Articles: hyperalgesia.
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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.
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Despite intense investigation, the mechanisms of the different forms of trigeminal neuropathic pain remain substantially unidentified. The transient receptor potential ankyrin 1 channel (encoded by TRPA1) has been reported to contribute to allodynia or hyperalgesia in some neuropathic pain models, including those produced by sciatic nerve constriction. However, the role of TRPA1 and the processes that cause trigeminal pain-like behaviours from nerve insult are poorly understood. ⋯ Nociception and hypersensitivity evoked by constriction of the infraorbital nerve was associated with intra- and perineural monocytic and macrophagic invasion and increased levels of oxidative stress by-products (hydrogen peroxide and 4-hydroxynonenal). Attenuation of monocyte/macrophage increase by systemic treatment with an antibody against the monocyte chemoattractant chemokine (C-C motif) ligand 2 (CCL2) or the macrophage-depleting agent, clodronate (both P < 0.05), was associated with reduced hydrogen peroxide and 4-hydroxynonenal perineural levels and pain-like behaviours (all P < 0.01), which were abated by perineural administration of HC-030031, α-lipoic acid or the anti-CCL2 antibody (all P < 0.001). The present findings propose that, in the constriction of the infraorbital nerve model of trigeminal neuropathic pain, pain-like behaviours are entirely mediated by the TRPA1 channel, targeted by increased oxidative stress by-products released from monocytes and macrophages clumping at the site of nerve injury.