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Assessment and Monitoring
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
Nociceptive pain is defined as “pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors” (IASP). It can be somatic or visceral and results from stimulation of specialized sensory nerve endings called nociceptors as a consequence of tissue damage and subsequent inflammation. Inflammatory mediators such as prostaglandins enhance the sensitivity of nociceptors, a process described as peripheral sensitization. Ongoing peripheral nociceptive stimuli will increase the excitability of neurons in the spinal cord, leading to central sensitization. Peripheral and central sensitization result in amplification of subsequent pain stimuli and a lowered pain threshold. Nociceptive pain is the most common type of pain seen in acute clinical settings.
Functional Rehabilitation
Published in James Crossley, Functional Exercise and Rehabilitation, 2021
Pain is not created within tissue. Pain is a subconscious response to a range of conditions that indicate that the brain feels we are under some sort of threat. Pain emerges in reaction to a raised subconscious evaluation of threat. Pain is an output of the brain – a subconscious mechanism designed to draw attention and change behavior. Nociceptors are not pain receptors, they are ‘threat’ receptors. Remember, nociceptors: Provide feedback regarding the state of tissuesAre not pain receptorsCould be considered ‘threat receptors’
Peripheral Mechanisms of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
A nociceptor is a peripherally localized neuron that is preferentially sensitive to a damaging or potentially damaging stimulus. Nociceptors are the first cells in pain pathways that lead to pain sensation. They are pseudo-unipolar in structure with distal and proximal axons arising from their cell bodies located in dorsal root and other sensory (e.g. trigeminal) ganglia. Membrane receptors and ion channels located on unmyelinated nerve endings transduce noxious input into transmembrane potential changes (depolarizations) which trigger the propagation of action potentials if the potential change is of sufficient magnitude. Action potentials are conducted to the dorsal horn of the spinal cord by two populations of nociceptors with fast and slow conduction velocities: myelinated Aδ fibres (5–25 m/s) which transmit well localized and ‘fast’ pain or unmyelinated C fibres (<2 m/s) which transmit diffuse and ‘slow’ pain. Nociceptors can be sensitized in damaged tissues.
Pharmacological approaches to treat intestinal pain
Published in Expert Review of Clinical Pharmacology, 2023
Mikolaj Swierczynski, Adam Makaro, Agata Grochowska, Maciej Salaga
Physiologically, pain originates from specialized sensory neurons (the nociceptors) exposed to mechanical, thermal, or chemical stimuli. However, pain is also classified into many different categories and types depending on its pathophysiology. The most important ones are nociceptive, inflammatory, nociplastic, and neuropathic pain [3]. Nociceptive pain is associated with tissue injury and activation of nociceptors. Autoimmune disorders or infections cause inflammatory pain. Nociplastic pain arises from altered nociception despite the absence of actual or imminent tissue damage. Neuropathic pain is a condition affecting the somatosensory nervous system, both peripheral and central, involving neural damage, irritation, or malfunction. Notably, many types of pain can coexist making suffering even more severe.
Is chronic pain as an autoimmune disease?
Published in Canadian Journal of Pain, 2022
The reasons for acquiring a mechanistic understanding of how sex influences pain have largely focused on nociceptors and neuronal signaling. Usually, nociceptors detect potentially harmful stimuli, including, for example, heat, noxious chemicals, or changes in pressure. In response to nerve injury, these neurons are aberrantly activated and can occur in the absence of such stimuli, with the possibility for a nonnoxious stimulus, such as gentle stroking of the skin, causing severe pain. Hyperexcitability of nociceptors, via N-methyl-d-aspartate receptor activation, eventually leads to the chronification of pain.8 Distinct hormone profiles between males and females may influence sex differences in hyperexcitability. For instance, glutamate currents in the dorsal root ganglia (DRG) were observed to be higher in female compared to male rats, possibly via a mechanism involving 17-β-estradiol.9 Also certain genes involved in ion transport, may be involved in producing a hyperexcitable response, are upregulated in female rats.10 In the field of pain research, the DRG have been of considerable interest, because these nodular enlargements of nerve bundles contain the somata of peripheral nociceptors. Electrical impulses produced by nociceptors are transmitted as action potentials along the axons to the DRG, with signals further relayed into the spinal cord. The ascending pain pathway continues with the spinal cord transmitting peripheral input to the brain, which processes the input, “interpreting” it as painful and initiating descending signals.
The slow medicine approach to chronic pain
Published in Physiotherapy Theory and Practice, 2022
Chronic pain is a mix of nociceptive, neuropathic, and nociplastic drivers that influence and are influenced by psychological and movement system factors (Chimenti, Frey-Law, and Sluka, 2018). While nociception signals an actual or perceived threat to non-neural tissues through the activation of nociceptors, neuropathic pain arises from threats to neurological structures or the somatorsensory system (International Association for the Study of Pain, 2020a). Nociplastic pain arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain (Trouvin and Perrot, 2019). Persistent stimulation by nociceptors and neural tissues may trigger the development of nociceptive pain (Kosek et al., 2016), and nociplastic pain includes nociceptive/neuropathic elements (International Association for the Study of Pain, 2020a).