%0 Journal Article
%T Voluntary activation failure is detectable in some myositis patients with persisting quadriceps femoris weakness: an observational study
%A Catherine B Molloy
%A Ahmed O Al-Omar
%A Kathryn T Edge
%A Robert G Cooper
%J Arthritis Research & Therapy
%D 2006
%I BioMed Central
%R 10.1186/ar1935
%X Polymyositis (PM) and dermatomyositis (DM) are the idiopathic inflammatory myositis subtypes most often treated by rheumatologists [1,2]. Corticosteroids and immunosuppressive drugs remain the mainstay of treatment [2], but the response to these agents is often disappointing, so chronic weakness and disability may persist despite treatment [3,4]. In chronic, end-stage myositis, in which muscle wasting may be radiologically and even clinically obvious, weakness may be explained by loss of muscle mass which, once established, often appears irreversible. In the early acute phase of myositis, when muscle histology might demonstrate the characteristic infiltration by T cells and macrophages, with secondary muscle fibre damage and myonecrosis [5], weakness is often at its most severe. Because early weakness usually improves with treatment, albeit to a variable degree, it has traditionally been assumed that muscle weakness prior to treatment results from inflammatory processes, although the actual mechanisms responsible for inflammatory weakness induction remain unelucidated. In treated myositis, recovery of strength is often incomplete, even though radiological and histological evidence suggests that inflammation has been suppressed. Here, especially in the absence of obvious wasting, persisting weakness is harder to explain. Thus, it is also increasingly recognised in myositis that any correlation between the observed weakness of a muscle and the degree of its inflammatory cell infiltration at biopsy may be very poor [6,7]. These discussions clearly suggest that mechanisms other than those related to inflammation are implicated in weakness induction in myositis [8]. Indeed, many recent studies present compelling evidence that abnormalities of energy metabolism [9,10], possibly due to disruption of local microcirculation [11], as well as cytokine dysfunction [12-14], are likely involved in weakness induction. More recently still, in murine and human myositis, activation o
%U http://arthritis-research.com/content/8/3/R67