December 2011 References   Devin J. Starlanyl   for http://www.sover.net/~devstar

Casale R, Rainoldi A. 2011. Fatigue and fibromyalgia syndrome: Clinical and neurophysiologic pattern. Best Pract Res Clin Rheumatol. 25(2):241-247. “The concept of 'fatigue' is strictly related to parameters of the setting in which fatigue is measured. Therefore, it is mandatory to provide a definition of fatigue and the modalities of its use. This is of pivotal importance with regard to the fibromyalgia (FM) syndrome, where fatigue is the most invalidating symptom and where, paradoxically, no clear and widely accepted definition of fatigue is available in the literature as yet. In the clinical setting, fatigue can be measured by different methods of various complexities. The simplest technique to assess fatigue involves the use of a visual analogue scale (VAS); however, a number of scales with differing levels of complexity are available for use. It is, often, difficult to detach the term 'fatigue' from tiredness and task failure, which correspond to two completely distinguished forms of fatigue: one with central origin (tiredness) and another which is localized within the muscle (peripheral muscle fatigue). The former is related to changes in motor-unit-recruitment strategies, whereas the latter is attributed to changes in membrane properties. To extensively assess fatigue and, partially, to avoid confusion among the types of fatigue described above, a number of laboratory tests have been developed; among these, there are multichannel surface electromyography (EMG) recordings. Using this type of an approach, it is possible the estimation of motor unit location within the muscle, the decomposition of the surface EMG (sEMG) interference signal into constituent trains of motor unit action potentials (MUAPs) and the analysis of single unit properties.” [One must take into consideration co-existing conditions such as myofascial trigger points, which could impact any conclusion considerably. DJS]

Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 25(2):185-198. “This article reviews the available published knowledge about the diagnosis, pathophysiology and treatment of myofascial pain syndromes from trigger points. Furthermore, epidemiologic data and clinical characteristics of these syndromes are described, including a detailed account of sensory changes that occur at both painful and nonpainful sites and their utility for diagnosis and differential diagnosis; the identification/diagnostic criteria available so far are critically reviewed. The key role played by myofascial trigger points as activating factors of pain symptoms in other algogenic conditions - headache, fibromyalgia and visceral disease - is also addressed. Current hypotheses on the pathophysiology of myofascial pain syndromes are presented, including mechanisms of formation and persistence of primary and secondary trigger points as well as mechanisms beyond referred pain and hyperalgesia from trigger points. Conventional and most recent therapeutic options for these syndromes are described, and their validity is discussed on the basis of results from clinical controlled studies.”

Ibarra JM, Ge HY, Wang C et al. 2011. Latent Myofascial Trigger Points are Associated with an Increased Antagonistic Muscle Activity during Agonist Muscle Contraction. J Pain. [Nov 9 Epub ahead of print]. “The current study provides the first evidence that increased motor unit excitability is associated with reduced antagonist reciprocal inhibition.” Even with latent TrPs, this inhibition existed. This “may contribute to the delayed and incomplete muscle relaxation following exercise. Disordered fine movement control, and unbalanced muscle activation.  Elimination of latent MTrPs and/or prevention of latent MTrPs from becoming active may improve motor functions.”

Kadetoff D, Lampa J, Westman M et al. 2011. Evidence of central inflammation in fibromyalgia - Increased cerebrospinal fluid interleukin-8 levels. J Neuroimmunol. [Nov 27 Epub ahead of print]. “Activation of glia cells resulting in intrathecal elevation of cytokines and chemokines has been hypothesized in chronic pain syndromes such as fibromyalgia. To our knowledge, this is the first study assessing intrathecal concentrations of pro-inflammatory substances in fibromyalgia. We report elevated cerebrospinal fluid and serum concentrations of interleukin-8, but not interleukin-1beta, in FM patients. This profile is in accordance with FM symptoms being mediated by sympathetic activity rather than dependent on prostaglandin associated mechanisms and supports the hypothesis of glia cell activation in response to pain mechanisms.”

Low LA, Schweinhardt P. 2012. Early Life Adversity as a Risk Factor for Fibromyalgia in Later Life. Pain Res Treat. 2012:140832. “This paper discusses risk factors from early life that may increase the occurrence or severity of FM in later life: pain experience during neonatal life causes long-lasting changes in nociceptive circuitry and increases pain sensitivity in the older organism; premature birth and related stressor exposure cause lasting changes in stress responsitivity; maternal deprivation affects anxiety-like behaviors that may be partially mediated by epigenetic modulation of the genome-all these adult phenotypes are strikingly similar to symptoms displayed by FM sufferers. In addition, childhood trauma and exposure to substances of abuse may cause lasting changes in developing neurotransmitter and endocrine circuits that are linked to anxiety and stress responses.”

Martinez-Lavin M. 2012. Fibromyalgia: When Distress Becomes (Un)sympathetic Pain. Pain Res Treat. 2012:981565. “...in fibromyalgia, distress could be converted into pain through forced hyperactivity of the sympathetic component of the stress response system.”

McGreevy K, Bottros MM, Raja SN. 2011. Preventing Chronic Pain following Acute Pain: Risk Factors, Preventive Strategies, and their Efficacy. Eur J Pain Suppl. 5(2):365-372. This paper from Johns Hopkins states: “Chronic pain is the leading cause of disability in the United States. The transition from acute to persistent pain is thought to arise from maladaptive neuroplastic mechanisms involving three intertwined processes, peripheral sensitization, central sensitization, and descending modulation. Strategies aimed at preventing persistent pain may target such processes. Models for studying preventive strategies include persistent post-surgical pain (PPP), persistent post-trauma pain (PTP) and post-herpetic neuralgia (PHN). Such entities allow a more defined acute onset of tissue injury after which study of the long-term effects is more easily examined. In this review, we examine the pathophysiology, epidemiology, risk factors, and treatment strategies for the prevention of chronic pain using these models. Both pharmacological and interventional approaches are described, as well as a discussion of preventive strategies on the horizon.”

Russell IJ. 2011. Future perspectives in generalized musculoskeletal pain syndromes. Best Pract Res Clin Rheumatol. 25(2):321-331. “This article describes contemporary controversies regarding two categories of soft-tissue pain (STP) - chronic widespread pain and fibromyalgia syndrome.... STP classification divides relevant painful conditions into three subgroups, depending on the extent of body involvement (localized, regional and generalized). Fibromyalgia syndrome, in the generalized STP category, is distinguished from other types of chronic widespread pain by virtue of its greater severity. During the past 20 years, the diagnosis of fibromyalgia was based on a research classification (1990 American College of Rheumatology Research Classification Criteria (1990 ACR RCC)) that requires a history of chronic widespread pain and the examination finding of widespread mechanical allodynia. A new approach (2010 American College of Rheumatology Fibromyalgia Diagnostic Criteria (2010 ACR FDC)), validated for clinical use, still requires a history of chronic widespread pain, but the examination is replaced by a historical assessment of co-morbid symptom severity. The populations identified by the two criteria are similar but not identical. Misuse of the new criteria could expand fibromyalgia from 2 to 10% of the general population. Avoidance of the term 'fibromyalgia' could return it to the obscurity from whence it came, leaving a much larger problem in its stead.”

Salgueiro M, Aira Z, Buesa I et al. 2011. Is psychological distress intrinsic to fibromyalgia syndrome? Cross-sectional analysis in two clinical presentations. Rheumatol Int. [Nov 8 Epub ahead of print]. “The present data suggest that associated psychological distress and maladaptive emotional responses that are commonly attributed to the general FMS population may be largely a distinguishing feature of one subset of patients.”

Spaeth M, Rizzi M, Sarzi-Puttini P. 2011. Fibromyalgia and sleep. Best Pract Res Clin Rheumatol. 25(2):227-239. “Chronic pain in fibromyalgia patients, together with its associated symptoms and co-morbidities, is now considered a result of dysregulated mechanisms in the central nervous system (CNS). As fibromyalgia patients often report sleep problems, the physiological processes that normally regulate sleep may be disturbed and overlap with other CNS dysfunctions. Although the mechanisms potentially linking chronic widespread pain, sleep alterations and mood disorders have not yet been proven, polysomnography findings in patients with fibromyalgia and non-restorative sleep and their relationships with clinical symptoms support the hypothesis of a conceptual common mechanism called 'central sensitization'. Food and Drug Administration (FDA)-approved drugs for the treatment of fibromyalgia may benefit sleep, but their label does not include the treatment of fibromyalgia-associated sleep disorders. Non-pharmacological therapies (including a thorough sleep assessment) can be considered in the first-line treatment of non-restorative sleep, although they have not yet been fully investigated in patients with fibromyalgia. Both pharmacological and non-pharmacological treatments should be used cautiously in patients with fibromyalgia, bearing in mind the patients' underlying disorders and the potential interactions of the therapies.”

Staud R. 2011. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol. 25(2):155-164. “Clinical symptoms of chronic widespread pain (CWP) conditions like fibromyalgia (FM), include pain, stiffness, subjective weakness, and muscle fatigue. Muscle pain in CWP is usually described as fluctuating and often associated with local or generalized tenderness (hyperalgesia and/or allodynia). This tenderness related to muscle pain depends on increased peripheral and/or central nervous system responsiveness to peripheral stimuli, which can be either noxious (hyperalgesia) or non-noxious (allodynia). For example, patients with muscle hyperalgesia will rate painful muscle stimuli higher than normal controls, whereas patients with allodynia may perceive light touch as painful, something that a 'normal' individual will never describe as painful. The pathogenesis of such peripheral and/or central nervous system changes in CWP is unclear, but peripheral soft tissue changes have been implicated. Indirect evidence from interventions that attenuate tonic peripheral nociceptive impulses in patients with CWP syndromes like FM suggest that overall FM pain is dependent on peripheral input. More importantly, allodynia and hyperalgesia can be improved or abolished by removal of peripheral impulse input. Another potential mechanism for CWP pain is central disinhibition. However, this pain mechanism also depends on tonic impulse input, even if only inadequately inhibited. Thus, a promising approach to understanding CWP is to determine whether abnormal activity of receptors in deep tissues is fundamental to the development and maintenance of this chronic pain disorder.....Most CWP patients present with focal tissue abnormalities including myofascial trigger points, ligamentous trigger points or osteoarthritis of the joints and spine. While not predictive for the development of CWP, these changes nevertheless represent important pain generators that may initiate or perpetuate chronic pain. Local chemical mediators, including lactic acid, adenosine triphosphate (ATP) and cytokines, seem to play an important role in sensitizing deep tissue nociceptors of CWP patients. Thus, the combination of peripheral impulse input and increased central pain sensitivity may be responsible for widespread chronic pain disorders including FM.”