Areas of Research
Peripheral neural mechanisms responsible for pelvic pain
We routinely employ the usage of quantitative sensory tests in our research (see Tu et al. 2008, and Tu et al. 2007 ). We are currently using equipment built by Olivier Monbureau to identify nociceptive mechanisms altered in women with pelvic pain.
Combined effects of alterations in pelvic floor mechanical thresholds and prolonged aftersensation on likelihood of CPP/PBS
Margin plot shows probability of chronic pelvic pain (CPP)/painful bladder syndrome (PBS) (Y axis) at different pelvic floor mechanical thresholds (X axis) given shorter or longer duration of painful aftersensation. Aftersensation duration up to 5 minutes (green), ≥5 and ≤10 minutes (black), and >10 minutes (red). Percent of overall population with each aftersensation range are shown in parentheses. Women with below-average levels of mechanical pain sensitivity (eg, 1.5 kg/cm2) are still likely to have CPP/PBS if they exhibit prolonged aftersensations.
From Nociceptive mechanisms in chronic pelvic pain. Am J Obstet Gynecol 2015.
Novel methods for evaluating bladder pain
We have developed a novel visceral pain testing paradigm, published in The Clinical Journal of Pain. Briefly, this involves voiding and obtaining baseline measurements of bladder volume with a 3D ultrasound abdominal transducer. The methodological appeal of our novel, noninvasive bladder pain test has allowed us to rapidly accumulate more participant repeat visits than the prevailing visceral pain testing methods, in addition to allowing us to identify a unique sub-phenotype in dysmenorrhea.
Example bladder volume measurement with 3d ultrasound.
Novel imaging based diagnostics for menstrual pain
In order to characterize viscero-somatic contributions to dysmenorrhea, we measured abdominal EMGs during menstruation in women reporting moderate-severe dysmenorrhea in an ongoing study. We combined this with repeated ultrasound observation of the abdominal wall and pelvic cavity as a complementary strategy to assess the uterine and abdominal wall musculature. Preliminary results suggest our method can distinguish different types of menstrual cramps and suggest specific nociceptive mechanisms.
Optic flow map of 3 different subjects. Color indicates magnitude of motion. White indicates stationary structure. Black/gray is ultrasound background. Left: Movement occurred in abdominal muscle (top of image). Middle: Most movement occurred in uterine and intestinal boundaries (bottom of image) in a subject experiencing menstrual cramps without somatic muscular events. Right: A subject experiencing temporary spontaneous remission from menstrual pain with overall reduced optic flow measurements.
Risk factors for chronic pelvic pain
Our work demonstrates that dysmenorrhea is one of the largest risk factors for pelvic pain. We are currently testing the hypothesis whether effectively treating dysmenorrhea can reduce bladder pain even in women that have not been yet diagnosed/treated for dysmenorrhea or bladder pain
Menstrual pain is associated with increased severity for other forms of pelvic pain (odds ratio: 13).
Westling AM, Tu FF, Griffith JW, Hellman KM. Am J Obstet Gynecol. 2013 Nov;209(5):422.e1-422.e10.
The mechanisms responsible for pain and analgesia
The traditional view of descending modulation [see here for more information] which purports that raphe magnus neurons in the brainstem perform like conventional brakes to provide sustained states of excitation or inhibition that either depress or facilitate nociception.The conventional model typically depicts ON cells facilitating dorsal horn neurons, whereas OFF cells provide analgesia by inhibiting dorsal horn neurons. Our work (published in The Journal of Neuroscience) casts doubt on the conventional model and implies that phasic changes in ON and OFF cell activity are responsible for the modulation of homeostasis and motor reflexes affecting cutaneous nociception. Rather, alterations in firing rates provide cues to elicit nociceptive or autonomic reflexes.