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In the skin surrounding a site of injury, hyperalgesia develops to mechanical stimuli. Two types of secondary hyperalgesia (to light touch and punctate stimuli) have recently been differentiated, based on different durations and sizes of the area involved. Secondary hyperalgesia refers to the increase in sensitivity to mechanical nociceptive stimuli delivered outside the area of tissue injury. Previous studies have suggested that secondary hyperalgesia is mediated by a specific class of myelinated nociceptors: slowly adapting A‐fibre mechano‐ and heat‐sensitive (AMH) type I nociceptors.

Secondary hyperalgesia physiology

The secondary neurons transmitting mechanosensory and. av T Jensen — Surgery and preparation for electrophysiology. 29 Secondary hyperalgesia is reflected in altered nociceptive transmission to SI in while a decreased acetylcholine release is associated with hyperalgesia, as seen after pharmacological and physiological mechanisms that regulate pain transmis- of pain. The secondary somatosensory cortex (SII), regions of the interior. Secondary mechanical hyperalgesia was used as an index of the magnitude of facilitation both in physiological conditions and in experimental model of PD. av L OLGART · Citerat av 1 — hyperalgesia in adult rats – dependence on enhanced cord transmission (secondary hyperalgesia, re- Dept of Physiology and Pharmacology, Karo-. Clinical physiology and functional imaging 2018;38(3):508-516 in women with fibromyalgia: secondary exploratory analyses from a randomized controlled trial perceptual analysis of cold dysesthesia and hyperalgesia in fibromyalgia. Characterizing pinprick-evoked brain potentials before and after experimentally induced secondary hyperalgesia.

Psychophysical studies were made, in humans, of the sensory characteristics and underlying mechanisms of the hyperalgesia (often termed “secondary hyperalgesia”) that occurs in uninjured skin surrounding a local cutaneous injury. The hyperalgesia was characterized by lowered pain thresholds and enhanced magnitude of pain to normally painful stimuli. Hyperalgesia A pain nervous pathway sometimes becomes excessively excitable; this gives rise to hyperalgesia, which means hypersensitivity to pain.

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Following an injury or cell damage two main things can occur. Primary hyperalgesiaand secondary hyperalgesia.

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Considerable progress has been made in developing clinically relevant animal models for identifying the most significant underlying mechanisms. 1. Psychophysical studies were made, in humans, of the sensory characteristics and underlying mechanisms of the hyperalgesia (often termed “secondary hyperalgesia”) that occurs in uninjured skin surrounding a local cutaneous injury. The hyperalgesia was characterized by lowered pain thresholds and enhanced magnitude of pain to normally painful 2020-12-18 The development of experimental models for the induction of secondary hyperalgesia in human subjects and animals has provided the basis to further explore the mechanisms of secondary hyperalgesia (Simone et al. 1989a,b).

Pain. 2013 Aug;154(8):1482-3.
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Five woollen fabrics (2 non-prickly, 2 prickly and 1 intermediate) were presented, in a blind manner, to the skin before and after the capsaicin injection.

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Psychophysical studies in humans supported the conclusions that the hyperalgesia was predominantly the secondary type and depended on one set of neurons sensitizing another (“neurogenic hyperalgesia”) and that the latter set of neurons is located in the central and not the peripheral nervous system. Secondary hyperalgesia refers to the sensitization that occurs because of changes in spinal cord processing. For example, through a process of central sensitization, the firing of dorsal horn nociceptors can change dramatically in the setting of injury (produced by either tissue or nerve damage).

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Orexin / hypokretinneurons integrerande roll i nociceptiv

One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves Secondary hyperalgesia refers to the increase in sensitivity to mechanical nociceptive stimuli delivered outside the area of tissue injury. Previous studies have suggested that secondary hyperalgesia is mediated by a specific class of myelinated nociceptors: slowly adapting A‐fibre mechano‐ and heat‐sensitive (AMH) type I nociceptors. Multiple mechanisms of secondary hyperalgesia. Treede RD(1), Magerl W. Author information: (1)Institute of Physiology and Pathophysiology, Johannes Gutenberg University, Mainz, Germany. treede@mail.uni-mainz.de PMID: 11098701 [Indexed for MEDLINE] Publication Types: Research Support, Non-U.S.