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Accessing care in multidisciplinary pain treatment facilities continues to be a challenge in Canada.
Multidisciplinary pain treatment facilities (MPTFs) are considered the optimal settings for the management of chronic pain (CP). This study aimed (1) to determine the distribution of MPTFs across Canada, (2) to document time to access and types of services, and (3) to compare the results to those obtained in 2005-2006.
Learn More >Resolvins (RvD1, RvD2 and RvE1) are endogenous anti-inflammatory lipid mediators that display potent analgesic properties in somatic pain by modulating transient receptor potential vanilloid 1 (TRPV1) activation. To what extent these molecules could also have a beneficial effect on TRPV1 sensitisation and visceral hypersensitivity (VHS), mechanisms involved in IBS, remains unknown.
Learn More >Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder associated with chronic abdominal pain and altered pain processing. The aim of this study was to examine whether attentional processes contribute to altered pain inhibition processes in patients with IBS. Nine female patients with IBS and nine age-/sex-matched controls were included in a pain inhibition paradigm using counter-stimulation and distraction with electroencephalography. Patients with IBS showed no inhibition of pain-related brain activity by heterotopic noxious counter-stimulation (HNCS) or selective attention. In the control group, HNCS and selective attention decreased the N100, P260 and high-gamma oscillation power. In addition, pain-related high-gamma power in sensorimotor, anterior cingulate and left dorsolateral prefrontal cortex was decreased by HNCS and selective attention in the control group, but not in patients with IBS. These results indicate that the central pain inhibition deficit in IBS reflects interactions between several brain processes related to pain and attention.
Learn More >PROMISE-2 was a phase 3, randomized, double-blind, placebo-controlled study that evaluated the efficacy and safety of repeat intravenous (IV) doses of the calcitonin gene-related peptide-targeted monoclonal antibody eptinezumab (ALD403) for migraine prevention in adults with chronic migraine. This report describes the results of PROMISE-2 through 24 weeks of treatment.
Learn More >Despite the important roles of protein kinase Cε (PKCε) and transient receptor potential vanilloind 1 (TRPV1) in inflammatory hypersensitivity, how PKCε is involved in the regulation of thermal hyperalgesia is not fully understood. We report here that PKCε is SUMOylated at a C-terminal lysine residue (K534), which enhances the sensitivity of the TRPV1 channel. We demonstrate that PKCε phosphorylation promotes its SUMOylation, which in turn regulates the phosphorylation level of TRPV1 serine 800 residue via controlling the binding of PKCε and TRPV1 and increased PKCε kinase activity. More importantly, the reduced ability of PKCε knockdown mice to develop inflammatory thermal hyperalgesia was rescued by viral infection of lumbar 4/5 dorsal root ganglia neurons of wild-type PKCε, but not the SUMOylation-deficient PKCε mutant. Therefore, the SUMOylation of PKCε potentiates inflammatory thermal hyperalgesia through stabilizing the interaction with TRPV1 to enhance its function by phosphorylation.
Learn More >The innate immune system responds to infections that give rise to pain. How the innate immune system interacts with the sensory nervous system and contributes to pain is poorly understood. Here we report that hyperactivity of innate immunity primes and initiates pain states via the TLR2-interleukin-33 (IL-33) axis. Toll-like receptors (TLRs) are upregulated in the complete Freund's adjuvant (CFA) pain model, and knockout of TLR2 abolishes CFA-induced pain. Selective activation of TLR2/6 triggers acute pain via upregulation of IL-33 in the hindpaw, dorsal root ganglia (DRG), and spinal cord in an NLRP3-dependent manner. The IL-33 increase further initiates priming of nociceptive neurons and pain states. Finally, blocking IL-33 receptors at the spinal level mediates analgesia during acute and chronic inflammatory pain, underscoring an important function of IL-33 in pain signaling. Collectively, our data reveal a critical role of the TLR2-IL-33 axis in innate immune activation for pain initiation and maintenance.
Learn More >The goal of this study is to determine the strength of association between treatment with triptans and acute myocardial infarction, heart failure, and death.
Learn More >Sensitization mechanisms are thought to play a role in the perception of pain in people with cluster headache. No study has investigated the relation between the spatial extent of pain in cluster headache and measures of sensitization or other clinical features. : Our aim was to investigate if the size of the painful area in people with cluster headache relates to widespread pressure sensitivity, headache features, and psychological outcomes. : Forty men with episodic cluster headache reported their symptoms on a digital body chart and pain extent was calculated. Pressure pain thresholds were assessed locally over the temporalis muscle and the C5-C6 joint and at a remote site over the tibialis anterior to assess widespread pressure sensitivity. Clinical features of headache attacks, and anxiety/depressive levels were also assessed. Patients were assessed during a period of remission 6 months after their last pain attack and after treatment discontinuation. : Thirty-two (80%) and thirty (75%) patients reported their headaches in the orbital and the frontal areas, respectively. No significant associations (rho values ranging from -0.228 to 0.187, values ranging from 0.157 to 0.861) were found between pain extent and pressure pain thresholds in trigeminal, extra-trigeminal, and distant pain-free areas, headache clinical features, and anxiety and depressive levels. : Pain extent in the trigemino-cervical area was not related to the degree of pressure pain sensitivity or headache features in men with episodic cluster headache during a period of remission.
Learn More >Low dose ketamine is a leading medication used to provide analgesia in pre-hospital and hospital settings. Low dose ketamine is increasingly used off-label to treat conditions such as depression. In animals, ketamine stimulates the sympathetic nervous system and increases blood pressure, but these physiological consequences have not been studied in conscious humans. Our data suggest that low dose ketamine administration blunts pain perception and reduces blood pressure, but not muscle sympathetic nerve activity burst frequency, responses during a cold pressor test in healthy humans. These mechanistic, physiological results inform risk-benefit analysis for clinicians administering low dose ketamine in humans.
Learn More >Cortical spreading depression (SD) is an intense depolarization underlying migraine aura. Despite the weight of evidence linking SD to the pain phase of migraine, controversy remains over a causal role of SD in cephalgia because of the invasive nature of previous SD induction methods. To overcome this problem, we employed a novel minimally invasive optogenetic SD induction method and examined the effect SD on behavior.
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