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Pain and (un)pleasantness
Published in Stephen Buetow, Rethinking Pain in Person-Centred Health Care, 2020
Endogenous pain inhibition can occur during and after activities such as intense exercise75 and by applying a pain stimulus to one body part to inhibit pain in a distal region. This phenomenon of “pain inhibits pain” has been demonstrated experimentally to result from conditioned pain modulation (diffuse noxious inhibitory control).76,77 Through activating the descending inhibitory system in the spinal cord,78 localized pain stimulation generates diffuse pain relief. Analgesia results from decreasing the perception of pain and because interrupting the noxious stimulus can produce a strong feeling of pleasantness.79 Cognitive modulation of endogenous pathways is also relevant to managing persistent pain, whose intensity depends less on tissue damage and nociception than on interacting emotional and social influences80 interpreted in a widely distributed neural network.81 Thus, potential increases for pain to be pleasant or at least not unpleasant, and innate aversion to pain may reverse hedonically.82
Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
In summary, the nociceptive system is not just a bottom-up system of connections that relays painful information to consciousness. Ascending and descending pathways exist to modulate the pain experience in real-time. There is a top-down component that allows for cognitive and emotional control over nociception. Importantly, the brain itself plays an active role in pain pathways and sculpting the pain experience. In this chapter, we reviewed the basics of the pain pathway. We have yet to discuss pain modulation which occurs both peripherally and centrally and is of critical importance when considering the chronic pain patient. Any effective strategy to treat patients with chronic pain must take these multiple variables into account.
Imaging Pain in the Brain: The Role of the Cerebral Cortex in Pain Perception and Modulation
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
M. Catherine Bushnell, Chantal Villemure, Irina Strigo, Gary H. Duncan
that emotional states and attitudes of patients have an effect on postsurgical analgesic requirements (50) and pain associated with chronic diseases (51-54). In the experimental context, manipulations that alter mood or emotional state, such as pleasant music or humorous films, reduce pain perception (55-58). Nevertheless, such studies do not clearly dissociate changes in mood from changes in attention, anxiety, or relaxation. Further, the neural circuitry underlying such pain modulation is not known. The findings from the hypnosis studies described above suggest that ACC might be an important region for hedonic modulation of pain. Further, a recent study revealed a region in the PFC that is activated by stimuli with either positive or negative hedonic value, independent of stimulus modality (59). This region is also sometimes activated by pain (10,25,30,60), so that it may possibly be important for hedonic alterations in pain states.
Pain extent is associated with Central Sensitization Inventory but not widespread pressure pain sensitivity or psychological variables in women with fibromyalgia
Published in Scandinavian Journal of Rheumatology, 2023
M Cigarán-Méndez, E Úbeda-D’Ocasar, JL Arias-Buría, C Fernández-de-Las-Peñas, M Barbero, GM Gallego-Sendarrubias, JA Valera-Calero
This study used pain drawing software to extract pain extent scores. The software used eliminates estimation errors; nevertheless, there are some limitations that should be recognized. First, we collected data only from women with FMS, in a cross-sectional design. Longitudinal studies investigating changes in pain extent would help to elucidate questions raised from the current findings. Secondly, although the assessment of pain extent has been shown to be highly reliable in people with temporomandibular pain (13), reliability data on pain drawings specifically in FMS are not available. Thirdly, we only collected PPTs as a neurophysiological outcome of sensitization. We do not know whether pain extent is associated with dynamic outcomes of sensitization e.g. wind-up, temporal summation, or conditioned pain modulation. Finally, we did not include cognitive outcomes e.g. kinesiophobia or catastrophizing, which could also be associated with pain extent, although current evidence does not support this in other chronic pain conditions (17).
Spinal and supraspinal modulation of pain responses by hypnosis, suggestions, and distraction
Published in American Journal of Clinical Hypnosis, 2021
Bérengère Houzé, Anouk Streff, Mathieu Piché, Pierre Rainville
Three hypotheses were tested in this study: 1) our four interventions are capable of pain modulation, such as a) hypoalgesia suggestions delivered with and without hypnotic induction, and distraction task are expected to reduce all pain responses compared to their respective neutral conditions, and b) hyperalgesia suggestions with hypnotic induction are expected to increase all pain responses compared to its respective neutral condition. Specifically, psychophysiological, and cerebral responses are expected to be reduced in the context of hypoalgesia compared to neutral context, and to be increased in the context of hyperalgesia compared to neutral context. 2) There is an additional effect of hypnotic induction on pain modulation resulting in a greater effectiveness of hypnotic hypoalgesia suggestions in reducing pain responses compared to non-hypnotic hypoalgesia suggestions and distraction task. Specifically, hypnotic hypoalgesia suggestions are expected to further reduce psychophysiological and cerebral responses compared to hypoalgesia suggestions and distraction conditions. 3) There is a directional effect depending on the type of suggestions. Specifically, hypnotic hyperalgesia suggestions are expected to amplify pain responses (both psychophysiological and cerebral) compared to hypnotic hypoalgesia suggestions. However, similar effects of hyperalgesia and hypoalgesia suggestions would imply the activation of general modulatory processes independent from directional changes in pain perception.
Depression, anxiety and acute pain: links and management challenges
Published in Postgraduate Medicine, 2019
Athena Michaelides, Panagiotis Zis
Monoamine transmitters such as serotonin and norepinephrine have a role in downregulating pain perception and their depletion results in comorbid pain and anxiety or depression. Studies have shown that pain signals are blocked when giving serotonin and norepinephrine intrathecally [20]. Similarly, antidepressants that work by increasing the amount of serotonin and norepinephrine in the brain also have a role in pain modulation. Although limited data exists on the use of anti-depressants for the treatment of concomitant depression and acute pain, the most commonly used antidepressants for neuropathic pain are the selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) [53]. In addition to the monoamine modulators, tricyclic antidepressant such as amitriptyline, imipramine and nortriptyline inhibit the reuptake of norepinephrine and serotonin and also enhance endogenous pain inhibition in the CNS [53]. Multiple studies have demonstrated its use in easing neuropathic pain such as postherpetic neuralgia [53].