Hyperalgesia
Hyperalgesia - Related Videos
04:22
Assessment of Knee Hyperalgesia in Mice using Pressure Application Measurement
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Cited by 2 •
2025
The protocol describes how to measure knee hyperalgesia in mice. We show examples in mouse models of acute knee pain as well as in models of osteoarthritis (OA).
07:23
Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
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Cited by 41 •
2014
We describe a protocol to examine the development of opioid-induced hyperalgesia and tolerance in mice. Based on the measurement of thermal and mechanical nociceptive responses of naïve and morphine-treated animals, it allows to quantify the increase in pain sensitivity (hyperalgesia) and decrease in analgesia (tolerance) associated with chronic opiate administration.
14:56
An Experimental Paradigm for the Prediction of Post-Operative Pain (PPOP)
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Cited by 107 •
2010
Diffuse noxious inhibitory control, temporal summation and wound hyperalgesia testing are demonstrated in the obstetric patient. These tests evaluate inhibitory and excitatory mechanisms of pain processing and are here utilized to evaluate endogenous analgesia at different time-points during pregnancy and the peripartum period to help reveal individual s risk for persistent pain.
06:46
Measurement of Tactile Allodynia in a Murine Model of Bacterial Prostatitis
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Cited by 23 •
2013
Infection of the prostate may be a contributing factor in mediating pelvic pain in chronic prostatitis. We describe the procedure for preparation of standardized bacterial inoculum, instillation of bacteria into the urethra of male mice and methodology for measuring tactile allodynia in mice over time.
08:19
In Vitro Characterization of the Electrophysiological Properties of Colonic Afferent Fibers in Rats
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2017
Abnormal sensory function underlies visceral pain and other symptoms of functional and inflammatory bowel diseases. A protocol for the electrophysiological recording of the colonic afferent nerves in an ex vivo rat colorectum preparation is presented here.
FAQs
Peripheral sensitization begins when inflammation or tissue injury makes nociceptors, the sensory neurons that detect potentially damaging stimuli, more responsive. Central sensitization occurs when spinal and brain pathways amplify incoming pain signals. These mechanisms can act together, so stronger pain may reflect altered processing at the injury site, within the central nervous system, or across both levels.
Inflammation can release immune mediators that change the excitability of peripheral nociceptors. Ion channels, which regulate electrical signaling in nerve cells, help determine how readily these neurons respond and transmit information. Studying their interaction connects tissue injury with altered sensory signaling and identifies biological components that may be relevant to analgesic treatment research.
The underlying site of altered signaling provides an important biological clue. Inflammatory pain is associated with sensitized peripheral nociceptors after inflammation or tissue injury, whereas neuropathic pain can involve altered neural pathways and signaling. Examining whether peripheral or spinal and brain mechanisms dominate can therefore help researchers compare pain categories and investigate their different therapeutic needs.
Changes in spinal and brain circuits can increase the impact of signals arriving from peripheral sensory neurons. Instead of simply reflecting the strength of stimulation at the tissue, the resulting response also reflects how central pathways process that input. This mechanism explains why research on hyperalgesia must consider neural circuits, not only injured tissue or peripheral receptors.
Researchers use the biological mechanisms associated with hyperalgesia to examine how potential analgesics influence pain signaling. Relevant targets include sensitized nociceptors, immune mediators, ion channels, and spinal or brain pathways. Comparing effects across these components can clarify whether a treatment acts on peripheral sensitivity, central amplification, or both, supporting more focused pain research.
These conditions illustrate why increased pain sensitivity is important beyond an acute injury. Hyperalgesia research links clinical pain states with changes in peripheral nociceptors, immune-related signaling, ion channels, and central neural circuits. In opioid-induced hyperalgesia, the same research framework helps investigate how pain processing may become amplified, while chronic pain and fibromyalgia provide broader contexts for studying persistent sensitivity.