Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although fatigue is common among multiple sclerosis (MS) patients, evaluation of this symptom is difficult due to the subjectivity and variability of the complaint. We proposed the Fatigue Descriptive Scale (FDS) as a tool to evaluate the severity and quality of fatigue in a group of patients suffering from MS. As a way to demonstrate the usefulness of this scale we applied the FDS in a group of 155 patients (105 women and 50 men) with clinically-definite multiple sclerosis, as outlined according to Poser's criteria. Age was 36.2 +/- 11.1 years (range 12-62) and time of evolution was 8.3 +/- 9.4 years (range 1-44). The Fatigue Severity Scale (FSS) was also used. Descriptive statistics techniques and techniques for nonparametric distribution (Spearman Rank, Kruskal-Wallis ANOVA) were used. One hundred and eighteen patients reported fatigue (73 spontaneously, 45 when questioned). All descriptions of fatigue were ranked according to FDS categories. Eighty-five patients defined the symptom as fatigue with exercise, 26 as asthenia and seven as the worsening of other symptoms. Fatigue by itself produced limited or disrupted activity in 78 patients; work-related functions were limited in 48 patients; social relations were limited in 29 patients; and self-care difficult for one patient. Fifty-six patients suffered fatigue daily. FDS score was 4.9 +/- 3.9 (range 0-13). FSS was 3.1 +/- 1.7 (range 0.2-6.6). FDS and FSS of Krupp were highly correlated (R = 0.87, p < 0.001). Therefore, in comparison with other scales, the FDS shows remarkable usefulness in classifying, periodicity, and severity of fatigue in MS patients. The high correlation with the FSS implies that it is a valid method to measure the severity of fatigue, as was demonstrated in our paper proposing the FDS. The importance of this new scale is its ability to inform the clinicians in a very quick, easy, and at the same time complete way, how severe the fatigue really is and how it affects the patient.
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PMID:The Fatigue Descriptive Scale (FDS): a useful tool to evaluate fatigue in multiple sclerosis. 1009 97

Although different factors are probably involved in the etiology of fatigue in multiple sclerosis patients, no definite mechanism has been proposed. We have proposed that fatigue is a complex symptom that includes three clinical different entities (asthenia, fatigability and worsening of symptoms with effort). The goal of this study is to demonstrate if there is a peculiar mechanism for each of the different varieties of fatigue. A control sample of 155 patients (105 women, 50 men) with clinically definite MS was studied. Fatigue was measured using the Fatigue Descriptive Scale (FDS) and the Fatigue Severity Scale (FSS). Treatment, depression, anxiety, sleep and cellular immune status were studied too. Fatigue was a symptom in 118 patients (76.13%); 26 patients (22.03%) described it as asthenia (fatigue at rest); 85 patients (72.03%) as fatigability (fatigue with exercise), and seven patients (5.9%) as worsening of symptoms. The severity of pyramidal involvement was significantly more severe in patients suffering from fatigue; some immunological parameters were associated with fatigue as well. The discriminant analysis of the data shows that some of the immunoactivation parameters are associated with asthenia (F=21.5, P<0.001), and pyramidal tract involvement is associated with fatigability (F=10.5, P<0.001). Sleep disorders, anxiety and depression were linked with fatigue in a few patients. No relationship with treatment was proven. In conclusion, fatigue in MS seems to be a heterogeneous entity. Asthenia and fatigability may be different clinical entities. Certain immunoactivation parameters correlate with the presence of asthenia while pyramidal involvement is associated with fatigability.
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PMID:Modalities of fatigue in multiple sclerosis: correlation with clinical and biological factors. 1077 59

The aims of this study were to investigate (i) the self-reported frequency and intensity of systemic side-effects and their impact on the daily lives of patients suffering from Multiple Sclerosis (MS) and undergoing interferon-beta therapy and (ii) the self-reported frequency and perceptions of any local-tissue reactions. Forty patients aged 22 - 59 years (27 females) with relapsing/remitting MS were consecutively recruited for the study (17 on interferon-beta-1a and 23 on interferon-beta-1b). Two self-administered questionnaires were used before and after 1, 4, 8 and 16 weeks of therapy. The interferon therapy was found to be associated with flu-like symptoms. Most systemic side-effects were reported to be mild and to have little impact on the patients' daily lives. Asthenia and fatigue were more often rated as moderate or severe. The most frequently reported local-tissue side-effects were redness and local pain at the injection sites. A considerable inter-individual variation was found among patients regarding the perceptions of both the systemic and local side-effects. This suggests that it is of importance to identify early those patients who may need more support or other interventions to maintain a successful compliance. Multiple Sclerosis (2000) 6 349 - 354
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PMID:Interferon-beta treatment for patients with multiple sclerosis: the patients' perceptions of the side-effects. 1106 46

Fatigue is a common complaint in patients affected by multiple sclerosis. Its mechanisms are poorly understood and are likely diverse. The term "fatigue" has been used for asthenia at rest but also for fatigability during exercise. Amantadine is the only drug that has a proven therapeutic benefit in randomized, double blind, controlled trials. Inhibitors of serotonin re-uptake are used pragmatically because of the relationship between fatigue and depression. Aminopyridins may improve fatigability, mainly at the level of lower limbs.
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PMID:[Therapeutic indications for managing symptoms: fatigue]. 1178 38

Fatigue is a very common symptom of multiple sclerosis (MS). Theoretically, fatigue may be related to neuromodulation by soluble products of the autoimmune process or by disruption of central nervous system pathways necessary for sustained activity, but little empirical evidence supports these possibilities. Amantadine, pemoline, and modafanil improved fatigue in placebo-controlled clinical trials, but these studies all had significant limitations. Difficulty measuring fatigue has impeded studies of its characteristics, mechanisms, and therapeutics. Most studies have relied on self-report questionnaires. These may be inappropriate, however, because they can be easily confounded by other symptoms of MS, they are entirely subjective, and they require patients to make difficult retrospective assessments. Studies of fatigue would be improved by including measures of more rigorously defined, quantifiable components of fatigue. For example, motor fatigue can be measured as the decline in strength during sustained muscle contractions. Cognitive fatigue can be measured as the analogous decline in cognitive performance during tasks requiring sustained attention. Lassitude is defined as a subjective sense of reduced energy, and it can be measured with the use of a visual analog diary. These measures provide reproducible results and demonstrate significant differences between MS patients and healthy controls. Dividing fatigue into these components can provide objective assessments that are less likely to be confounded by other symptoms of MS, such as weakness, spasticity, cognitive impairment, and depressed mood.
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PMID:Fatigue in multiple sclerosis: current understanding and future directions. 1205 65

Interferon-beta-1b (Betaseron, Betaferon) is a non-glycosylated recombinant human interferon-beta approved for high-frequency, subcutaneous (SC) administration in the treatment of multiple sclerosis (MS). Its mechanism of action is unknown, but may involve modulation of the autoimmune pathogenic processes of MS. In a randomised, double-blind trial in patients with relapsing-remitting MS (RRMS), SC interferon-beta-1b 250 micro g (8 million International Units [MIU]) every other day reduced the annual relapse rate and increased the proportion of relapse-free patients compared with placebo. It also reduced relapse severity, hospitalisations, and disease activity assessed by magnetic resonance imaging (MRI), and increased the time to first relapse. Progression of disability showed a trend towards reduction relative to placebo and baseline, but did not reach statistical significance. SC interferon-beta-1b 250 micro g every other day was shown in a randomised trial to be superior to intramuscular (IM) interferon-beta-1a 30 micro g (6 MIU) once weekly with respect to reductions in relapse-related parameters, disability progression and MRI-assessed disease activity. In patients with secondary progressive MS (SPMS), SC interferon-beta-1b 250 micro g every other day slowed progression of the disease relative to placebo in one randomised, double-blind trial, but not in another. In both studies, interferon-beta-1b 250 micro g recipients had fewer relapses and less MRI-assessed disease activity than placebo recipients. The difference in primary outcome may reflect differences in patient entry criteria. Interferon-beta-1b is generally well tolerated and the common adverse events (e.g. injection site reactions, asthenia and an influenza-like symptom complex) are clinically manageable. In a randomised trial, the tolerability of SC interferon-beta-1b 250 micro g every other day was generally similar to that of IM interferon-beta-1a 30 micro g once weekly, except for higher incidences of injection site reactions and neutralising anti-interferon-beta antibodies with SC interferon-beta-1b. In conclusion, SC interferon-beta-1b 250 micro g every other day reduces the frequency and severity of relapses and MRI measures of disease activity and may delay the progression of disability in RRMS. The drug appeared to be more effective than, and as well tolerated as, IM interferon-beta-1a 30 micro g once weekly. Interferon-beta-1b also has positive effects on relapse rates and disease activity in patients with SPMS, although its effects on disease progression remain uncertain. The drug is generally well tolerated, and the common adverse events are clinically manageable. Thus, interferon-beta-1b is a valuable first-line therapy for patients with RRMS and a potentially useful option in those with SPMS.
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PMID:Interferon-beta-1b: a review of its use in relapsing-remitting and secondary progressive multiple sclerosis. 1518 21

Interferon-beta-1b (Betaseron, Betaferon) is a non-glycosylated recombinant human interferon-beta approved for high-frequency, subcutaneous (SC) administration in the treatment of multiple sclerosis (MS). Its mechanism of action is unknown, but may involve modulation of the autoimmune pathogenic processes of MS. In a randomized, double-blind trial in patients with relapsing-remitting MS (RRMS), SC interferon-beta-1b 250 micro g (8 million International Units [MIU]) every other day reduced the annual relapse rate and increased the proportion of relapse-free patients compared with placebo. It also reduced relapse severity, hospitalizations, and disease activity assessed by magnetic resonance imaging (MRI), and increased the time to first relapse. Progression of disability showed a trend towards reduction relative to placebo and baseline, but did not reach statistical significance. SC interferon-beta-1b 250 micro g every other day was shown in a randomized trial to be superior to intramuscular (IM) interferon-beta-1a 30 micro g (6 MIU) once weekly with respect to reductions in relapse-related parameters, disability progression and MRI-assessed disease activity. In patients with secondary progressive MS (SPMS), SC interferon-beta-1b 250 micro g every other day slowed progression of the disease relative to placebo in one randomized, double-blind trial, but not in another. In both studies, interferon-beta-1b 250 micro g recipients had fewer relapses and less MRI-assessed disease activity than placebo recipients. The difference in primary outcome may reflect differences in patient entry criteria. Interferon-beta-1b is generally well tolerated and the common adverse events (e.g. injection site reactions, asthenia and an influenza-like symptom complex) are clinically manageable. In a randomized trial, the tolerability of SC interferon-beta-1b 250 micro g every other day was generally similar to that of IM interferon-beta-1a 30 micro g once weekly, except for higher incidences of injection site reactions and neutralizing anti-interferon-beta antibodies with SC interferon-beta-1b. In conclusion, SC interferon-beta-1b 250 micro g every other day reduces the frequency and severity of relapses and MRI measures of disease activity and may delay the progression of disability in RRMS. The drug appeared to be more effective than, and as well tolerated as, IM interferon-beta-1a 30 micro g once weekly. Interferon-beta-1b also has positive effects on relapse rates and disease activity in patients with SPMS, although its effects on disease progression remain uncertain. The drug is generally well tolerated, and the common adverse events are clinically manageable. Thus, interferon-beta-1b is a valuable first-line therapy for patients with RRMS and a potentially useful option in those with SPMS.
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PMID:Spotlight on Interferon-beta-1b in relapsing-remitting and secondary progressive multiple sclerosis. 1537 76

Weakness of the dorsiflexor muscles of the foot is a relatively common presentation. In most cases, the etiology involves a peripheral injury to the common peroneal nerve. These patients usually present with lower motor neuron findings on evaluation. In contrast, if upper motor neuron findings were present a central lesion should be suspected and appropriate imaging studies are performed. We describe a patient with painless foot drop and lower motor findings on examination that was diagnosed with multiple sclerosis. This case demonstrates that multiple sclerosis can masquerade as a peripheral process in some patients.
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PMID:Painless foot drop: an atypical etiology of a common presentation. 1688 21

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.
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PMID:[Possible mechanisms of chronic fatigue syndrome in multiple sclerosis]. 1717 41

A frequent manifestation of multiple sclerosis (MS) is chronic fatigue syndrome, which can be defined as a subjective decrease in the level of physical and/or mental energy. Chronic fatigue syndrome can be divided into asthenia (fatigue at rest), pathological fatigability (fatigue on physical loading), and fatigue on the background of deterioration of other symptoms (exacerbation of MS). There are both central and peripheral mechanisms for the formation of fatigue. The combination of fatigue and affective disturbances, especially depression and sleep disorders (insomnia, restless legs syndrome) is common in MS and may provide evidence that they share common mechanisms--decreases in the activity of the serotoninergic and noradrenergic systems. An important component in the formation of chronic fatigue syndrome consists of endocrine and autoimmune factors, the latter having a greater effect on asthenia than on pathological fatigue. Further studies of the pathogenetic mechanisms of the formation of asthenia and pathological fatigue and clarification of their differential diagnostic signs should allow not only a better understanding of the nature of this syndrome, but also better selection of individual treatment.
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PMID:Possible mechanisms of the formation of chronic fatigue syndrome in the clinical picture of multiple sclerosis. 1729 96


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