& Alberto Rainoldi2
1 Opusmedica, PC&R Patient, Care & Research Network, Piacenza, Italy
2 Motor Sciences Research Center, Interfaculty School of Motor Sciences, University of Turin, Italy
Using PubMed to go back in time, at the beginning of the publications of what at that time was called fibrositis and now defined as fibromyalgia, the muscle was always indicated as the pivot of the myriad of symptoms reported by fibromyalgic patients. Even sleep disturbances were referred to a lack of rest because of muscle pain, anxiety because of continuous pain in the muscle and even easier, fatigue was considered as the perfect condition that may follow continuous muscle pain. And when fibrositis was dropped out and myositis took its place, followed by muscle rheumatism and non-articular rheumatism, muscle remained the bad guy. In this period that we can define the “muscle era”, the pivotal point was to find out possible presence of alterations in the fibromyalgic muscle. All bioptic studies agreed on the presence of atrophy of type II fibers and of a phlogistic aspect. However, these features can be found regularly in the elderly, as well as in different pathologies and etiology: disuse and corticosteroids induced atrophy, corticospinal tract alterations and other diseases. Neither optical nor electronic microscopy revealed any inflammatory or pathognomonic pattern. Both techniques have in fact shown how, from this point of view, the fibromyalgic muscle may appear "normal" or show borderline characteristics as discrete and non-specific alterations. The use of ultrastructural electron microscopy techniques didn’t substantially change the idea that what can be found, were only secondary non-specific alterations. On this cul de sac are also modern non-invasive techniques such as fMR, failed to provide proof and sound diagnostic markers, again showing in one of the most recent papers only unspecific alterations in intramuscular ATP, PCr and fat content reflecting a combination of inactivity/atrophy-related to pain and dysfunction of muscle mitochondria i.e. a lack of function in oxidative muscle fibers [Gerdle et al 2013]. In more recent years and once again starting from the muscle we have succeeded in identifying patterns of muscular activation typical of fibromyalgia and not referred to a disorder of the muscle itself but to a wrong or better to say, non-appropriate or disfunctional motor command. This puts attention not on the effector organ rather that on the ability of the nervous system to match sensory information and to generate congruous motor output. These researches agreed with other lines of research where instead of looking at the periphery, researchers were looking into the CNS functioning with the more sophisticated technologies such as fMR. Indeed, this is the “brain era” in which the muscle doesn’t miss its important role but simply changes its role from the major and main actor to an important part of the interplay between sensory inputs and motor output in a continuous interplay. Moreover there are experimental evidences that indicate that when the bioelectrical phenomena known as localized muscular fatigue develop in the muscle, also in the central nervous system there are neuro-hormonal and excitability changes of the cerebral cortex, which suggest central factors that act upstream of the motoneuronal drive (Taylor JL, Gandevia 2008).In a simplistic and schematic representation: an incongruous motor output, triggered by a wide range of bio-psycho-social and person-related factors, generates an incongruous motor activation which generates incongruous sensory inputs to the brain which misinterpret the information and generates incongruous motor response (Casale & Rainoldi 2011). It turns that this abnormal sensory-motor coupling, if reiterated, can steadily modify the brain response to any motor task. This opens new questions on which type of rehabilitation is needed in fibromyalgia.