April 2014 References  Devin J. Starlanyl   for http://www.sover.net/~devstar

Arendt-Nielsen L, Nielsen TA, Gazerani P. 2014. Translational pain biomarkers in the early development of new neurotherapeutics for pain management. Expert Rev Neurother. 14(3):241-254. “Translation of the analgesic efficacy of investigational neurotherapeutics from pre-clinical pain models into clinical trial phases is associated with a high risk of failure. Application of human pain biomarkers in early stages of clinical trials can potentially enhance the rate of successful translation, which would eventually reduce both length and costs of drug development after the pre-clinical stage. Human pain biomarkers are based on the standardized activation of pain pathways followed by the assessment of ongoing and paroxysmal pain, plus evoked responses which can be applied to healthy individuals and patients prior to and after pharmacological interventions. This review discusses the rationality and feasibility of advanced human pain biomarkers in early phases of drug development for pain management which is still an unmet medical need.”

Broderick JE, Gold MS, Amin MM et al. 2014. The association of somatic arousal with the symptoms of upper airway resistance syndrome. Sleep Med. [Feb 15 Epub ahead of print.]

“We tested the hypothesis that the symptoms of upper airway resistance syndrome (UARS) are manifestations of chronic stress. …Our findings suggest that UARS patients have increased levels of the stress component, somatic arousal, proportionate to the severity of their symptoms.”

Boyer N, Dallel R, Artola A et al. 2014. General trigeminospinal central sensitization and impaired descending pain inhibitory controls contribute to migraine progression. Pain. [Mar 12 Epub ahead of print.]  “Migraine is a chronic disease with episodic manifestations. In a subgroup, attack frequency increases over time, leading to chronic migraine. One of the most important risk factors for migraine progression is frequency of headache attacks at baseline…. We investigated the behavioral, anatomical, and electrophysiological changes induced by repeated low- and high-intensity stimulation of meningeal nociceptor by injecting an inflammatory soup in rats. Single high-intensity, but not low-intensity, stimulation produces a reversible cephalic allodynia. Upon repetition, however, low-intensity stimulation, too, induces a reversible cephalic allodynia, and high-intensity, reversible cephalic and extracephalic allodynia. Moreover, cephalic allodynia becomes, in part, persistent upon repeated high-intensity stimulation. Fos expression reveals that a single high-intensity stimulation already leads to widespread, trigeminal, and spinal central sensitization, and that such general central sensitization potentiates upon repetition. Trigeminovascular nociceptive neurons become persistently sensitized and their diffuse noxious inhibitory controls (DNIC) concomitantly impaired. Thus, compared with single stimulation, repeated dural nociceptor activation specifically leads to: 1) a gradual worsening of cutaneous hypersensitivity and general neuronal hyperexcitability and 2) spreading of cutaneous hypersensitivity superimposed on 3) persistent cephalic cutaneous hypersensitivity and trigeminal central sensitization. Such repetition-induced development of central sensitization and its consequence, cutaneous allodynia, may arise from both the general neuronal hyperexcitability that results from DNIC impairment and hyperexcitability that likely develops in trigeminal nociceptive neurons in response to their repetitive activation. These neuronal changes may in turn elevate the risk for developing chronic migraine.”

Castaldo M, Ge HY, Chiarotto A et al. 2014. Myofascial trigger points in patients with whiplash-associated disorders and mechanical neck pain.  Pain Med.  [Mar 18 Epub ahead of print.]  “Active MTPs are more prominent in WAD (whiplash associated disorders) than MNP and related to current pain intensity and size of the spontaneous pain distribution in whiplash patients.  This may underlie a lower degree of sensitization in MNP than in WAD.” [We must get physicians and other care providers to recognize the myofascial trigger points that are causing the pain, and train them to treat these pain generators adequately. DJS]

Connelly M, Hoffart C, Schikler K et al. 2014. A84: Changes over Time in Symptoms and Treatment of Juvenile Primary Fibromyalgia Syndrome. Arthritis Rheumatol. 66 Suppl 11:S117. “Children with JPFS exhibit worsening pain and quality of life over time regardless of treatment modality recommendations or patient compliance to therapy. Patients returning for follow-up visits may be those whose symptoms are most refractory. Additional studies are needed to identify barriers to improvement in this patient population and to determine effective treatment approaches to improve health outcomes.”  [If the focus shifts to identifying the cause of the symptoms, including myofascial trigger points and their perpetuating factors, and then bring them under control, the prognosis of these patients may improve considerably.  DJS]

Diercks RL. 2014. [Practice guideline 'Diagnosis and treatment of the subacromial pain syndrome'].  Ned Tijdschr Geneeskd. 158:A6985. [Dutch] In shoulder pain there is often no direct relationship between the symptoms and the anatomical substrate; for this reason, the term 'subacromial pain syndrome' (SAPS) is better than 'impingement'. The diagnosis of SAPS can only be made using a combination of tests. Imaging diagnostics, preferably ultrasound, can be carried out if conservative treatment does not give the required result. Acute pain is treated by giving advice and if necessary analgesics; a subacromial injection of glucocorticoids is indicated if symptoms recur or are persistent. Exercise therapy should be specific, of low intensity and high frequency, including eccentric training, scapula stabilization and trigger point massage. Rehabilitation in a specialized unit may be considered if pain maintaining behavior is playing a role. There is no convincing evidence that surgical treatment is more effective than conservative management and there is no indication for the surgical treatment of asymptomatic rotator cuff tears.

Easton V, Bale P, Bacon H et al. 2014. A89: the relationship between benign joint hypermobility syndrome and developmental coordination disorders in children. Arthritis Rheumatol. 66 Suppl 11:S124. “The purpose of this study was to examine baseline data from an interventional study of BJHS in childhood to assess the relationship between joint hypermobility and motor control.

…The study subjects included 119 children between the ages of 5 and 16 years. All had documented joint hypermobility (assessed by a pediatric rheumatologist) and musculoskeletal pain or dysfunction. …Movement difficulty is a common independent component of BJHS in childhood. An evaluation of motor function needs to be included as part of the assessment of all children with BJHS and may merit targeted intervention as its presence represents a lower quality of functioning. Further research is needed into children with BJHS and movement difficulty, who may benefit from targeted interventions.” [It would be very useful if these children were assessed for trigger points that could be affecting their coordination. DJS]

Ferrari R, Russell AS. 2014. Perceived injustice in fibromyalgia and rheumatoid arthritis. Clin Rheumatol. [Mar 4 Epub ahead of print.] “Fibromyalgia is associated with a higher level of perceived injustice than is seen with rheumatoid arthritis. This difference appears to be associated with higher levels of pain reported by fibromyalgia patients, and therefore may not be specific to the diagnosis. Prospective studies may help to resolve this issue.”

Fillingim RB, Bruehl S Dworkin RH et al. 2014. The ACTTION-American Pain Society Pain Taxonomy (AAPT): An Evidence-Based and Multidimensional Approach to Classifying Chronic Pain Conditions. J Pain. 15(3):241-249. “Current approaches to classification of chronic pain conditions suffer from the absence of a systematically implemented and evidence-based taxonomy. Moreover, existing diagnostic approaches typically fail to incorporate available knowledge regarding the biopsychosocial mechanisms contributing to pain conditions. To address these gaps, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) public-private partnership with the U.S. Food and Drug Administration and the American Pain Society (APS) have joined together to develop an evidence-based chronic pain classification system called the ACTTION-APS Pain Taxonomy. This paper describes the outcome of an ACTTION-APS consensus meeting, at which experts agreed on a structure for this new taxonomy of chronic pain conditions. Several major issues around which discussion revolved are presented and summarized, and the structure of the taxonomy is presented. ACTTION-APS Pain Taxonomy will include the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors. In coming months, expert working groups will apply this taxonomy to clusters of chronic pain conditions, thereby developing a set of diagnostic criteria that have been consistently and systematically implemented across nearly all common chronic pain conditions. It is anticipated that the availability of this evidence-based and mechanistic approach to pain classification will be of substantial benefit to chronic pain research and treatment….The ACTTION-APS Pain Taxonomy is an evidence-based chronic pain classification system designed to classify chronic pain along the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors.”

Francois A, Laffray S, Pizzoccaro A et al. 2014. T-type calcium channels in chronic pain: mouse models and specific blockers. Pflugers Arch. 466(4):707-717. “Pain is a quite frequent complaint accompanying numerous pathologies. Among these pathological cases, neuropathies are retrieved with identified etiologies (chemotherapies, diabetes, surgeries…) and also more diffuse syndromes such as fibromyalgia. More broadly, pain is one of the first consequences of the majority of inherited diseases. Despite its importance for the quality of life, current pain management is limited to drugs that are either old or with a limited efficacy or that possess a bad benefit/risk ratio. As no new pharmacological concept has led to new analgesics in the last decades, the discovery of medications is needed, and to this aim the identification of new druggable targets in pain transmission is a first step. Therefore, studies of ion channels in pain pathways are extremely active. This is particularly true with ion channels in peripheral sensory neurons in dorsal root ganglia (DRG) known now to express unique sets of these channels. Moreover, both spinal and supraspinal levels are clearly important in pain modulation. Among these ion channels, we and others revealed the important role of low voltage-gated calcium channels in cellular excitability in different steps of the pain pathways. These channels, by being activated nearby resting membrane potential have biophysical characteristics suited to facilitate action potential generation and rhythmicity. In this review, we will review the current knowledge on the role of these channels in the perception and modulation of pain.”

Ghizzani A, Di Sabatino V Suman AL et al. 2014. Pain Symptoms in Fibromyalgia Patients with and without Provoked Vulvodynia. Pain Res Treat. [Jan 29 Epub ahead of print.] “The study reveals that increased vulvar pain excitability may occur in FMS patients independently of the presence of coital pain. Results suggest that coital pain develops in patients with higher FMS symptoms severity due to the cooperative effects of peripheral and central sensitization mechanisms.”

Haliloglu S, Carlioglu A, Akdeniz D et al. 2014. Fibromyalgia in patients with other rheumatic diseases: prevalence and relationship with disease activity. Rheumatol Int. [Mar 4 Epub ahead of print.] “Concomitant FM is a common clinical problem in rheumatologic diseases, and its recognition is important for the optimal management of these diseases. Increased pain, physical limitations, and fatigue may be interpreted as increased activity of these diseases, and a common treatment option is the prescription of higher doses of biologic agents or corticosteroids. Considerations of the FM component in the management of rheumatologic diseases increase the likelihood of the success of the treatment.”

Hayes AG, Arendt-Nielsen L, Tate S. 2014. Multiple mechanisms have been tested in pain – how can we improve the chances of success? Curr Opin Pharmacol. 14C:11-17. “Recent advances in understanding the pathophysiology of pain have led to a wealth of molecular targets for novel analgesic drugs and many clinical drug trials. There have been successes, like the gabapentinoids for neuropathic pain and calcium channel blockers for otherwise intractable pain states; and drugs which show promise in clinical trials, like nerve growth factor inhibitors and p38 kinase inhibitors. Unfortunately there have also been a number of failures. We suggest factors which might predispose to success, for example some clinical precedence for the mechanism in pain or a genetic link for the mechanism, for example a mutation linked to a pain syndrome. We also stress the importance of demonstrating molecular target engagement with a novel compound and suggest pain biomarkers which can be used for mechanistic drug profiling.”

Hirsch JK, Sirois FM. 2014.  Hope and fatigue in chronic illness: The role of perceived stress. J Health Psychol. [Mar 26 Epub ahead of print.] “Fatigue is a debilitating symptom of chronic illness that is deleteriously affected by perceived stress, a process particularly relevant to inflammatory disease. Hopefulness, a goal-based motivational construct, may beneficially influence stress and fatigue, yet little research has examined these associations. We assessed the relation between hope and fatigue, and the mediating effect of stress, in individuals with fibromyalgia, arthritis, and inflammatory bowel disease. Co-varying age, sex, and pain, stress partially mediated the association between hope and fatigue; those with greater hope reported less stress and consequent fatigue. Therapeutically, bolstering hope may allow proactive management of stressors, resulting in less fatigue.” [Hope often comes with identifying the causes of the fatigue and treating them, and the focus should be towards this goal. DJS]

Izumi M, Petersen KK, Arendt-Nielsen L et al. 2014. Pain referral and regional deep tissue hyperalgesia in experimental human hip pain models.  Pain. 155(4):792-800.  Hip pain and hyperalgesia was produced experimentally in health individuals by injecting them with hypertonic saline solution in the gluteus medius tendon, adductor longus tendon, or gluteus medius muscle.  [This experiment basically created referred pain patterns and hyperalgesia, such as occurs with myofascial trigger points in these muscles and tendons. DJS]

Kitagawa Y, Kimura K, Yoshida S. 2014. Spectral analysis of heart rate variability during trigger point acupuncture. Acupunct Med. [Mar 7 Epub ahead of print.] “These data suggest that acupuncture stimulation of trigger points of the tibialis anterior muscle transiently increases parasympathetic nerve activity.”  [This study may indicate that trigger point bodywork can be helpful to rebalance the sympathetic imbalance in fibromyalgia. DJS]

Koca I, Tutoglu A, Boyacı A. 2014. An evaluation of oxidative stress and antioxidant capacity in patients with myofascial pain syndrome. Mod Rheumatol. [Mar 26 Epub ahead of print.]

“The results of this study determined that the oxidant/antioxidant balance was impaired in MPS patients and thus MPS can be considered to be related to an increase in oxidative stress.”

Lachapelle DL, Lavoie S, Higgins NC et al. 2014. Attractiveness, Diagnostic Ambiguity, and Disability Cues Impact Perceptions of Women with Pain. Rehabil Psychol. [Mar 10 Epub ahead of print.]  “This experimental study investigated how physical attractiveness, disability cue, and diagnostic ambiguity stereotypes impact perceptions of a patient's pain/disability and personality….After viewing photographs of women pictured with or without a cane, accompanied by descriptions of the women's diagnosis (fibromyalgia or rheumatoid arthritis), 147 university students rated the women's pain/disability and personality….Analyses revealed that more attractive women received lower ratings on pain/disability and higher ratings (more positive) on personality. Moreover, those pictured with a disability cue got higher ratings on both pain/disability and personality, and those with medical evidence of pathology (less ambiguity) got higher ratings on pain/disability and lower ratings on personality. Examination of the 3 stereotypes in a single study enabled an evaluation of their interactions. An Attractiveness × Disability Cue × Diagnostic Ambiguity interaction for ratings of pain/disability revealed that the presence of both medical evidence and a disability cue were needed to override the strong "beautiful is healthy" stereotype. Significant 2-way interactions for ratings of personality indicated that the impact of the disability stereotype tends to be overshadowed by the attractiveness stereotype….The results indicate that these stereotypes have a large effect on perceptions of women with chronic pain and that attractiveness, a contextual variable unrelated to the pain experience, exerts an even stronger effect when there is less objective information available. This could have clinical ramifications for assessment and treatment of patients with chronic pain, which often occurs in the absence of "objective" medical evidence or any external cues of disability.”

Laursen JC, Cairns BE, Kumar U et al. 2013. Nitric oxide release from trigeminal satellite glial cells is attenuated by glial modulators and glutamate. Int J Physiol Pathophysiol Pharmacol. 5(4):228-238. “…these findings suggest that targeting SGCs (satellite glial cells) may provide a novel therapeutic approach for management of craniofacial pain conditions such as migraine in the future.”

Li YH, Wang FY, Feng CQ et al. 2014. Massage therapy for fibromyalgia: a systematic review and meta-analysis of randomized controlled trials. PLoS One. 9(2):e89304. “Massage therapy with duration ≥5 weeks had beneficial immediate effects on improving pain, anxiety, and depression in patients with FM. Massage therapy should be one of the viable complementary and alternative treatments for FM. However, given fewer eligible studies in subgroup meta-analyses and no evidence on follow-up effects, large-scale randomized controlled trials with long follow-up are warrant to confirm the current findings.”

McPartland JM, Guy GW, Di Marzo V. 2014. Care and Feeding of the Endocannabinoid System: A Systematic Review of Potential Clinical Interventions that Upregulate the Endocannabinoid System. PLoS One. 9(3):e89566. “Evidence indicates that several classes of pharmaceuticals upregulate the eCB system, including analgesics (acetaminophen, non-steroidal anti-inflammatory drugs, opioids, glucocorticoids), antidepressants, antipsychotics, anxiolytics, and anticonvulsants. Clinical interventions characterized as "complementary and alternative medicine" also upregulate the eCB system: massage and manipulation, acupuncture, dietary supplements, and herbal medicines. Lifestyle modification (diet, weight control, exercise, and the use of psychoactive substances-alcohol, tobacco, coffee, cannabis) also modulate the eCB system….Few clinical trials have assessed interventions that upregulate the eCB system. Many preclinical studies point to other potential approaches; human trials are needed to explore these promising interventions.”

Neziri AY, Bersinger NA, Andersen OK et al. 2014. Correlation between altered central pain processing and concentration of peritoneal fluid inflammatory cytokines in endometriosis patients with chronic pelvic pain. Reg Anesth Pain Med. [Apr 1 Epub ahead of print.] “The results suggest that inflammatory mechanisms may be important in the pathophysiology of altered central pain processes and that cytokines produced in the environment of endometriosis could act as mediators between the peripheral lesion and changes in central nociceptive processes.”

                       

Ohsawa M, Yamamoto S, Ono H. 2014. Contribution of the sensitization of supraspinal nociceptive transmission in chronic pain. Yakugaku Zasshi. 134(3):387-395. “Central sensitization in the spinal cord is well known to be involved in chronic pain. Recent investigations indicated that the protein expressions involving the synaptic plasticity are changed in several brain areas under a chronic pain condition. These changes in supraspinal neural function might cause the emotional and memory dysfunction. It is also possible that these changes are involved in the chronic pain. Indeed, since the improvement of spinal and peripheral sensitization showed limited relief in the neuropathic pain, the sensitization of supraspinal nociceptive transmission might be involved in the expression of chronic pain. We recently found that intra-thalamic treatment with excitatory neurotransmitter glutamate caused hyperalgesia, which is mediated by the stimulation of glutamate N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Moreover, intracerebroventricular treatment with gabapentin, a calcium channel alpha2delta-1 subunit blocker, attenuated the hyperalgesia in the nerve-injury model of mice. These results suggest that the sensitization of supraspinal nociceptive transmission is involved in neuropathic pain. It is also indicated that neuropathic pain is resulted from the activations of spinal glial cells. Likewise, the supraspinal glial activation was observed in the neuropathic pain. Therefore, the sensitization of supraspinal nociceptive transmission might be important for a chronic pain. In this review, we would like to discuss the possible involvement of the supraspinal sensitization in neuropathic pain and in its application for the curative treatment in chronic pain.” Free Article.

Olsen RV, Andersen HH, Moller HG et al. 2014. Somatosensory and vasomotor manifestations of individual and combined stimulation of TRPM8 and TRPA1 using topical L-menthol and trans-cinnamaldehyde in healthy volunteers. Eur J Pain. [Mar 25 Epub ahead of print.] “This study elucidates the potential of L-menthol as a counter-irritant to secondary neurogenic inflammation and provides evidence of an intricate interplay between cold receptors TRPA1 and TRPM8, warranting further investigation of the neural coding of cold pain perception.”

Pergolizzi JV Jr, Raffa RB, Taylor R Jr. 2014. Treating Acute Pain in Light of the Chronification of Pain. Pain Manag Nurs. 15(1):380-390. “The progression of acute to chronic pain, also known as pain chronification, remains incompletely understood. Biologic factors involved in this transition include central sensitization, neuroplastic changes, altered pain modulation, and changes to the "neuromatrix." Chronic pain may involve irreversible pathophysiologic changes, so interrupting the cascade of events that allows acute pain to advance to chronic pain is of crucial importance. This involves recognition and prompt treatment of acute pain, better awareness and application of evidence-based guidelines on pain management by all clinicians (not just pain specialists), and patient education. By interrupting nociceptive input in acute pain conditions, it might be possible to prevent transition to chronic pain syndromes.”

Relph N, Herrington L, Tyson S. 2013. The effects of ACL injury on knee proprioception: a meta-analysis. Physiotherapy. [Dec 4 Epub ahead of print.] ACL injuries may cause knee proprioception deficits compared to uninjured knees and control groups. Although differences were statistically significant, the clinical significance of findings can be questioned. Clinical practitioners using joint position sense or threshold to detect passive motion techniques need to consider the reliability and validity of data provided.  [This study indicates to me that there may be trigger points in the ACL affecting proprioception.  DJS]

Schuh-Hofer S, Wodarski R, Pfau DB et al. 2013. One night of total sleep deprivation promotes a state of generalized hyperalgesia: a surrogate pain model to study the relationship of insomnia and pain. Pain. 154(9):1613-1621. “Our findings show that a single night of TSD is able to induce generalized hyperalgesia and to increase State Anxiety scores. In the future, TSD may serve as a translational pain model to elucidate the pathomechanisms underlying the hyperalgesic effect of sleep disturbances.”

Sivertsen B, Lallukka T, Salo P et al. 2013.  Insomnia as a risk factor for ill health: results from the large population-based prospective HUNT Study in Norway. J Sleep Res. [Oct 30 Epub ahead of print.] “We conclude that insomnia predicts cumulative incidence of several physical and mental conditions. These results may have important clinical implications, and whether or not treatment of insomnia would have a preventive value for both physical and mental conditions should be studied further.”

Staud R. 2013. The important role of CNS facilitation and inhibition for chronic pain. Int J Clin Rheumtol. 8(6):639-646. “Multiple studies have demonstrated that the pain experience among individuals is highly variable. Even under circumstances where the tissue injuries are similar, individual pain experiences may vary drastically. However, this individual difference in pain sensitivity is not only related to sensitivity of peripheral pain receptors, but also to variability in CNS pain processing. Peripheral impulses derived from tissue receptors undergo modification in dorsal horn neurons that can either result in inhibition or facilitation of pain. Such influences are particularly apparent in inflammation where not only peripheral, but also central, pain modulatory mechanisms can significantly increase nociceptive pain. Emotional state, level of anxiety, attention and distraction, memories, stress, fatigue and many other factors can either increase or reduce the pain experience. Increasing evidence suggests that ‘bottom-up’ and ‘top-down’ modulatory circuits within the spinal cord and brain play an important role in pain processing, which can profoundly affect the experience of pain.”

Tanaka M, Ishii A, Watanabe Y. 2014. Regulatory mechanism of performance in chronic cognitive fatigue. Med Hypotheses. 82(5):567-571. “Chronic cognitive fatigue is characterized by a sensation of long-lasting fatigue that impairs cognitive functions. Facilitation and inhibition systems in the central nervous system play primary roles in determining the output to the peripheral system, that is, performance. Sensory input from the peripheral system to the central nervous system activates the inhibition system to limit performance, whereas motivational input activates the facilitation system to enhance performance. The dysfunction of the facilitation system and central sensitization and classical conditioning of the inhibition system play important roles in the pathophysiology of chronic cognitive fatigue. Because the dorsolateral prefrontal cortex receives input from both the facilitation and inhibition systems to determine performance, metabolic, functional, and structural impairments of the dorsolateral prefrontal cortex induced by repetitive and prolonged overwork, stress, and stress responses contribute to the impaired functioning and cognitive performance that occur in people with chronic cognitive fatigue. This hypothesis of the regulatory mechanism of performance provides a new perspective on the neural mechanisms underlying chronic cognitive fatigue.”

Terkelsen AJ, Gierthmuhlen J, Finnerup NB et al. 2014. Bilateral Hypersensitivity to Capsaicin, Thermal, and Mechanical Stimuli in Unilateral Complex Regional Pain Syndrome. Anesthesiology. [Mar 11 Epub ahead of print.] “Complex regional pain syndrome is multifactorial. Exaggerated inflammatory responses to limb injury may be involved. The authors hypothesized that capsaicin-induced pain and neurogenic inflammation (skin perfusion and flare area) are increased in patients with complex regional pain syndrome compared with that in controls….The main finding is bilaterally increased capsaicin-induced pain in patients compared with controls. The flare response to capsaicin was normal, suggesting that the increased pain response was not due to increased neurogenic inflammation. The bilateral hypersensitivity to painful chemical, thermal, and mechanical stimuli not confined to the innervation area of a peripheral nerve or root cannot be explained by a regional change and may partly be due to central sensitization.”

Trinanes Y, Gonzalez-Villar A, Gomez-Perretta C et al.  2014. Suicidality in chronic pain: Predictors of suicidal ideation in fibromyalgia. Pain Pract. [Apr 1 Epub ahead of print.]

“Fibromyalgia (FM) has been associated with a higher prevalence of suicidal behavior. Nevertheless, much remains unknown about suicide risk factors for this chronic pain disorder. In the present study, the relationship of suicidal ideation in FM with a number of sociodemographic, clinical, and psychological variables was analyzed....The prevalence of suicidal ideation among FM patients was 32.5%. Significant differences between patients with vs. without suicidal ideas emerged mainly for the various indices of depression. Patients with suicidal ideation also reported higher levels of anxiety, more day dysfunction due to sleepiness and more limitations due to emotional and physical problems. Logistic regression analysis revealed that cognitive depression symptoms such as BDI Self-Blame cluster are the more closely related to suicide ideation….The presence of suicidal ideation in FM patients is closely related to comorbid depression, anxiety and to a higher impact of the disease in daily life.”

           

Wang SY, Yue J, Xu YX et al. 2014. [Preliminary report of botulinum toxin type A injection at trigger point for treatment of trigeminal neuralgia:experiences of 16 cases]. Shanghai Kou Qiang Yi Xue. 23(1):117-119. [Article in Chinese]  “Botulium toxin type A injection is an effective way for treatment of patients with primary trigeminal neuralgia.”  [Note that the injections were given in trigger points, and not simply in pain areas.  DJS]

Watson DH, Drummond PD. 2014. Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex. Headache. [Mar 25 Epub ahead of print.] “Our findings corroborate previous results related to anatomical and functional convergence of trigeminal and cervical afferent pathways in animals and humans, and suggest that manual cervical modulation of this pathway is of potential benefit in migraine.”

Weiss JE, Schikler K, Boneparth A et al. 2014. A99: Symptom and treatment characteristics of juvenile primary fibromyalgia syndrome in the CARRA Registry: Are males and females created equal? Arthritis Rheumatol. 66 Suppl 11:S134. “Children and adolescents with juvenile primary fibromyalgia syndrome (JPFS) often present to pediatric rheumatologists for evaluation. Limited data are available on the characteristics of and treatments used for JPFS, particularly in males….We evaluated de-identified data from baseline visits of JPFS patients entered in the Childhood Arthritis & Rheumatology Research Alliance (CARRA) registry between May 2010 and September 2013. Data regarding demographics, symptoms, functional measures and treatment are compared as a function of gender.…Based on data from the largest known cohort of JPFS patients, there are few significant gender differences in physician assessment of disease activity. However, higher levels of disability reported by male patients suggest the need to consider gender when evaluating and treating JPFS patients. Possible explanations for the discrepancies in treatment include effects of gender on physician's perception of patient's pain leading to more medication use among males or females being more willing to try non-pharmacologic modes of treatment. Future studies on gender and treatment outcomes are needed to improve care for these patients.”