.0001), and more depressive symptoms (p less than 0.0001). Patients with CFS do not show evidence for a specific chronic EBV infection, but show altered sleep physiology, numerous tender points, diffuse pain, and depressive symptoms. These features are similar to those found in fibromyalgia syndrome.
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PMID:Sleep, Epstein-Barr virus infection, musculoskeletal pain, and depressive symptoms in chronic fatigue syndrome. 132 33

Sleep and fatigue characteristics were evaluated in 72 patients who met major criteria for the chronic fatigue syndrome (CFS), 57 multiple sclerosis (MS) patients preselected for fatigue complaints, and 40 healthy controls. Using previously validated rating scales, CFS patients had significant elevations in fatigue and sleep disturbance compared to the MS and healthy control groups. To confirm these subjective measures, polysomnography was carried out in a subgroup of CFS patients who included sleep disturbance as one of their symptoms on initial clinical interview. In 10 of 16 (62.5%) polysomnography revealed clinically significant and potentially treatable sleep abnormalities. Their sleep disorders included periodic movement disorder (4), excessive daytime sleepiness (3), apnea (2), and narcolepsy (1). We conclude that subjective sleep disturbance is common in CFS and some CFS patients may have objective sleep disorders.
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PMID:Sleep disturbance in chronic fatigue syndrome. 851 58

Traditional aetiological models in neuropsychiatry have placed little emphasis on the abnormal behavioural responses (decreased psychomotor activity, anorexia, weight loss, decreased social exploration and sexual behaviour, impaired cognitive function and increased somnolence) that are common to both psychiatric syndromes, notably depression, and the illness behaviour of sick animals. In recent years, the possible role of cytokines, as mediators of not only the immunological and metabolic responses to infection and inflammation but also a co-ordinated behavioural response, has been described. Further, a range of possible mechanisms for these effects has been postulated, notably involving corticotropin releasing factor (CRF) and prostaglandins of the E series (PgE) with the central nervous system (CNS). Here we outline a series of human clinical conditions where neuropsychiatric syndromes co-occur with a host response to infection or inflammation. These may be characterized by cytokine production (e.g. acute, recurrent and chronic viral illness, systemic autoimmune diseases and chronic fatigue syndrome). Other clinical situations characterized by exposure to or in vivo production of cytokines (e.g. treatment of chronic infections and malignancies, progression and/or recurrence of malignancies) are also discussed. We postulate that the stereotyped behavioural repertoire observed is mediated by cytokine-dependent mechanisms within the CNS. Systematic studies of the behavioural responses of such patient groups are suggested, noting specifically correlations between the time course and severity of immune and neuroendocrine and behavioural responses and dose-response effects.
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PMID:Are cytokines associated with neuropsychiatric syndromes in humans? 884 62

Periodic limb movements of sleep and the restless legs syndrome are not diagnoses but rather an indication that there is some CNS disturbance and are associated with an ever-growing number of conditions. They are very common, exist in many forms and are often overlooked by physicians. It is the author's opinion that they are parts of what has been called an akathisia syndrome in the most severe situations and may include the same mechanisms that underlie attention disorders, chronic fatigue syndrome and "sun-downing." They are likely parts of a syndrome caused by dysfunction in a complex brainstem center. This center's normal function is to maintain a smooth electrical template on which discrete neuronal impulses sculpture the rich repertoire we recognize as sensory and motor function awake and to effect a smooth "switching" mechanism allowing sleep to occur without motor and sensory input invading consciousness (awakening). While the DA-ergic CNS pathways have been thought to be the primary neurotransmitter involved, the opioids secondary, there is mounting evidence that the situation is far more complicated, that many neurotransmitter, including stimulating and inhibiting amino acids, play a part. These patients agonize with their indisposition but can be helped by various treatments. Treatment alleviates not only the distress caused by the symptoms but also the devastating insomnia and excessive daytime sleepiness associated with it.
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PMID:Periodic limb movements of sleep and the restless legs syndrome. 890 50

The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.
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PMID:Chronic fatigue syndrome--aetiological aspects. 946 37

The aim of this study was to identify factors other than objective sleep tendency associated with scores on the Epworth Sleepiness Scale (ESS). There were 225 subjects, of whom 40% had obstructive sleep apnoea (OSA), 16% had simple snoring, and 4.9% had snoring with sleep disruption (upper airway resistance syndrome); 9.3% had narcolepsy and 7.5% had hypersomnolence without REM sleep abnormalities; 12% had chronic fatigue syndrome; 7.5% had periodic limb movement disorder and 3% had diurnal rhythm disorders. ESS, the results of overnight polysomnography and multiple sleep latency test (MSLT) and SCL-90 as a measure of psychological symptoms were recorded. The ESS score and the mean sleep latency (MSL) were correlated (Spearman rho = -0.30, P < 0.0001). The MSL was correlated with total sleep time (TST) and with sleep efficiency but not with apnoea/hypopnoea index. There was no association between the MSL and any aspect of SCL-90 scores, except a borderline significant association with the somatisation subscale. The ESS was correlated with TST but not with sleep efficiency or apnoea/hypopnoea index. The ESS was correlated with all subscales of the SCL-90 except psychoticism. An ESS > or = 10 had poor sensitivity and specificity as a predictor of MSL < 10 min or MSL < 5 min. We conclude that the MSLT and the ESS are not interchangeable. The ESS was influenced by psychological factors by which the MSL was not affected. The ESS cannot be used to demonstrate or exclude sleepiness as it is measured by MSLT.
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PMID:Correlations among Epworth Sleepiness Scale scores, multiple sleep latency tests and psychological symptoms. 984 51

In order to study both the prevalence of Primary Sleep Disorders (PSD) and sleepiness, and their association to the Chronic Fatigue Syndrome (CFS), 46 unselected outpatients (34 women, mean age 36.5) were examined clinically and underwent two nights of all-night polysomnography and multiple sleep latency tests (MSLT). Forty-six percent presented with a Sleep Apnea/Hypopnea Syndrome Index (AHI>=5), 5% with a Periodic Limb Movements syndrome. No subject received a diagnosis of Narcolepsy or Idiopathic Hypersomnia. Thirty percent showed the presence of objective sleepiness as measured by MSLT<10 minutes. Objective and subjective measures of sleepiness were not associated with CFS, nor with the double diagnosis of CFS and a PSD. The presence of PSD or sleepiness was not associated with any of the clinical scales that were used to measure anxiety, depression, somatisation, physical or mental fatigue, or functional status impairment. Fifty-four percent of CFS patients had no PSD, and 69% no sleepiness. These patients could not be distinguished clinically from patients having a PSD or from those with sleepiness. Therefore, it is unlikely that CFS is simply a somatic expression of any PSD observed in our sample or of sleepiness per se.
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PMID:How significant are primary sleep disorders and sleepiness in the chronic fatigue syndrome? 1138 99

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

In humans, activation of the primary host defense system leads to increased or decreased NREM sleep quality, depending on the degree of early immune activation. Modest elevations of certain inflammatory cytokines are found during experimental sleep loss in humans and, in addition, relatively small elevations of cytokines are seen following commencement of pharmacological treatments with clozapine, a CNS active antipsychotic agent, known to have immunomodulatory properties. Cytokines such as TNF-alpha, its soluble receptors, and IL-6, present in the periphery and the CNS, comprise a link between peripheral immune stimulation and CNS-mediated behaviors and experiences such as sleep, sleepiness, and fatigue. The debilitating fatigue experienced in chronic fatigue syndrome and related diseases may also be related to altered cytokine profiles.
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PMID:Mediators of inflammation and their interaction with sleep: relevance for chronic fatigue syndrome and related conditions. 1200 21

Multiple sclerosis (MS) fatigue is one of the most common symptoms in MS, but its pathophysiology is still not understood Sympathovagal imbalance was suggested as a reason for fatigue in chronic fatigue syndrome. We examined the role of an imbalance in the central autonomic nervous system (ANS) as a cause of MS fatigue in 51 MS patients and a control group of 22 healthy volunteers. Fatigue was assessed with the revised MS Fatigue Severity Scale (FSS) and the Modified Fatigue Impact Scale (MFIS). Depression was evaluated with the Beck Depression Inventory (BDI). Disintegration of the central ANS expressed by pupillary fatigue waves was measured with pupillography and documented in the pupillary unrest index (PUI). All subjects had less than five points on the seven-point Stanford Sleepiness Scale and were therefore not sleepy. MS patients had significant higher mean FSS scores (p=0.001) and mean MFIS scores (p=0.003) than our control group. Mean BDI scores were significant higher (p=0.001) in the MS group, but were in the lowest score range (0-10 points) in both groups. Surprisingly, we found a statistically significant inverse correlation between PUI values and either FSS scores (p=0.001; r=-0.521) or MFIS scores (p=0.002; r=-0.423) in the MS group, but not in healthy participants. We therefore conclude that autonomic instability, as measured by pupillary unrest is not associated with MS fatigue severity.
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PMID:Autonomic instability, as measured by pupillary unrest, is not associated with multiple sclerosis fatigue severity. 1212 Jun 99


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