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Purpose: To validate a French translation of the Pain Sensitivity Questionnaire (PSQ), which is a valuable tool to predict an individual's natural disposition to feel pain that could be used after surgery., Methods: We studied content validity, internal consistency, convergent validity (anxiety, depression and catastrophism) and test-retest reliability of the French version of the PSQ (PSQ-F) in 146 patients either before scheduled surgery or during pregnancy; then, convergent and concurrent validity in 85 healthy volunteers submitted to nociceptive tests., Results: Internal consistency of the PSQ-F was found to be excellent, with Cronbach's α at 0.866, 0.886, and 0.927, respectively for its "minor", "moderate" and "total" scores. Test-retest reliability was significant, with intraclass correlation coefficients at 0.629, 0.629, and 0.635, respectively for the above- mentioned scores. These three scores correlated with anxiety, depression and catastrophizing scores in patients, but not in healthy volunteers, possibly because of low and few variant psychometric scores in this group. They were inversely correlated to the temperature needed to evoke heat pain rated 6 out of 10, but not to the mechanical pain threshold (electronic von Frey), nor to the heat pain threshold. Finally, they directly correlated to the pain induced by the cold pressor test (minor and total scores only)., Discussion: This validated version can now be used by French-speaking researchers and physicians., Trial Registration: www.ClinicalTrials.gov (NCT03113903); 14 April, 2017.

Background and Aims: Neuropathic pain has been shown to be accompanied by cognitive impairment, but the specific impact of postherpetic neuropathic pain on cognitive processes has not been explored. This study aims to evaluate the impact of pain on several domains of cognition in older patients with postherpetic neuralgia (PHN)., Methods: This cross-sectional study (clinicaltrial.gov NCT 00989040) included 84 individuals after signature of informed consent., Participants: 42 patients with PHN and 42 healthy volunteers. Of the 42 PHN patients, 21 received systemic treatment (antidepressants, anticonvulsants, opiates) and 21 had topical treatment with the 5% lidocaine medicated plaster. All participants performed a panel of four cognitive tests: reaction time, semantic memory, decision-making, and visual memory (Cantab, Cambridge)., Results: Forty men and 44 women with a mean age of 72 ± 8 years participated. Each PHN patient was matched by age and gender with a healthy volunteer. Vigilance, decision-making, and semantic memory were significantly impaired (P < 0.05) in patients on systemic treatment, especially with antidepressants, while no significant changes were noted between the lidocaine plaster group and their matched controls of healthy volunteers., Conclusion: This study shows the deleterious effect of systemic PHN treatment on several domains of cognition. Cognitive impairment associated with pain and antidepressants may be reversed by topical pain management. Topical treatment with 5% lidocaine medicated plaster is a valuable alternative for pain alleviation and maintains cognitive integrity in this vulnerable population., (© 2013 World Institute of Pain.)

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<⁄span>) were calculated and all data were compared between both groups; P<0.05 was considered to be statistically significant., Results: AUCCPM0-6 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.

Background and Objectives: Transient pain in humans is usually quantified using visual analog or numeric rating scales, but no assessment method has yet been validated in real time during such stimulation., Methods: To validate a transient pain monitor, healthy volunteers submitted to stimulations generated by a CO(2) laser at graded levels of stimulation were trained to close the dominant hand around a handgrip dynamometer as strongly as they felt the pain, and the signal was computerized.The parameters recorded for each response were the peak intensity, the area under the curve, and pain expressed on a visual analog scale as a control. The volunteers underwent a second session 1 week later to assess reproducibility., Results: The 3 parameters studied had a similar capacity to report the intensity of stimulation. The peak intensity showed many similarities with the visual analog scale, although a downward drift of the values throughout the session was observed. The area under the curve displayed a greater interindividual variability than other parameters, but it was better to assess low-intensity stimulation; a better fit for crossover designs was also suggested with the area under the curve., Conclusions: This study validates in human volunteers under a laser stimulation of skin the metrological properties of an electronic handgrip device to assess the intensity of transient punctuate pain (compared with visual analog scale). The transient pain monitor validated here should now be tested in the clinical context., (Copyright © 2011 by American Society of Regional Anesthesia and Pain Medicine)

Burning mouth syndrome (stomatodynia) is associated with changes of a neuropathic nature the main location of which, peripheral or central, remains unknown. A randomised, double-blind crossover design was used to investigate the effects of lingual nerve block on spontaneous burning pain and a possible correlation with the effects of topical clonazepam, the patient's response to a psychological questionnaire, and the taste and heat thresholds. The spontaneous burning was measured with a visual analogue scale (VAS) just before and 15 min after injection. The decreases in VAS score after lidocaine or saline injection were not significantly different (2.7+/-3.9 and 2.0+/-2.6, respectively; n=20). However, two groups of patients could be identified: in a "peripheral group" (n=10) the VAS decrease due to lingual nerve injection was 4.3+/-3.1cm after lidocaine and 0.9+/-0.3 cm after saline (p=0.02). In a "central group" (n=7), there were an increase in pain intensity score (-0.8+/-2.6 cm) after lidocaine and a decrease (1.5+/-3.0 cm) after saline (p=0.15). An increase in the hospital anxiety and depression (HAD) score and a decreased taste sensitivity and heat pain threshold of painful oral area were seen in patients compared with age-and-sex-matched controls (p<0.05). Topical clonazepam treatment tended to be more effective (p=0.07) and HAD score lower (p<0.03) in the peripheral than in the central group. These results suggest that the neuropathic disorder associated with stomatodynia may be predominantly peripheral, central or mixed depending on the individual. Topical application of clonazepam and HAD may serve as indicators of which mechanism is dominating., (Copyright 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.)

The mechanism of the analgesic action of acetaminophen involves the serotonergic system. This study explores how acetaminophen interferes with serotonergic descending pain pathways. Eighteen rapid metabolizers of tropisetron were included in this double-blind cross-over study. After ethical approval, the healthy volunteers took 1 g oral acetaminophen (A) or placebo (p) combined with either the 5-HT3 antagonist tropisetron (T) (5 mg) or saline, intravenously, at weekly intervals. Mechanical pain thresholds, determined before and after a cold pressor test (CPT), were repeated seven times during the three post-dosing hours, and area under the concentration-time curves (AUCs) of the three treatments were compared. After CPT, AUC (%*min) of Ap (1,561+/-429) was larger than before CPT (393+/-382, P<0.05); these effects were totally inhibited by tropisetron. Acetaminophen reinforces descending inhibitory pain pathways; it suggests a supraspinal target for acetaminophen's antinociceptive action. This study also confirmed that there is a central serotonergic mechanism of action for acetaminophen that is not stimulus-dependent.

In rats, a Mg(2+)-deficient diet, which in a few days dramatically decreased the Mg(2+) concentration in plasma, cerebrospinal fluid (CSF) and spinal cord, was accompanied by a significant lowering of the nociceptive threshold. After reloading, the Mg(2+) concentration was rapidly normalized in both spinal cord and CSF. In parallel, the neurological disturbances induced by Mg(2+) deficiency vanished in less that 24 h, but the reversal of the hyperalgesia was delayed for up to 11 to 20 days. In this model, repeated doses of dizocilpine (MK-801), a non-competitive NMDA receptor antagonist, given at start of the Mg(2+)-depleted diet, prevented hyperalgesia, suggesting the involvement of NMDA receptor channels. The delayed recovery of a normal pain threshold argues for long-term sensitization of the nociceptive pathways.

Background: An excess of excitatory pathway activation via N-methyl-D-aspartate (NMDA) receptors has been described in neuropathic pain that responds poorly to morphine. However, in this situation, several published data sets show that coadministration of NMDA receptor antagonists restores the efficacy of opioids. Considering that magnesium behaves like an NMDA receptor antagonist, we investigated the effect of the combination of magnesium and morphine in experimental models of chronic and tonic pain., Methods: Mechanical hyperalgesia was assessed with the paw-pressure test in mononeuropathic (chronic constrictive injury model) and diabetic rats. Behavioral reactions were scored in a model of inflammation induced by formalin. The animals were assigned to one of three groups according to the intraperitoneal pretreatment: magnesium (30 mg/kg x 3), magnesium (30 mg/kg), and saline. Before testing, morphine was injected intravenously in mononeuropathic (0.3 mg/kg) and diabetic rats (1 mg/kg) and by the subcutaneous route in rats with the formalin test (1.5 mg/kg)., Results: Magnesium alone induced a significant antihyperalgesic effect in mononeuropathic and diabetic rats after a cumulative dose of 90 mg/kg. Furthermore, it significantly increased morphine analgesia, regardless of the loading dose used (30 or 90 mg/kg) in the two models of neuropathic pain. In the formalin test, magnesium alone did not have a significant effect. However, in combination with morphine, it revealed the analgesic effect of this opiate., Conclusions: These data show that magnesium amplifies the analgesic effect of low-dose morphine in conditions of sustained pain. Considering the good tolerability of magnesium, these findings may have clinical applications in neuropathic and persistent pain.

Repeated application of capsaicin on the tongue has been used as a human oral pain model to assess topical anesthetic-analgesic drugs. The reliability of the model was evaluated by observing the variability of the response to repeated applications of capsaicin after three successive sessions at 1 day intervals. No session effect was observed for the time course of the visual analogue scale (VAS) scores and the area under the curve, but a significant decrease of VAS peak scores was noted from the first to the third session. The sensitivity of the model was assessed by mouth rinses with three doses of lidocaine (0.25, 0.5 and 1%). Lidocaine significantly reduced the burning pain. This effect was rapid, reversible and dose dependent. It is concluded that the oral capsaicin pain model displays good reliability and sensitivity and allows safe evaluation of candidate topical analgesic and anesthetic drugs.

The benefit of antidepressant treatment in human neuropathic pain is now well documented, but the effect is limited and slow to appear. It has been demonstrated that the association of a 5-HT(1A) antagonist and a serotoninergic antidepressant reduced the delay of action and increases the thymoanaleptic effect of the drug. The purpose of this work was to evaluate the combination of an antidepressant and a 5-HT(1A) antagonist in animal models of chronic neuropathic pain. We studied the antinociceptive effect of the co-administration of clomipramine and a 5-HT(1A) antagonist (WAY 100,635) in a pain test applied in normal rats and in two models of neurogenic sustained pain (mononeuropathic and diabetic rats). The results show an increase in the antinociceptive effect of acutely injected clomipramine due to WAY 100,635 in these models, which is majored when the two drugs are repeatedly injected. The 5-HT(1A) antagonist reduced the delay of onset and increased the maximal antinociceptive effect of clomipramine. These new findings argue for using the combination of an antidepressant and a 5-HT(1A) antagonist in human neuropathic pain therapy.

The aim of this study was to assess the effect of paradoxical sleep deprivation (PSD) and sleep recovery on the vocalization threshold in rats submitted to a mechanical noxious stimulus. Sixteen male Wistar rats were randomly assigned in two groups: controls (n=8), paradoxical sleep deprived rats (n=8). PSD was performed using the 'inverted flower pot' technique. Paw pressure test was used to assess the sensitivity to mechanical noxious stimulus (vocalization threshold). The experiment was divided into three periods: baseline (day 1, day 2), PSD (day 3, day 4, day 5) and recovery (day 6, day 7, day 8, day 9). After 48 and 72 h of PSD, the vocalization thresholds decreased significantly in comparison to the control rats (day 4: 245+/-21 vs. 303+/-20 g, P=0.05; day 5: 256+/-17 vs. 324+/-22 g, P=0.02). In PSD group, relative to controls, vocalization thresholds increased significantly after 48, 72, and 96 h of recovery sleep periods (day 7: 378+/-24 vs. 307+/-8 g P=0.01; day 8: 384+/-27 vs. 316+/-23 g, P=0.02; day 9: 395+/-24 vs. 328+/-15 g, P=0.02). Vocalization thresholds on day 6 were not significantly different in both groups (375+/-20 vs. 324+/-24 g, P=0.08). In conclusion, experimental PSD in rats induces a significant decrease in vocalization threshold to mechanical noxious stimulus, which is totally reversed during the sleep recovery period.

Rats (Sprague-Dawley), submitted to a mechanical noxious stimulus (paw pressure), were tested to determine 1) the antinociceptive effects of p.o. (200, 400 and 800 mg/kg), i.v. (50, 100, 200 and 300 mg/kg) and intrathecal (i.t.) (100 and 200 micrograms/rat) administrations of paracetamol; 2) the influence of i.t. administered tropisetron, a 5-hydroxytryptamine3 (5-HT3) receptor antagonist (0.5, 1 or 10 micrograms/rat) on paracetamol-induced antinociception; 3) the influence of indomethacin (25 mg/kg s.c.), naloxone (10 micrograms/rat i.t.) and yohimbine (1 mg/kg i.v.) on the effect of paracetamol (200 mg/kg i.v.) to determine the involvement of prostaglandins, opioids and alpha-2 adrenoceptors. The displacement by paracetamol of radioligand binding to various receptors was also investigated. Paracetamol induced a significant antinociceptive effect after p.o., i.v. and i.t. administration. A total inhibition of the effect of paracetamol, administered p.o. or i.t., occurred at the dose of 0.5 microgram/rat of tropisetron, whereas 10 micrograms/rat of this antagonist was needed to totally inhibit the action of i.v. administered paracetamol. Indomethacin, naloxone and yohimbine failed to modify paracetamol antinociceptive action. In vitro studies failed to show any binding of paracetamol to 5-HT3 and several other receptors and to 5-HT uptake sites. It is concluded that paracetamol has a central antinociceptive effect, based on an indirect involvement of spinal 5-HT3 receptors.

Unlabelled: Postoperative pain has rarely been assessed after ENT surgery for cancer. Its evaluation is difficult because of the frequent lack of speech after this type of surgery., Objectives: to assess postoperative pain after pharyngeal and laryngeal surgery for cancer., Patients and Method: prospective study in 13 men (38-71 ans) operated on by total laryngectomy with or without partial pharyngectomy. A standardised treatment using propacetamol and nalbuphine was systematically prescribed. Pain, anxiety and relief were assessed with the help of visual analogue scales (VAS). Heart rate, mean blood pressure and respiratory rate were evaluated too., Results: mean postoperative pain was maximal just after recovery (6,64 +/- 2,14 cm) then decreased regularly. Initial mean score of anxiety was 3,14 +/- 3 cm and then was decreasing too. Anxiety and pain did not correlate except in 2 cases. None of the 3 objective parameters correlated with pain., Conclusion: postoperative pain can be assessed reliably after pharyngolaryngeal cancer surgery and is probably underrated. Its high initial score indicates that efforts must be focused on pre-emotive analgesia. Its high individual variability let us hypothesise that PCA systems should be effective.

Literature on pain management in Alzheimer's disease is slowly emerging and this review deals with different aspects of pain in this growing population. Clinical pain, experimental pain and assessment of pain in cognitively impaired patients are presented. Treatment of pain is also discussed. This review calls for more studies and clinical trials with a view to improve the comfort and quality of life of patients suffering from Alzheimer's disease. [ABSTRACT FROM AUTHOR]