Models and Mechanisms of Hyperalgesia and Allodynia

Abstract

Hyperalgesia and allodynia are frequent symptoms of disease and may be useful adaptations to protect vulnerable tissues. Both may, however, also emerge as diseases in their own right. Considerable progress has been made in developing clinically relevant animal models for identifying the most significant underlying mechanisms. This review deals with experimental models that are currently used to measure (sect. II) or to induce (sect. III) hyperalgesia and allodynia in animals. Induction and expression of hyperalgesia and allodynia are context sensitive. This is discussed in section IV. Neuronal and nonneuronal cell populations have been identified that are indispensable for the induction and/or the expression of hyperalgesia and allodynia as summarized in section V. This review focuses on highly topical spinal mechanisms of hyperalgesia and allodynia including intrinsic and synaptic plasticity, the modulation of inhibitory control (sect. VI), and neuroimmune interactions (sect. VII). The scientific use of language improves also in the field of pain research. Refined definitions of some technical terms including the new definitions of hyperalgesia and allodynia by the International Association for the Study of Pain are illustrated and annotated in section I.

Analgesia to pressure–pain develops in the ipsilateral forehead after high- and low-frequency electrical stimulation of the forearm

“…Similarly, hyperalgesia to pinpricks and von Frey's monofilament developed at and around the HFSconditioned site, consistent with the development of central sensitisation (Klein et al 2008;Pfau et al 2011;Vo and Drummond 2013b, a;van den Broeke et al 2011;van den Broeke et al 2010). Central sensitisation is mediated, in part, by facilitatory influences on spinal nociception that emanate from the rostroventral medulla (Millan 2002;Sandkuhler 2009;Urban et al 1999;Pertovaara et al 1996;Burgess et al 2002). Thus, our findings suggest that the barrage of electrical impulses during HFS triggered this central facilitatory response.…”

Applications of sensory and physiological measurement in oral‐facial dental pain

“…In odontogenic pain, central sensitization begins from peripheral tissue injury at the site of tooth and supporting periodontium. At this site, inflammation modulates activation of afferent nociceptive nerve endings by lowering their firing threshold 47. Prolonged activation of nociceptive input to second‐order neurons facilitates augmentation of nociceptive impulses to higher brain centers.…”

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“…Hence, when potentially tissue-damaging impacts act on naive tissues, a warning signal that consists of a pain experience and an escape reaction such as a withdrawal reflex is generated [1][2][3]. If the impact does not produce tissue damage, the warning signal's pain component, called "acute nociceptive pain", ceases shortly after the termination of the insult [1][2][3].…”

“…If the impact does not produce tissue damage, the warning signal's pain component, called "acute nociceptive pain", ceases shortly after the termination of the insult [1][2][3]. However, if the insult does induce tissue damage, a different pain experience develops [1][2][3]. This tissue injury-associated pain usually lasts during the entire course of the underlying disease.…”

“…This tissue injury-associated pain usually lasts during the entire course of the underlying disease. Therefore, this type of pain is termed "prolonged pain" [1][2][3][4].…”