Abstract
Naloxone per se causes no pain in normal man, indicating that opioidergic antinociceptive systems are not tonically active, but this might not be the case in chronic pain conditions. The present investigation tested the hypothesis that pain in chronic headache is the result of insufficiently attenuated nociceptive impulses. Forty-seven patients suffering from chronic tension headache entered the present double-blind cross-over trial of naloxone 4 mg i.v. versus saline. Adverse effects were negligible. Patients scored headache pain on a 100 mm visual analog scale and change in headache on a 5-point verbal rating scale after 5, 15, 30, 60 and 90 min. Mean arterial blood pressure decreased 4.2 mm Hg (P < 0.05) after naloxone compared to saline, but naloxone had no effect on headache (P = 0.96). A bimodal distribution of acute pain patients into placebo responders and non-responders has been reported, but our chronic pain patients showed a homogeneous placebo response. Review of the literature indicates that acute clinical pain and stimulation-induced analgesia in experimental pain has a naloxone-responsive component. Chronic pain does not appear to be influenced by naloxone in moderate doses.