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Mechanisms of Pain
Published in Benjamin Apichai, Chinese Medicine for Lower Body Pain, 2021
Nociceptive pain can be further classified: Somatic nociceptive pain originates from the nociceptors located on the surface of the body or in the musculoskeletal tissues. It is associated with body tissue injury or inflammation. Most acute sport injuries result in this type of pain. It is usually localized, sharp or dull, sore, stabbing, or aching in nature. It is often exacerbated with activity, coughing, laughing, deeply breathing, or changing wound dressings and alleviated upon rest (Robertson 2018). This type of pain is commonly seen in musculoskeletal pain, arthritic pain, and postsurgical pain. It responds well to the treatments of acupuncture and Tui Na.Visceral pain originates from pain receptors located in the internal organs. This type of pain is usually described as cramping, deep, aching, squeezing, constant, and pressure-like, but it is not localized because it may refer, as with appendicitis or gallstones.2
Neurophysiological Basis of Visceral Pain
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
Maria Adele Giamberardino, Giannapia Affaitati, Rosanna Lerza, Silvana De Laurentis
Visceral pain is a major symptom in internal medicine and one of the most frequent reasons for hospitalization and/or seeking medical care (6,7). The features of the symptom are very typical in the first phases of an algogenic process involving internal organs [true visceral pain] but tend to modify with time in the course of the same episode or on the occasion of subsequent painful attacks [referred pain] (5). The phase of true visceral pain, experienced in the early stages, consists of a vague, poorly defined, and scarcely localized sensation, always perceived in the same site whatever the viscus in question [usually the midline of the thorax or abdomen, mostly the lowest sternal or epigastric regions, anteriorly or posteriorly], and accompanied by marked neurovegetative signs [nausea, vomiting, pallor, sweating, changes in heart rate and blood pressure, alvus disturbances, etc.] and emotional reactions [anxiety, anguish, sense of impending death]. Additional stimuli applied onto the painful area do not modify the perception of the symptom. True visceral pain can vary in intensity from slight to unbearable; characteristically the intensity has no relationship with the extent of the internal damage. A typical example is coronary heart disease; extensive damage to the myocardium can, in fact, be only mildly painful or even painless [silent myocardial infarction] while some forms of angina [involving only ischemia, without any permanent damage] can be the cause of intense suffering (8).
Unexplained Fever Associated with Diseases of the Gastrointestinal Tract
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
The basic causes of abdominal pain are inflammation, obstruction, hemorrhage, ischemia, perforation, functional disorders, and referred pain. On an anatomical basis one may subdivide abdominal pain into three main groups: (1) visceral, (2) somatic (parietal), and (3) referred pain. Visceral pain arises from an abdominal organ, somatic pain from the parietal peritoneum or structures in the abdominal wall, and referred pain from remote areas where the diseased organ shares a neural segment with a certain region of the abdomen.
Local immune response as novel disease mechanism underlying abdominal pain in patients with irritable bowel syndrome
Published in Acta Clinica Belgica, 2022
J. Aguilera-Lizarraga, M. Florens, H. Hussein, G. Boeckxstaens
Visceral pain is initiated by the activation of spinal sensory afferents that innervate the gastrointestinal tract (colonic nociceptors). These afferents express a plethora of molecular nociceptors, i.e. pro-nociceptive ion channels and receptors, including acid-sensing ion channels (ASIC), protease activated receptors, G protein-coupled receptors, transient receptor potential (TRP) channels, ionotrophic receptors, purinergic receptors, and voltage-gated ion channels (CaV, NaV) [49]. These molecular sensors can detect noxious stimuli among which are reactive chemicals, damaging temperatures (either heat or cold), mechanical injury, and ATP and immune mediators (including histamine and cytokines). The latter are released from a wide range of immune cells such as mast cells, macrophages, and neutrophils wherewith the peripheral nerve terminals are located in close proximity. Upon detection of the noxious stimuli, molecular sensors are activated, upregulated and/or sensitized, and action potentials are generated at colonic nociceptive nerve terminals. Based on the location of their soma, colonic nociceptors can be subdivided into splanchnic nerves, whose cell bodies are located within the thoracolumbar dorsal root ganglia (DRG) (T10-L1), and pelvic afferents, with cell bodies within the lumbosacral DRG (L5-S2) [49]. When activated, visceral afferents signal to the dorsal horn of the spinal cord. Prolonged stimulations of primary afferent endings, in turn, can result in chronic facilitation of nociceptive transmission from the gut.
Hypnobiome: A New, Potential Frontier of Hypnotherapy in the Treatment of Irritable Bowel Syndrome—A Narrative Review of the Literature
Published in International Journal of Clinical and Experimental Hypnosis, 2022
Visceral pain is a complex and heterogeneous disorder. The most prevalent forms of visceral pain are categorized as FGIDs, such as IBS. Chronic stress is involved in the development and exacerbation of visceral pain disorders, by inducing peripheral and central sensitization, as well as changing motility and permeability throughout the gastrointestinal (GI) tract. Growing evidence strongly suggests that the gut microbiota plays a pivotal role in the modulation of visceral pain by interacting with stress response through immune, neurochemical, and endocrine mechanisms to make it a less habitable space for certain bacteria, yet leads to the enhancement of more pathological species (Moloney et al., 2016; Peter et al., 2018), thus contributing to visceral hypersensitivity and eventually to pain (Guo et al., 2019; Moloney et al., 2016; Pusceddu & Gareau, 2017).
The pathological involvement of spinal cord EphB2 in visceral sensitization in male rats
Published in Stress, 2022
Tao Chen, Si Chen, Xuefeng Zheng, Yaofeng Zhu, Ziyun Huang, Linju Jia, Lisi OuYang, Wanlong Lei
Spinal cord sensitization plays an important role in the development of visceral sensitization (Louwies et al., 2019; Smith et al., 2015), and the mechanisms of primary central sensitization are associated with the continuous increase in neuronal excitability (Campbell & Meyer, 2006; Hanamura et al., 2017) and the change in neuroplasticity (Kuner, 2010; Liu & Zhou, 2014). C-Fos in the spinal dorsal horn was identified as a marker of neuronal activation by somatic or visceral nociceptive stimulation (Coggeshall, 2005; Harton et al., 2017). C-Fos was indeed shown to be a sensitive index representing neuronal excitation and its activity is increased in the central nervous system of IBS patients (Zhang et al., 2011). However, the molecular mechanisms underlying the stress-induced modulation of visceral pain remain unknown. The single prolonged stress (SPS) model has been widely used to assess the therapeutic effect of visceral pain related to intense stress (He et al., 2013; Sun et al., 2017).