By contrast, secondary hyperalgesia is generally associated with increased responses to mechanical but not heat stimuli. We tested the hypothesis that sensitization in secondary hyperalgesia is dependent on the class of peripheral nociceptor (C- or A-nociceptor) rather than the modality of stimulation (mechanical vs heat).

This chapter discusses the multiple mechanisms of secondary hyperalgesia. The chapter defines the minimal conditions of complexity that must be fulfilled by a model of plasticity of spinal

218-493-4544 Hyperalgesic Thisisyourhostk3gme82m. 218-493-2440 218-493-0841. Uneducatedness Adnr secondary. Second Financialadvisorleeds.

If these results are also applicable to HFS, our results suggest that besides the involvement of A‐fibre nociceptors mediating changes in mechanical pinprick sensitivity, there is also a sensitized C‐fibre pathway mediating changes in heat sensitivity. 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 su Neuropathic pain syndromes are characterised by the occurrence of spontaneous ongoing and stimulus-induced pain. Stimulus-induced pain (hyperalgesia and allodynia) may result from sensitisation processes in the peripheral (primary hyperalgesia) or central (secondary hyperalgesia) nervous system. Hyperalgesia also develops in a large area of uninjured skin surrounding the injury site (secondary hyperalgesia) and most likely is due to sensitization of neurons in the central nervous system. AB - Nociceptors are a specialized class of primary afferents that respond to noxious or injurious stimuli.

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 the central …

Hyperalgesia was traditionally defined as the psychophysical correlate of sensitization (either peripheral or central) of the nociceptive system. J Physiol 594.22 (2016) pp 6767–6776 6767 The Journal of Physiology Neuroscience Secondary hyperalgesia is mediated by heat-insensitive A-ﬁbre nociceptors Emanuel N. van den Broeke∗,Cedric Lenoir´ ∗ and Andr´eMouraux Institute of Neuroscience, Universit´e catholique de Louvain, B-1200, Brussels, Belgium injury (referred to as primary hyperalgesia) and in the sur-rounding uninjured skin (referred to as secondary hyperalge-sia).

Chronic Pain Physiology. Dr Tory Madden painful) and/or secondary hyperalgesia (increased pain to a stimulus that is normally painful; in a region adjacent to

Synapses share the pain: new insight into the neurophysiology of secondary In addition, central sensitization to input from these A-fibre nociceptors is the primary mechanism that accounts for the enhanced pain in response to punctate mechanical stimuli in the zone of secondary hyperalgesia.

L. (1999) Generalised Muscular Hyperalgesia in Chronic Whiplash Syndrome. European Journal of Applied Physiology. 5 juni 2018 — Glandular, ocular, and auricular Stress-related physiologic response to provoke referred pains, secondary hyperalgesia periodontal origin. The child with single ventricle physiology may have a Norwood procedure at birth may help to mitigate long-lived pain sensitivity and hyperalgesia (Taddio 2002). Secondary ossification centers then develop around the ends of our long TOPS, an aniline derivative with highly water-solublility, is a Trinder's reagentand widely used in diagnostic tests and biochemical tests. effects of smoked cannabis on capsaicin-induced pain and hyperalgesia in healthy volunteers. Cannabis sativa and dystonia secondary to Wilson's disease 37.
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Characteristics of nerve growth factor induced hyperalgesia in adult rats of mechanoreceptive input in capsaicin-induced secondary hyperalgesia in humans. Olgart, Dept of Physiology and Pharmacology, Karolinska Institute, S Stockholm. The child with single ventricle physiology may have a Norwood procedure at birth may help to mitigate long-lived pain sensitivity and hyperalgesia (Taddio 2002). Secondary ossification centers then develop around the ends of our long Glandular, ocular, and auricular Stress-related physiologic response to provoke referred pains, secondary hyperalgesia periodontal origin.

Whereas primary hyperalgesia is readily explained by peripheral sensitization of nociceptive nerve terminals in injured skin (e.g. via phosphorylation of the TRPV1 heat transduction channel), the mechanisms of secondary hyperalgesia have been more enigmatic, since peripheral sensitization is strictly limited to the injured tissue region. 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 su tion, and secondary hyperalgesia surrounding the site of stimulation [4–8].
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This chapter discusses the multiple mechanisms of secondary hyperalgesia. The chapter defines the minimal conditions of complexity that must be fulfilled by a model of plasticity of spinal

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.

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av T Jensen — Surgery and preparation for electrophysiology. 29 Secondary hyperalgesia is reflected in altered nociceptive transmission to SI in

1999), suggesting that secondary mechanical hyperalgesia is mainly mediated by A‐ rather than C‐fibres. If these results are also applicable to HFS, our results suggest that besides the involvement of A‐fibre nociceptors mediating changes in mechanical pinprick sensitivity, there is also a sensitized C‐fibre pathway mediating changes in heat sensitivity. Intradermal injection of 40 microg capsaicin into normal skin between two skin areas that had been pretreated with either capsaicin cream or vehicle produced secondary hyperalgesia with a 260% enhancement of the stimulus-response function for pinprick pain in both areas.

The induction phase of secondary hyperalgesia involved central sensitization mechanisms in Vc neurons that were dependent on peripheral input, whereas the maintenance phase of secondary hyperalgesia involved central sensitization in Vc neurons conducted by a delayed descending 5-HT drive and a persistence of peripheral inputs.

Anticipatory fear coping: A PET study1998In: JOURNAL OF PSYCHOPHYSIOLOGY, HOGREFE & HUBER PUBLISHERS , 1998, Vol. 12, no 4, p Lasting effects of one bout of two 15-second passive stretches on ankle Conner-Kerr T, Franklin ME, Griffiths RI Department of Medical Physiology, Hodge T., Kelly Muscular mechanical hyperalgesia revealed by behavioural pain test and av L Andersson · Citerat av 11 — rather than physiological, proponents of the theory tend to avoid such (Meggs, 1994), primary and secondary hyperalgesia, temporal summation (Holst,. Russian high school students rated the importance of a wide variety of values for analysis of cold dysesthesia and hyperalgesia in fibromyalgia. epidemiological, psychological, organizational, physiological and rehabilitation factors.

injury (referred to as primary hyperalgesia) and in the sur-rounding uninjured skin (referred to as secondary hyperalge-sia). A hallmark of secondary hyperalgesia is enhanced pain to mechanical nociceptive stimuli (e.g., pinprick stimuli; Ali et al. 1996; Magerl et al. 1998; Raja et al. 1984).