Amy L Shafrir1, Elena Martel2, Stacey A Missmer3, Daniel J Clauw4, Steven E Harte4, Sawsan As-Sanie5, Christine B Sieberg6. 1. Division of Adolescent and Young Adult Medicine, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA; Boston Center for Endometriosis, Boston Children's Hospital and Brigham and Women's Hospital, Boston, MA, USA. 2. Larner College of Medicine, University of Vermont, Burlington, VT, USA. 3. Division of Adolescent and Young Adult Medicine, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA; Boston Center for Endometriosis, Boston Children's Hospital and Brigham and Women's Hospital, Boston, MA, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, MI, USA. 4. Chronic Pain and Fatigue Research Center, Department of Anesthesiology, University of Michigan, Ann Arbor, MI, USA. 5. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA. 6. Departments of Anesthesiology, Critical Care, & Pain Medicine and Psychiatry, Boston Children's Hospital, Department of Psychiatry, Harvard Medical School, Boston, MA, USA; Biobehavioral Pediatric Pain Lab, Boston Children's Hospital, Boston, MA, USA. Electronic address: christine.sieberg@childrens.harvard.edu.
Abstract
OBJECTIVE: Pelvic floor pain, abdominal wall pain, and central nervous system pain amplification can be contributing factors in chronic pelvic pain (CPP), however; limited research has investigated the association of pelvic floor, abdominal, and uterine tenderness with central nervous system pain amplification. We assessed whether pressure pain thresholds on the non-dominant thumbnail, a marker of central nervous system pain amplification, were associated with pelvic floor, abdominal, and uterine tenderness among women with endometriosis or CPP. STUDY DESIGN: We conducted a cross-sectional study among 88 females with endometriosis and/or CPP. Abdominal (6 locations), pelvic floor (6 locations) and uterine (1 location) tenderness were assessed via a standardized physical exam. Participants reported their pain levels (0-10 scale) with application of 2 kg of pressure at each area, with a pain rating of ≥4 on the 0-10 scale considered moderate to severe pain. Pain sensitivity was measured on the non-dominant thumbnail by applying discrete pressure stimuli using a previously validated protocol. RESULTS: Overall, 50% (44/88), 42% (37/88), and 58% (51/88) of participants reported high pelvic floor, abdominal, and uterine tenderness, respectively. Pressure intensities needed to elicit 'faint' and 'mild' pain were lower for participants with high vs. low pelvic floor tenderness (median intensity for 'faint' pain = 0.50 kgf/cm2(min-max:0.25-3.25) vs. 1.06(0.25-3.00), p-value = 0.006; median intensity for 'mild' pain = 2.00(0.63-4.88) vs. 2.63(0.75-6.00), p-value = 0.03). No association was observed between pressure pain sensitivity and abdominal or uterine tenderness (p > 0.11). Participants with endometriosis without pain were less likely to have high pelvic floor (22.2%), abdominal (11.1%), and uterine (25.9%) tenderness compared to participants with endometriosis with pain (63.0%, 50%, 65.2%, respectively) and participants with chronic pelvic pain (60%, 73.3%, 93.3%, respectively). CONCLUSIONS: These results suggest that high pelvic floor tenderness among women with endometriosis/CPP may be a marker of heightened pain sensitivity suggestive of central nervous system pain amplification and may impact treatment response. Future research should examine whether this clinical phenotype predicts response to medical and behavioral treatments (e.g, anti-convulsants, behavioral therapy, Physical Therapy).
OBJECTIVE: Pelvic floor pain, abdominal wall pain, and central nervous system pain amplification can be contributing factors in chronic pelvic pain (CPP), however; limited research has investigated the association of pelvic floor, abdominal, and uterine tenderness with central nervous system pain amplification. We assessed whether pressure pain thresholds on the non-dominant thumbnail, a marker of central nervous system pain amplification, were associated with pelvic floor, abdominal, and uterine tenderness among women with endometriosis or CPP. STUDY DESIGN: We conducted a cross-sectional study among 88 females with endometriosis and/or CPP. Abdominal (6 locations), pelvic floor (6 locations) and uterine (1 location) tenderness were assessed via a standardized physical exam. Participants reported their pain levels (0-10 scale) with application of 2 kg of pressure at each area, with a pain rating of ≥4 on the 0-10 scale considered moderate to severe pain. Pain sensitivity was measured on the non-dominant thumbnail by applying discrete pressure stimuli using a previously validated protocol. RESULTS: Overall, 50% (44/88), 42% (37/88), and 58% (51/88) of participants reported high pelvic floor, abdominal, and uterine tenderness, respectively. Pressure intensities needed to elicit 'faint' and 'mild' pain were lower for participants with high vs. low pelvic floor tenderness (median intensity for 'faint' pain = 0.50 kgf/cm2(min-max:0.25-3.25) vs. 1.06(0.25-3.00), p-value = 0.006; median intensity for 'mild' pain = 2.00(0.63-4.88) vs. 2.63(0.75-6.00), p-value = 0.03). No association was observed between pressure pain sensitivity and abdominal or uterine tenderness (p > 0.11). Participants with endometriosis without pain were less likely to have high pelvic floor (22.2%), abdominal (11.1%), and uterine (25.9%) tenderness compared to participants with endometriosis with pain (63.0%, 50%, 65.2%, respectively) and participants with chronic pelvic pain (60%, 73.3%, 93.3%, respectively). CONCLUSIONS: These results suggest that high pelvic floor tenderness among women with endometriosis/CPP may be a marker of heightened pain sensitivity suggestive of central nervous system pain amplification and may impact treatment response. Future research should examine whether this clinical phenotype predicts response to medical and behavioral treatments (e.g, anti-convulsants, behavioral therapy, Physical Therapy).
Authors: Jacqueline V Aredo; Katrina J Heyrana; Barbara I Karp; Jay P Shah; Pamela Stratton Journal: Semin Reprod Med Date: 2017-01-03 Impact factor: 1.303
Authors: R Rolke; R Baron; C Maier; T R Tölle; - D R Treede; A Beyer; A Binder; N Birbaumer; F Birklein; I C Bötefür; S Braune; H Flor; V Huge; R Klug; G B Landwehrmeyer; W Magerl; C Maihöfner; C Rolko; C Schaub; A Scherens; T Sprenger; M Valet; B Wasserka Journal: Pain Date: 2006-05-11 Impact factor: 6.961
Authors: Hugh S Taylor; G David Adamson; Michael P Diamond; Steven R Goldstein; Andrew W Horne; Stacey A Missmer; Michael C Snabes; Eric Surrey; Robert N Taylor Journal: Int J Gynaecol Obstet Date: 2018-05-28 Impact factor: 3.561
Authors: Vânia Meira Siqueira-Campos; Mariana Siqueira Campos de Deus; Omero Benedicto Poli-Neto; Julio Cesar Rosa-E-Silva; José Miguel de Deus; Délio Marques Conde Journal: Int J Womens Health Date: 2022-02-18