April 2013 References    Devin J. Starlanyl   for          http://www.sover.net/~devstar

Bardal E, Olsen T, Ettema G et al. 2013. Metabolic rate, cardiac response, and aerobic capacity in fibromyalgia: a case-control study. Scand J Rheumatol. [Mar 26 Epub ahead of print]. “The current study indicates that patients with fibromyalgia (FM) have similar metabolic and cardiovascular responses to submaximal exercise as healthy controls (HCs). However, these patients have reduced ability to reach maximal oxygen consumption (VO2max) and a possible deficit in the metabolic system when exercising above the anaerobic threshold (AT).”

Bernstein CD, Albrecht KL, Marcus DA. 2013. Milnacipran for fibromyalgia: a useful addition to the treatment armamentarium. Expert Opin Pharmacother. [Mar 19 Epub ahead of print].

“Milnacipran provides modest fibromyalgia pain relief and is best used as part of a multidisciplinary treatment approach. While milnacipran was not studied in fibromyalgia patients with major depression, it may be a wise choice for fibromyalgia patients with depressive symptoms and patients for whom sedation, dizziness, edema or weight gain with gabapentin and pregabalin is a problem. Milnacipran has been found to be beneficial for treating some troublesome fibromyalgia-associated symptoms, including fatigue and cognitive dysfunction.”

Chopra P, Cooper MS. 2013. Treatment of Complex Regional Pain Syndrome (CRPS) Using Low Dose Naltrexone (LDN). J Neuroimmune Pharmacol. [Apr 2 Epub ahead of print].

“Complex Regional Pain Syndrome (CRPS) is a neuropathic pain syndrome, which involves glial activation and central sensitization in the central nervous system. Here, we describe positive outcomes of two CRPS patients, after they were treated with low-dose naltrexone (a glial attenuator), in combination with other CRPS therapies. Prominent CRPS symptoms remitted in these two patients, including dystonic spasms and fixed dystonia (respectively), following treatment with low-dose naltrexone (LDN). LDN, which is known to antagonize the Toll-like Receptor 4 pathway and attenuate activated microglia, was utilized in these patients after conventional CRPS pharmacotherapy failed to suppress their recalcitrant CRPS symptoms.”

Chung SD, Lin CC, Liu SP et al. 2013. Obstructive Sleep Apnea Increases the Risk of Bladder Pain Syndrome/Interstitial Cystitis: A Population-Based Matched-Cohort Study. Neurourol Urodyn. [Mar 28 Epub ahead of print]. “Previous studies indicated a possible association between bladder pain syndrome/interstitial cystitis (BPS/IC) and sleep disorders including sleep abnormalities with delayed onset of sleep, waking up before needed, and snoring. Nevertheless, no previous study has reported the association between obstructive sleep apnea (OSA) and BPS/IC....This study provides epidemiological evidence of a link between OSA and a subsequent BPS/IC diagnosis. We suggest that clinical practitioners treating subjects with OSA be alert to urinary complaints in this population.”

Climent JM, Kuan TS, Fenollosa P et al. 2013. Botulinum toxin for the treatment of myofascial pain syndromes involving the neck and back: a review from a clinical perspective. Evid Based Complement Alternat Med. [Feb 19 Epub ahead of print]. “Botulinum toxin inhibits acetylcholine (ACh) release and probably blocks some nociceptive neurotransmitters. It has been suggested that the development of myofascial trigger points (MTrP) is related to an excess release of ACh to increase the number of sensitized nociceptors. Although the use of botulinum toxin to treat myofascial pain syndrome (MPS) has been investigated in many clinical trials, the results are contradictory. The objective of this paper is to identify sources of variability that could explain these differences in the results....Sources of differences in studies were found in the diagnostic and selection criteria, the muscles injected, the injection technique, the number of trigger points injected, the dosage of botulinum toxin used, treatments for control group, outcome measures, and duration of followup. The contradictory results regarding the efficacy of botulinum toxin A in MPS associated with neck and back pain do not allow this treatment to be recommended or rejected. There is evidence that botulinum toxin could be useful in specific myofascial regions such as piriformis syndrome. It could also be useful in patients with refractory MPS that has not responded to other myofascial injection therapies.”

Diatchenko L, Fillingim RB, Smith SB et al. 2013. The phenotypic and genetic signatures of common musculoskeletal pain conditions. Nat Rev Rheumatol. [Apr 2 Epub ahead of print].

“Musculoskeletal pain conditions, such as fibromyalgia and low back pain, tend to coexist in affected individuals and are characterized by a report of pain greater than expected based on the results of a standard physical evaluation. The pathophysiology of these conditions is largely unknown, we lack biological markers for accurate diagnosis, and conventional therapeutics have limited effectiveness. Growing evidence suggests that chronic pain conditions are associated with both physical and psychological triggers, which initiate pain amplification and psychological distress; thus, susceptibility is dictated by complex interactions between genetic and environmental factors. Herein, we review phenotypic and genetic markers of common musculoskeletal pain conditions, selected based on their association with musculoskeletal pain in previous research. The phenotypic markers of greatest interest include measures of pain amplification and 'psychological' measures (such as emotional distress, somatic awareness, psychosocial stress and catastrophizing). Genetic polymorphisms reproducibly linked with musculoskeletal pain are found in genes contributing to serotonergic and adrenergic pathways. Elucidation of the biological mechanisms by which these markers contribute to the perception of pain in these patients will enable the development of novel effective drugs and methodologies that permit better diagnoses and approaches to personalized medicine.”

Dirckx M, Groeneweg G, van Daele PL et al. 2013. Mast Cells: A New Target in the Treatment of Complex Regional Pain Syndrome? Pain Pract. [Mar 14 Epub ahead of print]. “There is convincing evidence that inflammation plays a pivotal role in the pathophysiology of complex regional pain syndrome (CRPS). Besides inflammation, central sensitization is also an important phenomenon. Mast cells are known to be involved in the inflammatory process of CRPS and also play a role (at least partially) in the process of central sensitization. In the development of a more mechanism-based treatment, influencing the activity of mast cells might be important in the treatment of CRPS. We describe the rationale for using medication that counteracts the effects of mast cells in the treatment of CRPS.”

Hao J, Ruel J, Coste B et al. 2013. Piezo-electrically driven mechanical stimulation of sensory neurons. Methods Mol Biol. 998:159-170. “Mechanotransduction, the conversion of a mechanical stimulus into a biological response, constitutes the basis of a variety of physiological functions such as the senses of touch, balance, proprioception, blood pressure, and hearing. In vertebrates, mechanosensation is mediated by mechanosensory neurons, whose cell bodies are located in trigeminal and dorsal root ganglia. Here, we describe an in vitro model of mechanotransduction that provides an opportunity to explore the properties of mechanosensitive channels in mammalian sensory neurons. The mechano-clamp method allows applying local force on plasma membrane of whole-cell patch-clamped sensory neurons. This technique uses a mechanical probe driven by a computer-assisted piezoelectric microstage to repeatedly stimulate sensory neurons with accurate control of stimulus strength, duration, and speed.” [Considering the piezoelectrical properties of myofascia, this might prove interesting. DJS]

Homann D, Louzada FM, Goes SM. 2013. Acylated ghrelin: A potential marker for fibromyalgia? Eur J Pain. [Mar 8 Epub ahead of print]. “Fibromyalgia is characterized by chronic widespread pain and sleep disturbances. Overweight and obesity, which lead to metabolic changes, are additional comorbidities that are rarely explored, although they are highly prevalent in patients with fibromyalgia....These findings indicate that the decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity.”

Hoog SL, Cheng Y, Elpers J et al. 2013. Duloxetine and pregnancy outcomes: safety surveillance findings. Int J Med Sci. 10(4):413-419. “While limitations of these data are recognized, the information available to date from these two data sources suggest that the frequency of abnormal outcomes reported in duloxetine pregnancy cases is generally consistent with the historic control rates in the general population.” [This study was financed by Eli Lilly and Company, manufacturers of duloxetine]

Janssens L, Brumagne S, McConnell AK. 2013. Proprioceptive changes impair balance control in individuals with chronic obstructive pulmonary disease. PLoS One. 8(3):e57949.

“Individuals with COPD, especially those with inspiratory muscle weakness, increased their reliance on ankle muscle proprioceptive signals and decreased their reliance on back muscle proprioceptive signals during balance control, resulting in a decreased postural stability compared to healthy controls. These proprioceptive changes may be due to an impaired postural contribution of the inspiratory muscles to trunk stability. Further research is required to determine whether interventions such as proprioceptive training and inspiratory muscle training improve postural balance and reduce the fall risk in individuals with COPD.”

Jenewein J, Moergeli H, Sprott H et al. 2013. Fear-learning deficits in subjects with fibromyalgia syndrome? Eur J Pain. [Mar 7 Epub ahead of print]. “Contingency learning deficits represent a potentially promising and specific, but largely unstudied, psychopathological factor in FMS. Deficits in contingency learning may increase anxiety and, consequently, pain sensation. These findings have the potential to contribute to the development of novel therapeutic approaches for FMS.”

Juuso P, Skar L, Olsson M et al. 2012. Meanings of Feeling Well for Women with Fibromyalgia.

Health Care Women Int. [Nov 8 Epub ahead of print]. “Our interpretation of the findings shows that for women with FM meanings of feeling well can be understood as having strength to be involved. The women's experiences of feeling well meant being in control, having power, finding one's own pace, and experiencing feelings of belonging.”

Kim CH, Vincent A, Clauw DJ et al. 2013. Association between alcohol consumption and symptom severity and quality of life in patients with fibromyalgia. Arthritis Res Ther. 15(2):R42.

“Our study demonstrates that low and moderate alcohol consumption was associated with lower fibromyalgia symptoms and better quality of life (QOL) compared to no alcohol consumption. The reasons for these results are unclear. Since recent studies have demonstrated that gamma-Aminobutyric Acid (GABA) levels are low in fibromyalgia, and alcohol is known to be a GABA-agonist, future studies should examine whether alcohol could have a salutary effect on pain and other symptoms in fibromyalgia.”

Kojic Z, Stojanovic D. 2013. Pathophysiology of migraine--from molecular to personalized medicine.  Med Pregl. 66(1-2):53-57. “Understanding of migraine pathophysiology has substantially improved over the last two decades. As a result, migraine is now mainly considered to be a disorder of the brain, rather than one of the vasculature or the meninges....Although it remains speculative how exactly they relate to each other, the following three processes are important in migraine: 1. Cortical spreading depression is a wave of intense depolarization, it starts in the occipital lobe, propagates through the brain and is followed by a period of suppressed activity. 2. Activation of the trigemonovascular system causes the release of neuropeptides (e.g. calcitonin gene-related peptide, substance P) from the peripheral trigeminal nerve endings. These neuropeptides are thought to play a role in causing and maintaining headache. 3. Sensitization of peripheral and central brain areas, it is thought that pulsating quality of migraine headache is caused by a process of peripheral sensitization. Cutaneous allodynia is a marker of central sensitization....The view that the aura is caused by cortical spreading depression has become generally accepted, and the same is true for the view that activation of the trigemonovascular system underlies migraine headache. However, the relationship between the aura and the activation of the trigemonovascular system and the start of headache remains elusive....One of the most important aspects of the pathophysiology of migraine is the hereditary nature of the disorder....Identification of polymorphisms and genetic biomarkers should help us to understand migraine pathophysiology better and thus enable the development of specific, effective ‘individually-tailored treatment’ for each particular migraine patient (personalized medicine).”

Liedberg GM, Björk M. 2013. Symptoms of subordinated importance in fibromyalgia when differentiating working from non-working women. Work. [Mar 26 Epub ahead of print].

“The non-working (NW) women reported a significantly higher severity of symptoms compared with the working (W) women. The most important variable when differentiating the W from the NW women was social support from colleagues and employers. ...To change prevailing attitudes and values towards persons with a work disability, a process of active intervention involving staff is needed. Educating employers as to how a disability may influence a work situation, and the importance of social support, can be improved.” [In the case of women who have such severe pain and other disabling pain and dysfunctions that they cannot work, is it necessary to find another reason that such women who aren’t working have greater pain?  Where is the logic here?  DJS]

Magrey MN, Antonelli M, James N et al. 2013. High frequency of fibromyalgia in patients with psoriatic arthritis: a pilot study. Arthritis. [Feb 14 Epub ahead of print]. “FMS-associated pain and fatigue are significantly more frequent in patients with PsA compared to controls.”

Meeus M, Ickmans K, Struyf F et al. 2013. Does Acetaminophen Activate Endogenous Pain Inhibition in Chronic Fatigue Syndrome/Fibromyalgia and Rheumatoid Arthritis? A Double-Blind Randomized Controlled Cross-over Trial. Pain Physician. 16(2):E61-70. “Although enhanced temporal summation (TS) and conditioned pain modulation (CPM), as characteristic for central sensitization, has been proved to be impaired in different chronic pain populations, the exact nature is still unknown....We examined differences in TS and CPM in 2 chronic pain populations, patients with both chronic fatigue syndrome (CFS) and comorbid fibromyalgia (FM) and patients with rheumatoid arthritis (RA), and in sedentary, healthy controls, and evaluated whether activation of serotonergic descending pathways by acetaminophen improves central pain processing....After intake of acetaminophen, pain thresholds increased slightly in CFS/FM patients, and decreased in the RA and the control group. Temporal summation was reduced in the 3 groups and CPM at the shoulder was better overall, however only statistically significant for the RA group....This is the first study comparing the influence of acetaminophen on central pain processing in healthy controls and patients with CFS/FM and RA. It seems that CFS/FM patients present more central pain processing abnormalities than RA patients, and that acetaminophen may have a limited positive effect on central pain inhibition, but other contributors have to be identified and evaluated.”

Moller-Levet CS, Archer SN, Bucca G et al. 2013. Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcritome. Proc Natl Acad Sci USA. 110(12):E1132-1141. “…insufficient sleep affects the human blood transcriptome, disrupts its circadian regulation, and intensifies the effects of acute total sleep deprivation.  The identified biological processes may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness of sleep homeostasis, circadian rhythmicity, and metabolism.”  The change from 8 hours a night to 6 hours a night of sleep for even one week can cause drastic genetic effects.  After one week of the 6 hour a night sleep regimen, tests of the formerly healthy subjects showed that 711 of their genes had changed, including ones that regulate the immune system. 

Muscolino JE. 2013. Abdominal wall triggerpoint case study. J Bodyw Mov Ther 17(2):151-156. “When myofascial pain syndrome is responsible for a patient’s condition and is not recognized by the patient’s medical advisors, the patient may be put through a plethora of testing procedures to find the cause of the patient’s pain, and prescribed medications in an effort to treat the patient’s symptoms, The case review presented here involves a patient with severe anterior abdominal pain, with a history of Crohn’s disease, who experienced a long and difficult medical process before a diagnosis of myofascial pain syndrome was made.”

Neblett R, Cohen H, Choi Y et al. 2013. The Central Sensitization Inventory (CSI): Establishing Clinically-Significant Values for Identifying Central Sensitivity Syndromes in an Outpatient Chronic Pain Sample. J Pain. [Mar 9 Epub ahead of print]. “Central sensitization (CS) is a proposed physiological phenomenon in which central nervous system neurons become hyperexcitable, resulting in hypersensitivity to both noxious and non-noxious stimuli. The term central sensitivity syndrome (CSS) describes a group of medically indistinct (or nonspecific) disorders, such as fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome, for which CS may be a common etiology. In a previous study, the central sensitization inventory (CSI) was introduced as a screening instrument for clinicians to help identify patients with a CSS…. The CSI is a new self-report screening instrument to help identify patients with CSSs, including fibromyalgia. The present study investigated CSI scores in a heterogeneous pain population, with a large percentage of CSSs, and a normative nonclinical sample to determine a clinically relevant cutoff value.”

Nguyen BM. 2013. Myofascial trigger point falls in the elderly, idiopathic knee pain and osteoarthritis: An alternative concept. Med Hypotheses. [April 5 Epub ahead of print]. “Knee alignment and associated pathological abnormal forces transmitted through the knee is thought to provoke joint protective mechanism in reflex arthrogenic muscle inhibition (AMI) and the start of the idiopathic knee osteoarthritic process.  The current prevailing hypothesis is AMI initiates quadriceps muscle weakness, cause aberrant loading of the knee joint and focal cartilage destruction. This paper investigates for evidence in the literature if this conceptual framework is consistent with the clinical evidence, and if there is an alternative explanation to AMI hypothesis for the pathogenesis of idiopathic knee osteoarthritis.  One crucial question yet to be answered by the AMI hypothesis is; where are the initial aggravating factors of reflex AMI emanate from?  AMI hypothesis relies on joint damage and changes in joint homeostasis to provoke a reflex arthrogenous response which can be found late in the development of knee OA.  Myofascial trigger point (MTrP) hypothesis only relies on muscle tightness, pain and weakness to detect early pathological neuromuscular changes including knee instability and falls in the elderly.  AMI is implicated in the knee OA pathological process but much later on when there are changes in joint homeostasis and joint cartilage damage have occurred. Falls in the elderly are a result of early pathological neuromuscular changes.  The MTrP hypothesis is more sensitive and advanced in the early detection of neuromuscular impairment and pathological changes, allowing early intervention, prevention of falls in the elderly and idiopathic knee osteoarthritis.” [Researchers are discovering that bones follow muscles, and that it is the muscle contracture by TrPs causing the wear and tear on bony areas of joints that leads to osteoarthritis. DJS] 

Painter JT, Crofford LJ, Talbert J. 2013. Geographic variation of chronic opioid use in fibromyalgia. Clin Ther. 35(3):303-311. “Opioid use for the treatment of chronic nonmalignant pain has increased drastically over the past decade. Although no evidence of efficacy exists supporting the treatment of fibromyalgia (FM) with chronic opioid therapy, a large number of patients are receiving this therapy....Geographic variation in chronic opioid use among patients with FM exists at rates similar to those seen in other studies examining opioid use. This large level of geographic variation suggests that the prescribing decision is not based solely on physician-patient interaction but also on contextual and structural factors at the state level. The level of physician and condition prevalence suggest that information dissemination and peer-to-peer interaction may play a key role in adopting evidence-based medicine for the treatment of patients suffering from FM and related conditions. Level of diagnosis prevalence as a predictor of evidence-based practice has not been reported in the literature and is an important contribution to research on geographic variation.”

Rainey CE. 2013. The use of trigger point dry needling and intramuscular electrical stimulation for a subject with chronic low back pain: a case report. Int J Sports Phys Ther 8(2):145-161. The subject of this case report is a 30 year old female on active military duty, who developed low back and right posteriolateral hip pain after a lumbar flexion injury from picking up a barbell. Exam revealed a multi-segmental flexion movement pattern dysfunction, with TrPs in the right gluteus maximus and medius. Dry needling of the trigger points and intramuscular stimulation coupled with a home program of core stability exercises helped the patient return to full military duty without pain.

Timmerman GM, Calfa NA, Stuifbergen AK. 2013. Correlates of body mass index in women with fibromyalgia. Orthop Nurs. 32(2):113-119. “The findings support a growing body of evidence that excess weight is negatively related to quality of life and pain in women with FMS.”

Turo D, Otto P, Shah JP et al. 2013. Ultrasonic characterization of the upper trapezius muscle in patients with chronic neck pain. Ultrason Imaging. 35(2):173-187. “Localization, diagnosis, and clinical outcome measures of painful MTrPs (myofascial trigger points) can be improved by objectively characterizing and quantitatively measuring their properties. The goal of this study was to evaluate whether ultrasound imaging and elastography can differentiate symptomatic (active) MTrPs from normal muscle.....results suggest that active MTrPs have more homogeneous texture and heterogeneous stiffness when compared with normal, unaffected muscle. Our methods enabled us to improve the imaging contrast between suspected MTrPs and surrounding muscle. Our results indicate that in subjects with chronic neck pain and active MTrPs, the abnormalities are not confined to discrete isolated nodules but instead affect the milieu of the muscle surrounding palpable MTrPs. With further refinement, ultrasound imaging can be a promising objective method for characterizing soft tissue abnormalities associated with active MTrPs and elucidating the role of MTrPs in the pathophysiology of MPS.”

Vallejo M, Martinez-Martínez LA, Grijalva-Quijada S et al. 2013. Prevalence of fibromyalgia in vasovagal syncope. J Clin Rheumatol. 19(3):111-114. “Fibromyalgia was relatively frequent in these women with vasovagal syncope and could be associated with dysautonomic symptoms. Therefore, it seems important to search for dysautonomic comorbidities in patients with vasovagal syncope and/or fibromyalgia, to provide a patient-centered holistic approach, instead of the often currently used therapeutic partition.”

Woller SA, Hook MA. 2013. Opioid administration following spinal cord injury: Implications for pain and locomotor recovery. Exp Neurol. [Mar 15 Epub ahead of print]. “Approximately one-third of people with a spinal cord injury (SCI) will experience persistent neuropathic pain following injury. This pain negatively affects quality of life and is difficult to treat. Opioids are among the most effective drug treatments, and are commonly prescribed, but experimental evidence suggests that opioid treatment in the acute phase of injury can attenuate recovery of locomotor function. In fact, spinal cord injury and opioid administration share several common features (e.g. central sensitization, excitotoxicity, aberrant glial activation) that have been linked to impaired recovery of function, as well as the development of pain. Despite these effects, the interactions between opioid use and spinal cord injury have not been fully explored. A review of the literature, described here, suggests that caution is warranted when administering opioids after SCI. Opioid administration may synergistically contribute to the pathology of SCI to increase the development of pain, decrease locomotor recovery, and leave individuals at risk for infection. Considering these negative implications, it is important that guidelines are established for the use of opioids following spinal cord and other central nervous system injuries.”

Zamanillo D, Romero L, Merlos M et al. 2013. Sigma 1 receptor: A new therapeutic target for pain. Eur J Pharmacol. [Mar 13 Epub ahead of print]. “Sigma 1 receptor... is a unique ligand-regulated molecular chaperone located mainly in the endoplasmic reticulum and the plasma membrane. (Sigma 1) receptor is activated under stress or pathological conditions and interacts with several neurotransmitter receptors and ion channels to modulate their function. The effects reported preclinically with (Sigma 1) receptor ligands are consistent with a role for (Sigma 1) receptor in central sensitization and pain hypersensitivity and suggest a potential therapeutic use of (Sigma 1) receptor antagonists for the management of neuropathic pain as monotherapy. Moreover, data support their use in opioid adjuvant therapy: combination of (Sigma 1) receptor antagonists and opioids results in potentiation of opioid analgesia, without significant increases in opioid-related unwanted effects. Results from clinical trials using selective (Sigma 1) receptor antagonists in several pain conditions are eagerly awaited to ascertain the potential of (Sigma 1) receptor modulation in pain therapy.”