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 (AUC<span style="vertical-align: sub">CPM<⁄span>) were calculated and all data were compared between both groups; P<0.05 was considered to be statistically significant. RESULTS: AUC<span style="vertical-align: sub">CPM0-6 min<⁄span> 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.
RCT Entities:
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 PHNpatients with healthy controls. METHODS: Nine PHNpatients 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 (AUC<span style="vertical-align: sub">CPM<⁄span>) were calculated and all data were compared between both groups; P<0.05 was considered to be statistically significant. RESULTS: AUC<span style="vertical-align: sub">CPM0-6 min<⁄span> was significantly lower in PHNpatients 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.
Authors: Sarah J Love-Jones; Marie Besson; Charlotte E Steeds; Peter Brook; Boris A Chizh; Anthony E Pickering Journal: Eur J Pain Date: 2008-12-30 Impact factor: 3.931
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