A Model of Neural Cross-Talk and Irritation in the Pelvis: Implications for the Overlap of Chronic Pelvic Pain Disorders

Convergence of bladder and colon sensory innervation occurs at the primary afferent level

“…the distal colon and urinary bladder), could contribute to the common clinical overlap of IBS, IC, and other CPP disorders (Alagiri et al 1997;Prior et al 1989;Whorwell et al 1986). As we have recently shown, cross-organ pelvic reflexes, as well as, cross-organ alterations in physiological functioning and sensation following irritation (bladder-to-bowel and vice versa), suggested the involvement of pre-existing dichotomous afferent pathways in the pelvis (Pezzone et al 2005). This putative role of afferent pathways was further verified by single unit recordings of C-fiber bladder afferents within the pelvic nerve that exhibited sensitized mechanical and chemogenic response properties following acute colonic irritation with trinitrobenzenesulfonic acid (TNBS) (Ustinova et al 2006).…”

“…We recently provided evidence of pre-existing neural pathways in the development of pelvic organ cross-sensitization by demonstrating that colonic hypersensitivity develops following the induction of acute cystitis and vice versa (Pezzone et al 2005). Follow-up studies in our laboratory employing single unit C-fiber bladder afferent recording revealed that acute colonic irritation is capable of sensitizing urinary bladder afferents to mechanical and chemical stimuli, and interruption of the neural input to the bladder can ameliorate this effect, suggesting a direct afferent pathway from the colon (Ustinova et al 2006).…”

Visceral and Somatic Hypersensitivity in TNBS-Induced Colitis in Rats

“…The somatic hypersensitivity present is likely to be a result of central sensitization of spinal dorsal horn neurons that receive somatovisceral convergence [6][7][8][9][10]36]. An additional factor could be related to neural cross-talk in the pelvis [10].…”

“…An additional factor could be related to neural cross-talk in the pelvis [10]. The persistent colitis may result in the peripheral and/or central release of some excitatory mediator that produces and maintains central sensitization, eventually leading to somatic hypersensitivity.…”

“…Patients with visceral pain often exhibit a wide variety of somatic symptoms including back pain, migraine headaches, and muscle pain. These symptoms may be consistent with central sensitization; referral of visceral pain to somatic tissues outside the area of immediate referral [1][2][3][4][5] or neural cross-talk in which afferent activation of one visceral structure influences efferent output in other structures and organs and is mediated by convergence of sensory pathways in the spinal cord [6][7][8][9][10].. Somatic hypersensitivity may also occur in clinical conditions where visceral pain is directly referred to a corresponding area of somatic tissue. Referred visceral hypersensitivity is most often related to visceral pain being directly referred to the corresponding area of the abdominal wall [2,11, and 12].…”