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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Improved treatments and rehabilitation for cerebral palsy (CP) have led to an increased number of children with CP surviving into adulthood. Adults with CP show an increased prevalence of pain, fatigue, and musculoskeletal dysfunction, leading to a decrease in ambulatory function. Recent work has demonstrated the potential benefits of intensive task-specific gait training, including the use of robotic-driven gait orthoses, on motor recovery in children with CP. In contrast, reports of interventions aimed at improving motor function in adults with CP are lacking. This case study reports on the outcomes of a 6-week intervention of robotic-assisted gait training administered to a 52-year-old woman with right hemiplegia attributable to CP. Improvements were noted in balance, walking speed, and time to negotiate stairs at posttraining and follow-up. Gait analysis showed an increase in step length and a reduction in the period of double support. In conclusion, robotic-assisted gait training may be beneficial in enhancing locomotor function in adults with CP.
PM R 2010 Jan
PMID:Robotic gait training in an adult with cerebral palsy: a case report. 2012 16

Aid in understanding issues surrounding the construct validity of fatigue including the distinction between pathological versus nonpathological fatigue. Fatigue is a universal symptom reported by individuals in the general population as well as by those suffering from different medical and psychological illnesses, including cancer, multiple sclerosis, chronic fatigue syndrome, depression, and anxiety. Chronic fatigue is a significant problem in many primary care settings, and the debilitating and prolonged nature of fatigue can pose significant economic consequences for society. Researchers have struggled to better assess and understand the etiology and classification of fatigue within different illness groups.
PM R 2010 May
PMID:What is fatigue? Pathological and nonpathological fatigue. 2065 13

Describe and define the concept of central fatigue, as well as discuss the behavioral and neuroimaging studies that attempt its assessment and measurement. A brief description of how fatigue can be differentiated from psychiatric symptoms and from sleepiness is also provided. Promising directions for future research will be outlined in the final portion of this review. Despite its popular clinical use as a descriptor of certain symptomatology, fatigue is not a unitary construct. Describing central fatigue as distinct from peripheral fatigue represents one way of understanding the underlying neural and behavioral concomitants of fatigue.
PM R 2010 May
PMID:Central fatigue: issues related to cognition, mood and behavior, and psychiatric diagnoses. 2065 14

Peripheral fatigue results from an overactivity-induced decline in muscle function that originates from non-central nervous system mechanisms. A common symptom of fatigue is a feeling of tiredness or weariness because of overexertion, such as that associated with intense or prolonged physical exercise. Fatigue is worsened by low physical fitness and chronic illnesses. These conditions may intensify fatigue to levels that limit physical and social functioning and severely diminish health-related quality of life. Although etiologic aspects of peripheral fatigue are often associated with regulatory system (neurologic, endocrine, immunologic, muscular) and support system (cardiovascular, pulmonary, metabolic, renal, digestive, skeletal) limitations, final mediation occurs in muscle cells as a result of altered crossbridge functioning. Specifically, the final product and ionic metabolite accumulation that result from adenosine triphosphate hydrolysis appear to inhibit crossbridge formation and activation. Thus, clinical manifestations of peripheral fatigue often can be observed as limitations placed upon muscle or cardiorespiratory endurance, here defined as fatigue resistance. An overview of the common pathways by which peripheral fatigue can be mediated is provided. Product inhibition of contractile chemistry is brought into focus as a common pathway through which the mechanisms of peripheral fatigue often act.
PM R 2010 May
PMID:Peripheral fatigue: high-energy phosphates and hydrogen ions. 2065 16

Central fatigue, a persistent and subjective sense of tiredness, generally correlates poorly with traditional markers of disease. It is frequently associated with psychosocial factors, such as depression, sleep disorder, anxiety, and coping style, which suggest that dysregulation of the body's stress systems may serve as an underlying mechanism in the maintenance of chronic fatigue (CF). This article addresses the endocrine, neural, and immune factors that contribute to fatigue and describes research regarding the role of these factors in chronic fatigue syndrome as a model for addressing the biology of CF. In general, hypoactivity of the hypothalamic-pituitary-adrenal axis, autonomic nervous system alterations characterized by sympathetic overactivity and low vagal tone, as well as immune abnormalities, may contribute to the expression of CF. Noninvasive methods for evaluating endocrine, neural, and immune function are also discussed. Simultaneous evaluation of neuroendocrine and immune systems with noninvasive techniques will help elucidate the underlying interactions of these systems, their role in disease susceptibility, and progression of stress-related disorders.
PM R 2010 May
PMID:Neuroendocrine and immune contributors to fatigue. 2065 15

The shared goal of all clinical disciplines is to optimize the well-being of people who become patients and find themselves diminished by illness and recovery. This goal relies on sound tools to evaluate both real and perceived deficits in a way that can be used for a particular patient over time and also across medical disciplines and patient populations. Fatigue is a critical and notoriously subjective aspect of many illnesses. Although the soundness of research is often correlated with the objectivity of data, certain clinical measures must, by definition, be patient centered, with all the complexities and challenges of patient-reported evaluations. Measurement of fatigue has been an important and evolving component of symptom management in the field of oncology. The Functional Assessment of Chronic Illness Therapy Fatigue Scale is a self-administered fatigue-assessment tool that has found wide application across diverse medical fields and that has demonstrated validity and utility across a broad range of populations. The Functional Assessment of Chronic Illness Therapy Fatigue Scale has become one in a repository of tools in the item banks that are accumulating under the auspices of The Patient-Reported Outcomes Measurement Information System, a National Institutes of Health initiative to deploy the most clinically relevant and technologically agile tools that we have to advance research in medicine and patient care. As much as with any other discipline, physical medicine and rehabilitation stands to gain from the collective knowledge and creative horizons in the assessment and treatment of fatigue.
PM R 2010 May
PMID:Building a measure of fatigue: the functional assessment of Chronic Illness Therapy Fatigue Scale. 2065 17

Cancer-related fatigue (CRF) is a disabling and distressing symptom that is highly prevalent across the cancer continuum from a patient's diagnosis and treatment through survivorship and end of life. It has a multifactorial etiology and significant individual variability in its clinical expression, determinants, and sequelae. Despite the significance of CRF, it is often underdiagnosed, and management is frequently suboptimal. This review synthesizes the state of the science concerning the features, possible mechanisms, and predictors of CRF; offers recommendations for the evaluation of CRF; and appraises the strength of the evidence for a wide range of pharmacologic and nonpharmacologic interventions to prevent and manage fatigue during and after cancer and its treatment. There is evidence from methodologically rigorous controlled trials that exercise, psycho-educational interventions, and cognitive-behavioral therapy for insomnia are effective in the treatment of CRF, and a wide range of pharmacologic and nonpharmacologic interventions has shown initial promise in single-arm pilot studies with small, heterogeneous samples. Rigorously designed and adequately powered randomized trials are warranted to (1) determine the effectiveness of promising approaches and (2) identify the interventions that are most effective in treating CRF in specific subpopulations (eg, stem cell transplant recipients, older adults, patients with lung or colorectal cancers, survivors, and those at the end of life). Studies to elucidate the biologic expression profiles of CRF, to explicate the mechanisms through which particular interventions impact CRF, and to identify the mediators and moderators of fatigue outcomes will ultimately permit individually tailored approaches for the treatment of CRF.
PM R 2010 May
PMID:Cancer-related fatigue: state of the science. 2065 18

Two inflammatory autoimmune diseases, systemic lupus erythematosus and rheumatoid arthritis, are characterized by fatigue. Patient reports support the significant negative impact of the symptom on functioning and well-being. The prevalence, trajectory, mechanism, and correlates of fatigue in each disease are reviewed. Some disease-focused treatments have demonstrated a reduction in fatigue. However, until recently, clinical trials have not routinely assessed fatigue. Analyses and interpretation of data have been hindered by variability in the reliability and validity of fatigue measures. Empirically based fatigue treatment guidelines are needed in both conditions.
PM R 2010 May
PMID:Fatigue in systemic lupus erythematosus and rheumatoid arthritis. 2065 19

Fatigue is a frequent reason for seeking medical attention. Endocrine dysfunction is a common etiology of fatigue. In fact, thyroid function is usually one of the first explanations on the list of possible diagnoses. The symptoms associated with endocrinopathies are frequently "nonspecific," and psychiatric disease or psychological disorders need to be differentiated. Often, this can be accomplished using biological measures of hormone function, such as measures of thyroid, pituitary, parathyroid, and adrenal hormone levels. The field of endocrinology is highly dependent on an algorithmic approach to differential diagnosis using hormone levels as the guide. The use of self-reports helps identify at-risk patients, and raises suspicions about whether there is an abnormality, but diagnosis is dependent on laboratory values. Metabolic abnormalities, such as hyper- or hypoglycemia, dyslipidemia, and gonadal dysfunction can also contribute to fatigue. A better understanding of the interactions among hormones, their releasing factors, and regulation of inflammation will help identify abnormalities early and help distinguish endocrinopathies from other causes of fatigue. Early identification of these abnormalities may reduce end-organ damage and improve treatment strategies.
PM R 2010 May
PMID:Fatigue, endocrinopathies, and metabolic disorders. 2065 20

Fatigue is a feature of several chronic diseases of the central and peripheral nervous system. The pathophysiology of central fatigue is complex and often not well-defined. In contrast, peripheral fatigue is more objectively defined and measured. Fatigue can be part of the primary disease process, but there are often contributions from comorbid factors such as depression, sleep disturbance, medication, or deconditioning. Multiple sclerosis (MS) offers an example of central fatigue. More than 40% of MS patients complain of fatigue. Validated questionnaires are used to assess fatigue severity and comorbid factors. Although fatigue is believed to be a primary process in MS, depression and sleep disturbance are often comorbid problems. Magnetic resonance imaging (MRI), positron emission tomography, and functional MRI studies suggest that fatigue is related to gray matter disease, particularly of the cerebral cortex, but also of the thalamus and caudate. Disruption of impulse propagation from demyelination is also a likely factor. It is uncertain if pro-inflammatory cytokines have a specific effect on the genesis of MS fatigue. Several medications have been reported to alleviate fatigue in MS, but controlled studies show contradictory results. Treatment of depression and sleep disturbance, use of exercise programs and rehabilitation therapies as well as treatment of other comorbid conditions is necessary for optimal alleviation of fatigue. Myasthenia gravis (MG) patients exhibit peripheral fatigue. In contrast to MS, the mechanism of weakness and fatigue in MG is well-defined. Antibodies to the postsynaptic acetylcholine receptor at the myoneural junction cause diminution of the force of muscle contractions. This leads to a feeling of fatigue. MG treatments increase the availability of acetylcholine and reduce antibody formation. Evaluation for comorbid conditions, especially thymoma and hyperthyroidism, are mandatory in patients with MG.
PM R 2010 May
PMID:Central and peripheral fatigue: exemplified by multiple sclerosis and myasthenia gravis. 2065 21


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