Abstract
There is increasing recognition that mechanisms in the nervous system common to other persistent pain conditions and inflammation of neurogenic origin play a major role in chronic pelvic pain. For either somatic or visceral pain, an understanding of the processes of peripheral and central sensitization mechanisms, common to both acute and persistent pain, should help explain difficult pain conditions and open new therapeutic options. This review aims to correlate knowledge regarding persistent pain causation and pain conditions in gynecology. Although there is emerging evidence about the pathophysiology and management of persistent pain, there is still a dearth of evidence-based practice for chronic pelvic pain in women.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Notes
Gabapentin does not cause gastric irritation; it may absorb better after food. Gabapentin increases amount of Phase IV (deep restorative) sleep. Gabapentin is not metabolized, and does not react with other medications. Renal excretion unchanged – curtail dose if renal failure. Dose of more than 3600 mg/day usually does not increase efficacy.