Search

Background: Neuropathic pain is associated with abnormal sensitivity of the central nervous system. Although the mechanism underlying the development of sensitization remains to be fully elucidated, recent studies have reported that neuroplastic changes in the pain circuitry may be involved in hypersensitivity associated with neuropathic pain. However, it is difficult to investigate such phenomena in existing animal pain model. Therefore, in this study, we developed a novel animal model - the circuit plasticity reconstruction (CPR) model - to mimic central sensitization associated with neuroplastic changes.Method: NMDA and Ro 25-6981 were injected into the right insular cortex of Sprague-Dawley rats, while electrical stimulation was delivered to the contralateral hind paw. Mechanical allodynia was tested by von Frey test with up-down method, and neuroplastic changes were confirmed by PSA-NCAM-positive immunostaining.Result: The mechanical withdrawal threshold of the left hind paw decreased beginning 1 day after CPR modelling and persisted until day 21 comparing to the modified CPR 1 (mod-CPR 1) group (CPR: 91.68 ± 1.8%, mod-CPR 1: 42.71 ± 3.4%, p < 0.001). In contrast, mod-CPR 2 surgery without electrical stimulation did not induce mechanical allodynia. Immunostaining for PSA-NCAM also revealed that neuroplastic changes had occurred in the CPR group.Conclusion: Our results demonstrated that CPR modelling induced neuroplasticity within the insular cortex, leading to alterations in the neural circuitry and central sensitization.Significance: This article represents that the CPR model can mimic the neuropathic pain derived by neuroplastic changes. Our findings indicate that the CPR model may aid the development of novel therapeutic strategies for neuropathic pain and in elucidating the mechanisms underlying pain induced by central sensitization and neuroplastic changes. [ABSTRACT FROM AUTHOR]

Background An objective measurement of scar is important for evaluating treatment outcomes. However, to date, there is no 'gold standard' for quantitative measurement of properties of hypertrophic scar. Existing objective modalities are neither portable nor easy to use. Objective This study aims to validate the correlation between objective measurements with SkinFibrometer®, SkinGlossMeter®, and Mexameter® and subjective assessment with Vancouver Scar Scale ( VSS) of keloid and hypertrophic scar. Methods A total of 25 patients with keloids and hypertrophic scars were enrolled in this study. Patients were treated with intralesional triamcinolone acetonide at 2-6 week intervals. Scar assessments using VSS, Skinfibrometer, Skinglossmeter, and Mexameter were performed in both scars and contralateral normal skin at each treatment session. Correlations between the measurements by these tools and VSS parameters were examined. Results We found statistically significant differences between scar and contralateral normal skin using Skinfibrometer, Skinglossmeter, and Mexameter. A strong correlation was found between the VSS pliability scores and the stiffness of skin of Skinfibrometer ( r = 0.628, P < 0.001). VSS vascularity scores showed weak correlation with erythema index of Mexameter ( r = 0.372, P < 0.001). However, no correlation appeared to exist between any parameters of VSS and Skinglossmeter and between VSS pigmentation scores and the melanin index of Mexameter. Conclusion In our study, Skinfibrometer can be an objective noninvasive evaluation tool for pliability of the scar. [ABSTRACT FROM AUTHOR]