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

Primary fibromyalgia syndrome (PFS) is characterized by widespread chronic pain that affects the musculoskeletal system, fatigue, anxiety, sleep disturbance, headache and postural hypotension. The pathophysiology of PFS is unknown. The hypothalamic-pituitary-adrenal (HPA) axis seems to play an important role in PFS. Both hyperactivity and hypoactivity of the HPA axis have been reported in patients with PFS. In this study we assessed the HPA axis by 1 microg ACTH stimulation test and metyrapone test in 22 patients with PFS and in 15 age-, sex-, and body mass index (BMI)- matched controls. Metyrapone (30 mg/kg) was administered orally at 23:00 h and blood was sampled at 08:30 h the following morning for 11-deoxycortisol. ACTH stimulation test was carried out by using 1 microg (iv) ACTH as a bolus injection after an overnight fast, and blood samples were drawn at 0, 30 and 60 min. Peak cortisol level (659.4 +/- 207.2 nmol/l) was lower in the patients with PFS than peak cortisol level (838.7 +/- 129.6 nmol/l) in the control subjects (p < 0.05). Ten patients (45%) with PFS had peak cortisol responses to 1 microg ACTH test lower than the lowest peak cortisol detected in healthy controls. After metyrapone test 11-deoxycortisol level was 123.7 +/- 26 nmol/l in patients with PFS and 184.2 +/- 17.3 nmol/l in the controls (p < 0.05). Ninety five percent of the patients with PFS had lower 11-deoxycortisol level after metyrapone than the lowest 11-deoxycortisol level after metyrapone detected in healthy controls. We also compared the adrenal size of the patients with that of the healthy subjects and we found that the adrenal size between the groups was similar. This study clearly shows that HPA axis is underactivated in PFS, rather than overactivated.
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PMID:Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome. 1505 42

In the 1991 Gulf War less than 150 of nearly 700,000 deployed US troops were killed in action. Today, however, over 1 in 7 US veterans of the war has sought federal healthcare for related-health concerns, and fully 17% of UK Gulf War veterans describe themselves as suffering from the 'Gulf War syndrome', a set of poorly defined and heterogeneous ailments consisting mainly of chronic pain, fatigue, depression and other symptoms. Even though over 250 million dollars of federally funded medical research has failed to identify a unique syndrome, the debate regarding potential causes continues and has included oil well smoke, contagious infections, exposure to chemical and biological warfare agents, and posttraumatic stress disorder. Historical analyses completed since the Gulf War have found that postwar syndromes consisting of chronic pain, fatigue, depression and other symptoms have occurred after every war in the 20th century. These syndromes have gone by a variety of names such as Da Costa's syndrome, irritable heart, shell shock, neurocirculatory asthenia, and battle fatigue. Though the direct causes of these syndromes are typically elusive, it is clear that war sets in motion an undeniable cycle of physical, emotional, and fiscal consequences for war veterans and for society. These findings lead to important healthcare questions. Is there a way to prevent or mitigate subsequent postwar symptoms and associated depression and disability? We argue that while idiopathic symptoms are certain to occur following any war, a population-based approach to postwar healthcare can mitigate the impact of postwar syndromes and foster societal, military, and veteran trust. This article delineates the model, describes its epidemiological foundations, and details examples of how it is being adopted and improved as part of the system of care for US military personnel, war veterans and families. A scientific test of the model's overall effectiveness is difficult, yet healthcare systems for combatants and their families are already being put to pragmatic tests as troops return from war in Iraq and Afghanistan and from other military challenges.
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PMID:Can we prevent a second 'Gulf War syndrome'? Population-based healthcare for chronic idiopathic pain and fatigue after war. 1524 70

The terms myofascial pain, fibromyalgia and fibrositis are critically examined. They constitute diagnostic labels for non-specific musculoskeletal aches and pains. Analysis of the evidence shows that none of these labels is substantiated by hard physical signs or by laboratory evidence of consistent pathological or biochemical abnormality. What is the objective evidence for disorder(s) of muscle, fascia or fibrous tissues, so clearly indicated by these diagnostic names? Alternative terms such as 'regional pain syndrome' or 'chronic pain syndrome' merely redefine the clinical problem without providing a mechanism or basis for diagnosis. Despite different diagnostic criteria, these conditions, along with chronic fatigue syndrome, have many demographic and clinical similarities, most notably tender trigger points. Indeed, the terms are often used interchangeably. There are few differences in the symptoms, physical findings, laboratory tests, functional status, psychosocial features and psychiatric disorders. This paper seeks not to deny the existence of aches and pains, but to critically examine the utility of these terms. The only claimed physical sign is the presence of tender trigger points over muscles or muscle attachments. Research suggests that tender points are a measure of general distress related to pain complaints but separately associated with fatigue and depression. They are present in some normal subjects and are variable in occurrence in time in the same individual. They reflect no demonstrable pathology. It is therefore argued that none of these commonly used diagnoses represent distinct disease entities. A possible but unproven alternative hypothesis is that such symptoms relate to neural pain with both peripheral and central components, and in some instances psychological or wilful embellishment.
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PMID:Myofascial pain, fibromyalgia or fibrositis? 1525 26

Fatigue is a symptom that is frequently found in chronic pain patients with low back pain and/or neck pain. At the present time, no specific psychopharmacological treatment for this problem has been identified. Modafinil is a wakefulness-promoting agent that the FDA has approved for the treatment of excessive daytime sleepiness associated with narcolepsy. There have been reports on the use of modafinil for the treatment of fatigue in various neurological syndromes. This literature is reviewed. As such, modafinil treatment was initiated for a patient with severe fatigue associated with chronic low back pain and neck pain. There was dramatic improvement in fatigue and associated function. This case is described. It is the first such case report in the literature. The significance of this finding to the treatment of pain-associated fatigue is discussed.
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PMID:Modafinil for the treatment of pain-associated fatigue: review and case report. 1525 74

Stressful events occur in the lives of millions of individuals each year. Such events, or "stressors", are experiences that threaten personal well-being, and include traumatic events such as motor vehicle collision, infectious illness, and situations such as military deployment. While most individuals recover from such events, others develop persistent somatic symptoms, such as chronic pain and fatigue, and/or psychological disturbances, such as posttraumatic stress disorder. Recent findings from the study of risk factors for the development of chronic somatic symptoms after a traumatic, infectious, or situational stressor suggest that similar pre-event, event-related, and post-event risk factors influence the development of chronic symptoms in each condition. Females, and those with pre-event distress or psychological factors, may be at higher risk of developing chronic symptoms after such events. Regarding the event, or "stressor", it appears as though the intensity or specific characteristics of exposure may be a relatively unimportant predictor of patient outcome. Instead, other factors such as the worry, or expectation, of chronicity may increase the risk of chronic symptom development. After the event, inactivity and time off work appear to increase the risk of chronic symptoms. Health care providers have an important role in emphasizing the benefits of resuming usual activities, and downplaying potential benefits of continuing in the sick role (e.g., time off work, increased family attention). While many aspects of the complex interaction of biological, psychological, and social factors that influence patient outcome after a stressful event remain to be elucidated, it appears that for the present, one of the most important interventions is to continue to emphasize to patients the old saying, "rest makes rust".
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PMID:Predicting chronic symptoms after an acute "stressor"--lessons learned from 3 medical conditions. 1532 10

Because of the high prevalence and the refractory nature of pain following spinal cord injury (SCI), it is important to increase the understanding of what factors aggravate different types of pain. This information is related to pain generating mechanisms and may thus be useful in the diagnosis and management of these difficult pain conditions. The aims of the present study were to (1) identify variables (factors) that exacerbate chronic pain associated with SCI and (2) define the relationships among these patterns of pain exacerbation, specific pain characteristics, and psychological features. A sample out of 159 (75.5%) people with SCI and chronic pain, volunteered to participate in a mail survey. Over 50% of the sample indicated that prolonged sitting, infections, fatigue, muscle spasms, cold weather, and sudden movements exacerbated their pain. A principal components analysis detected five sets of factors that were reported to magnify pain: negative mood, prolonged afferent activity (bowel, bladder, somatic), weather, voluntary physical activity, and transient somatic afferent activity. Negative mood and prolonged afferent activity were frequently and significantly associated with both pain characteristics and psychosocial issues. A multiple regression analysis revealed that a combination of decreased activity levels due to pain (t = 3.54; p < 0.001), pain located in the frontal aspects of torso (including genitals) (t = 2.29; p < 0.05), "burning" (t = 2.26; p < 0.05), or "electric" (t = 2.09; p < 0.05) pain, and a limited perception of life control (t = -2.16; p < 0.05) was significantly associated with a high extent of pain aggravation (R2 = 0.39; p < 0.000).
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PMID:Exacerbation of chronic pain following spinal cord injury. 1567 29

Disturbed sleep is a key complaint of people experiencing acute and chronic pain. These two vital functions, sleep and pain, interact in complex ways that ultimately impact the biological and behavioral capacity of the individual. Polysomnographic studies of patients experiencing acute pain during postoperative recovery show shortened and fragmented sleep with reduced amounts of slow wave and rapid eye movement (REM) sleep, and the recovery is accompanied by normalization of sleep. Objective assessments of sleep in patients with various chronic pain conditions have been less definitive with some studies showing fragmented and shortened sleep and others showing normal sleep. Although daytime fatigue is a frequent complaint associated with complaints of pain-related disturbed sleep, objective assessments of daytime sleepiness reveal minimally elevated levels of sleepiness and emphasize the importance of distinguishing sleepiness and fatigue. The pain-sleep nexus has been modeled in healthy pain-free subjects and the studies have demonstrated the bidirectionality of the sleep-pain relation. Given this bidirectionality, treatment must focus on alleviation of both the pain and sleep disturbance. Few of the treatment studies have done such, and as a result no clear consensus on treatment approaches, much less on differential etiology-based treatment strategies, has emerged.
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PMID:Sleep and pain: interaction of two vital functions. 1579 43

In order to react adequately to any new challenge, it is necessary to stop all ongoing activity. The first phase in the orienting response to a novel stimulus is an arrest of all ongoing activity. Inhibition is also necessary to switch from one behaviour to another, and from one cognitive activity to another. Inhibition was a difficult phenomenon to handle until the role of inhibitory synapses was demonstrated, and that many brain areas have an inhibitory function for overt behaviour and for establishing new responses in learning experiments. The role of these areas for learning and for plasticity of the brain has been well established. Recently, the role of inhibition, or lack of inhibition, for cognitive activities has been discussed for the understanding of somatization and sensitization to afferent somatic impulses. It has been postulated that muscle pain is maintained by positive feed back loops between muscles, the spinal cord, and the brain areas for pain and interpretation of pain. Activity in these loops may lead to sensitisation of the neural circuits, leading to chronic pain states. Similar models have been presented for non-specific gastric and intestinal complaints, and for fatigue and depression. Rumination and perseveration of negative thoughts may maintain the activity in these loops.
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PMID:Press stop to start: the role of inhibition for choice and health. 1596 45

Fibromyalgia syndrome (FM) is a common chronic pain condition that affects at least 2% of the adult population in the USA and other regions in the world where FM is studied. Prevalence rates in some regions have not been ascertained and may be influenced by differences in cultural norms regarding the definition and attribution of chronic pain states. Chronic, widespread pain is the defining feature of FM, but patients may also exhibit a range of other symptoms, including sleep disturbance, fatigue, irritable bowel syndrome, headache, and mood disorders. Although the etiology of FM is not completely understood, the syndrome is thought to arise from influencing factors such as stress, medical illness, and a variety of pain conditions in some, but not all patients, in conjunction with a variety of neurotransmitter and neuroendocrine disturbances. These include reduced levels of biogenic amines, increased concentrations of excitatory neurotransmitters, including substance P, and dysregulation of the hypothalamic-pituitary-adrenal axis. A unifying hypothesis is that FM results from sensitization of the central nervous system. Establishing diagnosis and evaluating effects of therapy in patients with FM may be difficult because of the multifaceted nature of the syndrome and overlap with other chronically painful conditions. Diagnostic criteria, originally developed for research purposes, have aided our understanding of this patient population in both research and clinical settings, but need further refinement as our knowledge about chronic widespread pain evolves. Outcome measures, borrowed from clinical research in pain, rheumatology, neurology, and psychiatry, are able to distinguish treatment response in specific symptom domains. Further work is necessary to validate these measures in FM. In addition, work is under way to develop composite response criteria, intended to address the multidimensional nature of this syndrome. A range of medical treatments, including antidepressants, opioids, nonsteroidal antiinflammatory drugs, sedatives, muscle relaxants, and antiepileptics, have been used to treat FM. Nonpharmaceutical treatment modalities, including exercise, physical therapy, massage, acupuncture, and cognitive behavioral therapy, can be helpful. Few of these approaches have been demonstrated to have clear-cut benefits in randomized controlled trials. However, there is now increased interest as more effective treatments are developed and our ability to accurately measure effect of treatment has improved. The multifaceted nature of FM suggests that multimodal individualized treatment programs may be necessary to achieve optimal outcomes in patients with this syndrome.
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PMID:Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. 1607 56

The fibromyalgia syndrome (FM) seems an unlikely candidate for classification as a neuropathic pain. The disorder is diagnosed based on a compatible history and the presence of multiple areas of musculoskeletal tenderness. A consistent pathology in either the peripheral or central nervous system (CNS) has not been demonstrated in patients with FM, and they are not at higher risk for diseases of the CNS such as multiple sclerosis or of the peripheral nervous system such as peripheral neuropathy. A large proportion of FM sufferers have accompanying symptoms and signs of uncertain etiology, such as chronic fatigue, sleep disturbance, and bowel/bladder irritability. With the exception of migraine headaches and possibly irritable bowel syndrome, the accompanying disorders are clearly not neurological in origin. The impetus to classify the FM as a neuropathic pain comes from multiple lines of research suggesting widespread pain and tenderness are associated with chronic sensitization of the CNS. An examination of how the term neuropathic pain is defined reveals a conceptual split into 2 partially overlapping groups of disorders: those with demonstrable pathology in the nervous system and those characterized primarily by enduring dysfunction in the nervous system. Requiring demonstrable pathology in the nervous system in the definition of neuropathic pain is the traditional approach. The expansion of the definition to require only enduring nervous system dysfunction is less palatable because it opens the classification to many disorders of uncertain etiology, including complex regional pain syndrome. As it is uncertain which of the many different chronic pain syndromes include an enduring component of central sensitization, restricting the term "neuropathic pain" to those disorders with a primary etiology clearly related to the peripheral or CNS is prudent and consistent with clinical practice.
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PMID:Is fibromyalgia a neuropathic pain syndrome? 1607 59


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