Publications by authors named "Katlyn E Dillane"

7 Publications

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Cortical mechanisms of visual hypersensitivity in women at risk for chronic pelvic pain.

Pain 2021 Aug 27. Epub 2021 Aug 27.

Department of Ob/Gyn, NorthShore University HealthSystem, Evanston, IL, United States Department of Ob/Gyn, Pritzker School of Medicine, University of Chicago, Chicago, IL, United States Department of Psychology, Loyola University Chicago, Chicago, IL, United States Chronic Pain and Fatigue Research Center, Department of Anesthesiology, University of Michigan, Ann Arbor, MI.

Abstract: Increased sensory sensitivity across non-nociceptive modalities is a common symptom of chronic pain conditions and is associated with chronic pain development. Providing a better understanding of the brain-behavior relationships that underlie multimodal hypersensitivity (MMH) may clarify the role of MMH in the development of chronic pain. We studied sensory hypersensitivity in a cohort of women (n=147) that had diary confirmation of menstrual status and were enriched with risk factors for chronic pelvic pain, such as dysmenorrhea and increased bladder sensitivity. We administered two experimental tasks to evaluate the cross-modal relationship between visual and visceral sensitivity. Visual sensitivity was probed by presenting participants with a periodic pattern-reversal checkerboard stimulus presented across five brightness intensities during EEG recording. Self-reported visual unpleasantness ratings for each brightness intensity were simultaneously assessed. Visceral sensitivity was evaluated with an experimental bladder-filling task associated with early clinical symptoms of chronic pelvic pain. Visually evoked cortical activity increased with brightness intensity across the entire scalp, especially at occipital electrode sites. Visual stimulation-induced unpleasantness was associated with provoked bladder pain and evoked primary visual cortex activity. However, the relationship between unpleasantness and cortical activity was moderated by provoked bladder pain. These results demonstrate that activity in primary visual cortex is not greater in individuals with greater visceral sensitivity. We hypothesize that downstream interpretation or integration of this signal is amplified in individuals with visceral hypersensitivity. Future studies aimed at reducing MMH in chronic pain conditions should prioritize targeting of cortical mechanisms responsible for aberrant downstream sensory integration.
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http://dx.doi.org/10.1097/j.pain.0000000000002469DOI Listing
August 2021

Noninvasive bladder testing of adolescent females to assess visceral hypersensitivity.

Pain 2021 Apr 12. Epub 2021 Apr 12.

Department of Ob/Gyn, NorthShore University HealthSystem Evanston, IL, United States, Department of Ob/Gyn, University of Chicago, Pritzker School of Medicine, Chicago, IL, United States, Department of Psychology, Loyola University of Chicago, Chicago, IL, United States, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, United States.

Abstract: Excess pain after visceral provocation has been suggested as a marker for chronic pelvic pain risk in women. However, few noninvasive tests have been validated that could be performed readily on youth in early risk windows. Therefore, we evaluated the validity and reliability of a noninvasive bladder pain test in 124 healthy premenarchal females (median age 11, [interquartile range 11-12]), as previously studied in adult women. We explored whether psychosocial, sensory factors, and quantitative sensory test results were associated with provoked bladder pain and assessed the relation of bladder pain with abdominal pain history. Compared with findings in young adult females (age 21 [20-28]), results were similar except that adolescents had more pain at first sensation to void (P = 0.005) and lower maximum tolerance volume (P < 0.001). Anxiety, depression, somatic symptoms, and pain catastrophizing predicted provoked bladder pain (P's < 0.05). Bladder pain inversely correlated with pressure pain thresholds (r = -0.25, P < 0.05), but not with cold pressor pain or conditioned pain modulation effectiveness. Bladder pain was also associated with frequency of abdominal pain symptoms (r = 0.25, P = 0.039). We found strong retest reliability for bladder pain at standard levels of sensory urgency in 21 adolescents who attended repeat visits at 6 to 12 months (intraclass correlations = 0.88-0.90). Noninvasive bladder pain testing seems reproducible in adolescent females and may predict abdominal pain symptomatology. Confirmation of our findings and further investigation of the bladder test across menarche will help establish how visceral sensitivity contributes to the early trajectory of pelvic pain risk.
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http://dx.doi.org/10.1097/j.pain.0000000000002311DOI Listing
April 2021

Development and validation of a real-time method characterizing spontaneous pain in women with dysmenorrhea.

J Obstet Gynaecol Res 2021 Apr 15;47(4):1472-1480. Epub 2021 Feb 15.

Department of Obstetrics and Gynecology, NorthShore University HealthSystem, Evanston, Illinois, USA.

Aim: Prior research has primarily focused on static pain assessment, largely ignoring the dynamic nature of pain over time. We used a novel assessment tool for characterizing pain duration, frequency, and amplitude in women with dysmenorrhea and evaluated how these metrics were affected by naproxen treatment.

Methods: Dysmenorrheic women (n = 25) rated their menstrual pain by squeezing a pressure bulb proportional to the magnitude of their pain. To evaluate whether bulb squeezing was affected by naproxen, we compared parameters before and after naproxen. We also analyzed the correlation between pain relief on a numerical rating scale to changes in bulb squeezing parameters. Random bulb-squeezing activity in pain-free participants (n = 14) was used as a control for nonspecific effects or bias.

Results: In dysmenorrheic women, naproxen reduced the duration of the squeezing during a painful bout, the number of painful bouts and bout intensity. Before naproxen, the correlation between these bulb squeeze parameters and self-reported pain on numeric rating scale was not significant (R = 0.12, p = 0.304); however, there was a significant correlation between changes in bulb squeeze activity and self-reported pain relief after naproxen (R = 0.55, p < 0.001).

Conclusion: Our study demonstrates a convenient technique for continuous pain assessment, capturing three different dimensions: duration, frequency, and magnitude. Naproxen may act by reducing the duration and frequency of episodic pain in addition to reducing the severity. After further validation, these methods could be used for other pain conditions for deeper phenotyping and assessing novel treatments.
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http://dx.doi.org/10.1111/jog.14663DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8317258PMC
April 2021

Cortical Mechanisms of Visual Hypersensitivity in Women at Risk for Chronic Pelvic Pain.

medRxiv 2021 Jan 18. Epub 2021 Jan 18.

Multisensory hypersensitivity (MSH), which refers to persistent discomfort across sensory modalities, is a risk factor for chronic pain. Developing a better understanding of the neural contributions of disparate sensory systems to MSH may clarify its role in the development of chronic pain. We recruited a cohort of women ( =147) enriched with participants with menstrual pain at risk for developing chronic pain. Visual sensitivity was measured using a periodic pattern-reversal stimulus during EEG. Self-reported visual unpleasantness ratings were also recorded. Bladder pain sensitivity was evaluated with an experimental bladder-filling task associated with early clinical symptoms of chronic pelvic pain. Visual stimulation induced unpleasantness was associated with bladder pain and evoked primary visual cortex excitation; however, the relationship between unpleasantness and cortical excitation was moderated by bladder pain. Thus, future studies aimed at reversing the progression of MSH into chronic pain should prioritize targeting of cortical mechanisms responsible for maladaptive sensory input integration.
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http://dx.doi.org/10.1101/2020.12.03.20242032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7836135PMC
January 2021

Low Serum Naproxen Concentrations Are Associated with Minimal Pain Relief: A Preliminary Study in Women with Dysmenorrhea.

Pain Med 2020 11;21(11):3102-3108

Department of Obstetrics and Gynecology, NorthShore University HealthSystem & Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.

Objective: Incomplete pain relief after administration of nonsteroidal anti-inflammatory drugs (NSAIDs) is common, but it is unknown whether malabsorption or heightened metabolism contributes to NSAID resistance. To explain the etiology of NSAID resistance, we evaluated naproxen absorption and metabolism in relation to pain relief in a pilot study of women with dysmenorrhea.

Methods: During menses, participants completed before and after naproxen ingestion pain assessments. Analgesic effectiveness was calculated as a percent change in pain rating before and after naproxen administration. To evaluate the impact of malabsorption, the correlation between analgesic effectiveness and serum naproxen was analyzed. To identify whether hypermetabolism contributes to NSAID resistance, we also analyzed the metabolite O-desmethylnaproxen.

Results: Serum naproxen and O-desmethylnaproxen concentrations of the dysmenorrheic cohort (N = 23, 126 ± 10 µg/mL, 381 ± 56 ng/mL) and healthy controls (N = 12, 135 ± 8 µg/mL, 355 ± 58 ng/mL) were not significantly different (P > 0.05), suggesting that menstrual pain does not affect drug absorption and metabolism. However, nine dysmenorrhea participants had levels of analgesic effectiveness <30%. Among dysmenorrheic women, analgesic effectiveness was correlated with serum naproxen (r = 0.49, P = 0.019) and O-desmethylnaproxen (r = 0.45, P = 0.032) concentrations. After controlling for other gynecological diagnoses, a multivariate model analysis confirmed that lower serum naproxen concentrations were associated with reduced pain relief (P  = 0.038).

Conclusions: Our preliminary findings suggest that poor drug absorption contributes to ineffective pain relief in dysmenorrheic women. Future studies should explore whether malabsorption contributes to NSAID resistance for other pain conditions.
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http://dx.doi.org/10.1093/pm/pnaa133DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784249PMC
November 2020

Dysmenorrhea subtypes exhibit differential quantitative sensory assessment profiles.

Pain 2020 06;161(6):1227-1236

Department of Ob/Gyn, Northshore University HealthSystem, Evanston, IL, United States.

Women who develop bladder pain syndrome (BPS), irritable bowel syndrome, or dyspareunia frequently have an antecedent history of dysmenorrhea. Despite the high prevalence of menstrual pain, its role in chronic pelvic pain emergence remains understudied. We systematically characterized bladder, body, and vaginal mechanical sensitivity with quantitative sensory testing in women with dysmenorrhea (DYS, n = 147), healthy controls (HCs) (n = 37), and women with BPS (n = 25). Previously, we have shown that a noninvasive, bladder-filling task identified a subset of women with both dysmenorrhea and silent bladder pain hypersensitivity, and we repeated this to subtype dysmenorrhea sufferers in this study (DYSB; n = 49). DYS, DYSB, and BPS participants had lower vaginal mechanical thresholds and reported more pain to a cold stimulus during a conditioned pain modulation task and greater pelvic examination after-pain than HCs (P's < 0.05). DYSB participants also had reduced body mechanical thresholds and less conditioned pain modulation compared to HCs and DYS participants (P's < 0.05). Comparing quantitative sensory testing results among the DYS and HC groups only, provoked bladder pain was the only significant predictor of self-reported menstrual pain (r = 0.26), bladder pain (r = 0.57), dyspareunia (r = 0.39), and bowel pain (r = 0.45). Our findings of widespread sensory sensitivity in women with dysmenorrhea and provoked bladder pain, much like that observed in chronic pain, suggest a need to study the trajectory of altered mechanisms of pain processing in preclinical silent visceral pain phenotypes to understand which features convey inexorable vs modifiable risk.
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http://dx.doi.org/10.1097/j.pain.0000000000001826DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7230023PMC
June 2020

Cine MRI during spontaneous cramps in women with menstrual pain.

Am J Obstet Gynecol 2018 05 2;218(5):506.e1-506.e8. Epub 2018 Feb 2.

Department of Radiology, Northshore University HealthSystem, Evanston, IL; Department of Radiology, Pritzker School of Medicine, University of Chicago, Chicago, IL.

Background: The lack of noninvasive methods to study dysmenorrhea has resulted in poor understanding of the mechanisms underlying pain, insufficient diagnostic tests, and limited treatment options. To address this knowledge gap, we have developed a magnetic resonance imaging-based strategy for continuously monitoring the uterus in relationship to participants' spontaneous pain perception.

Objective: The study objective was to evaluate whether magnetic resonance imaging can detect real-time changes in myometrial activity during cramping episodes in women with dysmenorrhea, with a handheld squeeze bulb for pain reporting.

Study Design: Sixteen women with dysmenorrhea and 10 healthy control women both on and off their menses were evaluated with magnetic resonance imaging while not taking analgesic medication. Continuous magnetic resonance imaging was acquired using half-Fourier acquisition single-shot turbo spin echo sequence along with simultaneous reporting of pain severity with a squeeze bulb. Pearson's coefficient was used to compare results between reviewers. Proportional differences between women with dysmenorrhea and controls on/off menses were evaluated with a Fisher exact test. The temporal relationships between signal changes were evaluated with Monte Carlo simulations.

Results: Spontaneous progressive decreases in myometrial signal intensity were more frequently observed in women on their menses than in the absence of pain in the same women off their menses or participants without dysmenorrhea (P < .01). Women without reductions in myometrial signal intensity on their menses either had a history of endometriosis or were not in pain. Observations of myometrial events were consistently reported between 2 raters blinded to menstrual pain or day status (r = 0.97, P < .001). Episodes of cramping occurred either immediately before or 32-70 seconds after myometrial signal change onset (P < .05).

Conclusion: Transient decreases in myometrial uterine T2-weighted signal intensity can be reliably measured in women with menstrual pain. The directionality of signal change and temporal relationship to pain onset suggest that cramping pain may be caused by a combination of uterine pressure and hemodynamic dysfunction.
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http://dx.doi.org/10.1016/j.ajog.2018.01.035DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916049PMC
May 2018
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