This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This protocol is part of a Pain Center Grant that focuses on how pain itself, especially chronic neuropathic pain, alters the response to traditional and non-traditional analgesics. The way that nerve fibers carry the information of pain to the brain is thought to change after surgery and in chronic pain. For this reason, some medicines work better to relieve pain in healthy people who have a sudden painful injury compared to those after surgery or those with chronic pain. Currently available pain medications may not relieve all types of pain or may relieve pain only at doses that produce side effects and potential complications.
The aim of this protocol is to understand the mechanisms by which intrathecal clonidine increases in potency and efficacy by looking at the cerebrospinal fluid of healthy individuals before and after clonidine administration as well as looking at the spinal fluid of people that have chronic neuropathic nerve pain.
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