Articles: hyperalgesia.
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Anesthesia and analgesia · May 2016
Electroacupuncture Enhances the Antiallodynic and Antihyperalgesic Effects of Milnacipran in Neuropathic Rats.
Milnacipran, a selective serotonin/norepinephrine-reuptake inhibitor, has been shown to elicit a beneficial effect in various models of neuropathic pain. Previously, we reported that repetitive electroacupuncture (EA) significantly ameliorates neuropathic pain induced by L5 spinal nerve ligation (SNL). In the present study, we sought to determine whether a single treatment with EA produces analgesia and whether EA in combination with a subeffective dosage of milnacipran exhibits an additive effect in SNL rats. ⋯ The study shows that, in male rats with SNL, spinal administration of milnacipran effectively alleviates mechanical allodynia and thermal hyperalgesia, and that a single treatment of EA has an antihyperalgesic effect. Furthermore, our findings suggest that coapplication of EA and milnacipran enhanced antiallodynia and antihyperalgesia by activating spinal noradrenergic systems coupled with spinal α2-adrenoceptors and prolongs the duration of analgesia.
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Am J Phys Med Rehabil · May 2016
Randomized Controlled TrialSymptom-Based Treatment of Neuropathic Pain in Spinal Cord-Injured Patients: A Randomized Crossover Clinical Trial.
The objective of this study was to identify the differences in medication effect according to pain characteristics in spinal cord-injured patients. ⋯ In summary, the phenotype of neuropathic pain was associated with the efficacy of different pharmacologic treatments. Symptom-based treatment, therefore, can lead to more efficient analgesia.
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Am J Phys Med Rehabil · May 2016
Randomized Controlled TrialEffects of Virtual Walking Treatment on Spinal Cord Injury-Related Neuropathic Pain: Pilot Results and Trends Related to Location of Pain and at-level Neuronal Hypersensitivity.
Previous studies have shown that virtual walking to treat spinal cord injury-related neuropathic pain (SCI-NP) can be beneficial, although the type of SCI-NP that may benefit the most is unclear. This study's aims were to (1) determine the effect of location of SCI-NP on pain outcomes after virtual walking treatment and (2) examine the potential relationship between neuronal hyperexcitability, as measured by quantitative sensory testing, and pain reduction after virtual walking treatment. Participants were recruited from a larger ongoing trial examining the benefits of virtual walking in SCI-NP. ⋯ In addition, quantitative sensory testing was performed on a subset of individuals at a nonpainful area corresponding to the level of their injury before virtual walking treatment and was used to characterize treatment response. These pilot results suggest that when considered as a group, SCI-NP was responsive to treatment irrespective of the location of pain (F1, 44 = 4.82, P = 0.03), with a trend for the greatest reduction occurring in at-level SCI-NP (F1, 44 = 3.18, P = 0.08). These pilot results also potentially implicate cold, innocuous cool, and pressure hypersensitivity at the level of injury in attenuating the benefits of virtual walking to below-level pain, suggesting certain SCI-NP sensory profiles may be less responsive to virtual walking.
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Patellofemoral pain (PFP) is common among young individuals. Female adolescents with PFP present typically with localized mechanical hyperalgesia around the knee, but the effect of central pain mechanisms are unknown. This study aimed to compare temporal summation of pain, conditioned pain modulation (CPM), and widespread hyperalgesia in young female adults with PFP and age-matched pain-free controls. ⋯ Young female adults with long-standing PFP demonstrated impaired CPM. This is important because PFP, a peripheral pathology, might have important central components that need to be studied in order to understand its extent and therapeutic implications.
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Tissue injury enhances pain sensitivity both at the site of tissue damage and in surrounding uninjured skin (secondary hyperalgesia). Secondary hyperalgesia encompasses several pain symptoms including pain to innocuous punctate stimuli or static mechanical allodynia. How injury-induced barrage from C-fiber nociceptors produces secondary static mechanical allodynia has not been elucidated. ⋯ Sensitization of lamina IIi PKCγ interneurons is required for the manifestation of secondary static mechanical allodynia but not for spontaneous pain. Such sensitization is driven by ROS and GABAAergic disinhibition. ROS released during intense C-fiber nociceptor activation might produce a GABAAergic disinhibition of PKCγ interneurons. Innocuous punctate inputs carried by Aδ low-threshold mechanoreceptors onto PKCγ interneurons can then gain access to the pain transmission circuitry of superficial MDH, producing pain.