Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CFIDS (chronic fatigue and immune disfunction syndrome) is also known as CFS (chronic fatigue syndrome), CEBV (chronic Epstein-Barr virus), M.E. (myalgic encephalomyelitis), yuppie flu and by other names. It is a complex illness characterized by incapacitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems and a constellation of symptoms that can resemble many disorders, including; mononucleosis, multiple sclerosis, fibromyalgia, AIDS-related complex (ARC) and autoimmune diseases such as lupus. These symptoms tend to wax and wane, but any often severely debilitating and may last for many months or years. All sections of the population (including children) are at risk, but women under 45 seem to be most susceptible. The investigators suggest that CFIDS results from dysfunction of the immune system. The exact nature of this dysfunction is not yet well defined, but it can generally be viewed as an unregulated or overactive state which is responsible for most of the symptoms. There is also evidence of some immune suppression in CFIDS. None of the treatments is consistently satisfactory, but some may be helpful: psychotherapy, physiotherapy, exercise programs, acupunctures, small doses of antidepressants, etc.
 ...
PMID:[The chronic fatigue syndrome]. 790 Apr 53

Fatigue is a common symptom in patients with multiple sclerosis. Rapid exhaustion and reduced exercise tolerance leads to difficulties in maintaining a normal daily life for many patients. Regular resting and short breaks can help to compensate this to a certain degree. The pathophysiology of fatigue is currently unknown. Damage of specific neuroanatomic regions or a more generalized effect of inflammatory mediators in the central nervous system could be the causes of fatigue. Some drugs (e.g. amantadine) have proven effective in therapy of fatigue. Recent therapeutic approaches have begun using aminopyridines (4-aminopyridine, 3,4-diaminopyridine). These two substances are thought to improve nerve conduction, but there might be a central stimulatory effect as well. Overdosage leads to an elevated risk of epileptic seizures and confusion.
 ...
PMID:['Fatigue' in multiple sclerosis]. 1041 4

In multiple sclerosis (MS), one of the most frequent demyelinating diseases in man, remyelination of demyelinating lesions exists but is often incomplete. Also reported in experimental models of demyelination, this phenomenom confirms the regenerating potential of the demyelinated central nervous system (CNS) and, in particular, the existence of an endogenous mechanism of oligodendrocyte renewal. Failure in efficient remyelination could result from exhaustion of the pool of remyelinating cells, loss of axons and absence of a permissive environment for remyelination. Identifying the nature and the origin of the cells capable of generating new oligodendrocytes for remyelination could contribute to strategies to activate these cells, and thereby enhance their potential for myelin repair. Within the adult CNS, several cell types are capable of generating new oligodendrocytes following myelin damage: post-mitotic oligodendrocytes frequently found at the lesion site, oligodendrocyte progenitors whose existence has been confirmed both in vitro and in vivo, and multipotent cells localized in the germinative areas of the brain and the spinal cord. Although restricted to particular sites of the CNS, these multipotent cells, which maintain the capacity to self-renew and to migrate throughout adulthood, could constitute a powerful source of remyelinating cells. The study of the mechanisms of proliferation, migration and differentiation of these cells in response to demyelination should allow the definition of new strategies to promote endogenous remyelination and develop therapeutic approaches for demyelinating diseases such as MS. This goal is an appealing alternative to the transplantation of myelin-forming cells and should efficiently complement strategies aimed at reducing neuronal loss and inflammation.
 ...
PMID:Do central nervous system axons remyelinate? 1072 14

A widely quoted hypothesis for the failure of remyelination in multiple sclerosis (MS) is the exhaustion of the oligodendrocyte progenitor cell (OPC) pool that is strongly implicated as the source of remyelinating oligodendrocytes in demyelinating lesions. Despite this, little is known about the responses of adult OPCs to adjacent areas of the CNS from which their numbers are depleted. We have developed an experimental model to study the pattern and rate of repopulation of OPC-depleted zones, by endogenous OPCs in the adult rat spinal cord. By X-irradiating short lengths of the spinal cord with 40 Gy of X-irradiation, we were able to produce a highly localised depletion of OPCs that allowed us to study the responses of cells located in adjacent normal areas, to this local depletion. Using both NG2 immunohistochemistry and PDGFalphaR in situ hybridisation to identify OPCs, we demonstrate that endogenous OPCs repopulated the depleted areas slowly, but completely. This repopulation occurred at the rate of approximately 0.5 mm/week in the first month. Most cells at the leading edge of repopulation had complex, branching morphologies. The repopulation process was capable of restoring the density of progenitors in repopulated areas to that of normal tissue and was not associated with a secondary progenitor loss in tissue from which progenitor cells were generated. These findings indicate that depletion of the OPC population around lesions is not likely to be the primary explanation for remyelination failure in MS.
 ...
PMID:Efficient recolonisation of progenitor-depleted areas of the CNS by adult oligodendrocyte progenitor cells. 1187 Aug 70

Fatigue is a common disabling symptom of multiple sclerosis (MS). It is often considered a state of exhaustion distinct from depressed mood or physical weakness. Fatigue can be assessed by either self-report scales or performance-based measures; however, neither method captures all features of fatigue. Fatigue in MS frequently leads to unemployment. It is associated with a sense of loss of control over one's environment, low positive affect, psychological distress and neurological impairment. To date there is no reproducible neuroimaging marker or biological correlate that has been identified. Proposed pathological mechanisms of fatigue in MS include neuronal factors such as dysfunction of premotor, limbic, basal ganglia or hypothalamic areas; disruption of the neuroendrocrine axis leading to low arousal; alteration in serotoninergic pathways; changes in neurotransmitter levels; and altered CNS functioning caused by a disruption of the immune response. Treatment of fatigue is best approached in a multidisciplinary fashion that incorporates nonpharmacological interventions as well as medication. Amantadine and modafinil are among the most commonly used medications for fatigue associated with MS. Both medications have been studied with positive results in controlled clinical trials. Additional research towards measurement and pathogenesis of fatigue will hopefully lead to improved therapies.
 ...
PMID:Fatigue in multiple sclerosis: definition, pathophysiology and treatment. 1266 96

More than 50 % of patients with multiple sclerosis (MS) suffer from cognitive deficits. Attention is one of the most frequently affected cognitive functions. It has been shown that MS patients suffer from a specific but not necessarily from a generalized decrease in performance and that different severity grades of impaired attentional processing can be distinguished. Little is known about patterns of brain activation in MS patients with different grades of attentional deficits. The objective was to examine if different severity grades in attentional impairment are reflected by altered patterns of brain activation in specific attention tasks. In the present study cerebral activation induced by three attention tasks of different complexity was assessed in 14 MS patients and seven healthy controls by functional MRI (fMRI). Based on their performance on the tests recorded off-line with a computerized test battery and during the fMRI investigation, patients were classified as mildly and severely impaired. MS patients with mild impairment showed increased and additional activation of brain areas which were in part not activated in normal subjects. Those were located mainly in the frontal cortex and posterior parietal cortex. This effect decreased with increasing task complexity and was strongest for the alertness task. In MS patients with severe impairment no additional activation was found in prefrontal structures and activation in the premotor cortex was not significantly different from controls. These findings suggest that compensation in MS patients is in part achieved by functional integration of frontal and parietal association areas. The extent of compensation seems to depend on the brain's capacity to access additional brain structures. Exhaustion of this capacity may finally lead to severe cognitive impairment.
 ...
PMID:Analysis of impairment related functional architecture in MS patients during performance of different attention tasks. 1270 Sep 13

High-load coordination dynamics were measured in athletes, physiotherapists, gymnasts, musicians, patients with spinal cord injury and a patient with multiple sclerosis during exercise on a special coordination dynamic therapy device to quantify improvement in the central nervous system (CNS) organization due to therapy in patients and to quantify differences in the CNS organization between healthy subjects and patients with CNS injury. The values of high-load coordination dynamics for the group of athletes were two times better than those of physiotherapists, gymnasts and musicians, but still two times poorer than the best value achieved so far in a patient with a spinal cord injury after 10 months of continuous intensive coordination dynamics therapy. Especially the physiotherapists, gymnasts and musicians had poor coordination between arms and legs for the difficult intermediate coordinations between pace and trot gait for high load. Exhaustion of the CNS and improvement of CNS functioning in the short-term memory could be made visible using hysteresis-like curves for load increase and decrease. When not receiving therapy, patients with CNS injury could not turn at high loads, and showed poor coordination at lower loads only. After exercising 7,000 coordinated arm and leg movements per month, the CNS organization for high load improved in 3 healthy subjects by 36%. In patients with CNS injury, such improvements of high-load coordination dynamics took several months of intensive coordination dynamics therapy including 350,000 coordinated movements per months. The rate of learning may differ in healthy subjects and patients very approximately by a factor of 50 depending on the severity of the injury. On the other hand however, the high-load coordination between arms and legs, necessary for walking could be improved during therapy even in patients with multiple sclerosis, with the consequence that they could manage better in every day life.
 ...
PMID:High-load coordination dynamics in athletes, physiotherapists, gymnasts, musicians and patients with CNS injury. 1453 48

Patients suffering from multiple sclerosis (MS) frequently complain of fatigue (53 to 92 percent depending on studies). Fatigue can be one of the most disabling symptoms of MS and presents as physical or mental fatigue in daily living activities. Besides this permanent feeling of exhaustion, MS patients can suffer from an abnormal tiredness and lack of energy after a given motor or mental task, which defines fatigability. A number of studies explored the origins of fatigue and fatigability by means of subjective and objective tools. The implication of central nervous system dysfunctions has been established in several studies; however the contribution of peripheral nervous system factors and systemic abnormalities associated with inflammatory and immunological parameters was also suggested. The aim of this review is to present the different types of fatigue and fatigability occurring in MS patients, their origins, the investigation tools which allow the quantification of fatigue and fatigability and characterization of their mechanisms. The currently available therapeutic strategies that have been proposed to relieve this disabling symptom are presented.
 ...
PMID:[Pathophysiology and treatment of fatigue in multiple sclerosis]. 1658 84

Functional magnetic resonance imaging (fMRI) is being widely used to study recovery of function in patients with several neurological conditions, including multiple sclerosis, stroke and Alzheimer's disease. The application of this MR technique has shown that plastic cortical changes do occur after central nervous system (CNS) injury of different aetiology, that such changes are related to the extent of CNS damage and that they can contribute in limiting the clinical consequences of brain damage. Conversely, the failure or exhaustion of the adaptive properties of the cerebral cortex might be among the factors responsible for the accumulation of 'fixed' neurological deficits. New studies aimed at investigating the effect of therapies devoted to promote brain plasticity are now warranted.
 ...
PMID:Functional MRI to study brain plasticity in clinical neurology. 1670 77

One of frequent presentations of multiple sclerosis (MS) is chronic fatigue that may be determined as a subjective decrease of the physic and/or psychic energy level. Fatigue can be divided into asthenia (fatigue in resting state), pathological fatigability (exhaustion during physical loading) and fatigue concomitant with other symptoms (MS exacerbation). There are central as well as peripheral mechanisms of fatigue formation. Frequent is a combination of fatigue and affective disorders in MS, in particular depression, as well as sleep disturbances (insomnia, restless legs syndrome) that may indicate the common origin of their mechanisms, i.e. reduction of serotoninergic and noradrenergic systems activity. Endocrinal and autoimmune components are considered as important in fatigue syndrome formation, the latter exerting more influence on asthenia than on pathological fatigability. Further investigation into pathogenetic mechanisms of asthenia (fatigue in resting state), pathological fatigability (fatigue in active state) and specification of their differential diagnostic features allow not only to understand the essence of this syndrome but to choose an adequate individualized therapy.
 ...
PMID:[Possible mechanisms of chronic fatigue syndrome in multiple sclerosis]. 1717 41


1 2 3 4 5 Next >>