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eBook details

• Title: Managing Fatigue: Clinical Correlates, Assessment Procedures and Therapeutic Strategies (Report)
• Author : The International MS Journal
• Release Date : January 01, 2010
• Genre: Health & Fitness,Books,Health, Mind & Body,
• Pages : * pages
• Size : 215 KB

Description

Introduction Fatigue is estimated to affect 75 to 95% of patients with multiple sclerosis (MS). For 50 to 60% of these, fatigue is one of the most incapacitating symptoms (1,2) and one of the major reasons for social and occupational problems. Fatigue can be present at all stages of the disease, (3) is often even a symptom of disease onset (4) and may persist throughout the disease course. The knowledge about its presence and substantial impact on quality of life is disproportionate to the knowledge about the symptom itself. The pathophysiology is still unknown although several suggestions have been made. It was assumed that peripheral abnormalities provoke fatigue due to a decrease in maximal voluntary force (5,6) and lower muscle force during repetitive peripheral nerve stimulation (6). On the other hand, central abnormalities such as demyelination and axonal damage in the reticular formation, (7,8) disturbed metabolism in the basal ganglia and the frontal cortex (9) as well as brain atrophy (10,11) are also discussed. Though some immune-related factors (12,13) and neuroendocrine abnormalities (14) are also thought to contribute to fatigue they nevertheless do not fully explain the entire symptom-complexity. Existing evidence so far supports a multicausal aetiology of MS fatigue with a strong contribution of central factors. Further, taking into account data from imaging studies in chronic fatigue syndrome and patients with MS (8,9,15) it can be assumed that fatigue is not an uni-dimensional phenomenon which is focused on physical symptoms, but consists in addition of a cognitive component. Changes in the frontal and temporal cortex as well as in the basal ganglia and thalamus have been reported to be present in patients with fatigue. Although cognitive fatigue was not assessed explicitly in these studies, the authors conclude that the observed abnormalities belong to circuits highly involved in cognitive processing.

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