Hypoalgesia following intrathecal morphine: a segmental dependent effect.

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.