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: To study chronic widespread pain (CWP) over time in patients with spondyloarthritis (SpA), and to identify risk factors for development and persistence of CWP. : In this cohort study with baseline and 2.5 year follow-up postal surveys, patients with ankylosing spondylitis (AS) and undifferentiated spondyloarthritis (USpA) (47% women) answered questions regarding pain, and were categorized as no chronic pain (NCP), chronic regional pain (CRP), or CWP. For each risk factor candidate (disease duration, body mass index, smoking, and patient-reported outcome measures), logistic regression analyses with CWP as the main outcome were performed separately, together with a basic model including age, gender, and SpA subgroup. : Altogether, 644 patients could be categorized at both time-points, yielding similar prevalence estimates at baseline and follow-up, although 38% transitioned between pain groups. Risk factors (odds ratio; 95% confidence interval) for development of CWP included more pain regions (1.36; 1.20‒1.53), higher pain intensity (1.35; 1.20‒1.52), worse fatigue (1.25; 1.13‒1.38), and worse global health (1.35; 1.19‒1.54). Persistent CWP was reported by 72%. In addition to factors predicting development of CWP, higher age (1.02; 1.00‒1.04), female gender (1.82; 1.06‒3.10), and anxiety (1.07; 1.00-1.14) also predicted persistence. : The prevalence of CWP remained high over time, but with individual transitions between the pain groups. The development and persistence of CWP were predicted by more pain and worse health, with the addition of female gender and higher age for persistent CWP. Special attention and treatment alternatives for patients with SpA and concomitant CWP are essential in the clinic.
Learn More >Poor sleep quality has been associated with greater pain and fatigue in people living with osteoarthritis (OA). The objective of this micro-longitudinal study was to determine whether sleep impacts the diurnal pattern of next-day OA-related pain and fatigue. Community-dwelling older adults (≥65 years) with hip and/or knee OA provided data over 5 days using daily diaries and wrist-worn actigraphs. Pain and fatigue intensity were measured on awakening, at 11 am, 3 pm, 7 pm, and bedtime. Subjective previous night sleep quality was measured on awakening. Multilevel linear regression models examined interactions between sleep variables and time of next-day symptom reports. One hundred sixty participants provided 785 days of data (median age = 71 years; 62% female). Analysis of time interaction effects identified an association between poor sleep quality and more morning pain and fatigue. Although the effect on awakening was more pronounced for fatigue, differences in both symptoms attributable to sleep quality attenuated as the day progressed. Investigation of actigraphy-based sleep parameters revealed no significant interactions with time of symptom measurement. These findings observed in a sample of older adults with mild-to-moderate OA symptoms warrant further investigation in a sample with more severe symptoms and more pronounced sleep dysfunction and/or sleep disorders. PERSPECTIVE: This article investigates the impact of sleep on next-day pain and fatigue of older adults with OA. On awakening from a night of poor quality sleep, pain and fatigue intensity were heightened. However, the effect was not sustained throughout the day, suggesting the morning may be an optimal time for symptom interventions.
Learn More >Recent animal research suggests that mild traumatic brain injury (mTBI) facilitates abnormal endogenous modulation of pain, potentially underlying the increased risk for persistent headaches following injury. However, no human studies have directly assessed the functioning of endogenous facilitory and inhibitory systems in the early stages after an mTBI.
Learn More >This article outlines key features of diagnosis and treatment of migraine in children and adolescents. It emphasizes techniques that can be used by clinicians to optimize history taking in this population, as well as recognition of episodic conditions that may be associated with migraine and present in childhood. Acute treatment strategies include use of over-the-counter analgesics and triptan medications that have been approved by the US Food and Drug Administration for use in children and adolescents. Preventive treatment approach includes lifestyle modifications, behavioral strategies, and consideration of preventive medications with the lowest side effect profiles.
Learn More >This analysis assessed migraine-related burden and treatment decisions in Chronic Migraine Epidemiology and Outcomes (CaMEO) Study survey respondents who stopped taking acute prescription medications for migraine.
Learn More >Adenosine is a signaling molecule induced under stress such as energy insufficiency and ischemic/hypoxic conditions. Adenosine controls multiple physiological and pathological cellular and tissue function by activation of four G protein-coupled receptors (GPCR). Functional role of adenosine signaling in acute pain has been widely studied. However, the role of adenosine signaling in chronic pain is poorly understood. At acute levels, adenosine can be beneficial to anti-pain whereas a sustained elevation of adenosine can be detrimental to promote chronic pain. In recent years, extensive progress has been made to define the role of adenosine signaling in chronic pain and to dissect molecular new insight underlying the development of chronic pain. In this review, we summarize the differential role of adenosine signaling cascade in acute and chronic pain with a major focus on recent studies revealing adenosine ADORA2B receptor activation in the pathology of chronic pain. We further provide a therapeutic outlook of how multiple adenosine signaling components can be useful to treat chronic pain.
Learn More >Pituitary adenylate cyclase-activating polypeptide (PACAP) has emerged as an important signaling peptide in migraine pathogenesis. Recently, we have shown that the less-abundant PACAP isoform, PACAP27, induced migraine and headache in patients equipotently to PACAP38. The present study examined the effect of PACAP27 on cerebral hemodynamics in healthy volunteers using high resolution magnetic resonance angiography (MRA). Eighteen healthy volunteers received infusion of PACAP27 (10 pmol/kg/min) or placebo over 20 min and were scanned repeatedly in fixed intervals for 5 hours in a double-blind, randomized, placebo-controlled study. The circumference of extra-intracerebral arteries was measured and compared with PACAP38 data. We found significant dilation of middle meningeal artery (MMA) (p = 0.019), superficial temporal artery (p = 0.001) and external carotid artery (p = 0.039) after PACAP27 infusion compared to placebo. Whereas the middle cerebral artery (MCA) (p = 0.011) and internal carotid artery (ICA) (p = 0.015, p = 0.019) were constricted. No effects on basilar artery (p = 0.708) and cavernous portion of ICA were found. Post hoc analyses revealed significant larger area under the curve for MMA after PACAP38 compared to PACAP27 (p = 0.033). We also found that PACAP27 induced headache in nine out of twelve (75%) volunteers and one (17%) after placebo. In conclusion, PACAP27 induced headache and dilated extracerebral arteries (>5 h) and slightly constricted MCA in healthy volunteers. Post hoc analysis of PACAP38 data compared with PACAP27 showed that PACAP isoforms dilates MMA with significantly different magnitude.
Learn More >Vagus nerve stimulation (VNS) is a common treatment for medically intractable epilepsy, but response rates are highly variable, with no preoperative means of identifying good candidates. This study aimed to predict VNS response using structural and functional connectomic profiling.
Learn More >: Given our improved understanding of the role of central sensitization (CS) in many patients with chronic pain, it seems rational to account for CS during treatment. : First, the treatment rationale based on the complex mechanisms underlying CS in patients having chronic pain is presented. Second, emphasis is given to explaining the concept of CS when providing treatment, as well as why patients and clinicians should focus on long-term rather than short-term treatment effects. Third, possible pharmacological and non-pharmacological treatment options are discussed. : Centrally acting drugs such as tricyclic compounds, serotonin-norepinephrine reuptake inhibitors, and αδ ligands each target mechanisms that are often dysfunctional in patients having chronic pain and CS, but decades of clinical practice and clinical trials have not resulted in satisfactory outcomes. This comes as no surprise; CS comprises complex psycho-neuro-immunological interactions, while each of the tested drugs targets one or two of those mechanisms from a purely biomedical viewpoint. Clinicians willing to take CS into account should design an individually tailored multimodal treatment plan comprising pain neuroscience education, cognition-targeted exercise therapy, sleep management, stress management, and/or dietary intervention.
Learn More >The amygdala plays a critical role in emotional-affective aspects of behaviors and pain modulation. The central nucleus of amygdala (CeA) serves major output functions, and neuroplasticity in the CeA is linked to pain-related behaviors in different models. Activation of G-coupled group II metabotropic glutamate receptors (mGluRs), which consist of mGluR2 and mGluR3, can decrease neurotransmitter release and regulate synaptic plasticity. Group II mGluRs have emerged as targets for neuropsychiatric disorders and can inhibit pain-related processing and behaviors. Surprisingly, site and mechanism of antinociceptive actions of systemically applied group II mGluR agonists are not clear. Our previous work showed that group II mGluR activation in the amygdala inhibits pain-related CeA activity, but behavioral and spinal consequences remain to be determined. Here we studied the contribution of group II mGluRs in the amygdala to the antinociceptive effects of a systemically applied group II mGluR agonist (LY379268) on behavior and spinal dorsal horn neuronal activity, using the kaolin/carrageenan-induced knee joint arthritis pain model. Audible and ultrasonic vocalizations (emotional responses) and mechanical reflex thresholds were measured in adult rats with and without arthritis (5-6 h postinduction). Extracellular single-unit recordings were made from spinal dorsal horn wide dynamic range neurons of anesthetized (isoflurane) rats with and without arthritis (5-6 h postinduction). Systemic (intraperitoneal) application of a group II mGluR agonist (LY379268) decreased behaviors and activity of spinal neurons in the arthritis pain model but not under normal conditions. Stereotaxic administration of LY379268 into the CeA mimicked the effects of systemic application. Conversely, stereotaxic administration of a group II mGluR antagonist (LY341495) into the CeA reversed the effects of systemic application of LY379268 on behaviors and dorsal horn neuronal activity in arthritic rats. The data show for the first time that the amygdala is the critical site of action for the antinociceptive behavioral and spinal neuronal effects of systemically applied group II mGluR agonists.
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