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Pain Research and Management
Volume 19, Issue 1, Pages e19-e23
Original Article

Impaired Modulation of Pain in Patients with Postherpetic Neuralgia

Gisèle Pickering,1,2,3 Bruno Pereira,1 Elodie Dufour,1 Sylvie Soule,1 and Claude Dubray1,2,3

1Centre Hospitalier Universitaire de Clermont-Ferrand, Centre de Pharmacologie Clinique, France
2Inserm, CIC 501, UMR 766, France
3Clermont Université, Laboratoire de Pharmacologie, Faculté de médecine, Clermont-Ferrand, France

Copyright © 2014 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BACKGROUND: The efficiency of inhibitory pain descending pathways (evaluated using conditioned pain modulation [CPM]) has not been studied in postherpetic neuralgia (PHN).

OBJECTIVE: To compare CPM in PHN patients with healthy controls.

METHODS: Nine PHN patients and nine control individuals were matched according to age and sex. Amplitudes of cortical thermal-evoked potentials were recorded on the surface of the scalp; clinical pain and thermal pain were evaluated on a 0 to 10 numerical rating scale, at baseline and at intervals during the 6 min after CPM (elicited by a cold pressor test, 8°C). A battery of cognitive tests was performed. Amplitude differences, percentages and related areas under the curve (AUCCPM) were calculated and all data were compared between both groups; P<0.05 was considered to be statistically significant.

RESULTS: AUCCPM0–6 min was significantly lower in PHN patients compared with controls (−39±51 μV/min versus −144±66 μV/min; P=0.0012) and correlated (P=0.04) with clinical pain intensity. Pain ratings before CPM were similar in both groups but were significantly lower in the control group 3 min after the cold pressor test. Cognitive test results were not significantly different.

CONCLUSION: Psychophysical and electrophysiological approaches have shown that patients with PHN exhibit a deficiency of pain inhibition modulation, which could signal a predisposing factor to developing chronic pain. This deficiency was not linked to the cognitive performance but rather to subtle in situ cognitivoemotional adaptations, which remain to be investigated.