Articles: hyperalgesia.
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The Journal of physiology · Mar 1992
Central changes in processing of mechanoreceptive input in capsaicin-induced secondary hyperalgesia in humans.
1. Capsaicin, the algesic substance in chilli peppers, was injected intradermally in healthy human subjects. A dose of 100 micrograms given in a volume of 10 microliters caused intense pain lasting for a few minutes after injection and resulted in a narrow area of hyperalgesia to heat and a wide surrounding area of hyperalgesia to mechanical stimuli (stroking) lasting for 1-2 h. 2. ⋯ Electrical intraneural microstimulation normally eliciting non-painful tactile sensations was accompanied by pain when the sensation was projected to skin areas within the region of mechanical hyperalgesia induced by capsaicin injection. 4. The threshold for pain evoked by intraneural microstimulation was reversibly lowered and pain from suprathreshold stimulation was exaggerated during the period of mechanical hyperalgesia, regardless of lidocaine anaesthesia of the cutaneous innervation territory of the stimulated fibres. 5. The results indicate that hyperalgesia to stroking on a skin area surrounding a painful intradermal injection of capsaicin is due to reversible changes in the central processing of mechanoreceptive input from myelinated fibres which normally evoke non-painful tactile sensations.
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Progress in neurobiology · Jan 1992
ReviewPeripheral and central mechanisms of cutaneous hyperalgesia.
Hyperalgesia after cutaneous injury can be divided into two phenomena: Primary hyperalgesia occurs at the site of injury and is characterized by hyperalgesia to mechanical and heat stimuli. Secondary hyperalgesia occurs outside the injury site and is characterized by mechanical hyperalgesia only. Hyperalgesia in inflammatory processes corresponds to primary hyperalgesia. ⋯ This form of sensitization may account for the pain to light touch associated with neuropathic pain. Receptive field plasticity is a prevalent property of dorsal horn neurons and probably plays a vital role with regard to hyperalgesia. The molecular mechanisms of synaptic plasticity are currently subject to intense experimental investigation and may provide new insights on the mechanisms of pain and hyperalgesia.
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J Reconstr Microsurg · Jan 1992
ReviewThe adrenergic pharmacology of sympathetically-maintained pain.
The authors seek to highlight some of the recent advances in understanding the pharmacology and pathophysiology of sympathetically-maintained pain, and to develop alternate, and possibly more specific, diagnostic tests for this phenomenon. Mechanical hyperalgesia in sympathetically-maintained pain can be explained by central sensitization so that the activation of A-beta mechanoreceptors now causes pain. ⋯ The authors propose that an ongoing input from peripheral nociceptive afferents is necessary to maintain central sensitization. This nociceptive input may be due to an alpha-adrenoceptor mediated excitatory action of sympathetic efferents on sensory nerves that is independent of neurovascular transmission.
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Neuroscience letters · Dec 1991
Sympathectomy alleviates mechanical allodynia in an experimental animal model for neuropathy in the rat.
We attempted to determine the effects of surgical sympathectomy on an animal model for neuropathic pain. The L5 and L6 spinal nerves on one side were tightly ligated in anesthetized rats. ⋯ The sympathectomy produced an immediate and almost complete reversal of the increased mechanical sensitivity, whereas sham sympathectomy had no effect. The data suggest that sympathectomy alleviates mechanical allodynia in this experimental animal model.
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Case Reports
Topical application of clonidine relieves hyperalgesia in patients with sympathetically maintained pain.
Patients with reflex sympathetic dystrophy or causalgia characteristically have ongoing pain and pain to light touch (hyperalgesia). Some of these patients obtain relief of their pain following interruption of sympathetic function to the affected area and, therefore, have sympathetically maintained pain (SMP). Evidence suggests that the pain and hyperalgesia in SMP are related to activation of peripheral adrenergic receptors. ⋯ In two SMP patients, intradermal injection of norepinephrine or phenylephrine (a specific alpha 1-adrenergic agonist) at a site treated with clonidine evoked intense pain and rekindled the pre-clonidine hyperalgesia at that site. It is likely that clonidine locally blocks the release of norepinephrine via activation of alpha 2 receptors on the sympathetic terminals. This study suggests, therefore, that SMP is mediated via alpha 1-adrenergic receptors located in the affected tissue.