Abstract
Nowadays, there are three main pain descriptors: nociceptive pain, neuropathic pain, and nociplastic pain. The last one is the newest expression defining pain as ‘Pain that 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’ (International Association for the Study of Pain). The implementation of modern pain neuroscience in practice is said to be the most important for musculoskeletal physical therapists around the world. One of the examples of the nociplastic pain mechanism can be myofascial trigger points that are connected with central sensitization (one of the subtypes of nociplastic pain). Central sensitization (CS) is defined as an amplification of neural signaling within the central nervous system that elicits pain hypersensitivity and ongoing neuronal excitation which outlasts the initial nociceptor input. Features typical of that state are abnormally low peripheral thresholds for pain from pressure, temperature, electrical, and other stimuli and it has been proposed that trigger points may function as peripheral mediators of CS.
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