Proinflammatory Peptides in Sensory Nerves of the Airways
Sami I. Said in Proinflammatory and Antiinflammatory Peptides, 2020
Traditionally, the four classical signs of inflammation are redness, heat, swelling, and pain. The first two signs result from the dilatation of arterioles and increased blood flow, whereas swelling, or tissue edema, results from plasma leakage, mainly from postcapillary venules. Pain results from the stimulation of nociceptive sensory nerve fibers, which are mostly unmyelinated C-fibers and small-diameter myelinated A-δ fibers. Many inflammatory stimuli and conditions can cause these physical signs to be manifested to different extents in various organs. A role for the sensory nervous system itself in inflammation has been recognized for more than a century, but for many years the only inflammatory sign believed to result from stimulation of sensory nerves was vasodilatation, as evidenced by redness observed in the skin after electrical or chemical stimulation of sensory nerves. For interesting historical accounts of the early studies of the involvement of sensory nerves in inflammation, see Refs. 1 and 2.
Biopsychosocial approaches to pain
Elizabeth Marks, Myra Hunter, John Chambers in CBT for Managing Non-cardiac Chest Pain, 2017
In chronic pain, since the brain does not clearly differentiate between ‘normal’ nociception and ‘acute pain’ stimuli, it may respond as if there is acute pain (and current harm). However, since there is no actual harm occurring, these typical responses will neither resolve nor explain why pain is being experienced, and so the pain persists. The individual will experience this as a failure to reduce pain, and may continue to feel as if the body is experiencing harm. This can understandably lead to negative and worrying thoughts and emotions about the pain. Patients are also more likely to begin to pay more attention to sensations in the body, in an effort to explain their experiences. They may change their behaviour in an attempt to reduce the pain, or they may seek help for it. Unfortunately, these psychosocial changes can further sensitize the pain system.
Ethical Issues in Chronic Pain Research
Michael E. Schatman in Ethical Issues in Chronic Pain Management, 2016
The extent to which animals (e.g., rats) provide a model of conscious pain experiences remains a matter of uncertainty among most pain researchers and controversy among others. It is relatively well known that nociception, the basic capacity for sensing noxious stimuli, is widespread in the animal kingdom. Even relatively primitive animals such as leeches and sea slugs possess functionally specialized mechanisms for sensing noxious stimuli (17). Vertebrate spinal cords play a sophisticated role in processing and modulating nociceptive signals, providing direct control of some motor responses to noxious stimuli and a basic capacity for Pavlovian and instrumental conditioning (18,19). Higher brain systems provide additional layers of association, top-down control, and cognition. In humans, at least, these higher brain systems also give rise to the conscious experiences that are characteristic of pain.
Differentiating primary dry eye disease from ocular neuropathic pain: implications for symptom management
Published in Clinical and Experimental Optometry, 2023
Mark T Forristal, Kirk A J Stephenson
1. Nociceptive pain (pain in response to a noxious stimulus, such as heat, cold, mechanical force or chemical irritants), 2. Inflammatory pain (pain caused by activation of immune cells, such as macrophages, neutrophils, mast cells, and granulocytes in response to tissue injury or infection) and 3. Pathological pain (pain due to abnormal functioning of peripheral pain nerves leading to abnormal central processing).12 Pathological pain can be further divided into neuropathic pain and dysfunctional pain. Neuropathic pain is the abnormal function of the peripheral or central nervous system which occurs due to damage to the nervous system, while dysfunctional pain is the abnormal function of the nervous system which occurs in the absence of damage or inflammation (See Figure 1).13 DED can lead to nerve damage via sensitisation of nociceptors, leading to altered gene expression in ion channels of corneal nerve endings and trigeminal ganglion cells. This causes the formation of corneal neuromas leading to dysaesthesia and neuropathic pain.14 Ocular pain can therefore be simply classified as helpful (physiological) pain, which stimulates a response to physical insult, or pathological where pain results from sensitisation of nociceptors (Figure 1).
The association between myofascial orofacial pain with and without referral and widespread pain
Published in Acta Odontologica Scandinavica, 2022
Anna Lövgren, Corine M. Visscher, Frank Lobbezoo, Negin Yekkalam, Simon Vallin, Anders Wänman, Birgitta Häggman-Henrikson
Since 2014, the Diagnostic Criteria for TMD (DC/TMD) has provided a reliable and valid method for diagnosis of the most common TMDs. In the DC/TMD, the diagnosis of ‘myalgia’ can be further specified as the subdiagnosis ‘myofascial pain with referral’ in cases where pain spreads beyond the muscle border during palpation [7]. Such referred pain has been suggested related to a decrease in thresholds to nociceptive stimuli, potentially caused by general hyperalgesia and central sensitisation [26–28]. In dentistry, a diagnosis of referred pain was suggested to be relevant for differential diagnosis for the identification of pain in other anatomical locations such as muscular pain referred to the teeth [7]. However, there is a gap of knowledge regarding the association between a clinical diagnosis of pain referral and the presence of widespread pain in community samples with TMD.
Spider toxins targeting ligand-gated ion channels
Published in Toxin Reviews, 2021
The P2X receptor has trimeric structure where three subunits form functional receptor. The receptor can be homomeric (P2X1, P2X2, P2X3, P2X4, P2X5, P2X7) or heteromeric (P2X2/P2X3, P2X4/P2X6, P2X1/P2X5) (North 2002, 2016). The composition of the receptor determines its agonist- and antagonist- binding properties, as well kinetics of ion channel gating (Kaczmarek-Hajek et al. 2012). The receptors are widely distributed throughout the body, within and outside the central nervous system (Burnstock and Knight 2004). They have been implicated in physiological as well as pathophysiological conditions, such as synaptic transmission, smooth muscle contraction, taste, hearing, platelet activation, nociception, and inflammation (Khakh and North 2006, Surprenant and North 2009, Burnstock et al. 2014). P2X3-containing receptors are known to be expressed in small diameter afferents which activate in response to peripheral injury and thus mediate pain. These receptors were shown to be involved in developing of mechanical hypersensitivity after nerve injury (Fabbretti 2013). Multiple experiments with P2X3-selective antagonists as well as with knock-out mice demonstrate the contribution of P2X3-containing receptors to nociception, especially to chronic inflammatory and neuropathic pain (Cockayne et al. 2000, Souslova et al. 2000, North 2003, 2004, Burnstock 2009). Inhibition of these receptors reduced the activity of nociceptive Aδ and C- fibers.
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