PHILADELPHIA Interim pain management is likely to become even more difficult for people addicted to morphine. But the same technology used to treat Tourettes Syndrome and severe depression could provide new pharmacological damage treatment for morphine-inhaled neuropathic pain according to a study published April 27 in the Journal of Clinical Investigation.

Opioid pain relievers are commonly used to manage pain in critically ill patients undergoing surgery but their use for this purpose is becoming increasingly restricted by limiting opioid-drug interactions.

Researchers at 19 sites in North America Europe and Asia and at five National Institutes of Health Institutes of Health awarded at least 500000 National Institute of Health-funded research funds for opioid addiction research including this study. The study identifies a promising case in which a minivac that provides access to morphine but does not cope with morphine-induced withdrawal symptoms prevented opioid-induced neuropathic pain in rats. Nurses and human volunteers participated. The results were presented at the American Physiological Society (APS) Annual Meeting in Chicago.

Opioid pain relievers and morphine activate the N pain pathway deeply damaging the body including the brain yet they also can trigger this pathway leading to harmful withdrawal symptoms. While morphine does not present the same negative side effects as morphine or sedatives opioid agonists (orphan drugs) such as methadone and Naloxone work by blocking a receptor found on unoccupied opioid receptors leading to opioid-induced pain. The N-pain receptor ligands can also activate a receptor found on the released rats sodium-glucose transporter membrane. Thus they represent a potential therapeutic target for preventing opioid-induced neuropathic pain. Although it has been well established that opioid agonists modify the pathways of the N-pain pathway this technology also targets an already-defeated receptor so that morphine or a purified synthetic agonist can be administered intravenously. This is the case for Adoxone-induced Neuropathic Pain Syndrome (ANSS) a non-opioid acute pain-related neuroinflammation syndrome that has been unsuccessfully treated with opioids and is especially vulnerable to the adverse effects of opioids.

Each opioid agonist receptor is a bad man vulnerable to -blockers like Aducan and Valium but resistant to morphine-psoralen. The -blockers bind to the -interacting receptor and impair dopamine signaling. The -blockers activate the N-pain pathway activating a calcium channel to prevent this agonist receptor from functioning.

Administration of agonists to some mice results in a state similar to morphine treatment plus -blocker naloxone which is OK. Positron emission tomography and PET scans and PET imaging to detect opioid-induced neuropathic pain in these mice suggest that the nerves receiving the opioid signal are not behaving as normally as they would in morphine-naired patients.

Peter Van de Water PhD senior author professor of neurosurgery MedUni ViennaVienna General Hospital and the Technical University of Vienna.