Oxycodone provided better analgesia but also more side effects, suggesting that the doses used in the present study may not be equipotent.

Subhypnotic doses of thiopentone are considered to have a hyperalgesic effect, while propofol has a hypoalgesic effect. We investigated the effect of these drugs on the nociceptive system by measuring the pain threshold to laser stimulation and the pain evoked potential (power and latency). Nineteen patients (ASA group I) participated. Twelve patients received thiopentone 0.5 mg kg-1 and propofol 0.25 mg kg-1 in random order separated by an interval of 14 h, and seven patients received saline. Immediately after the injection of both agents, the pain threshold was increased significantly (P less than 0.001) and the amplitude of the evoked potential was reduced significantly (P less than 0.05), while the latency of the evoked potential remained constant. It is concluded that, in subhypnotic doses, both thiopentone and propofol decrease the acute pain evoked by argon laser stimulation.

Subhypnotic doses of thiopentone are considered to have a hyperalgesic effect, while propofol has a hypoalgesic effect. We investigated the effect of these drugs on the nociceptive system by measuring the pain threshold to laser stimulation and the pain evoked potential (power and latency). Nineteen patients (ASA group I) participated. Twelve patients received thiopentone 0.5 mg kg-1 and propofol 0.25 mg kg-' in random order separated by an interval of 14 h, and seven patients received saline. Immediately after the injection of both agents, the pain threshold was increased significantly (P < 0.001) and the amplitude of the evoked potential was reduced significantly (P < 0.05), while the latency of the evoked potential remained constant. It is concluded that, in subhypnotic doses, both thiopentone and propofol decrease the acute pain evoked by argon laser stimulation.

In 20 patients a continuous block of the lumbar plexus was administered after knee-joint surgery, and the analgesic effect of two different concentrations of bupivacaine was compared. The same volume of bupivacaine was given to both groups of patients: a bolus dose of 0.4 ml/kg, 0.5% or 0.25%, followed by infusion of 0.14 ml/kg/h, 0.25% or 0.125%, respectively, via a catheter placed in the neurovascular fascial sheath of the femoral nerve according to the "3-in-1 block" technique. The median morphine consumption during the first 16 h postoperatively was 6.0 mg when bupivacaine 0.5/0.25% was used and 9.5 mg when 0.25/0.125% was used. This difference is not significant. The visual analogue pain scores were also similar in the two groups (P greater than 0.05). All plasma concentrations were below 4 micrograms/ml, the highest concentration measured being 3.6 micrograms/ml. It is concluded that when used for a continuous block of the lumbar plexus after knee-joint surgery, bupivacaine in a concentration of 0.125% offers the same pain relief as a concentration of 0.25%, and the risk of toxic reactions is reduced.

Analgesia was assessed quantitatively at various dermatomes (C7, T8, T10, T12, L1, L3, S1) for the first 30 min after subarachnoid administration of 0.5% bupivacaine 3.5 ml. Stimulation with 10 needles and laser stimulation could evoke pain in dermatomes with adequate analgesia to single needle stimulation. Analgesia was assessed by thresholds (sensory and pain) and by pain-related brain potentials (amplitude and latency) to laser stimulation. Little analgesia was found at T10, but it increased gradually towards caudal segments. The dermatome related to the site of the injection (L3) was not blocked to a greater extent than the surrounding dermatomes. Conduction time (the latency of the evoked brain potential) was increased relatively more from the S1 dermatome compared with L1.

The onset phase of hypoalgesia, following intrathecal morphine, was assessed by experimental argon laser-induced pain. A dose of 0.4 mg morphine was injected pre-operatively at the L3-L4 level into nine patients. The thresholds to laser-induced pain and pain-evoked brain potentials were monitored for 2 h at the S1, L1, and C7 dermatomes. Hypoalgesia was detected at the S1 and L1 dermatomes after 5 and 15 min, respectively. No hypoalgesic effect was found at C7. This indicates that hypoalgesia was caused predominantly by segmental spinal mechanisms during the onset phase, and not by a general widespread effect. No latency changes (conduction delay) of the brain potentials evoked from the hypoalgesic dermatomes were found. Cutaneous pain, induced experimentally by laser stimulation, has the advantage of being quantitative and is useful to assess the onset and the segmental spread of hypoalgesia.

The study was done to see if it was possible to predict the level of analgesia in repeated spinal blocks with our routine technique where the patient is seated during injection of plain 0.5% bupivacaine 3.5 ml at the L3-L4 interspace and placed in the lithotomy position after 0.5 min. Thirty patients with tumour of the bladder had two spinal blocks during a 13-month period. The segmental spread of sensory loss was tested with the pin-prick technique. A wide range of height of blocks was found, increasing with age. Regression analysis on maximum cephalad spread of the second spinal analgesia against the first had a slope of 0.48 (P less than 0.01 for the hypothesis that the slope is zero). A significant correlation between the time for maximal cephalad spread was found, while the correlation between duration of thoracal analgesia was non-significant.