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Multicenter assessment of quantitative sensory testing (QST) for the detection of neuropathic-like pain responses using the topical capsaicin model
Background: The use of quantitative sensory testing (QST) in multicenter studies has been quite limited, due in part to lack of standardized procedures among centers.
Aim: The aim of this study was to assess the application of the capsaicin pain model as a surrogate experimental human model of neuropathic pain in different centers and verify the variation in reports of QST measures across centers.
Methods: A multicenter study conducted by the Quebec Pain Research Network in six laboratories allowed the evaluation of nine QST parameters in 60 healthy subjects treated with topical capsaicin to model unilateral pain and allodynia. The same measurements (without capsaicin) were taken in 20 patients with chronic neuropathic pain recruited from an independent pain clinic.
Results: Results revealed that six parameters detected a significant difference between the capsaicin-treated and the control skin areas: (1) cold detection threshold (CDT) and (2) cold pain threshold (CPT) are lower on the capsaicin-treated side, indicating a decreased in cold sensitivity; (3) heat pain threshold (HPT) was lower on the capsaicin-treated side in healthy subjects, suggesting an increased heat pain sensitivity; (4) dynamic mechanical allodynia (DMA); (5) mechanical pain after two stimulations (MPS2); and (6) mechanical pain summation after ten stimulations (MPS10), are increased on the capsaicin-treated side, suggesting an increased in mechanical pain (P < 0.002). CDT, CPT and HPT showed comparable effects across all six centers, with CPT and HPT demonstrating the best sensitivity. Data from the patients showed significant difference between affected and unaffected body side but only with CDT.
Conclusion: These results provide further support for the application of QST in multicenter studies examining normal and pathological pain responses
Insights into the electrochemistry of (CoxNi(1−x))2Al-NO3LayeredDouble Hydroxides
International audienceA series of (CoxNi1−x)2Al-NO3 (0 ≤ x ≤ 1) Layered Double Hydroxides (LDH) has been synthesized by the coprecipitation method. Their chemistry, structure and morphology were characterized using Inductively Coupled Plasma Atomic Emission and Energy-Dispersive X-ray Spectroscopies, Powder X-Ray Diffraction, Fourier Transformed Infrared spectroscopy, Raman spectroscopy and Scanning Electron Microscopy. The electrochemical behaviors of the LDH were investigated by Cyclic Voltammetry, Electrochemical Impedance Spectroscopy and Galvanostatic Charge/discharge with Potential Limitation measurements. The relationship between chemical composition of the LDH compounds (i.e. substituted samples vs physical mixtures) and their electrochemical properties is discussed. Special attention was paid to i) the role of the electrolyte cation (0.1 M COH, C+ = K+, Li+ and Na+) and to ii) the contribution of (CoxNi1−x)2Al-NO3@graphene nanocomposites (x = 0, 0.5, 1) in improving electron transfer in the materials
Effect of isoflurane on the auditory steady-state response and on consciousness in human volunteers.
BACKGROUND: The auditory steady state response (ASSR) is a sustained electrical response of the brain to auditory stimuli delivered at fast rates (30-50 responses/s). The aim of this study was to evaluate the effect of 0.26-0.50% isoflurane on the ASSR and on consciousness, defined as responsiveness to verbal commands. METHODS: Ten volunteers (21-31 yr) participated. Isoflurane was administered at three stable, end-tidal concentrations: 0.26%, 0.38%, and 0.50%. The ASSR in response to 18,000 stimuli (500-Hz tonebursts, 10 ms, 82-dB, the right ear, 35-45 bursts/s) was recorded from the vertex with reference to the right mastoid. Recordings were made during baseline, at each isoflurane concentration, and during recovery. RESULTS: The mean (SD) ASSR amplitudes were 0.32 (0.23) microV during baseline, 0.24 (0.17) microV during 0.26% isoflurane, 0.09 (0.05) microV during 0.38% isoflurane, 0.04 (0.03) microV during 0.50% isoflurane, and 0.29 (0.33) microV during recovery. The amplitude during baseline and recovery was larger than during 0.38% and 0.50% isoflurane (P < 0.001). The amplitude at 0.26% was larger than at the other concentrations (P < 0.025). The logarithm of the ASSR amplitude was related linearly to the concentration of isoflurane (r = 0.85; P < 0.0001). The prediction probability (Pk) for loss of consciousness was 0.95 for both ASSR and measured isoflurane concentration. An ASSR amplitude < 0.07 microV was always associated with unconsciousness. CONCLUSIONS: The ASSR is attenuated in a concentration-dependent manner by isoflurane. Suppression of consciousness and maximal attenuation of ASSR occur in the same isoflurane concentration range. Profound attenuation of ASSR appears to reflect unconsciousness, defined as unresponsiveness to verbal commands