Chronic pain is common after thoracotomy and its neuropathic component is infrequent. As age, ASA scores, number of drains, and situations relating to daily life seem to play a role in pain occurrence, a multifaceted approach against the onset of chronic pain is advisable.

Minocycline strongly inhibits microglial activation, which contributes to central sensitization, a major mechanism underlying chronic pain development. We hypothesized that the perioperative administration of minocycline might decrease persistent pain after lumbar discectomy. We randomly assigned 100 patients undergoing scheduled lumbar discectomy to placebo and minocycline groups. The minocycline group received 100mg minocycline orally, twice daily, beginning the evening before surgery and continuing for 8 days. The primary outcome was the change in lower limb pain intensity at rest between baseline and 3 months. Secondary outcomes were pain intensity on movement, the incidence of persistent pain and chronic neuropathic pain, back pain intensity at rest and on movement, and changes in Neuropathic Pain Symptom Inventory, Brief Pain Inventory, and Roland-Morris scores at 3 months. An intention-to-treat analysis was performed for patients assessed from the day before surgery to 3 months. The decrease in lower limb pain intensity was similar in the placebo and minocycline groups, both at rest -1.7 ± 1.6 vs -2.3 ± 2.4 and on movement -2.5 ± 2.1 vs -3.4 ± 2.9. The incidence and intensity of neuropathic pain and functional scores did not differ between the minocycline and placebo groups. Exploratory analysis suggested that minocycline might be effective in a subgroup of patients with predominantly deep spontaneous pain at baseline. Perioperative minocycline administration for 8 days does not improve persistent pain after lumbar discectomy.

Local anesthetic infiltration has been proposed to decrease postoperative pain. The aim of this study was to determine whether scalp infiltration with bupivacaine or ropivacaine would improve analgesia after supratentorial craniotomy for tumor resection. Eighty patients were recruited into a randomized double-blind study. Infiltration was performed after skin closure with 20 mL of saline 0.9% (placebo group, n = 40), of 0.375% bupivacaine with epinephrine 1:200,000 (bupivacaine group, n = 20), or of 0.75% ropivacaine (ropivacaine group, n = 20). Postoperative analgesia was provided with patient-controlled morphine IV analgesia (PCA). The study was continued until PACU discharge, which occurred early in the morning following surgery. Results are reported on 37 patients in the placebo group, 20 in the bupivacaine group, and 19 in the ropivacaine group because 4 patients experienced postoperative complications and were excluded from the study. Morphine titration at arrival in the postanesthesia care unit was necessary more often in the placebo group (62% of the patients) than in the 2 treated groups (19% in each, P = 0.02). The median quantity of morphine administered during the first 2 postoperative hours, including initial titration administered by a nurse and PCA-administered morphine, was lower in each treated group than in the placebo group (P < 0.01). The median morphine consumption up to the 16th postoperative hour was not significantly different among the 3 groups. There was no difference in the visual analogue scale scores among the 3 groups at any time. Scalp infiltration with either bupivacaine or ropivacaine had a statistically significant effect on morphine consumption during the first 2 postoperative hours.

Twenty-eight patients presenting for aortic surgery were randomly assigned in a double-blind, placebo-controlled protocol to receive placebo (n = 14) or clonidine (4.7 +/- 1.2 micrograms.kg-1 po; n = 14), in addition to flunitrazepam 120 min before induction of anesthesia. Plasma catecholamines (CA) and hemodynamic variables were determined at 7 stages during surgery. In the placebo group, plasma epinephrine (E) and norepinephrine (NE) had risen twofold at skin closure compared to baseline (E: from 109 +/- 51 pg.ml-1 to 294 +/- 161 pg.ml-1; NE: from 658 +/- 226 to 1150 +/- 494 pg.ml-1). Plasma CA were significantly lower in the clonidine group (P less than 0.001 and 0.01 vs placebo for NE and E respectively). In both groups, similar directional changes were observed for the circulatory variables, upon aortic clamping and declamping. In the clonidine group, however, mean arterial pressure was lower at most stages (P less than 0.05 vs placebo); moreover, stroke volume index was greater in the clonidine group (P less than 0.05) upon declamping. This improved stability in the clonidine group was achieved with a halving in the number of anesthetic/circulatory interventions (P less than 0.05 vs placebo). Provided intravascular volume is adequate, clonidine suppresses the increase in plasma catecholamines induced by aortic surgery and improves circulatory stability, with a reduced number of anesthetic, circulatory adjustments.

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