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Sodium channel Na1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and functional studies. However, little is known about Na1.7 trafficking or membrane distribution along sensory axons, which can be a meter or more in length. We show here with single-molecule resolution the first live visualization of Na1.7 channels in dorsal root ganglia neurons, including long-distance microtubule-dependent vesicular transport in Rab6A-containing vesicles. We demonstrate nanoclusters that contain a median of 12.5 channels at the plasma membrane on axon termini. We also demonstrate that inflammatory mediators trigger an increase in the number of Na1.7-carrying vesicles per axon, a threefold increase in the median number of Na1.7 channels per vesicle and a ~50% increase in forward velocity. This remarkable enhancement of Na1.7 vesicular trafficking and surface delivery under conditions that mimic a disease state provides new insights into the contribution of Na1.7 to inflammatory pain.
Learn More >To estimate the prevalence of co-occurring pain sites among older adults with persistent back pain and associations of multisite pain with longitudinal outcomes.
Learn More >Children of chronic pain patients run greater risk for developing chronic pain themselves. Exposure to chronic pain of the parent might install cognitive (e.g., pain catastrophizing, interpretation and attentional bias) and affective (e.g., pain anxiety) vulnerability which increase the risk for the development of chronic pain complaints in offspring. This study examines whether pain-free offspring of parents with chronic pain complaints make more health-threatening interpretations and display a stronger pain-related attentional bias compared to the offspring of pain-free parents. We furthermore examined differences between both groups on pain catastrophizing, pain anxiety, and somatic symptoms, and explored the relations between parental pain catastrophizing and aforementioned pain vulnerability measures in offspring.
Learn More >The McGill Pain Questionnaire (MPQ) pain quality descriptors have been analyzed to characterize the sensory, affective, and evaluative domains of pain, but have not been differentiated by pain location.
Learn More >Topical application of lidocaine and prilocaine (LP) cream attenuates the functionality of small cutaneous nerve fibers. The aim of this human study was to measure the underlying excitability modulation of small cutaneous nerve fibers using a novel and fast perception threshold tracking (PTT) technique.
Learn More >To determine if the perioperative administration of valproic acid reduces the incidence of chronic pain three months after amputation or revision surgery.
Learn More >The International Classification of Headache Disorders lists different subtypes of medication overuse headache (MOH), according to the medication overused. The aim of this study is to evaluate whether the different subtypes correspond to clinically distinguishable phenotypes in a large population.
Learn More >Post-traumatic headache (PTH) is a highly disabling secondary headache disorder and one of the most common sequelae of mild traumatic brain injury, also known as concussion. Considerable overlap exists between PTH and common primary headache disorders. The most common PTH phenotypes are migraine-like headache and tension-type-like headache. A better understanding of the pathophysiological similarities and differences between primary headache disorders and PTH could uncover unique treatment targets for PTH. Although possible underlying mechanisms of PTH have been elucidated, a substantial void remains in our understanding, and further research is needed. In this Review, we describe the evidence from animal and human studies that indicates involvement of several potential mechanisms in the development and persistence of PTH. These mechanisms include impaired descending modulation, neurometabolic changes, neuroinflammation and activation of the trigeminal sensory system. Furthermore, we outline future research directions to establish biomarkers involved in progression from acute to persistent PTH, and we identify potential drug targets to prevent and treat persistent PTH.
Learn More >To determine whether synchronous video-based telemedicine visits with specialists are feasible and to evaluate clinical effectiveness, patient perceptions, and other benefits of telemedicine visits for follow-up migraine care in a tertiary headache center.
Learn More >Detecting and avoiding noxious heat is crucial to prevent burn injury. While the nociceptor neurons involved in conveying heat-induced pain were identified more than a century ago, the molecular sensors responsible for detecting noxious heat had remained elusive. In a recent study, important progress was made in our understanding of the molecular basis of acute noxious heat sensing, with the identification of a set of three transient receptor potential (TRP) ion channels, TRPV1, TRPA1 and TRPM3, which have crucial but largely redundant roles in acute heat sensing. Most strikingly, combined elimination of all three TRP channels causes a complete loss of the acute avoidance reaction to noxious heat, without affecting pain responses to painful mechanical or cold stimuli. Here, we provide a brief account of the current model of acute noxious heat sensing, and discuss possible implications for analgesic drug development.
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