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hyperalgesia/atrophy
Veza se sprema u međuspremnik
Stranica 1 iz 358 rezultatima
Wallerian degeneration and hyperalgesia after peripheral nerve injury are glutathione-dependent.
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Experimental inflammatory compression injury to the sciatic nerve (chronic constriction injury, CCI) induces Wallerian degeneration of axons and damages non-neuronal cells at the injury site in association with the development of exaggerated pain-like behavior, or hyperalgesia, to noxious thermal
Mechanical allodynia in postherpetic neuralgia: evidence for central mechanisms depending on nociceptive C-fiber degeneration.
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In 12 zoster patients who had developed postherpetic neuralgia with dynamic mechanical allodynia and in six zoster patients who had recovered without pain, the functional role of nociceptive C-fibers in allodynia was assessed by quantifying axon reflex reactions induced by histamine iontophoresis
Salmon calcitonin exerts better preventive effects than celecoxib on lumbar facet joint degeneration and long-term tactile allodynia in rats.
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Physiological and pathological characterization of capsaicin-induced reversible nerve degeneration and hyperalgesia.
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The study aimed to investigate the physiology, psychophysics, pathology and their relationship in reversible nociceptive nerve degeneration, and the physiology of acute hyperalgesia.
We enrolled 15 normal subjects to investigate intraepidermal nerve fibre (IENF) density, contact heat-evoked
Treadmill running and static stretching improve long-lasting hyperalgesia, joint limitation, and muscle atrophy induced by cast immobilization in rats.
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The effects of exercise on chronic pain induced by immobilization are incompletely understood. The purpose of this study was to investigate whether 30min of treadmill running (TR; active exercise) and 10min of static stretching (SS; passive exercise) of the immobilized hindlimb reduce widespread
Depletion of macrophages reduces axonal degeneration and hyperalgesia following nerve injury.
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Inflammatory mechanisms are believed to play an important role in hyperalgesia resulting from nerve injury. Hyperalgesia following nerve injury is temporally linked with Wallerian degeneration and macrophage recruitment, and is reduced in WLD mice, in which Wallerian degeneration is delayed. We
Reduced hyperalgesia in nerve-injured WLD mice: relationship to nerve fiber phagocytosis, axonal degeneration, and regeneration in normal mice.
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The pathogenesis of neuropathic pain states is influenced by inflammatory factors associated with nerve injuries and may be mediated in part by the macrophage-dependent process of Wallerian degeneration. Macrophages play a dominant role in the Wallerian (axonal) degeneration that characterizes the
Combinatorial Prg4 and Il-1ra Gene Therapy Protects Against Hyperalgesia and Cartilage Degeneration in Post-Traumatic Osteoarthritis.
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Osteoarthritis (OA) is a degenerative disease of synovial joints characterized by progressive loss of articular cartilage, subchondral bone remodeling, and intra-articular inflammation with synovitis that results in chronic pain and motor impairment. Despite the economic and health impacts, current
Cutaneous nerve terminal degeneration in painful mononeuropathy.
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Nociceptive nerves innervate the skin and play an important role in the generation of neuropathic pain. However, it remains elusive whether and how nociceptive nerve terminals degenerate in neuropathic pain conditions. To address this issue, we investigated cutaneous innervation in a model of
Axonal viability and the persistence of thermal hyperalgesia after partial freeze lesions of nerve.
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Partial freeze injuries of rat sciatic nerve have been used to investigate the relationship between the amount of tissue injured and the magnitude and duration of the resulting thermal hyperalgesia. Complete freeze injury of peripheral nerve produces temporary anesthesia to peripheral stimuli and is
Mechanical hyperalgesia after an L5 ventral rhizotomy or an L5 ganglionectomy in the rat.
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An L5 spinal nerve ligation (SNL) in the rat leads to behavioral signs of mechanical hyperalgesia. Our recent finding that an L5 dorsal root rhizotomy did not alter the mechanical hyperalgesia following an L5 SNL suggests that signals originating from the proximal stump of the injured nerve are not
Physical disuse contributes to widespread chronic mechanical hyperalgesia, tactile allodynia, and cold allodynia through neurogenic inflammation and spino-parabrachio-amygdaloid pathway activation.
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Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other
Thiamine, pyridoxine, cyanocobalamin and their combination inhibit thermal, but not mechanical hyperalgesia in rats with primary sensory neuron injury.
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Neuropathic pain after nerve injury is severe and intractable, and current drugs and nondrug therapies offer substantial pain relief to no more than half of affected patients. The present study investigated the analgesic roles of the B vitamins thiamine (B1), pyridoxine (B6) and cyanocobalamin (B12)
EVALUATION OF HYPERALGESIA AND HISTOLOGICAL CHANGES OF DORSAL ROOT GANGLION INDUCED BY NUCLEUS PULPOSUS.
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To evaluate the hyperalgesia and histological abnormalities induced by contact between the dorsal root ganglion and the nucleus pulposus.
METHODS
Twenty Wistar rats were used, divided into two experimental groups. In one of the groups, a fragment of autologous nucleus pulposus was removed from the
Degeneration of myelinated efferent fibers induces spontaneous activity in uninjured C-fiber afferents.
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We demonstrated recently that uninjured C-fiber nociceptors in the L4 spinal nerve develop spontaneous activity after transection of the L5 spinal nerve. We postulated that Wallerian degeneration leads to an alteration in the properties of the neighboring, uninjured afferents from adjacent spinal
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