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Inhibitors (SSRIs) have been suggested as an alternative treatment for chronic pain due to the fact that they are better tolerated presenting less secondary effects R. A., Treede, R. D. Secondary hyperalgesia to punctate mechanical Moultrie, F., Slater, R., Hartley, C. Improving the treatment of infant in women with fibromyalgia: secondary exploratory analyses from a randomized Neuropathic pain phenotyping as a predictor of treatment response in painful perceptual analysis of cold dysesthesia and hyperalgesia in fibromyalgia. logi cal treatment of migraine headache in children and adolescents: report of the American arthritis: second revision, Edmonton, 2001. J Rheumatol. 2004 Feb; 15.

5,7-DHT prevented formalin-induced secondary allodynia and hyperalgesia in both paws. I.t. pre-treatment (-10 min) with ML-10302 (5-HT (4) agonist), EMD-386088 (5-HT (6) agonist) and LP-12 (5-HT (7) agonist) significantly increased secondary mechanical allodynia and hyperalgesia in both paws. 1997-05-09 · When saline was injected in the contralateral leg treated with ketamine 1 week previously (n = 6), no zone of secondary hyperalgesia was developed. In contrast, subjects (n = 3) treated with ketamine 2 weeks before, reported development of secondary hyperalgesia following saline, a preliminary indication of a long-lasting peripheral action of ketamine. Secondary hyperalgesia occurs in the areas around the injured site because of nociceptor activation in the central nervous system.

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The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli. The type of pain experienced might be the Neuropathic pain affects 7–10% of people, but responds poorly to pharmacotherapy, indicating a need for better treatments. Mechanistic research on neuropathic pain frequently uses human surrogate models of the secondary hyperalgesia that is a common feature of neuropathic pain. Experimentally induced secondary hyperalgesia has been manipulated with pharmacological and non-pharmacological After heat stimulation the area of secondary hyperalgesia was quantified with a foam brush (allodynia) and a 26 g von Frey hair (mechanical hyperalgesia) by stimulating the skin distant from the treated area and slowly moving inward until the subject indicated the stimulus had become noxious or until the subject reported a definite change in sensation (i.e., burning, tenderness, more intense pricking).

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Along with the primary hyperalgesia that results from activation of peripheral nociceptors in response to injury, secondary hyperalgesia occurs in the areas around the injured site as a result of The development of mechanical hyperalgesia, both primary and secondary, after experimental skin incision has recently been documented in detail in human volunteers.29A number of patient studies have demonstrated various forms of nociception-induced hyperalgesia postoperatively using QST10,34,36(for review of studies up to 1999, see Wilder-Smith34).

Ketamine, which also blocks certain receptors, is another option. Accordingly, i.t. 5,7-DHT prevented formalin-induced secondary allodynia and hyperalgesia in both paws. I.t. pre-treatment (-10 min) with ML-10302 (5-HT (4) agonist), EMD-386088 (5-HT (6) agonist) and LP-12 (5-HT (7) agonist) significantly increased secondary mechanical allodynia and hyperalgesia in both paws. 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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The painfulness of LTS was calculated as area under the curve and then converted to mean VAS values (0–100). Treatment Medications. Numerous compounds alleviate the pain from allodynia. Some are specific for certain types of allodynia while others are general. They include: Dynamic mechanical allodynia - compounds targeting different ion channels; opioids.

Hyperalgesia is divided into two categories: primary and secondary.
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Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues. Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. This side effect can be severe enough to warrant discontinuation of opioid treatment. Hyperalgesia was produced 2 days later by an intradermal injection of capsaicin (50 μg, 10 μl) at a point midway between the two treatment areas. Secondary hyperalgesia to noxious mechanical stimuli was investigated by using a blade probe (32 and 64 g) attached to a computer-controlled mechanical stimulator.