IPPS 2012 Program Book PDF

Basics Course for General Gynecologists, Physical Therapists, Nurses and Residents Thursday, October 18, 2012 2012
IPPS Annual Fall Meeting on Pelvic Pain: Merging Science and Clinical Care for Pelvic Pain Disorders October 19 20, 2012 The Palmer House Hilton Chicago, Illinois IPPS Post-Conference Course Explain Pain Sunday, October 21, 2012 Featuring guest lecturer Lorimer Moseley PhD, B.App.Sc.(Phty)(hons)
PROGRAM COMMITTEE: Stephanie Prendergast, MPT Program Committee Chair Sawsan As-Sanie, MD, MPH Basics Course Chair Sarah Fox, MD Georgine Lamvu, MD, MPH, FACOG Amy Stein, MPT, BCB-PMD Frank Tu, MD, MPH
PROGRAM BOOK
Welcome to the 2012 IPPS Annual Fall Meeting
IPPS
INTERNATIONAL PELVIC PAIN SOCIETY 2012 IPPS Annual Fall Meeting on Pelvic Pain: Merging Science and Clinical Care for Pelvic Pain Disorders October 19 20, 2012 Chicago, Illinois
President Georgine Lamvu, MD, MPH, welcomes you to the 2012 IPPS Annual Fall Meeting on Pelvic Pain.
PROGRAM CHAIRS
Stephanie Prendergast, MPT
Sawsan As-Sanie, MD, MPH
Georgine Lamvu, MD, MPH
International Pelvic Pain Society
Schedule-at-a-Glance
THURSDAY, OCTOBER 18
7:00 a.m. 7:50 a.m. Continental Breakfast Location: Adams Foyer Registration/Information Desk Open Location: Adams Foyer Exhibit Hall Open Location: Monroe Ballroom Welcome from the Basics Course Chair Introduction to the Physiology of Chronic Pain Q&A Evaluation of the Chronic Pelvic Pain Patient Q&A Break Location: Monroe Ballroom Diagnosis and Treatment of Gynecologic Causes of Chronic Pelvic Pain Q&A Diagnosis and Treatment of Vulvar Pain Q&A Diagnosis and Treatment of Abdominal and Pelvic Peripheral Neuropathies Discussion Lunch (on your own) Diagnosis and Treatment of Urologic Causes of Chronic Pelvic Pain Q&A Diagnosis and Treatment of Musculoskeletal Causes of Chronic Pelvic Pain Q&A Diagnosis and Treatment of Functional Bowel Disorders Discussion Break Location: Monroe Ballroom Medical and Behavioral Therapies for Chronic Pain Q&A
IPPS
7:00 a.m. 5:00 p.m.
10:00 a.m. 5:30 p.m. 8:00 a.m. 8:05 a.m. 8:05 a.m. 8:35 a.m. 8:35 a.m. 8:40 a.m. 8:40 a.m. 9:50 a.m. 9:50 a.m. 10:00 a.m. 10:00 a.m. 10:20 a.m. 10:20 a.m. 11:00 a.m. 11:00 a.m. 11:05 a.m. 11:05 a.m. 11:35 a.m. 11:35 a.m. 11:40 a.m. 11:40 a.m. 12:10 p.m. 12:10 p.m. 12:20 p.m. 12:20 p.m. 1:20 p.m. 1:20 p.m. 1:50 p.m. 1:50 p.m. 1:55 p.m. 1:55 p.m. 2:35 p.m. 2:35 p.m. 2:40 p.m. 2:40 p.m. 3:10 p.m. 3:10 p.m. 3:20 p.m. 3:20 p.m. 3:40 p.m. 3:40 p.m. 4:20 p.m. 4:20 p.m. 4:25 p.m. 4:25 p.m. 5:00 p.m. 6:00 p.m. 9:00 p.m.
Psychological Aspects of Living with Chronic Pelvic Pain: Evaluation and Treatment of Comorbid Anxiety and Depression IPPS Board of Directors Meeting Location: The Hancock Parlor
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FRIDAY, OCTOBER 19
7:00 a.m. 7:50 a.m. 7:00 a.m. 5:30 p.m. 7:00 a.m. 7:30 p.m. 7:50 a.m. 8:00 a.m. 8:00 a.m. 8:10 a.m. 8:10 a.m. 9:05 a.m. 9:05 a.m. 9:45 a.m. 9:45 a.m. 10:25 a.m. 10:25 a.m. 10:45 a.m. 10:45 a.m. 11:15 a.m. 11:15 a.m. 12:30 p.m. 12:30 p.m. 2:00 p.m. 2:00 p.m. 3:25 p.m. 3:25 p.m. 3:55 p.m. 3:55 p.m. 5:10 p.m. 5:15 p.m. 7:00 p.m. Continental Breakfast in Exhibit Hall Location: Monroe Ballroom Registration/Information Desk Open Location: Adams Foyer Exhibit Hall Open Location: Monroe Ballroom Welcome from the Scientific Program Chair Presidential Address James E. Carter Memorial Lecture: An Update on the Pathogenesis and Treatment of Endometriosis Innovative Injection Therapies for Pain Syndromes of Pelvic Floor Fascia The Acute Anus Discussion Break & Poster Session I in Exhibit Hall (Odd numbered posters) Location: Monroe Ballroom Clinical Updates and Latest Research Lunch (on your own) Translational Science Symposia Part I Break & Poster Session I in Exhibit Hall (Odd numbered posters) Location: Monroe Ballroom Translational Science Symposia Part II Welcome Reception & Poster Session II in Exhibit Hall (Even numbered posters) Location: Monroe Ballroom
IPPS
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SATURDAY, OCTOBER 20
6:15 a.m. 7:15 a.m. Yoga Class Location: Chicago Room Continental Breakfast in Exhibit Hall Location: Monroe Ballroom Registration/Information Desk Open Location: Adams Foyer Exhibit Hall Open Location: Monroe Ballroom Welcome and Announcements
IPPS
7:00 a.m. 7:50 a.m.
6:00 a.m. 5:30 p.m.
7:00 a.m. 11:00 a.m. 7:50 a.m. 8:00 a.m. 8:00 a.m. 8:55 a.m. 8:55 a.m. 9:35 a.m. 9:35 a.m. 10:15 a.m. 10:15 a.m. 10:30 a.m. 10:30 a.m. 11:00 a.m. 11:00 a.m. 11:40 a.m. 11:40 a.m. 12:10 p.m. 12:10 p.m. 12:25 p.m. 12:25 p.m. 1:40 p.m. 1:40 p.m. 2:20 p.m. 2:20 p.m. 3:00 p.m. 3:00 p.m. 3:10 p.m. 3:10 p.m. 3:30 p.m. 3:30 p.m. 4:10 p.m. 4:10 p.m. 4:40 p.m. 4:40 p.m. 5:00 p.m. 5:00 p.m. 5:10 p.m. 5:10 p.m. 5:30 p.m.
C. Paul Perry Memorial Lecture: Rethinking Pelvic Pain Lessons From Two Decades of Explaining Pain Simultaneous Pelvic Floor Physical Therapy and Functional Brain Imaging: Applications to Mind-Body Interactions in Chronic Pain Optimizing Organ-Related Pelvic Pain: Making a Difference With Visceral Manipulation Discussion Break & Poster Session II in Exhibit Hall (Even numbered posters) Location: Monroe Ballroom Opioids: Part of a Polymoidal Pain Treatment: Which Patent, Which Drug, and Patient Monitoring Hysterectomy Differential Diagnosis Discussion Lunch (on your own) The Management of Chronic Pelvic Pain: Neuromodulation and Other Novel Techniques Nutritional Considerations in Treating Patients with Pain Discussion Break Location: Adams Foyer Medical Management of Sexual Dysfunction/Pelvic Pain Leveraging the Intersection Between Sexuality and Chronic Pelvic Pain in Treatment Design Discussion Closing Remarks Annual Business Meeting Location: Adams Ballroom
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SUNDAY, OCTOBER 21
7:00 a.m. 7:50 a.m. Continental Breakfast Location: Adams Foyer Registration/Information Desk Open Location: Adams Foyer What is Pain? Conceptual Change in Action What Modulates Pain? Break Location: Adams Foyer When Pain Persists Lunch (on your own) The Cortical Body Matrix in Health and Disease Break Location: Adams Foyer Explaining Pain
IPPS
7:00 a.m. 5:00 p.m. 8:00 a.m. 9:00 a.m. 9:00 a.m. 10:30 a.m. 10:30 a.m. 10:50 a.m. 10:50 a.m. 12:50 p.m. 12:50 p.m. 1:45 p.m. 1:45 p.m. 3:15 p.m. 3:15 p.m. 3:30 p.m. 3:30 p.m. 5:00 p.m.
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Table of Contents
IPPS
Page # Schedule-at-a-Glance................................................................. 1 Course Description..................................................................... 6 Needs Statement ...................................................................... 6 Objectives ................................................................................. 6 Accreditation Statement ............................................................ 6 Conflict Resolution Statement.................................................... 7 General Disclaimer ..................................................................... 7 Special Assistance ..................................................................... 7 Thank You to Promotional Partners ............................................ 8 Thank You to Exhibitors ............................................................. 9 IPPS Board of Directors .............................................................. 10 Faculty Listing ........................................................................... 11 Program Schedule ..................................................................... 13 Biosketches ............................................................................... 22 Abstracts .................................................................................. 33 Presentations ............................................................................ 77
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Course Description
IPPS
Course Description The 20th Annual Scientific Meeting has been designed to provide a thorough overview on the evaluation and management of chronic pelvic pain disorders. The meeting emphasizes the multidisciplinary and collaborative approach to the management of chronic pelvic pain. Presentations will combine research findings and clinical care recommendations important to the care of women and men afflicted by chronic pelvic pain. For providers who need a more broad understanding of musculoskeletal, neurological, and visceral causes of pelvic pain, and available multidimensional treatments, additional workshops will provide a more basic overview of the evaluation of chronic pelvic pain. Target Audience Gynecologists, physical therapists, urologists, primary care physicians, nurses, surgeons, pain management physicians, psychologists, neurologists, basic science researches Needs Statement It is known that millions of patients suffer with disorders that cause chronic pelvic pain. The social, psychological and financial costs associated with treatments of these disorders are enormous. Yet, less than 10% of patients are receiving care from a provider trained in management of chronic pain disorders. Many patients endure being misdiagnosed or receiving inappropriate treatment because of the practitioners lack of knowledge on this subject. Unless practitioners and researchers are educated about factors that affect patient care, treatment outcomes and research in chronic pelvic pain disorders, it is likely that patients with chronic pelvic pain will continue to lack appropriate treatment in the future. Furthermore, without exchange of clinical and research information across all disciplines encompassing the treatment of chronic pelvic pain, advances in treatment options for these patients will not be possible. Recently, a study was published stating that less than 10 % of medical students are prepared to treat pain patients when graduating from medical school. This conference serves as a sit for post-graduate education on complex topics. Course Objectives At the completion of this course, attendees should be able to: Describe the latest evidence of evaluation and surgical management of endometriosis Interpret the clinical updates on Interstitial Cystitis, Vulvodynia, Irritable Bowel Syndrome, Anal Pain Recognize the role the central nervous system plays in CPP Integrate exposure to new treatment techniques for CPP Integrate improved knowledge of how to evaluate and treat patients with sexual dysfunction
Accreditation Statement This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the American College of Legal Medicine and the International Pelvic Pain Society. The American College of Legal Medicine is accredited by the ACCME to provide continuing medical education for physicians.
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Course Description
IPPS
The American College of Legal Medicine designates this live activity for a maximum of 28.50 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Conflict Resolution Statement The American College of Legal Medicine CME Office has reviewed this activitys speaker and planner disclosures and resolved all identified conflicts of interest, if applicable. CE Accreditation Statement The Illinois Chapter Continuing Education Committee has approved this course according to the Criteria for Approval of Continuing Education offerings established by the Illinois Physical Therapy Association. The 2012 IPPS Annual Fall Meeting on Pelvic Pain: Merging Science and Clinical Care for Pelvic Pain Disorders, has been accredited for a maximum of 28.50 Continuing Education hours. Attendees who reside in a state other than Illinois should inquire with their state board regarding acceptance of Illinois accreditation. General Disclaimer The statements and opinions contained in this program are solely those of the individual authors and contributors and not of the IPPS. The appearance of the advertisements is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality, or safety. The content of this publication may contain discussion of offlabel uses of some of the agents mentioned. Please consult the prescribing information for full disclosure of approved uses. The IPPS disclaims responsibility for any injury to persons or property resulting from any ideas or products referred to in the abstracts or advertisements. Special Assistance We encourage participation by all individuals. If you have a disability, advance notification of any special needs will help us better serve you. Call (847) 517-7225 if you require special assistance to fully participate in the meeting. Copyright Notice Individuals may print out single copies of abstracts or slides contained in this publication for personal, non-commercial use without obtaining permission from the author or the IPPS. Permission from both the IPPS and the author must be obtained when making multiple copies for personal or educational use, for reproduction for advertising or promotional purposes, for creating new collective works, for resale or for all other uses. Filming/Photography Statement No attendee/visitor at the IPPS 2012 annual meeting may record, film, tape, photograph, interview, or use any other such media during any presentation, display, or exhibit without the express, advance approval of the IPPS Executive Director. This policy applies to all IPPS members, non-members, guests, and exhibitors, as well as members of the print, online, or broadcast media.
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Thank You to Our Promotional Partners
IPPS
Thank You to Our 2012 Promotional Partner Gold Level Neogyn, Inc.
Thank You to Our 2012 Contributor KevMed, LLC
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Thank You to Our Exhibitors
IPPS
Thank You to Our 2012 Exhibitors

Abbott Laboratories Athletico Physical Therapy Chicagoland Pelvic Floor Research Consortium Current Medical Technologies, Inc. Endometriosis Association Innovation Compounding Interstitial Cystitis Association Neogyn, Inc. Section On Womens Health, APTA The Barral Institute The COMMANDO Group, Inc. Vital Health Institute
Thank You to Our 2012 Educational Grant Providers

Abbott Laboratories Allergan, Inc. Endo
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2012 2013 Board of Directors

2012 2013 IPPS Board of Directors
OFFICERS Chairman of the Board Fred M. Howard, MD, MS President Georgine Lamvu, MD, MPH Vice President Stephanie Prendergast, MPT Treasurer Frank Tu, MD, MPH Secretary Sarah Fox, MD Past President Maurice K. Chung, RPh, MD BOARD OF DIRECTORS International Director Juan Diego Villegas-Echeverri, MD Directors Sawsan As-Sanie, MD, MPH Charles W. Butrick, MD Elizabeth Dee Hartmann, PT, DPT Michael Hibner, MD, PhD Andrea Rapkin, MD Howard T. Sharp, MD Amy Stein, MPT, BCB-PMD Denniz Zolnoun, MD, MPH Advisory Board Members Stanley J. Antolak, Jr., MD James F. Carter, MD, FACOG Margaret A. Coffman, MSN, ARNP Beverly J. Collett, MD Melissa Kubic, PT Susan Parker, PT John C. Slocumb, MD, SMH Jerome M. Weiss, MD Executive Director Wendy J. Weiser Managing Director Sue OSullivan Associate Director Pam Murphy
IPPS
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Faculty Listing
Faculty Listing
Sawsan As-Sanie, MD, MPH University of Michigan Ann Arbor, MI Erkut Attar, MD Istanbul University Medical Center Istanbul, Turkey Robert L. Barkin, PharmD University Pain Centers Rush Oak Park Hospital Oak Park, IL Hal Blatman, MD Blatman Pain Clinic Cincinnati, Ohio Mario Castellanos, MD Dignity Health St. Josephs Hospital and Medical Center Phoenix, AZ Thomas C. Chelimsky, MD Medical College of Wisconsin Milwaukee, WI Melissa Farmer, PhD McGill University Montreal, Quebec, Canada Colleen Fitzgerald, MD Rehabilitation Institute of Chicago Chicago, IL Sarah M. Fox, MD Women & Infants Hospital of Rhode Island Providence, RI Nel E. Gerig, MD The Pelvic Solutions Center Denver, CO Elizabeth Dee Hartmann, PT, DPT Dee Hartmann Physical Therapy for Women Chicago, IL Dana Hayden, MD, MPH Loyola University Medical Center Chicago, IL Kevin Hellman, PhD North Shore University Health System Evanston, IL
IPPS
Heather Howard, MBA, PhD, ACS The Center for Sexual Health and Rehabilitation San Francisco, CA Barry K. Jarnagin, MD Center for Pelvic Health Franklin, TN Susan Kellogg-Spadtt, CRNP, PhD The Pelvic and Sexual Health Institute Philadelphia, PA Daniel Kirages, DPT, OCS, FAAOMPT University of Southern California Los Angeles, CA Brandi Kirk, PT, BCB-PMD Kirk Center for Healthy Living Lockport, IL Jason Kutch, PhD University of Southern California Los Angeles, CA Georgine Lamvu, MD, MPH Advanced Minimally Invasive Surgery and Gynecology Specialists Orlando, FL Stacy T. Lindau, MD, MAPP The University of Chicago Chicago, IL Geeta Maker-Clark, MD Northshore Medical Group Evanston, IL
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Faculty Listing
Joseph M. Maurice, MD Rush University Medical Center Chicago, IL Lorimer Moseley PhD, B.App.Sc.(Phty)(hons) University of South Australia Adelaide, Australia Kenneth Peters, MD William Beaumont Hospital Royal Oak, MI Stephanie Prendergast, MPT Pelvic Health & Rehabilitation Center San Francisco, CA Andrea Rapkin, MD David Geffen School of Medicine at UCLA Los Angeles, CA Ja Hyun Shin, MD Albert Einstein College of Medicine Bronx, NY Devon M. Shuchman, MD University of Michigan Ann Arbor, MI Matthew T. Siedhoff, MD, MSCR University of North Carolina Chapel Hill, NC
IPPS
Alain Watier, MD Centre Hospitalier Universitaire Sherbrooke Sherbrooke, Quebec, Canada Gail Wetzler, RPT, CVMI Wetzler Integrative Physical Therapy Center Newport Beach, CA Kathryn M. Witzeman, MD Denver Health Medical Center Denver, CO Denniz M. Zolnoun, MD, MPH University of North Carolina Chapel Hill, NC
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Program Schedule
IPPS
2012 IPPS Annual Fall Meeting Program Schedule

*All sessions will be located in the Adams Ballroom unless otherwise noted *Speakers and times are subject to change Thursday, October 18, 2012
Basics Course Case Studies for General Gynecologists, Physical Therapists, Nurses and Residents
7:00 a.m. 7:50 a.m. 7:00 a.m. 5:00 p.m. Continental Breakfast Location: Adams Foyer Registration/Information Desk Open Location: Adams Foyer Exhibit Hall Open Location: Monroe Ballroom
10:00 a.m. 5:30 p.m.
8:00 a.m. 8:05 a.m.
Welcome from the Basics Course Chair Sawsan As-Sanie, MD, MPH University of Michigan Ann Arbor, MI Introduction to the Physiology of Chronic Pain Thomas C. Chelimsky, MD Medical College of Wisconsin Milwaukee, WI Q&A Evaluation of the Chronic Pelvic Pain Patient Part I: Essential Elements of the History Kathryn M. Witzeman, MD Denver Health Medical Center Denver, CO Q&A Part II: Essential Elements of the Gynecologic Exam Ja Hyun Shin, MD Albert Einstein College of Medicine Bronx, NY
8:05 a.m. 8:35 a.m.
8:35 a.m. 8:40 a.m. 8:40 a.m. 9:50 a.m. 8:40 a.m. 9:00 a.m.
9:00 a.m. 9:05 a.m. 9:05 a.m. 9:25 a.m.
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Program Schedule
Thursday, October 18, 2012 9:25 a.m. 9:30 a.m. 9:30 a.m. 9:50 a.m. Q&A
IPPS
Part III: Essential Elements of the Musculoskeletal Exam Elizabeth Dee Hartmann, PT, DPT Dee Hartmann Physical Therapy for Women Chicago, IL Q&A Break Location: Monroe Ballroom Diagnosis and Treatment of Gynecologic Causes of Chronic Pelvic Pain Matthew T. Siedhoff, MD, MSCR University of North Carolina Chapel Hill, NC Q&A Diagnosis and Treatment of Vulvar Pain Frank Tu, MD, MPH North Shore University Health System Evanston, IL Q&A Diagnosis and Treatment of Abdominal and Pelvic Peripheral Neuropathies Mario Castellanos, MD Dignity Health Phoenix, AZ Discussion Lunch (on your own) Diagnosis and Treatment of Urologic Causes of Chronic Pelvic Pain Barry K. Jarnagin, MD Center for Pelvic Health Franklin, TN Q&A
9:50 a.m. 10:00 a.m. 10:00 a.m. 10:20 a.m.
10:20 a.m. 11:00 a.m.
11:00 a.m. 11:05 a.m. 11:05 a.m. 11:35 a.m.
11:35 a.m. 11:40 a.m. 11:40 a.m. 12:10 p.m.
12:10 p.m. 12:20 p.m. 12:20 p.m. 1:20 p.m. 1:20 p.m. 1:50 p.m.
1:50 p.m. 1:55 p.m.
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Program Schedule
Thursday, October 18, 2012 1:55 p.m. 2:35 p.m.
IPPS
Diagnosis and Treatment of Musculoskeletal Causes of Chronic Pelvic Pain Brandi Kirk, PT, BCB-PMD Kirk Center for Healthy Living Lockport, IL Colleen Fitzgerald, MD Rehabilitation Institute of Chicago Chicago, IL Q&A Diagnosis and Treatment of Functional Bowel Disorders Alain Watier, MD Centre Hospitalier Universitaire Sherbrooke Sherbrooke, Quebec, Canada Discussion Break Location: Monroe Ballroom Medical and Behavioral Therapies for Chronic Pain Devon M. Shuchman, MD University of Michigan Ann Arbor, MI Q&A Psychological Aspects of Living with Chronic Pelvic Pain: Evaluation and Treatment of Comorbid Anxiety and Depression Sarah M. Fox, MD Women & Infants Hospital of Rhode Island Providence, RI IPPS Board of Directors Meeting Location: The Hancock Parlor
2:35 p.m. 2:40 p.m. 2:40 p.m. 3:10 p.m.
3:10 p.m. 3:20 p.m. 3:20 p.m. 3:40 p.m.
3:40 p.m. 4:20 p.m.
4:20 p.m. 4:25 p.m. 4:25 p.m. 5:00 p.m.
6:00 p.m. 9:00 p.m.
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Program Schedule
Friday, October 19, 2012 7:00 a.m. 7:50 a.m. Continental Breakfast in Exhibit Hall Location: Monroe Ballroom Exhibit Hall Open Location: Monroe Ballroom Registration/Information Desk Open Location: Adams Foyer
IPPS
7:00 a.m. 7:00 p.m.
7:00 a.m. 5:30 p.m.
7:50 a.m. 8:00 a.m.
Welcome from the Scientific Program Chair Stephanie Prendergast, MPT Pelvic Health & Rehabilitation Center San Francisco, CA Presidential Address Georgine Lamvu, MD, MPH Advanced Minimally Invasive Surgery and Gynecology Specialists Orlando, FL James E. Carter Memorial Lecture: An Update on the Pathogenesis and Treatment of Endometriosis Erkut Attar, MD Istanbul University Medical Center Istanbul, Turkey Innovative Injection Therapies for Pain Syndromes of Pelvic Floor Fascia Hal Blatman, MD Blatman Pain Clinic Cincinnati, Ohio The Acute Anus Dana Hayden, MD, MPH Loyola University Medical Center Chicago, IL Discussion Break & Poster Session I in Exhibit Hall (Odd numbered posters) Location: Monroe Ballroom
8:00 a.m. 8:10 a.m.
8:10 a.m. 9:05 a.m.
9:05 a.m. 9:45 a.m.
9:45 a.m. 10:25 a.m.
10:25 a.m. 10:45 a.m. 10:45 a.m. 11:15 a.m.
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Program Schedule
Friday, October 19, 2012 11:15 a.m. 12:30 p.m. 11:15 a.m. 11:35 a.m. Clinical Updates and Latest Research Irritable Bowel Syndrome Alain Watier, MD Centre Hospitalier Universitaire Sherbrooke Sherbrooke, Quebec, Canada Vulvodynia Andrea Rapkin, MD David Geffen School of Medicine at UCLA Los Angeles, CA Interstitial Cystitis Nel E. Gerig, MD The Pelvic Solutions Center Denver, CO Discussion
IPPS
11:35 a.m. 11:55 a.m.
11:55 a.m. 12:15 p.m.
12:15 p.m. 12:30 p.m. 12:30 p.m. 2:00 p.m. 2:00 p.m. 3:25 p.m. 2:00 p.m. 2:40 p.m.
Lunch (on your own) Translational Science Symposia - Part 1 Visceral Pain Models Kevin Hellman, PhD North Shore University Health System Evanston, IL Vulvar Pain Mechanisms Melissa Farmer, PhD McGill University Montreal, Quebec, Canada Discussion Break & Poster Session I in Exhibit Hall (Odd numbered posters) Location: Monroe Ballroom Translational Science Symposia - Part 2 Dyspareunia in Women With Cancer Stacy T. Lindau, MD, MAPP The University of Chicago Chicago, IL
2:40 p.m. 3:10 p.m.
3:10 p.m. 3:25 p.m. 3:25 p.m. 3:55 p.m.
3:55 p.m. 5:10 p.m. 3:55 p.m. 4:25 p.m.
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Program Schedule
Friday, October 19, 2012 4:25 p.m. 4:55 p.m. Neurobiology of Complex Painful Dysautonomias Thomas C. Chelimsky, M.D. Medical College of Wisconsin Milwaukee, WI Discussion Welcome Reception & Poster Session II in Exhibit Hall (Even numbered posters) Location: Monroe Ballroom
IPPS
4:55 p.m. 5:10 p.m. 5:15 p.m. 7:00 p.m.
Saturday, October 20, 2012 6:15 a.m. 7:15 a.m. Yoga Class Location: Chicago Room Continental Breakfast in Exhibit Hall Location: Monroe Ballroom Exhibit Hall Open Location: Monroe Ballroom Registration/Information Desk Open Location: Adams Foyer
7:00 a.m. 7:50 a.m.
7:00 a.m. 11:00 a.m.
6:00 a.m. 5:30 p.m.
7:50 a.m. 8:00 a.m.
Welcome and Announcements Stephanie Prendergast, MPT Pelvic Health & Rehabilitation Center San Francisco, CA C. Paul Perry Memorial Lecture: Rethinking Pelvic Pain Lessons From Two Decades of Explaining Pain Lorimer Moseley PhD, B.App.Sc.(Phty)(hons) University of South Australia Adelaide, Australia Simultaneous Pelvic Floor Physical Therapy and Functional Brain Imaging: Applications to Mind-Body Interactions in Chronic Pain Daniel Kirages, DPT, OCS, FAAOMPT University of Southern California Los Angeles, CA Jason Kutch, PhD University of Southern California Los Angeles, CA
8:00 a.m. 8:55 a.m.
8:55 a.m. 9:35 a.m.
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Program Schedule
Saturday, October 20, 2012 9:35 a.m. 10:15 a.m.
IPPS
Optimizing Organ-Related Pelvic Pain: Making A Difference With Visceral Manipulation Gail Wetzler, RPT, CVMI Wetzler Integrative Physical Therapy Center Newport Beach, CA Discussion Break & Poster Session II in Exhibit Hall (Even numbered posters) Location: Monroe Ballroom Opioids: Part of a Polymoidal Pain Treatment: Which Patent, Which Drug, and Patient Monitoring Robert L. Barkin, PharmD University Pain Centers Rush Oak Park Hospital Oak Park, IL Hysterectomy Differential Diagnosis Joseph M. Maurice, MD Rush University Medical Center Chicago, IL Discussion Lunch (on your own) The Management of Chronic Pelvic Pain: Neuromodulation and Other Novel Techniques Kenneth Peters, MD William Beaumont Hospital Royal Oak, MI Nutritional Considerations in Treating Patients With Pain Geeta Maker-Clark, MD Northshore Medical Group Evanston, IL Discussion Break Location: Adams Foyer
10:15 a.m. 10:30 a.m. 10:30 a.m. 11:00 a.m.
11:00 a.m. 11:40 a.m.
11:40 a.m. 12:10 p.m.
12:10 p.m. 12:25 p.m. 12:25p.m. 1:40 p.m. 1:40 p.m. 2:20 p.m.
2:20 p.m. 3:00 p.m.
3:00 p.m. 3:10 p.m. 3:10 p.m. 3:30 p.m.
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Program Schedule
Saturday, October 20, 2012 3:30 p.m. 4:10 p.m. Medical Management of Sexual Dysfunction/Pelvic Pain Susan Kellogg-Spadtt, CRNP, PhD The Pelvic and Sexual Health Institute Philadelphia, PA
IPPS
4:10 p.m. 4:40 p.m.
Leveraging the Intersection Between Sexuality and Chronic Pelvic Pain in Treatment Design Heather Howard, MBA, PhD, ACS The Center for Sexual Health and Rehabilitation San Francisco, CA Discussion Closing Remarks Annual Business Meeting Location: Adams Ballroom
4:40 p.m. 5:00 p.m. 5:00p.m. 5:10 p.m. 5:10 p.m. 5:30 p.m.
Sunday, October 21, 2012 7:00 a.m. 5:00 p.m. Registration/Information Desk Open Location: Adams Foyer Continental Breakfast Location: Adams Foyer
7:00 a.m. 7:50 a.m.
8:00 a.m. 9:00 a.m. 9:00 a.m. 10:30 a.m.
What Is Pain? Conceptual Change in Action What Modulates Pain? Nociception Versus Pain Protection Versus Symptom The Representing Brain (Or, How Does It Happen?) Peripheral Sensitisation Break Location: Adams Foyer When Pain Persists Humoral Sensitivity Central Sensitisation Sensitivity and Disinhibition Lunch (on your own)
10:30 a.m. 10:50 a.m. 10:50 a.m. 12:50 p.m.
12:50 p.m. 1:45 p.m.
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Program Schedule
Sunday, October 21, 2012 1:45 p.m. 3:15 p.m.
IPPS
The Cortical Body Matrix in Health and Disease Imprecise Body Maps - Or 'Clinical Manifestations of Disinhibition' Break Location: Adams Foyer Explaining Pain Principles of Conceptual Change Integrating Modern Pain Science with Clinical Assessment and Management
3:15 p.m. 3:30 p.m.
3:30 p.m. 5:00 p.m.
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Speaker Biosketches
Speaker Biosketches
(in alphabetical order)
IPPS
Sawsan As-Sanie, MD, MPH, is an assistant professor and the director of the Minimally Invasive Gynecology Program and Fellowship in the Department of Obstetrics and Gynecology at the University of Michigan. She is also the director the University of Michigan Endometriosis Center. Dr. As-Sanie received her medical degree from the Johns Hopkins School of Medicine in 1998 and completed her residency in obstetrics and gynecology at MetroHealth Medical Center and the Cleveland Clinic Foundation in 2002. Following residency, she completed a three year clinical and research fellowship in advanced laparoscopy and chronic pelvic pain at the University of North Carolina. During this time, she also received her MPH in epidemiology. Dr. As-Sanie is dedicated to the care of women with complex gynecologic conditions, including the treatment of women with various chronic pain disorders. She has a particular interest in endometriosis, as well as minimally invasive surgery techniques including robotic surgery. Dr. As-Sanie is actively engaged in numerous research studies. Her research interests are aimed at defining the underlying mechanisms involved in the initiation and maintenance of pelvic pain disorders, with a focus on endometriosis-associated chronic pelvic pain. She is the principal investigator for several studies evaluating the neurobiological mechanism of pain processing in endometriosis-associated chronic pelvic pain. Dr. As-Sanie has spoken at many national and international conferences on pelvic pain and endometriosis, and has authored and co-authored research articles published in peer reviewed literature. Erkut Attar, MD, is a professor at Istanbul University in the Department of Reproductive Endocrinology and Infertility and the Department of Obstetrics and Gynecology. In 2001, Dr. Attar received a certificate of IVF in obstetrics and gynecology from the Ministry of Health. Dr. Attar graduated in 1986 from Istanbul University Cerrahpasa. He completed a fellowship in 1995 at Yale University School of Medicine in New Haven, Connecticut. From 1995 1999, Dr. Attar was a research assistant at Istanbul University in the Department of Obstetrics and Gynecology and the Department of Reproductive Endocrinology and Infertility. In 2001, Dr. Attar was a doctoral student in the Department of Molecular Medicine at Istanbul University Institute of Health Sciences. From 2005 2006, Dr. Attar was a visiting scholar at Northwestern University Feinberg School of Medicine in the Division of Reproductive Research. Robert L. Barkin, MBA, PharmD, FCP, DAAPM, DABFE, DABFM, DABPS, is professor of anesthesiology, pharmacology and family medicine at Rush University Medical Center in Chicago, Illinois. He is also a clinical pharmacologist in a collaborative practice with five physician pain specialists at the NorthShore University Health System Department of Anesthesiology Pain Centers of Skokie and Evanston Hospitals in Illinois. Dr. Barkins extensive practice is both outpatient and in-patient. Dr. Barkin designs patient-specific pharmacotherapeutic treatment plans. Following graduation from St. Louis College of Pharmacy, Dr. Barkin earned a Master of Business Administration degree in healthcare administration from DePaul University in Chicago, Illinois. He then earned his Doctor of Clinical Pharmacy degree from Purdue University in West Lafayette, Indiana.
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Speaker Biosketches
IPPS
Dr. Barkin is the author of more than 150 abstracts, CD-Rom programs, textbook chapters and peer reviewed articles. He is associate editor for the American Journal of Therapeutics He also serves as a reviewer for 28 peer-reviewed journals and on the Editorial Board of nine peer reviewed journals. He is frequently invited to speak on a wide variety of topics at both national and international conferences and seminars. Dr. Barkin is a Diplomate of the American Academy of Pain Management, a Fellow of the American College of Clinical Pharmacology, Diplomate of American Board of Forensic Medicine, Examiners, Psychologic Specialties in Psychopharmacology. Dr. Barkin was granted scientific status with the American Academy of Pain Medicine. Hal S. Blatman, MD, is the founder and medical director of the Blatman Pain Clinic in Cincinnati, Ohio, a nationally recognized specialist in myofascial pain, and co-author of The Art of Body Maintenance: Winners' Guide to Pain Relief, a reference for treating myofascial pain, from migraine headaches to plantar fasciitis. He is credentialed in pain management, occupational and environmental medicine, and integrative holistic medicine. After receiving his medical degree from the Medical College of Pennsylvania in 1980, Dr. Blatman completed two years of training in orthopedic surgery. He later studied ergonomics and toxicology during his residency in occupational and environmental medicine at the University of Cincinnati Medical Center. In the early 1990s, he studied with the late Dr. Janet Travell, pain physician to former President Kennedy. Dr. Blatman currently leads a team that specializes in the holistic and comprehensive rehabilitation and treatment of pain, ligament and tendon injury, fibromyalgia and chronic fatigue syndrome. He is a past president of the American Holistic Medical Association. Mario E. Castellanos, MD, is a faculty physician at St. Josephs Hospital and Medical Center in Phoenix, Arizona. He received his MD from the University of Texas Southwestern in Dallas. He completed a residency in obstetrics and gynecology in 2010 from the University of Texas Southwestern Parkland Memorial Hospital in Dallas. In 2012, Dr. Castellanos completed an AAGL fellowship in minimally invasive gynecologic surgery at St. Josephs Hospital and Medical Center in Phoenix, Arizona, as well as a fellowship in chronic pelvic pain. Dr. Castellanos received an excellence award in 2010 for excellence in gynecologic surgery and two excellence awards in medical student teaching in 2007 and 2008. Thomas C. Chelimsky, MD, is on staff in the Department of Neurology at University Hospitals of Cleveland in Ohio. He is a professor of neurology, anesthesiology and of pediatrics at Case Western Reserve University School of Medicine in Cleveland, Ohio. Dr. Chelimsky is also the director of the Division of Autonomic Disorders at University Hospitals of Cleveland in Ohio and has been since 1990. Dr. Chelimsky graduated from Harvard University with a degree in biochemistry in 1979. He received his MD from Washington University in 1983. He completed two residencies at the Mayo Clinic: one in internal medicine and the other in neurology. He also completed a fellowship at the Mayo Clinic in autonomic research. Melissa A. Farmer, PhD, is a postdoctoral fellow in the Department of Physiology at Northwestern University Feinberg School of Medicine in Evanston, Illinois. She received her PhD in clinical psychology from McGill University in 2011. Dr. Farmer attended the University of Texas at Austin for undergrad, where she was a research assistant. She is on the Editorial Board of Archives of Sexual Behavior.
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Speaker Biosketches
IPPS
Beginning in 2011 and lasting until 2013, Dr. Farmer is receiving a research grant from the National Vulvodynia Association. Dr. Farmers areas of interest and specializations are neuroimaging of urogenital and visceral pain conditions; pain psychophysiology; sex differences in sexual motivation; animal models of post-infectious pain; human sexuality; sexual dysfunction; and philosophy of science. Colleen M. Fitzgerald, MD, is the medical director of Womens Health Rehabilitation at the Rehabilitation of Chicago (RIC) and assistant professor at the Northwestern University Feinberg School of Medicine in the Department of Physical Medicine and Rehabilitation. Dr. Fitzgeralds areas of clinical expertise and research include pregnancy-related pain disorders, pelvic pain, pelvic floor dysfunction and pelvic rehabilitation. Dr. Fitzgerald received her medical degree from Northwestern University Feinberg School of Medicine in 1996 and completed her post-graduate training at the RIC and Northwestern University Feinberg School of Medicine in 2000, where she served as chief resident. Dr. Fitzgerald provides consultations to inpatients at Prentice Womens Hospital and Northwestern Memorial Hospital, where she also serves on the medical staff. She is currently funded on the Building Interdisciplinary Research Careers in Womens Health (BIRCWH) K12 HD055884 from the National Institute of Child Health and Human Development. Her study is on the use of pelvic musculoskeletal ultrasound to investigate the etiology of pregnancy related pelvic girdle pain. She is also researching pelvic floor muscle dysfunction and pain, chronic pelvic pain, pelvic joint injections and the instruction of pelvic floor muscle examination for physicians. She is the co-chair for the past 2010 and upcoming 2013 World Congress on Low Back and Pelvic Pain in Dubai. She is an active member of the American Academy of Physical Medicine and Rehabilitation and the International Pelvic Pain Society. She serves on the Advisory Council for the Womens Health Foundation. Sarah Fox, MD, received her undergraduate degree from Brown University and her MD from Robert Wood Johnson Medical School in New Brunswick, NJ. She completed her residency in obstetrics and gynecology at Allegheny University in Pittsburgh, and her fellowship in Urogynecology at St. Georges Hospital in London. She developed an interest in pelvic pain after working with patients with interstitial cystitis and joined the Ambulatory Division at Women & Infants Hospital to open a multidisciplinary Chronic Pelvic Pain Clinic. She is also the secretary of the International Pelvic Pain Society and has lectured nationally and internationally. She has special interests in medical and alternative management of pelvic pain as well as resident education in pelvic pain. She is also director of the Cervical Cancer Screening and Prevention service at W&I. She has been actively involved in advocacy, testifying both in RI and Washington, DC, about womens reproductive health. She also teaches an undergraduate course at Brown University: Reproductive Health: Science, Politics and the Media. Nel E. Gerig, MD, is a Diplomate of the American Board of Urology. She graduated from the UCLA School of Medicine and completed a residency in urological surgery at the University of Colorado Health Sciences Center in Denver, Colorado. She has since been in the private practice of urology in the Denver area. Dr. Gerigs passion is the treatment of pelvic pain disorders, including interstitial cystitis/painful bladder syndrome, pelvic floor dysfunction, pudendal neuralgia, chronic prostatitis, dyspareunia, vulvodynia, vulvar vestibulitis, endometriosis, sacroiliac dysfunction,and other manifestations of the pelvic and low back pain syndrome.
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Speaker Biosketches
IPPS
Her approach is interdisciplinary, involving physical therapists and many other medical specialists in the care of those suffering from various aspects of the pelvic pain syndrome. Dr. Gerig is the founder and medical director of the Pelvic Solutions Network, a group of providers working together to help those with pelvic pain. Elizabeth Dee Hartmann, PT, DPT, has been in private practice in the Chicagoland area for over 20 years. Her practice focuses on the treatment of both women and men with chronic pelvic pain and dysfunction, with a special interest in treating women with chronic vulvar pain and sexual dysfunction. She is a past Board Counselor for the International Society for the Study of Vulvovaginal Disease (ISSVD) and is currently a counselor for the North American Chapter of the ISSVD and is on the Advisory Board of the International Pelvic Pain Society (IPPS). Past positions include Director of Programming, original Director of the CAPP Pelvic Committee and a member of the Vulvar Pain Task Force for the Section on Women's Health of the American Physical Therapy Association (APTA) and an Advisory Board Member for the National Vulvodynia Association. Dana Hayden, MD, MPH, is currently an attending surgeon at Rush University Medical Center in Chicago, Illinois, and has been since 2011. Dr. Hayden is also assistant professor of surgery at Rush University Medical Center. Dr. Hayden received her MPH from the University of Illinois at Chicago in 2000. She received her MD from Rush Medical College in 2004. She interned at Rush University Medical Center in Chicago, Illinois, from 2004 to 2005. In 2010, Dr. Hayden completed her residency at Rush University Medical Center. She went on to complete a fellowship in colon and rectal surgery at Cleveland Clinic Florida in 2011. Dr. Hayden is a member of the American Society of Colon and Rectal Surgeons and a candidate member of the American College of Surgeons. Kevin M. Hellman, PhD, is an assistant professor in the Department of Obstetrics and Gynecology at the University of Chicago. Dr. Hellman is also a research scientist in the Department of Obstetrics and Gynecology at NorthShore University HealthSystem. He received his BS in computer science from the University of Wisconsin-Madison in 1998. Dr. Hellman graduated from the University of Pennsylvania in 2004 with a Doctor of Philosophy in Neuroscience. Since 2010, Dr. Hellman has been a member of the International Pelvic Pain Society and the International Association for the Study of Pain. Heather S. Howard, MBA, PhD, ACS, Heather Howard, PhD, MPH, is a board certified sexologist and mind-mind health facilitator. She founded the Center for Sexual Health and Rehabilitation to help clients adjust sexually to challenges and transitions such as chronic health conditions, trauma, and family building. She uses an educational approach to support embodiment, intimacy, comfort and pleasure and recently launched www.Ergoerotics.com to provide ergonomic sexual adjustments related to physical limitations and pain.
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Speaker Biosketches
IPPS
In addition to her private practice work, Heather is an associate professor of clinical sexology at The Institute for Advanced Study of Human Sexuality (IASHS); a clinical skills instructor for Herman & Wallace Pelvic Rehabilitation Institute; a clinical skills instructor in the OSCE Program for the Stanford School of Medicine Obstetrics & Gynecology Department; and a gynecological teaching associate at Stanford, Tauro and UCSF medical schools through Project Prepare, where she teaches medical students to perform comfortable and effective breast and pelvic exams. She received her BA from the University of California at Berkeley (1993), her MBA from New York Universitys Stern School of Business (1995), and her PhD and MPH in human sexuality from IASHS (2008, 2012), where her doctoral research explored the potential for sexual response to augment the impact of pain management interventions for chronic pelvic pain. She is board certified through the American College of Sexologists (ACS) and is a certified sexuality counselor and educator through the American Association of Sexuality Educators, Counselors and Therapists (AASECT). Barry K. Jarnagin, MD, is a clinical associate professor at Vanderbilt University Medical Center in Nashville, Tennessee. He is also the medical director of the Center for Pelvic Health at Saint Thomas Health Services where he is also the fellowship coordinator. Dr. Jarnagin is part of the Public Health Committee of the Tennessee Medical Association. And Dr. Jarnagin is the adjunct associate professor in the OB/GYN department of the Meharry Medical College. Dr. Jarnagin attended Union University in Jackson, Tennessee, for his undergraduate degree in chemistry with a minor in biology. He went on to receive his MD from the University of Tennessee in Memphis in 1984. Dr. Jarnagin interned at the Naval Hospital in San Diego, California, in obstetrics and gynecology. He completed a residency in obstetrics and gynecology in 1989 at the National Naval Medical Center in Bethesda, Maryland. Susan Kellogg-Spadt CRNP, PhD, is the co-founder of The Pelvic and Sexual Health Institute of Philadelphia, where she is managing partner and the director of Vulvar and Sexual Medicine. In this capacity, Dr. Kellogg performs direct patient care, consultative services as a vulvovaginal specialist, vulvoscopist, researcher, preceptor and sexual dysfunction consultant. Dr. Kellogg is professor of OB/GYN at Drexel University College of Medicine in Philadelphia; professor of Human Sexuality at Widener University in Chester, Pa., and clinical associate faculty at the University of Pennsylvania and Thomas Jefferson University in Philadelphia. She is the course director for the Female Sexual Health Preceptorship and faculty for the Pelvic & Reconstructive Surgery Fellowship at Drexel University. She is a member of the Board of Directors, education, certification and scientific program committees of the International Society for the Study of Womens Sexual Health and on the Editorial Board of the Journal of Sexual Medicine. Dr. Kellogg received her Ph.D. in Human Sexuality; certificate as an OB/GYN practitioner from the University of Pennsylvania; and MSN in Maternal Child Health from Loyola University in Chicago. She is an active researcher and has been an investigator in a NIH trial and several industry trials investigating female sexual dysfunction and pelvic pain syndromes.
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Speaker Biosketches
IPPS
Daniel J. Kirages, DPT, OCS, FAAOMPT, is an instructor of clinical physical therapy at the University of Southern California in Los Angeles. He is also part of the clinical faculty at the Kaiser Permanente Los Angeles Medical Center in California.
Dr. Kirages received his Doctor of Physical Therapy in 1998 from the University of Southern California in Los Angeles, where he also received his BS in exercise science in 1994. Dr. Kirages is a member of the International Pelvic Pain Society, International Continence Society, American Physical Therapy Association and a fellow of the American Academy of Orthopaedic Manual Physical Therapists. In 2008, he received the outstanding teacher award in the Division of Biokinesiology and Physical Therapy at the University of Southern California in Los Angeles. Brandi Kirk, PT, BCB-PMD, began her undergraduate work at Ohio State University and she completed her studies at Finch University of Health Sciences/Chicago Medical School, graduating from their acclaimed Physical Therapy program in 1996. She started practicing women's health in 1997 and became a women's health coordinator in 2003. It was at this time that she created the Womens Health program at Northwest Community Hospital's Wellness Center in Arlington Heights, Illinois. During 2004 and 2005 she was the Women's Health Specialist at Womens Physical Therapy Institute in Lake Zurich, Illinois. In 2006 Ms. Kirk founded Kirk Center for Healthy Living, which is a specialty center focusing on pelvic and visceral conditions for men and women. Ms. Kirk earned certification in Pelvic Muscle Dysfunction Biofeedback through the Biofeedback Certification Institute of America in 2009. She is a member of the APTA Section on Womens Health, the APTA Private Practice Section and the International Pelvic Pain Society. She is currently pursuing her Visceral Manipulation Technician Certification and her Visceral Manipulation Practitioner Certification through the Barral Institute. She is also a faculty member for the Herman and Wallace Pelvic Rehabilitation Institute and was a 2008-2011 board member for the Chicagoland Pelvic Floor Research Consortium. She has just recently been accepted as a Teaching Assistant for the Barral Institute. Ms. Kirk has lectured for numerous professional organizations and she is currently conducting research with Dr. Denise Elser, of Womens Health Institute of Illinois, for future publication. Jason Kutch, PhD, received a BSE in mechanical engineering from Princeton University in 2001 and his PhD in applied and interdisciplinary mathematics in 2008 from the University of Michigan, Ann Arbor. He was mentored by Tony Bloch (Mathematics), Art Kuo (Mechanical & Biomedical Engineering), and Zev Rymer (Northwestern University Physiology and the Rehabilitation Institute of Chicago). From 2008-2010 he was a postdoctoral research associate, and from 2010-2011 he was a research assistant professor in biomedical engineering at the University of Southern California (USC) working with Francisco Valero-Cuevas. In August 2011, he became assistant professor of biokinesiology and physical therapy at USC. His research interests include the neural mechanisms for muscle activation, engineering of non-invasive systems to study human motor function, and neuromuscular disorders, particularly chronic pain.
Page 27
Speaker Biosketches
IPPS
Georgine Lamvu, MD, MPH, received her undergraduate and medical degrees from Duke University. She completed her residency in obstetrics and gynecology at the University of North Carolina at Chapel Hill (2001). She received her MPH in epidemiology and completed a fellowship in advanced laparoscopy and pelvic pain at UNC in 2003. During this time she served as a fellow scholar in the NIH T-32 Training in Epidemiology and Clinical Trials Program, as a UNC Simmons Minority fellow and as an NIH Womens Reproductive Health Research Scholar. From 2003 2006 Dr. Lamvu began her clinical practice at UNC Healthcare Hospitals as an assistant professor, and she served as director of Grand Rounds and director of the NICHD Triangle Clinical Research Fellowship in Reproductive Health. Her clinical practice and research focused on gynecologic care of women with chronic pelvic pain disorders. As assistant professor at UNC, Dr. Lamvu was the teacher and mentor for many medical students, residents and fellows and she used her expertise to provide training opportunities with an emphasis on clinical trials methodology, womens health research and advanced laparoscopic surgical techniques. Currently, Dr. Lamvu is vice president of the International Pelvic Pain Society and a contributing committee member of the American Association of Gynecologic Laparoscopists. She is board certified in Ob-Gyn by the American College of Obstetricians and Gynecologists. She maintains an active teaching role as the director of the Fellowship in Advanced Minimally Invasive Surgery and Gynecology at Florida Hospital in Orlando. She also serves as medical unit director of Gynecology. Stacy T. Lindau, MD, MAPP, is a tenured associate professor of obstetrics and gynecology and medicine-geriatrics at The University of Chicago. She is a leader in the field of womens health, specifically in the context of aging, cancer and urban issues. Dr. Lindau is a practicing gynecologist, directing a clinical and research program that treats sexual problems and dysfunction in women and girls affected by cancer and other complex diseases. She is founder and chair of the international Scientific Network on Female Sexual Health and Cancer, an interdisciplinary organization that collaborates to accelerate science to improve sexual outcomes for women and girls affected by cancer. Dr. Lindaus research draws from national, local and clinical populations. She is an expert in the field of biosocial survey research and is the founding director, since 2003, of the Chicago Core on Biomeasures in PopulationBased Aging Research at the National Institute on Aging-funded Center on Demography and Economics of Aging at the University of Chicago and NORC. Dr. Lindau is the PI for the South Side Health and Vitality Studies and leads CommunityRx, an effort supported by the 2012 Centers for Medicare and Medicaid Services Healthcare Innovation Challenge. She is a Research Economist at the National Bureau of Economic Research, serves as a peer-reviewer for the National Institutes of Health and more than a dozen medical journals, and is currently a member of the Scientific Advisory Board for the Irish Longitudinal Study on Ageing. Geeta Maker-Clark, MD, is a board certified integrative family physician, who sees adults and children at 909 Davis St. in Evanston and attends births at Highland Park Hospital. She is the coordinator of Integrative Medical Education and clinical assistant professor at Pritzker School of Medicine, University of Chicago and faculty at the U of C NorthShore Family Medicine Residency program. Dr. Maker-Clark received her undergraduate degree in English literature at Northwestern University
Page 28
Speaker Biosketches
IPPS
and received her MD from Rush Medical College in Chicago, IL, where she was president of the Alpha Omega Alpha Honor Society. She was very active in international health, alternative medicine and underserved medicine. She then completed a residency in family medicine and a fellowship in Maternal-Child Health and Obstetrics at West Suburban Hospital in Oak Park, IL. After graduating, she then practiced for 6 years in Ventura ,CA at the UCLA affiliated Ventura County Medical Center, primarily seeing women and children and teaching the art of natural birthing to Family Medicine residents and UCLA medical students, as well as teaching prenatal yoga. Dr. Maker-Clark has always held the belief that any meaningful healing must involve the mind, body and spirit, and that whenever possible the most natural and least invasive intervention serves the highest good of the patient. She has pursued studies with traditional healers in India, midwives, herbalists and energy healers. She has found that the practice of Integrative Medicine, combining the best of conventional medicine and alternative therapies, offers an opportunity for healing, wellness and disease prevention that neither modality can achieve alone. For this reason, she spent 2 years training at the University of Arizona Fellowship in Integrative Medicine, under the supervision and mentorship of Dr. Andrew Weil, a world renowned pioneer in this field. Dr. Maker-Clark relies heavily on the use of food as medicine in her approach to healing, as well as herbs, botanicals, breathwork, conventional medicines and healing practitioners in the community. She has taught on the use of food as medicine at hospitals, residencies, conferences and yoga festivals. She has been featured as an expert in widely viewed documentaries on family centered maternity care and the health of children of farmworkers, and is deeply involved in the communities she serves. Currently she sits on the boards of multiple organizations that work to create access to high quality health care for all. She has always been active in teaching students and residents, and feels that this is a very important part of furthering integrative medical work for the future. Joseph M. Maurice, MD, serves as director, Division of Gynecology, director, Minimally Invasive Gynecologic Surgery and assistant professor at Rush University Medical Center in Chicago. Dr Maurice completed his residency in Obstetrics and Gynecology at Cook County Hospital in Chicago. He completed his fellowship in Minimally Invasive Gynecologic Surgery at St Joseph's Hospital and Medical Center in Phoenix, Arizona, under the direction of his Fellowship Director Dr. Michael Hibner. Dr. Maurice's practice is centered on female pelvic pain, and he works with a multi-specialty group at Rush addressing female pelvic pain care. Lorimer Moseley PhD, B.App.Sc.(Phty)(hons), is a physiotherapist and clinical pain scientist who has worked in chronic pain rehabilitation for 20 years. He completed a PhD from Sydney University in 2002 and a post-doctoral fellowship at Royal Brisbane & Womens Hospital/University of Queensland. In 2004, he was appointed Nuffield Research Fellow at Oxford University UK. In 2007 he was judged by the International Association for the Study of Pain, as the outstanding mid-career clinical scientist working in a pain-related field. In 2011, he was appointed professor of clinical neurosciences and foundation chair in physiotherapy at the University of South Australia. He has written over 100 articles and book chapters and three books. He is associate editor for PAIN, the European Journal of Pain and British Journal of Sports Medicine.
Page 29
Speaker Speaker Biosketches Biosketches
IPPS IPPS
Kenneth Peters, MD, became chairman of the department of urology at Beaumont Hospital in Royal Oak in 2007. He joined Beaumont in 1991 as a urology resident, and completed an additional urology fellowship at the hospital after his residency. Widely recognized as a leader in conducting research, Dr. Peters is internationally known for his work on nerve rerouting surgery, interstitial cystitis and neuromodulation. He has written numerous peer-reviewed journal articles and book chapters on incontinence, interstitial cystitis and neuromodulation. He has twice won the Society for Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction (SUFU) clinical research award. Dr. Peters has research grants from the National Institutes for Health and Industry, and he is a grant reviewer for the National Institutes of Health. He received his medical degree from Case Western Reserve University School of Medicine. He is an active and well-respected resident educator. He is a member of the American Urological Association, Michigan Urological Society, the Society for Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction, International Continence Society and International Society for Pelvic Neuromodulation. He was recently voted by the American Urological Association to serve on its research council. Dr. Peters has a private practice in Royal Oak, Michigan, and lives in Huntington Woods. Stephanie A. Prendergast, MPT, received her Master of Physical Therapy degree from the Medical College of Pennsylvania and Hahnemann University in 2000. She is co-founder of the Pelvic Health and Rehabilitation Center, which has three locations in San Francisco, Oakland, and Los Gatos, California, treating patients from all over the United States and abroad. In 2002, she was elected to the Board of Directors for the International Pelvic Pain Society, where she currently serves on the Executive Board as the vice-president and program chair. Ms. Prendergast will be the first physical therapist to be president of the society in 2013. As an acknowledged leader in the field, she was invited to become one of the founding Board members of the Society for Pudendal Neuralgia in 2005 and subsequently co-developed and teaches De-mystifying Pudendal Neuralgia, a continuing education course attended by doctors, physical therapists and other allied health professionals around the world. In 2009 she joined the Department of Urology at Stanford University where she is currently working on two NIH-funded grants. Ms. Prendergast is internationally recognized in the field of pelvic floor dysfunction, lectures regularly and has numerous publications in textbooks, journals, and magazines. Andrea J. Rapkin, MD, is a professor and vice chair in the Department of Obstetrics and Gynecology at the David Geffen School of Medicine at UCLA. She is director of the UCLA Pelvic Pain Clinic and the Premenstrual Disorders Research Program. She has published extensively in the areas of premenstrual syndrome, chronic pelvic pain, menopause and womens reproductive health with numerous research articles and contributions to textbooks in the areas of menstrual cycle-related nerve disorders and pelvic pain. Dr. Rapkin is a member of several professional societies, including the Society for Gynecologic Investigation, American Pain Society, the International Association for the Study of Pain, the International Society of Psychoneuroendocrinology and the Society for Sexual Medicine, and serves as a reviewer for numerous medical journals. Dr. Rapkin received her undergraduate degree from Cornell University and went on to study medicine at the State University of New York in Buffalo and completed residency in Obstetrics and Gynecology at the UCLA School of Medicine.
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Speaker Biosketches
IPPS
Ja Hyun Shin, MD, is an assistant professor of minimally invasive gynecologic surgery at Albert Einstein College of Medicine. Dr. Shin received her BS from Massachusetts Institute of Technology in 1999. She completed an MS at Harvard School of Public Health in 2002 and received her MD from SUNY Downstate College of Medicine in 2006. Dr. Shin completed an internship in obstetrics and gynecology at Washington University/Barnes-Jewish Hospital in 2007. In 2010, she completed a residency in obstetrics and gynecology at Columbia University Medical Center/New York Presbyterian. And this past year, Dr. Shin finished an AAGL minimally invasive gynecologic surgery fellowship at the University of Rochester School of Medicine and Dentistry and the Albert Einstein College of Medicine. She is a member of the American Association of Gynecologic Laparoscopists and the International Pelvic Pain Society. Devon N. Shuchman, MD, is a physiatrist at Associates in Physical Medicine & Rehabilitation (APM&R) in Ypsilanti, Michigan. Dr. Shuchman completed a BS in movement science from the University of Michigan in Ann Arbor in 2000. She received an MS in applied physiology in 2003 from Rosalind Franklin University Chicago Medical School in North Chicago, Illinois, where she received her MD in 2007. Then, in 2011, Dr. Shuchman received a certificate from the University of Michigans Graduate Medical Education Scholars Program. She completed an internal medicine internship at Advocate Lutheran General Hospital in Park Ridge, Illinois, in 2008. She then finished a residency and fellowship at the University of Michigan in Ann Arbor in 2011 and 2012. The residency was in physical medicine and rehabilitation and the fellowship was in pain management. Matthew T. Siedhoff, MD, MSCR, is an assistant professor in obstetrics and gynecology at the University of North Carolina at Chapel Hill. He is the director of the UNC Fibroid Care Center and the residency rotation director of gynecology. Dr. Siedhoff received his BA in biology with minors in chemistry and art from Covenant College in Lookout Mountain, Georgia, in 2001. He received his MD from Stanford University School of Medicine in 2005 and in 2011, Dr. Siedhoff received his MSCR in epidemiology from UNC Gillings School of Public Health. He completed an internship and residency in obstetrics and gynecology at New York University in New York City in 2009. He pursued a fellowship in advanced laparoscopy and pelvic pain at the University of North Carolina in Chapel Hill in 2011. Alain Watier, MD, is currently professor of gastroenterology and director of the pelvic floor unit at Universite de Sherbrooke in Quebec, Canada. He is co-founder of Convergences-PP, an international French society interested in pelvi-perineal pain. Dr. Watiers areas of interests include irritable bowel syndrome, constipation and fecal incontinence, but mainly chronic pelvi-perineal pain. Mind-body medicine, post-traumatic syndrome and chronic pain, alternative management of pelviperineal pain are other fields of activity.
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Speaker Biosketches
IPPS
Gail P. Wetzler, RPT, CVMI, has a private practice called Wetzler Integrative Physical Therapy Center specializing in orthopedics, womens health, sports and manual therapy. She is the director of curriculum and program development at the Barral Institute in Palm Beach Gardens, Florida, where she is also the director of research. She is also the director of physical therapy at the Susan Samueli Center for Integrative Medicine. She is part of the faculty of the American Physical Therapy Association in the Womens Health Section. Ms. Wetzler received her BS in physical therapy at Long Beach State University in California in 1973. She became certified as an instructor of visceral manipulation in 1991 from the Upledger Institute, Inc. in Palm Beach Gardens, Florida. She was also certified in 1995 in equine sports massage therapy from the Sullivan Institute in Lake Forest, California. Then in 1998, Ms. Wetzler received a certification as an instructor mechanical link from Upledger Institute, Inc. In 2000, Ms. Wetzler became the curriculum director of visceral manipulation at the Barral Institute and became a Barral Institute Diplomate in 2008. She was also the equine diplomate in osteopathy in 2009 at the Vluggen Institute in San Marcos, Texas. Ms. Wetzler is currently enrolled in a doctoral program for physical therapy at Rosalind Franklin University in Chicago, Illinois. Kathryn M. Witzeman, MD, is an assistant professor in the Department of OBGYN at the University of Colorado. She completed her OBGYN Residency training at the University of North Carolina, Chapel Hill, and has practiced general obstetrics and gynecology for eight years at Denver Health Medical Center in Denver, CO. She started a multidisciplinary Chronic Pelvic Pain clinic at Denver Health approximately four years ago. This multimodal clinic gives patients with chronic pelvic pain access to medical and surgical treatments, physical therapy, a health psychologist, a psychiatrist with a focus on womens issues, sexual therapy, pain anesthesia and nurse coordination of their integrative care. This clinic is a recruitment site for The National Provider-Based Vulvodynia Outcomes Registry. Dr. Witzeman has also served on the Denver Health Ethics Committee for six years, serving as co-chair of the committee for the last year. She is the site director for the University of Colorado School of Medicines Womens Care Clerkship at Denver Health and has developed curricula for the Womens Healthcare clerkship and the OBGYN Residents training program both in approaches to chronic pelvic pain and bioethics as it applies to womens healthcare issues. Denniz Zolnoun, MD, MPH is board certified in Obstetrics and Gynecology. She received her MD from the University of Illinois, Chicago. Dr. Zolnoun completed her residency at Rochester General Hospital, NY, specifically in Obstetrics and Gyneocology. She also completed a fellowship at the University of North Carolina, Chapel Hill, in Advanced Laparoscopy & Gynecologic Surgery. She is the director of the Vulvar Pain Clinic at the University of North Carolina, School of Medicine, as well as the director of research in the Division of Advanced Laparoscopy & Pelvic Pain.
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Abstracts
Abstract #1 3D, INTERACTIVE, GRAPHIC DISPLAY OF PUDENDAL NERVE ANATOMY Courtney McKenna, BA, MFA; Georg Furtmueller, M; A Lee Dellon Johns Hopkins University Presented By: A Lee Dellon
IPPS
Objective: To depict, in an interactive, threedimensional (3D) graphic interface, the anatomy of the pudendal nerve from its sacral roots, between the sacrospinous and sacrotuberous ligaments, through Alcocks canal, and on to its rectal, perineal and dorsal branches, permitting doctors and patients to understand this complex anatomy and the different surgical routes required for pudendal nerve block and surgical intervention. Methods: Cadaver dissections of 10 fresh, sagitally split, hemipelvises were completed to study the multiple branching patterns and varied course of the pudendal nerve, in the male (5) and the female (5). A detailed anatomic pen and ink illustration of each dissection was created and converted into a colored diagram documenting measurements relating the exit of the perineal and dorsal branches at the inferior pubic ramus with respect to the ischial tuberosity. High resolution (3Tessla) MR Neurography and CT scans were taken of one additional, not sagitally split, male and one female pelvis block pre and post surgical dissection in which pudendal nerve branches were identified and marked. Data from the magnetic imaging were imported into the DICOM viewing program OsiriX. The pelvis structure was exported to 3D modeling program ZBrush to sculpt the nerves. Twelve hundred sliceswere animated for the graphic interface. For comparison, the final 3D graphic depicts the traditionalanatomic pattern on the right and the most common observedpattern on the left side of the model. Results: Each hemipelvis demonstrated considerable variation in branching patterns adjacent to the sacrospinous ligament: 50% had 2 trunks present, 40% had 3 trunks present, 1 had 1 trunk present. 60% had a separate rectal branch. A common perineal/dorsal trunk and common rectal/ perineal trunk were seen most often. Variation of the level at which the dorsal nerve to the clitoris/penis exited Alcocks canal in relation to the ischial tuberosity ranged from 25mm to 45mm in the 10 hemipelvises, demonstrating a bimodal distribution, such that there are two exits from Alcocks canal, one for the perineal branch and one for the dorsal branch. Conclusions: The complex anatomy of the pudendal nerve can explain variations in patients symptoms and surgical results related to pudendal nerve compression and decompression, and encourages a rethinking of traditional operative approaches. Summary: A 3D graphic interface of pudendal nerve anatomy has been created and facilitates teaching of pelvic pain problems related to the pudendal nerve. Key Words: Pudendal nerve anatomy
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Abstract #2 THE USEFULNESS OF MINILAPAROSCOPIC CYSTECTOMY FOR SMALL ENDOMETRIOMA IN ADOLESCENT WOMEN HeungYeol Kim, PHDMD2; SungTack Oh, MD, PhD1 1 College of medicine, Chonnam National University; 2College of Medicine, Kosin University Presented By: HeungYeol Kim Objective: Minilaparoscopy is lesser invasive and more cosmetic than conventional laparoscopy, and simple surgical procedure is possible by development of instrument. It is very important point in adolescent women. This study was done to evaluate the usefulness of minilaparoscopic cystectomy for treatment for small endometrioma in adolescence. Methods: The prospective, randomized study was done in 54 adolescence patients with for small endometrioma of lesser than 2 cm diameter. The minilaparoscopic cystectomy with 3 mm telescope and 3 mm instruments was performed in 18 patients (Group A), and conventional laparoscopic cystectomy with 10 mm telescope and 5 mm instruments was performed in 20 patients (Group B). The Anesthesia of laparoscopy was general anesthesia in all 38 cases. The operating time, average operating room costs, average ancillary department costs, instrument and supply costs, and length of hospital stay were compared. Postoperative pain score of each patient was estimated by visual analog scale (VAS). The recurrence was observed for 2 years. The statistical analysis was done by student's ttest and Fisher's exact test. Results: The procedures were performed satisfactorily in all patients of both groups without any difficulty. However in 8 patients (44.4%) of Group A, skillful doctor was necessary due to weak illumination of scope. There was no significant difference in operating time, average operating room costs, average ancillary department costs, instrument and supply costs, or length of hospital stay. Postoperative pain was significantly lesser in Group A than B (VAS 1.3 +/ 1.1 vs. 5.8 +/ 2.1; P <0.01), and patients requiring analgesia were lesser in Group A than B (2/18 vs. 20/20; P <0.01). The satisfaction of operation scar was higher in Group A than B (18/18 vs. 5/20; P <0.01). There was no postoperative complication and no recurrence of cyst for 2 years in both groups. Conclusions: The success rate of minilaparoscopic cystectomy of cyst wall does not differ from conventional laparoscopy, but acceptability and satisfaction of patients are more and postoperative pain is lesser. Therefore minilaparoscopy seems to be better than conventional laparoscopy for the management of adolescence patients with small endometrioma of lesser than 2 cm diameter.
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Abstract #3 OBGYN RESIDENT ATTITUDES AND PERCEPTIONS ABOUT CHRONIC PELVIC PAIN: A TARGETED NEEDS ASSESSMENT FOR FUTURE CURRICULUM REVISION Kathryn Witzeman, MD2;Jenifer E. Kopfman, PhD1 1 College of Charleston; 2Denver Health Presented By: Kathryn Witzeman
IPPS
Objective: Resident education in the area of chronic pelvic pain (CPP) historically has been inconsistent. Pelvic pain accounts for at least 10% of all general gynecologic visits and is a common presenting complaint in resident training clinics. Furthermore, community surveys report between 15 and 24% of women aged 18 to 50yearsold experienced CPP within the last 3 months. (3,4) However, both anecdotally and reviewing the limited literature, OBGYN physicians and residents demonstrate predominantly negative perceptions of patients perceived to have CPP.(2,5,6) Attitudes and perceptions may create barriers to interest and learning about CPP and potentially to thorough and compassionate treatment of women with CPP. In the current literature, no studies specifically evaluate OBGYN residents attitudes and perceptions. When creating or revising existing curriculum, a targeted needs assessment is an integral step prior to developing appropriate goals and objectives of the curriculum. (7) Hence, determining current OBGYN Resident attitudes, selfperceived knowledge, and potential educational barriers regarding CPP will help focus future curriculum design. Methods: This educational study was IRB exempt or approved at involved hospitals. PHASE 1 FOCUS GROUP A focus group of 7 OBGYN Residents was performed to understand the attitudes, perceptions, challenges, and obstacles OBGYN residents have in seeing patients with CPP. Participation was voluntary. The focus group format utilized Dr. Kruegers recommendations from Designing and Conducting Focus Group Interviews (8). The focus group was digitally recorded and moderated by the primary researcher; an assistant moderator took notes describing nonverbal behavior of the participants. The primary researcher and a second nonbiased reviewer reviewed the transcription and identified 8 primary themes. PHASE 2 SURVEY Three statements were written to evaluate each major theme to assess reliability. A 7point Likert scale assessed agreement with each statement. (7 = Strongly Agree; 1=Strongly Disagree) The survey was voluntarily administered to OBGYN Residents at both a Universitybased and a Communitybased program. SPSS data analysis software was used to determine Cronbachs for reliability of the question groupings. Each grouping demonstrated high or acceptable reliability ratings. Descriptive statistics examined the mean for each question grouping. Independent samples ttests assessed differences between training levels and between University and Community training sites. Results: Survey response rate was 72% (41/57). Residents demonstrated consistently high scores on items measuring negative attitudes toward CPP patients, feeling overwhelmed by CPP patients, and lack of time to see them. Low scores indicated a lack of confidence in their own knowledge base and high scores indicated residents desire to learn more in this area. There was variation in preferred learning methods but a trend toward one on one clinical time and diagnostic algorithms. No significant differences between training levels (i.e. PGY1 to PGY4) were observed, nor were there any significant differences between the University and Communitybased training sites in any of the groupings. Conclusion: The majority of OBGYN Residents surveyed felt inadequately prepared to address the needs of women presenting with CPP. Curriculum revision is needed and should focus on addressing these areas. Key Words: Pelvic pain; attitudes; perceptions; OBGYN Resident
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Summary: The majority of OBGYN Residents surveyed feel inadequately prepared to address the needs of women presenting with CPP. Curriculum revision is needed and should focus on addressing these areas.
Abstract #4 IS THERE AN ASSOCIATION BETWEEN ONGOING DOMESTIC ABUSE AND CHRONIC PELVIC PAIN IN WOMEN? Lena Braginsky, MD; Sondra Summers, MD Loyola University Medical Center, Department of Obstetrics and Gynecology, 2160 South First Avenue, Maywood, IL 60153 Objective: There is a known correlation between women suffering from chronic pelvic pain and a history of physical or sexual abuse. However, no studies have yet examined the relationship between ongoing domestic abuse and chronic pelvic pain. The primary goal of the current study is to determine whether there is as association between ongoing domestic abuse and chronic pelvic pain syndrome. Methods: All participants were recruited from the womens chronic pelvic pain clinic at Loyola University Medical Center. Patients experiencing chronic pelvic pain of at least 3 months duration were asked to complete a Womens Abuse Screening Tool (WAST) to assess for current domestic violence. The eight question WAST survey has been validated for use in the outpatient setting, and was chosen for this study to identify victims of any type of domestic abuse. Demographic data was also collected. Statistical analysis was performed to investigate prevalence of current domestic abuse amongst patients experiencing chronic pelvic pain. Results: Thirty-one women were enrolled, and twenty-eight completed the entire WAST questionnaire. Two out of thirty-one (6.5%) women screened positive for current abuse using WAST. Pain scores for women experiencing current abuse were not significantly different from women screening negative for abuse using WAST. Prior studies in the healthcare setting have demonstrated a prevalence range of 7-26% current domestic abuse in all surveyed female participants. Conclusions: Our pilot study did not demonstrate an increased prevalence of ongoing intimate partner abuse amongst female patients with chronic pelvic pain syndrome using the WAST questionnaire. Larger, randomized controlled studies will be needed to further investigate this issue and make treatment recommendations. We plan to continue collecting data on our patients presenting to the chronic pelvic pain clinic. Key Words: Pelvic Pain, Domestic Abuse Summary: A pilot study of 31 female chronic pelvic pain patients self-reported prevalence of ongoing domestic abuse found a 6.5% prevalence of abuse, which is lower than reported in the general population.
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Abstract #5 AUTONOMIC TESTING DOES NOT DIFFERENTIATE SUBJECTS WITH INTERSTITIAL CYSTITIS FROM HEALTHY CONTROLS Gisela Chelimsky2; Di Zhang1, Sarah Ialacci1; N. Patrick McCabe1; Melissa Kwitowski1; Jeffrey Janata3; Thomas Chelimsky2 1 Case Western Reserve University; 2Medical College of Wisconsin; 3University Hospitals Case Medical Center Presented By: Gisela Chelimsky Objective: Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) presents with medically unexplained urinary urgency, frequency, nocturia, and elevated pelvic pain when the bladder is full. Autonomic dysfunction associated comorbid disorders include irritable bowel syndrome, migraine and fibromyalgia. We therefore postulated that abnormal autonomic function may characterize IC/BPS and intend to determine whether IC/BPS belongs to a larger family of disorders sharing a common predisposition to aberrant central autonomic control. Methods: This prospective, IRB approved study evaluated at rest autonomic function of adult females with IC/BPS and matched female healthy controls. The healthy controls underwent a detailed neurologic evaluation prior to enrollment to ensure their true healthiness. All subjects underwent the cardiac response to deep breathing (DB) and Valsalva maneuver (VM), tilt table test and sudomotor function (QSART). The Composite Autonomic Severity Score (CASS) includes a sudomotor index, an adrenergic index and a cardiovascular heart rate index. Results: 17 healthy females (mean age 35 +/ 16 yrs; mean BMI 35) and 15 females (mean age 39 +/ 18 yrs; mean BMI 29) with IC/BPS were enrolled. There was no statistical difference in the sudomotor or cardiovascular heart rate index. The adrenergic function was significantly different due to 1 severely abnormal Valsalva response in the IC/BPS group. The heart rate increase in the first 10 minutes of tilt was also not different between the 2 groups. Conclusion: Based on this initial sample, IC/BPS cannot, at this time, be characterized by abnormalities of autonomic testing. Completed enrollment for this study could change this preliminary conclusion. A dysautonomia (defined by classical autonomic test findings) may not be the linchpin that connects and explains the associated symptoms of IC/BPS. This study does not exclude other types of autonomic dysfunction. Key words: Interstitial Cystitis/Bladder Pain Syndrome Autonomic Function Autonomic Testing Summary: In this pilot study of 32 subject autonomic testing did not differentiate subjects with interstitial cystitis from healthy controls, including parasympathetic, cardiac, sympathetic cardiovascular and sudomotor functions.
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Abstract #6 PELVIC PAIN: PERIMETER NEUROPATHIES THAT AFFECT PUDENDAL NEUROPATHY: SCIENTIFIC ANALYSIS OF PELVIC PAIN BEGINS WITH A PROPER DIAGNOSIS. Stanley Antolak, MD1; Christopher Antolak, MD2 1 MAPS PAIN CLINIC; 2Silver Lake Clinic Presented By: Stanley Antolak
IPPS
Objective: To demonstrate in both genders, using physical examination, that multiple neuropathies may surround the pudendal nerve territory and can aggravate pelvic pain caused by pudendal neuropathy. Methods: This review is limited to the first, consecutive 26 women and 25 men evaluated for pelvic pain in 2010. Data was collected prospectively. Each patient had standard examination for pudendal neuropathy including sensory pinprick examination and two neurophysiologic tests. Abdominal examination is performed for thoracolumbar junction (TLJ) syndrome, abdominal cutaneous nerve entrapment and ilioinguinal neuropathy. The back is examined at the sacrum for middle cluneal neuropathy; tender vertebrae are sought for the TLJ syndrome; and iliac crest is examined for tenderness of T12 branches. Pressure at the posterior femur searched for perineal pain caused by the perineal branch of the posterior femoral cutaneous nerves. Results: Sensory testing using pinprick was abnormal in 92%. Objective neurophysiologic testing was abnormal in 100%. All patients were found to have pudendal neuropathy. Of these, 64% had additional painful perimeterneuropathies at consultation that required treatment to attempt complete pain relief. Perimeterneuropathies, the secondary pain generators, varied by gender. In females the two most common perimeterneuropathies were the thoracolumbar junction syndrome or Maigne syndrome (57.6%) and middle cluneal neuropathy (56%). In males the most common perimeterneuropathies were unilateral ilioinguinal neuropathy (35.3%) and middle cluneal neuropathy (also 35.3%). Conclusions: In both genders, pudendal neuropathy is a consistent cause of neuropathic pelvic pain. In addition, multiple peripheral nerves can cause pains that overlap the pudendal territory and can aggravate the pudendal pain and confound the treating physician. These finding are compelling and should encourage all clinical researchers to evaluate for neuropathic pain in order to categorize treatment strategies into specific diagnostic groups. Hopefully defining specific painful neuropathies will lead to a paradigm change in research of chronic pelvic pain.
Abstract #7 MUSCULOSKELETAL EVALUATION OF PATIENTS WITH INTERSTITIAL CYSTITIS Tatiana Sanses4; Gisela Chelimsky2; Di Zhang1; Jeffrey Janata4; Tina Mahajan4; Bradford Fenton3; Ali Askari4; Robert Elston1; Thomas Chelimsky2 1 Case Western Reserve University; 2Medical College of Wisconsin; 3Summa Health Systems; 4University Hospitals Case Medical Center Presented By: Tatiana Sanses Objectives: To determine the distribution and correlations of pain across five body locations in women with Interstitial Cystitis (IC) and healthy agematched women. Background: We hypothesized that deep muscular pelvic pain in patients with IC is due to a generalized pain disorder with altered afferent signaling. Therefore, the pain is not limited to the pelvic area, but rather a more centralized disorder.
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Methods: Interstitial Cystitis Elucidation of Psychophysiologic and Autonomic Characteristics study (ICEPAC) is a multicenter prospective cohort trial. Subjects underwent muscular tender point assessment in 5 areas: general body, abdomen, inguinal, inner thigh, and pelvic area. Pain was assessed using a 010 Numeric Rating Scale (NRS). We calculated the overall intraclass correlation (ICC), where the classes are the body locations, and the 10 pairwise correlations across the 5 locations of pelvic, body, lower extremity, abdominal and inguinal tender points. Positive pairwise correlations and overall ICC would support our hypothesis. Results: We examined 17 patients with IC and 20 healthy agematched women. We found no difference in age and weight between the groups. The range of mean NRS pain scores for different body locations in subjects with IC was 4.15.2 and in healthy controls 0.21.0. The mean pelvic NRS pain score in subjects with IC was higher 4.91 3.34 than in healthy controls 0.19 0.31, p<0.01. The ICC coefficients for women with IC and healthy agematched controls were positive 0.58 and 0.541, respectively. Within the group of women with IC, the pairwise correlation coefficients were high between pelvic and abdominal (0.70), and between pelvic and inguinal (0.73) muscle groups. Similar but smaller correlations were noticed in healthy controls. Conclusions: Muscular, including pelvic, pain in women with IC could be due to a generalized pain disorder with altered afferent signaling. These results will be confirmed after the final enrollment is completed. Summary: Deep Muscular pelvic pain in Interstitial Cystitis patients could be part of a generalized pain disorder and not limited to the pelvic area. Keywords: Pelvic Pain, Interstitial Cystitis, Tender Point Assessment
Abstract #8 LAPAROSCOPIC INGUINAL EXPLORATION AND MESH FOR CHRONIC PELVIC PAIN Paul Yong, MD, PhD, FRCSC1; Christina Williams, MD, FRCSC1,2; Catherine Allaire, MDCM, FRCSC1,2 1 BC Women's Centre for Reproductive Health; 2University of British Columbia Presented By: Paul Yong Objective: Chronic pelvic pain affects 15% of women. Our objective was to evaluate empiric laparoscopic inguinal exploration in this population. Methods: Retrospective cohort with followup questionnaire of women with lateralizing chronic pelvic pain (right or left), ipsilateral inguinal tenderness on pelvic exam, no clinical hernia on abdominal exam, and ipsilateral empiric laparoscopic inguinal exploration with mesh placement (20032009). Primary outcome was pain level at the last postoperative visit. Secondary outcomes were pain level and SF36 scores from the followup questionnaire. Fortyeight cases met the study criteria. Surgery was done empirically for all patients, with only 7 patients (15%) found to have an ipsilateral patent processus vaginalis (shallow peritoneal dimple or a deeper defect (occult hernia)), and the remaining found to have normal appearing inguinal regions.
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Results: Of 43 cases informative for the primary outcome, there was pain improvement in 15 patients (35%); pain improvement then return of the pain in 18 patients (42%); and pain unchanged in 9 patients (21%) and worse in 1 patient (2%). Improvement in pain was associated with a positive Carnetts test in the ipsilateral abdominal lower quadrant (p = .024). Thirteen patients returned the questionnaire (27%), and the pain was now described as improved in 9 patients (69%), unchanged in 4 patients (31%), and worse in none. Three SF36 subscales showed improvement (physical functioning, social functioning, and pain). There were no intraoperative complications, and the postoperative complications were mild and uncommon (10%): hospitalization for postop pain (n = 2), bladder infection (n = 1), endometritis (n = 1), and slow recovery(n = 1). Three patients requested mesh removal which resulted in no change in their pain. Conclusion: In selected women with chronic pelvic pain, empiric laparoscopic inguinal exploration and mesh results in moderate improvement in outcome. A positive Carnetts test in the ipsilateral abdominal lower quadrant is a predictor of better outcome. Keywords: pelvic pain, laparoscopy, inguinal Summary: Empiric laparoscopic inguinal decompression & mesh appears to be safe and may be useful in women with lateralizing pelvic pain, no clinical hernia, and ipsilateral inguinal tenderness on pelvic exam.
Abstract #9 RECTUS ABDOMINIS MUSCLE ENDOMETRIOSIS Yong Jin Na, MD; Yong Jung Song, MD Pusan National University Yangsan Hospital Presented By: Yong Jin Na Objectives: Endometriosis is defined as the presence of functional endometrial glands and stroma outside the uterine cavity. Most frequently endometriosis occurs within the pelvis. However, the extrapelvic implantation of endometrial tissue has been described in virtually every organ. Endometriosis of rectus abdominis muscle is extremely rare. It should be considered in the differential diagnosis of abdominal wall masses in women with cyclic pain. Methods: We experienced a case of endometriosis of the rectus abdominis muscle in a 35 years old woman who had a tender nodular lesion on right mid portion abdominal wall, fluctuating with her menstrual cycles for 4 years. Results: She had received Cesarean section twice 6 years ago. The physical examination revealed an ill defined, about 1 cm sized mass on her right mid portion abdominal wall above 3 cm of surgical scar. MRI showed an irregular margined mass which had high signal intensity on T1 weighted image and low signal intensity on T2 weighted image at the right rectus abdominis muscle. We performed a resection of rectus abdominis muscle mass by abdominal approach and diagnostic laparoscopy. There was a small subtle white lesion in pelvic cavity. Conclusion: The histological confirmation of rectus abdominis muscle mass and pelvic peritoneal lesion are consistent with endometriosis. She had no more cyclic pain after operation. Key words: Endometriosis, rectus abdominis muscle
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Abstract #10 17 PELVIC SURGERIES (OR 16, 14, 11, 5, ETC.): ENDOMETRIOSIS, ADHESIONS OR NEUROPATHY? Stanley Antolak, MD1; Christopher Antolak, MD2 1 MAPS PAIN CLINIC; 2Silver Lake Clinic Presented By: Stanley Antolak
IPPS
Objective: To present women with multiple previous laparotomies and laparoscopies who had neuropathic causes for pains; and to demonstrate physical examination to identify the multiple neuropathic pain generators; and to demonstrate office neural blockades for pain control. Methods: Women with chronic pelvic pain were referred by physicians, physical therapists or selfreferral. A consistent examination of the abdomen, pelvis and back, searched for pudendal neuropathy, the Maigne syndrome (thoracolumbar junction syndrome), abdominal cutaneous nerve entrapment, ilioinguinal and iliohypogastric neuropathies, and middle cluneal neuropathy. Examination equipment included a Wartenberg pinwheel and a safety pin. Pudendal neuropathy is confirmed using a warm detection threshold test and the pudendal nerve terminal motor latency test. Neural blockades were performed. 1. Pudendal nerve blocks of bupivacaine and corticosteroids were done via fluoroscopic, transgluteal approach. 2. Subcutaneous nerve pain generators were treated two hours later at office examination. Injection was done at each tender nerve site using 3 or 4 mL of a mixture of bupivacaine 0.25% and lidocaine 1.0%. A nerve protection program is used for pudendal neuropathy and a postural correction program is used for abdominal wall nerves. Results: Seven women had 5, 5, 5, 11, 14, 16 and 17 gynecologic surgeries. Five women had pudendal neuropathy plus one or more additional peripheral neuropathic pain generators. Two women with only abdominal cutaneous neuropathy had pains that persisted after hysterectomy. No patients had neuropathy of the perineal branch of the posterior femoral cutaneous nerve. Five women had pudendal nerve blocks followed by injection of their secondary nerve pain generators. Two women with only abdominal cutaneous neuropathy were treated at consultation. Early pain reduction followed infiltration of the painful nerves with 3 to 6mL of a mixture of equal parts bupivacaine 0.25% and lidocaine 1.0% . Pain control lasted hours to months. Most women require long term treatment to relieve chronic pelvic pain. Pudendal neuropathy responds to a series of three PNPI in up to 70% of patients. A selfcare, nerve protection program may improve pudendal neuropathy symptoms rapidly. The Maigne syndrome responds slowly to postural care and nerve blocks. Gradually, the extent and intensity of pain decreases and fewer sites require injections Conclusions: In patients with multiple previous gynecologic surgeries careful office physical examination can demonstrate neuropathic pain generators. Inoffice nerve blocks can be diagnostic and therapeutic and eliminate the need for multiple surgeries. How many of the surgeries were necessary? Summary: Women who had previously undergone multiple gynecologic surgeries had consistent physical examination for neuropathic pain generators. Abdominal and pelvic neuropathies were identified. Diagnostic and therapeutic nerve blocks can provide temporary or permanent pain relief. Key Words: Chronic pelvic pain, pudendal neuropathy; Maigne syndrome, abdominal cutaneous nerve entrapment, middle cluneal neuropathy
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Abstract #11 LAPAROSCOPIC PUDENDAL NERVE DECOMPRESSION AND TRANSPOSITION COMBINED WITH PROTECTION USING OMENTAL FLAP IN CHRONIC PELVIC PAIN SYNDROME Tibet Erdogru2; Egemen Avc2; Murat Akand4; Dilek Uslu Erdogru3;Gul Koknel Talu1 1 Istanbul University Istanbul Faculty of Medicine Dept. of Algology; 2Memorial Istanbul Atasehir Hospital Dept. of Urology, Minimally Invasive & Robotic Surgery Center; 3Memorial Istanbul Sisli Hospital Female Sexual Function Center; 4Selcuklu University Faculty of Medicine Dept. of Urology Presented By: Tibet Erdogru Purpose: Chronic pelvic pain (CPP) is a challenging and devastating syndrome that affects patients daily functions and quality of life, and can be caused by pudendal neuralgia. With the increasing use of laparoscopy in urology, laparoscopic pudendal nerve decompression and transposition (LPDT) is an optional treatment modality besides conservative options. This study is aimed to evaluate the efficacy of LPNDT in the treatment of CPP. Patient and Methods: Consecutive, 31 patients had diagnosis of PNE, who were refractory to conservative treatment modalities, underwent LPDT. Laparoscopic pudendal nerve decompression and transposition with omental protection for preventing longterm refibrosis around the nerve was performed. The degree of the pain was assessed with visual analog scale (VAS) and the impact of the pain was evaluated with the Impact of Symptoms and Quality of Life (QoL), pre and postoperatively. Results: Preoperative pain scores during daily life and pain attacks were compared with postoperative VAS. The mean VAS scores of 31, 31, 24 and 13 patients were 0.8, 1.6, 1.8 and 1.4 in the 1st, 3rd, 6th and 12th month. Statistically significant reduction in VAS scores was observed in overall patients (p<0.0001). In 24 patients who were followed for more than 6 months, the decrease in VAS scores and the increase in QoL indices in the postoperative period were statistically significant (p<0.0001). The same situation has been found to be valid for the 13 patients who were followed for more than 12 months postoperatively. Conclusions: LPDT seems to be a new treatment modality when compared the previously described open surgical decompression techniques for the cautiously selected patients with PNE. In addition, using omental flap and protection of the nerve is one of the most important advantages of laparoscopy. As minimal invasive surgery, laparoscopic approach can be offered with its promising results in the treatment of the selected patient with CPP syndrome due to PNE. Table: Patients demographics, operative results and pre and postoperative VAS scores Patients Age (year) 44.710.9 (2067) Duration of the PNE (year) 6.94.8 (116) Operation time (minute) 197.249.7 (115325) Hospitalization (day) 1.60.6 (13) Oral intake (day) 1.50.7 (13) Followup (month) 14.75.7 (322) Postoperative VAS results VASBasal (n:31) 5.51.4 (38) VASCrisis (n:31) 9.00.9(710) VAS1st M (n:31) 0.80.9 (02) VAS3rd M (n:31) 1.62.3(07) VAS6th M (n:24) 1.82.1(07) VAS12th M (n:13) 1.41.9(06)
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Abstract 12 LONGTERM OUTCOMES OF HYSTERECTOMY IN CHRONIC PELVIC PAIN PATIENTS Katina Foster, MD; Miya Yamamoto, M; Fred Howard, MD University of Rochester Presented By: Katina Foster
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Objective: Analyze outcomes with patients receiving hysterectomy as treatment for chronic pelvic pain (CPP) Methods: Study design is a retrospective cohort study. Patients were recruited to the study by review of surgical billing forms from 20042009 at a single center that specialized in treatment of pelvic pain. Study inclusion criteria were as follows: patient completed the initial intake visit for CPP, they possessed at least one ovary, and their hysterectomy was performed through the center. Outcomes were analyzed with a goal of 24 months of follow up. Results: 106 women were identified to have a hysterectomy for chronic pelvic pain, 80 completed the initial intake visit, and 49 patients had follow up greater than or equal to 24 months. With an average of 46 months of follow up, 67% (33) had 50% or better improvement in their pain levels. 45% (22) had complete resolution of their pain, and 22% (11) had a 63% improvement in pain. Of the 16 patients whose pain did not improve, 8% (4) had their pain worsen and 24% (12) had an 18% improvement in their pain. Comparison of the clinically improved group to the minimally or worsened group, the average age of hysterectomy was not significantly different (38 vs 35), but the number of previous surgeries (2.8 vs 3.5) and the beck depression scale were different (13 vs 20). Mcgill pain scores were similar at the initial visit (23 in improved vs 25 in nonimproved group). Histologically, the patients with improved pain of 50% or more were more likely to have had endometriosis (30 versus 13%), and the group with minimal/no improvement had higher incidence of adenomyosis (44 versus 33%). Conclusion: A retrospective cohort analysis of patients diagnosed with chronic pelvic pain that underwent hysterectomy as treatment and followed postoperatively. Of these patients, 67% had clinically significant improvement of pain and had a higher rate of endometriosis. 8% had clinically worsening of pain and 24% had minimal improvement of pain and these patients had a higher rate of adenomyosis. Key Words: (limit 5): chronic pelvic pain, hysterectomy Summary: With an average of 46 months of follow up after hysterectomy for CPP, 67% had clinically significant improvement of pain by 50% or more, while 8% had worsening of pain.
Abstract #13 MTDNA DELETION IN ENDOMETRIOSIS Elnaz Salahi, Msc2; Zivar Salehi, PhD2; Ziba Zahiri1 1 Guilan University of Meidcal Science; 2University of Guilan Presented By: Elnaz Salahi Purpose: Endometriosis is a multifactorial gynecological condition characterized by the presence of ectopic endometrial and stromal tissue outside the uterus. It is frequently associated with debilitating pelvic pain and infertility. Free radicals and Oxidative stress have been proposed to be involved in the pathogenesis of the disease. The mitochondrial DNA (mtDNA) has been hypothesized to be a major target for ROS damage. The aim of this study was to investigate the association of oxidative stress, mitochondrial DNA (mtDNA) deletion mutation (4977 bp deletion), and endometriosis in northern Iran. Methods: The mitochondrial genotype of 40 women with endometriosis and 50 healthy controls were compared. Total DNA was extracted from endometriotic bioptic tissues of patients and controls.
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Results: Assessing indicate that 60% of patients and 8% of controls show mtDNA deletion through Gap PCR based assay. (Odds Ratio [OR] = 17.25, P<0.0001, confidence interval [CI] = 5.1857.36). There was a significant difference in distribution of 4977 bp deletion in this research. Conclusion: According to this study apparently mtDNA 4977 bp deletion associated with endometriosis in northern Iran. However larger populationbased studies are needed to determine the relation between this deletion and endometriosis.
Abstract #14 CHARACTERISTICS OF FEMALE PATIENTS WITH PELVIC FLOOR MUSCLE SPASM IN A CHRONIC PELVIC PAIN CLINIC Anthony Gyang, MD; Jose Carugno, MD; Frederick Hoover, MD, FACOG; Georgine Lamvu, MD, MPH Florida Hospital, Orlando Presented By: Anthony Gyang Objectives: To determine the prevalence of pelvic floor muscle spasm, the relationship between pelvic floor muscle spasm and painful pelvic conditions and to describe the demographic characteristics and treatments received by these patients. Methods: A descriptive retrospective study of two hundred and twenty consecutive female patients with pelvic floor muscle spasm over a 30 month period from January 2008 to June 2011 in a chronic pelvic pain clinic. All women between the ages of 18 to 75 years with the diagnosis of chronic pelvic pain were eligible for inclusion. Each patients visit was recorded in an electronic medical record. Records were reviewed for patient demographics, current painful pelvic conditions were recorded using CPT codes. The prevalence of these painful pelvic conditions was estimated. Current treatment modalities of pelvic physical therapy referral, medication therapy and pelvic physical examination findings were recorded. A univariate analysis of the study group was performed. Setting: An urban hospital that is a main referral center for patients with chronic pelvic pain in central Orlando area. Key words: Pelvic floor muscle spasm, chronic pelvic pain, medical therapy, physical therapy referral. Results: Of 739 women eligible for review, 220 patients were included in this review. The prevalence of pelvic floor muscle spasm was 29.7%. A univariate analysis revealed that the study group was mostly composed of Caucasian women 66.4%(95%CI 59.772.6, N=146). The mean age of this study group was 42.8 (SD13.6) years, mean BMI of 25.3 (SD 5.6).The commonest painful pelvic condition described with pelvic floor muscle spasm was dyspareunia 35.9% (95%CI 29.6% 42.6%) with the highest prevalence in the 31 year age group. Pelvic floor physical therapy referral was made in 95.5% (95% CI 92.398.1) of all patients. The most common medication used was muscle relaxants 50.5%(95%CI 43.757.2)of patients. Levator ani muscle tenderness was the most common physical examination finding in 86.5% (95%CI 78.792.2) of patients with pelvic floor muscle spasm. Conclusion: Pelvic floor muscle spasm is a prevalent disorder often described in patients with dyspareunia. These patients were found to have increased pelvic floor muscle tone with the most common muscle group being the levators. This information brings to attention the high prevalence of musculoskeletal disorders as a source of chronic pelvic pain and the need for a pelvic musculoskeletal examination in patients with dyspareunia. As expected pelvic floor most often was treated with a combination of medication and pelvic physical therapy. Further studies are needed to validate therapies employed to treat this disorder.
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Abstract #15 HIGHLIGHTS BETWEEN CATALASE GENE POLYMORPHISM & ENDOMETRIOSIS Samin Saboohi, Msc; Zivar Salehi, PHD; Elnaz Salahi, Msc University of Guilan Presented By: Samin Saboohi
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Objective: Endometriosis manifested via the flourishing of endometrial glands and stroma in outer part of uterine cavity. Recent studies are shown Oxidative stress imposes an unretaliated damage which leads to oxidative enzymopathies. Therefore the role of Catalase as an antioxidant is noteworthy. Catalase exclusively breaks down hydrogen peroxide to H2O and O2 .The aim of this study was to delineate whether a single nucleotide polymorphism (SNP) of Catalase gene could have impact on endometriosis or not. Methods: In this study, we assessed the distribution of a functional polymorphism in the gene for Catalase C262T SNP in Iranian population. DNA was extracted from peripheral blood leukocytes and the presence of the polymorphism, was assigned with Allele specific PCR (ASPCR) based assay. Result: The prevalence of genotype frequencies of the CAT CC/CT/TT were 67.5%, 32.5%, 0% respectively, in infertile subjects, whiles in healthy volunteers were 12%, 68% and 20% respectively Significant differences in allele and genotype distribution among healthy controls and endometriosis patients were found (p<0/0001). Conclusion: The result of our study proposed that Catalase gene may have vindicative impact with respect to endometriosis. The findings of this study have a number of important implications for future practice. Key Words: catalase, endometriosis, gene polymorphism, oxidative stress
Abstract #16 PERIOPERATIVE INTRAVENOUS LIDOCAINE INJECTION PROVIDES POSTOPERATIVE PAIN RELIEF AND DECREASES OPIOID REQUIREMENT AFTER LAPAROSCOPIC CHOLECYSTECTOMY FangLin Chang and Shinn Long Lin Presented By: FangLin Chang Objective: Systemically administered local anesthetics and other sodium channel blockers produce analgesia in patients with hypersensitivity disorders. In the present study, we examined whether perioperative treatment with intravenous lidocaine provides the better postoperative analgesia. Methods: Fortyfour patients undergoing laparoscopic cholecystectomy were studied with one half of the patients receiving a lidocaine bolus (1.5 mg/kg) and infusion 3 mg/kg/hr; the other half received a saline infusion. Meperidine (1 mg/kg IM) was given for postoperative pain relief as required. A blind observer recorded the times to first meperidine injection, total meperidine consumption, worst pain score and side effects were recorded for 48 h after surgery. At the same time, patients were instructed to write down the exact time of bed rest (the interval between the end of the surgery and end of bed rest) and bowel movement.
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Results: Times to first meperidine injection were 8.4 16.1 and 1.4 0.6 h for the lidocainetreated group and saline group, respectively. The total meperidine consumption was 49.5 32.4 and 80.2 33.8 mg for the lidocainetreated group and saline group, respectively. The worst visual analog pain scores were 4.5 1.1 and 6 0.9 for the lidocainetreated group and saline groups, respectively. The average time of bed rest and bowel movement were not significant. The time of bed rest was 19.73.4 and 21.32.5 h for the lidocainetreated group and saline group, respectively(P >0.05). The time of bowel movement was22.13.2 and 22.33.0h for the lidocainetreated group and saline group, respectively(P >0.05). Seven and three patients suffered from either meperidineassociated nausea, vomiting, dizziness, or headache in the saline group and lidocainetreated group, respectively. Conclusions: In the study, we conclude perioperative intravenous lidocaine injection provides postoperative pain relief and decreases opioid requirement after laparoscopic cholecystectomy.
Abstract 17 SEVERITY OF DYSMENORRHEA IS CORRELATED WITH OVERALL ELEVATED PAIN REPORT Allyson Westling2; James Griffith, PhD1; Julia Resnick, MPH2; Kevin Hellman, PhD2,3; Frank Tu, MD, MPH2,3 1 Medical Social Sciences, Northwestern University; 2Ob/Gyn, NorthShore University HealthSystem; 3 Ob/Gyn, University of Chicago Presented By: Frank Tu, MD, MPH Objective: Dysmenorrhea remains a poorly understood risk factor for chronic pelvic pain (CPP). One in every five women with menstrual pain will develop a CPP disorder such as endometriosis, interstitial cystitis, or irritable bowel syndrome, but menstrual pain has largely been ignored as a potential target for risk reduction. As part of a broader survey, we investigated the relationship of dysmenorrhea to 7 CPPlike pains: bladder, intercourse, urination, bowel, abdominal, pelvic, and overall pain categories. Methods: A webbased assessment of nonpregnant women (age 1845) was administered. Demographic questions and menstrual timing questions were queried, as well as items addressing pertinent constructs based on prior literature and focus group results: fatigue, mood, pain, somatic symptomatology, and physical functioning. Multivariable linear regression was used for statistical evaluation. Results: Among 1021 participants, mean age was 35.06 years old (SD 7.78), with an average parity of 1.3 (SD 1.4). Over 70% of the women reported having a regular, 2135 day interval menstrual cycle, with the typical menses lasting 5 days (SD 1.54). Over 40% of these subjects indicated moderate or worse dysmenorrhea, and 10% had severe dysmenorrhea. The overall VAS pain score among this cohort at the time of the survey was 2.4 (SD 2.57). The reported severity of dysmenorrhea and the seven different types of CPPlike pain symptoms were significantly correlated (R2=0.19). Only a weak relationship exists between reported pain intensity in these seven pain categories and being on the menses at time of assessment (R2=0.01), suggesting that the severity of dysmenorrhea is associated with regional pain sensitivity throughout the entire menstrual cycle. Multivariable linear regression identified that a combined model that includes anxiety and dysmenorrhea, but not depression best predicts CPP severity (R2=0.35). Conclusion: Self reported intensity of abdominopelvic pain in a general population sample of menstruating women is positively associated with dysmenorrhea intensity. Given the wellknown phenomenon of crossorgan sensitization, earlier identification of women with more severe dysmenorrhea may permit preclinical detection of future CPP patients, opening the door to prevention.
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Summary: In a sample of over 1,000 women, half were found to have moderate or worse dysmenorrhea. Severity of dysmenorrhea was associated with CPP like symptoms and pain sensitivity throughout the menstrual cycle.
Abstract #18 ATTRIBUTES AND BARRIERS TO CARE OF PELVIC PAIN IN UNIVERSITY WOMEN Julie Mann, MPH1; Nash Moawad, MD, MS2 1 University of Florida; 2University of Florida College of Obstetrics and Gynecology Presented By: Julie Mann Objective: The objective of this protocol is to describe rates of pelvic pain in university women ages 18 and older, as well as to explore the barriers to adequate healthcare which exist for women in this population who suffer from pelvic pain. Methods: A crosssectional study was designed to assess chronic pelvic pain (CPP) in female students 18 years or older attending the University of Florida. The questionnaire was created online using REDCap electronic data capture tool hosted at the University of Florida. The questionnaire included demographic items, general health and health behavior questions, measures to assess different types of pelvic pain (dysmenorrhea, dyspareunia, urinary, bowel and vulva), items regarding barriers to care for pelvic pain problems, and quality of life measures. A randomized sample of 2000 female university students email addresses was compiled, and they received instructions and the questionnaire hyperlink via REDCap. Data were exported into SAS statistical package for analysis. Results: Of the 2000 subjects who received the questionnaire invitation, 390 filled out the questionnaire, yielding a response rate of 19.5%. Respondents ages ranged from 18 to 51, with a mean of 23.28 years. A total of 79.3% of respondents reported experiencing pelvic pain over the past 12 months. Dysmenorrhea was reported by nearly 80% of participants; vulvar symptoms, including superficial dyspareunia, were reported by 21.5% of participants; over onethird of participants noted deep dyspareunia; and a significant proportion of participants reported symptoms related to bowel movements. Most participants with pelvic pain (78.8%) have not received any diagnosis for their pain, while 73.6% report not yet having visited a doctor. Significant barriers to receiving adequate medical care were reported, including difficulty with insurance coverage, and physicians lack of time and knowledge or interest in CPP conditions. Conclusion: Pelvic pain in younger women is a critical public health issue experienced by a significant portion of the population. Careful study of the barriers to receiving adequate medical care reported by these women will allow researchers to describe how best to improve care for these syndromes. Key Words: Chronic pelvic pain, university women Summary: A substantial number of young women experience chronic pelvic pain and various barriers to adequate health care while seeking diagnosis and treatment.
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Abstract #19 LOW DOSE U50488 RESTORES THE ANTINOCICEPTIVE EFFECT OF MORPHINE VIA UPREGULATION OF ANTIINFLAMMATORY CYTOKINE IL10 EXPRESSION IN MORPHINETOLERANT RATS ShinnLong Lin, MD, PhD2; ChunChang Yeh, MD2; FangLin Chang, MD1; ChenHwan Cherng, MD, PhD1; ChihShung Wong, MD, PhD2 1 anesthesia physician; 2pain specialist & anesthesia physician Presented By: ShinnLong Lin Objective: Combination of opioid agonist and antagonist administration was demonstrated to inhibit opioid tolerance, however, the mechanisms remain unclear. Chronic morphine treatment induces both proinflammatory and antiinflammatory cytokines expression, which plays a role in tolerance development. The aim of our study was to examine the effect of low dose kappa agonist (U50488) on morphine tolerance and the possible role of antiinflammatory cytokine IL10. Methods: Male Wistar rats implanted with intrathecal catheter were used. Morphine tolerance was induced by chronic intrathecal infusion of morphine (15 ug/hr), and the effect of low dose U50488 (0.5 ug/hr) on morphine tolerance was examined by coinfusion with morphine. The effect of IL10 was examined by additional intrathecal IL10 antibody (10 mg once daily) administration. Behavioral tailflick test, immunohistochimstry staining and real time PCR for cytokine IL10 expression were examined. Results: Low dose U50488 coinfusion with morphine attenuated morphine tolerance and IL10 antibody injection reversed this effect. Tail flick latency decreased under IL10 antibody administrated in an apparent accumulated manner. Immunohistochemistry staining revealed an increasing of IL10 expression in the rat spinal cord by the low dose U50488 coinfusion. Moreover, astrocytes and microglials were activated by IL10 antibody administration in rats which prior coinfused with morphine and low dose U50488. Conclusions: The expression of antiinflammatory cytokine IL10 is contributed to the restoration of morphines antinociceptive effect by low dose U50488 treatment in morphinetolerant rats and involves immunologically specific cellular alterations. Key Word: U50488, morphine tolerance, IL10,
Abstract #20 COMMON INFLAMMATORY CYTOKINES IN ENDOMETRIOSIS, INTERSTITIAL CYSTITIS, AND IRRITABLE BOWEL SYNDROME Jessica Ritch, MD; Maryann Masone, MD; Wilkens Mondesir, MD; Barry Jarnagin, MD; Jennifer Tatalovich, MD Center for Pelvic Health Presented By: Jessica Ritch Objective: Chronic pelvic pain can have several etiologies including, but not limited to endometriosis, interstitial cystitis, and irritable bowel syndrome. There is significant overlap between these conditions and patients with chronic pelvic pain often suffer with two or more conditions. While several studies have noted increased prevalence of each condition when another is present, most still evaluate these three conditions as separate entities and target diagnosis and treatment to individual problems. We believe that these chronic conditions of the pelvis stem from an inflammatory process that affects one or more organ systems. Our aim was to identify elevations in inflammatory cytokines that are common to endometriosis, interstitial cystitis, and irritable bowel syndrome.
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Methods: Comprehensive searches of Pub Med and Ovid Medline were conducted using the search terms endometriosis AND cytokines, interstitial cystitis AND cytokines, and irritable bowel syndrome AND cytokines. Over 8000 results were initially identified. All nonjournal references, nonEnglish references and duplicates were eliminated. The remaining titles and abstracts were reviewed for relevance. Fulltext articles of relevant abstracts were then reviewed to identify specific cytokine alterations and these were compiled in a table to reference across diagnoses. Results: Common proinflammatory cytokine elevations noted in all three diagnoses (endometriosis, interstitial cystitis, and irritable bowel syndrome) included interferon, interleukin1, interleukin2, interleukin6, interleukin8 and tumor necrosis factor. Antiinflammatory cytokines, interleukin4, interleukin10, and transforming growth factor were also noted to be altered, typically decreased. Interleukin4 was altered in all three diagnoses. Interleukin10 was altered in both endometriosis and irritable bowel syndrome, but has not been described in interstitial cystitis. Transforming growth factor was altered in interstitial cystitis and irritable bowel syndrome, but not endometriosis. Conclusion: Several inflammatory cytokines are common to endometriosis, interstitial cystitis, and irritable bowel syndrome. This may suggest that these conditions are part of a similar inflammatory process. While it remains unclear whether the inflammatory process is the cause of these conditions or a result of them, evidence exists to warrant more investigation into the inflammatory process and to evaluate inflammatory pelvic conditions as a whole, rather than as separate entities. Targeting a common inflammatory process may provide more relief to patients suffering from chronic pelvic pain. Key Words: endometriosis, interstitial cystitis, irritable bowel syndrome, cytokines Summary: Inflammatory cytokines are found to be elevated in endometriosis, interstitial cystitis, and irritable bowel syndrome.
Abstract #21 ASSOCIATIONS BETWEEN GYNECOLOGICAL CHARACTERISTICS AND TEMPOROMANDIBULAR DISORDERS: INSIGHTS FROM THE OPPERA STUDY Erin Carey, Denniz Zolnoun, Gary Slade, Richard Ohrbach, Naomi Brownstein, Ron Dubner, Joel Greenspan, Roger Fillingim, William Maixner and Eric Bair UNCChapel Hill Presented By: Eric Bair Objective: Chronic pain conditions, such as temporomandibular disorders (TMD), are more common in women than in men. The aim of this study is to explain gender difference by evaluating gynecological characteristics that are putative risk factors for TMD: parity, use of hormonal contraception, and pain levels and psychological symptoms over the course of the menstrual cycle. Methods: OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) is a prospective cohort study designed to identify risk factors for the onset of TMD. Subjects were recruited at four U.S. study sites from 20062008. The present analysis was based on 155 women with chronic TMD and 925 women without TMD. Each study participant provided questionnaires to evaluate their gynecological history in addition to a Prospective Record of the Impact and Severity of Menstruation (PRISM) diary to investigate pain and psychological distress over 28 days. Logistic regression models were used to evaluate the association between TMD case status and each risk factor, and mixed effects models were used to evaluate the association between each symptom measured by the PRISM diary and TMD case status and the phase of the menstrual cycle.
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Results: Current use of hormonal contraception (HC) was weakly associated with TMD, although the association was no longer statistically significant after adjusting for race and age (OR 1.6, 95% CI=1.0, 2.4). The use of HC for five years or longer was significantly associated with TMD case status (OR 2.9, 95% CI=1.9, 4.3) as well as using HC to treat pain (OR 2.5, 95% CI=1.3, 4.6), however using HC for other reasons (bleeding, contraception) was not associated with case status (OR 1.6, 95% CI=1.0, 2.5). Dysmenorrhea was associated with a higher risk of TMD (OR 3.0, 95% CI=1.3, 6.7). Severe premenstrual symptoms (PMS) were also associated with a higher risk of TMD (OR 2.3, 95% CI=1.1, 4.7). Women with TMD reported higher levels of abdominal pain (p<0.0001) and pelvic pain (p<0.0001) as well as psychological distress throughout the month on their PRISM diary compared to women without TMD. Women with TMD also reported more severe pain in several bodily regions during the follicular phase of the menstrual cycle than TMDfree women. Conclusions: Though a weak associated with current HC use and TMD case status was noted, a stronger association was observed with longterm use (>5 years) and TMD case status. Further study on the association between HC use and TMD is needed. Dysmenorrhea has been associated with other functional pain syndromes, and dysmenorrhea and severe PMS symptoms are both strongly associated with TMD. These results suggest that the higher prevalence of TMD in women may be influenced by female reproductive hormones and provide evidence that pain during menstruation may increase womens risk of developing more serious chronic pain conditions. Summary: A prospective cohort study of TMD reveals an association between TMD and dysmenorrhea, PMS, and elevated levels of pain/psychological symptoms during menstruation. Key Words: temporomandibular disorders, dysmenorrhea, PMS, hormonal contraception Supported by NIH/NIDCR U01DE017018.
Abstract #22 OPPERA STUDY IDENTIFIES AN ASSOCIATION BETWEEN THE USE OF HORMONAL CONTRACEPTIVES AND OROFACIAL PAIN AND HEADACHES Sheila Gaynor, Denniz Zolnoun, Erin Carey, Gary Slade, Naomi Brownstein, Richard Ohrbach, Roger Fillingim, Joel Greenspan, Ron Dubner, William Maixner and Eric Bair UNCChapel Hill Presented By: Eric Bair Objective: Previous studies have identified an association between the use of hormonal contraceptives (HC) and painful conditions such as migraine headaches and temporomandibular disorders (TMD), although the nature of this association remains unclear. This analysis sought to determine the relationship between hormonal contraceptive use and painful symptoms (particularly headaches and orofacial pain) using data from a largescale prospective cohort study. Methods: OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) is a prospective cohort study designed to identify risk factors for the onset of TMD. Participants were recruited at 4 study sites from 20062008. A total of 3,263 initially TMDfree individuals were enrolled, including 1863 women. Each OPPERA participant completed a questionnaire every three months that evaluated the frequency and severity of the painful symptoms in the orofacial region. Participants also reported the presence of pain in other bodily regions and whether they were using any medications, including HC. Mixed effects regression models were used to evaluate the association between HC use and orofacial pain. Each model included all female OPPERA participants who had completed at least one follow up questionnaire. HC use was modeled as a fixed effect with a random effect for each participant. Standard linear mixed effects models were used for continuous outcomes, and logistic generalized linear mixed models were used for binary outcomes.
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Results: There was a significant association between HC use and the presence of cheek and jaw pain (OR=1.5, 95% CI=1.3,1.7) and headaches (OR=1.7, 95% CI=1.5,1.9). When participants were asked to rate the intensity of their orofacial pain on a scale from 0 to 10, HC users reported greater pain intensity (mean difference=0.25, 95% CI=0.15,0.35). There was also a statistically significant difference between HC users and nonusers in the number of months with 5 or more days with orofacial pain (mean difference=0.03, 95% CI=0.01,0.04). When participants were asked to report which regions of the body experienced aches and pains, HC use was significantly associated with pain in the face (OR=1.4, 95% CI=1.0,1.8) and head (OR=1.4, 95% CI=1.1,1.6). There was no significant association (at the p<0.05 level) between HC use and pain in other regions of the body. These results remained essentially unchanged after excluding women with severe menstrual pain and those who had used HC to treat pain prior to enrollment. Conclusions: HC use was associated with the presence, severity, and duration of orofacial pain. No association was observed between HC use and pain in other bodily regions. Since the association remained after excluding women with severe menstrual pain, it is unlikely that the association between HC use and orofacial pain can be explained by the fact that HC is used to treat dysmenorrhea and other painful conditions. Summary: A prospective cohort study of TMD reveals an association between HC use and orofacial pain. No such association was observed between HC use and pain in other bodily regions. Key Words: orofacial pain, headaches, dysmenorrhea, hormonal contraception Supported by NIH/NIDCR U01DE017018.
Abstract #23 PUTATIVE RISK FACTORS FOR DYSMENORRHEA: RESULTS FROM THE OPPERA STUDY Frank Tu, Donna Wilson, Saswan AsSanie, Erin Carey, Denniz Zolnoun, Lia Weiner, Gary Slade, Richard Ohrbach, Joel Greenspan, Ron Dubner, Roger Fillingim, William Maixner and Eric Bair UNCChapel Hill Presented By: Eric Bair Objective: Dysmenorrhea is the most common gynecological problem of menstruating women. The aims of this investigation are to identify putative risk factors for dysmenorrhea and investigate differences in the severity of menstrual pain among different demographic groups. Methods: Baseline, selfreported data were analyzed from females aged 1844 years who enrolled in the OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) prospective cohort study. Participants were recruited at 4 U.S. study sites from 20062008. The present analysis was based on 1,831 females who reported at least one menstrual period in the prior 60 days, including 1,690 individuals with no history of temporomandibular disorder (TMD) and 141 chronic TMD cases. They reported the severity of abdominal pain experienced during menstrual periods over the previous three months, which was used to identify women with dysmenorrhea. The putative risk factors for dysmenorrhea in this analysis included demographic variables, namely race, age, income, education level, and whether the individual had health insurance, and gynecological variables, including parity, age of menarche, use of hormonal contraceptives (HC), and severity of premenstrual syndrome (PMS). The association between dysmenorrhea case status and each putative risk factor was evaluated using logistic regression.
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Results: AfricanAmericans (OR=1.4, 95% CI=1.1,1.7) and those without health insurance (OR=1.4, CI=1.1,1.9) had greater odds of dysmenorrhea. Those with postgraduate degrees had lower odds of dysmenorrhea (OR=0.7, 95% CI=0.5,0.9). There was slight evidence that those with an income of less $60,000 had higher risk of dysmenorrhea, but the association was no longer significant after adjusting for age, race, and HC use (OR=1.0, 95% CI=0.8,1.3). No consistent relationship was observed between age and dysmenorrhea. Severity of PMS was strongly associated with dysmenorrhea. Even mild PMS significantly increased the risk of dysmenorrhea (OR=2.7, 95% CI=1.9,4.0), and severe PMS was very strongly associated with dysmenorrhea (OR=46.3, 95% CI=24.7,87.1). There was evidence of a weak association between nulliparity and dysmenorrhea (OR=1.3, 95% CI=1.0,1.8). No association was observed between the age of menarche and dysmenorrhea. Use of HC was protective against dysmenorrhea (OR=0.5, 95% CI=0.4,0.7). Conclusions: The putative risk factors that were most strongly associated with dysmenorrhea include AfricanAmerican race, lack of health insurance, and severity of PMS. HC use and postgraduate education were protective. Interestingly, the associations between dysmenorrhea and race, health insurance, and education remained significant after adjusting for HC use, suggesting that the association cannot be entirely explained by lower HC use in the highrisk groups. Although age, parity, and age of menarche have been associated with dysmenorrhea in previous studies, they were at best weakly associated with dysmenorrhea in the present cohort. Summary: A prospective cohort study of TMD reveals socioeconomic and gynecological risk factors for dysmenorrhea. Key Words: dysmenorrhea, hormonal contraception, demographics Supported by NIH/NIDCR U01DE017018.
Abstract #24 HISTORY OF COMORBID OROFACIAL PAIN AMONG WOMEN WITH VULVAR VESTIBULITIS SYNDROME Eric Bair, Elizabeth Simmons, William Maixner, Andrea Nackley and Eric Bair UNCChapel Hill Presented By: Eric Bair Objective: In an earlier study, we identified an association between orofacial pain (OFP) and its associated clinical characteristics and vulvar vestibulitis syndrome (VVS). The aim of the present study was to evaluate the stability of this association after a period of two years in hopes of uncovering additional clues in the underlying mechanisms of both conditions. Methods: This retrospective cohort study was conducted between July 20, 2006 and January 2, 2007, which is two years after the previous parent study. The analysis included 71 out of 137 women in the parent study who consented to participate in the followup study. Each participant completed each questionnaire that was administered in the parent study, which included assessments for psychological characteristics, selfreported pain, and signs and symptoms of OFP. Each subject was classified as having OFP, subclinical OFP, or no OFP. Fishers exact test was used to determine if there were differences in categorical patient characteristics amongst the OFP classifications, and ANOVA was used for numeric patient characteristics. Differences in psychological characteristics amongst the OFP classifications were identified using ANOVA and subgroup differences were identified after making appropriate adjustments for multiple comparisons.
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Results: OFP was highly prevalent (66%) among women with VVS and women with OFP symptoms experienced higher levels of anxiety (P=0.005) and somatization (P<0.001) than women with no OFP symptoms, which is consistent with our earlier study. No significant differences in demographics were observed in the subgroups, which is also consistent with our earlier results. 73% of OFPfree patients at baseline remained free of symptoms, whereas only 39% and 53% of VVS patients with subclinical and clinical OFP stayed within their respective category. 33% of VVS patients with OFP symptoms at baseline showed reduced OFP symptoms over the course of the twoyear followup period. However, 13% of VVS patients either developed new symptoms or transitioned from subclinical to clinical OFP classification by the time of the followup study. Women with OFP symptoms showed less improvement in their VVS symptoms than women without OFP. Conclusions: OFP is a common comorbidity among women with VVS. There is an association between psychological variables and OFP subgroups, and women with OFP were less likely to respond to treatment for VVS. This is possible evidence that VVS patients with OFP have a centrally mediated subtype of VVS with poorer treatment outcomes. The relationship between VVS and OFP is a subject for further research. Summary: OFP is comorbid with VVS, and VVS patients with high levels of psychological distress are more likely to have comorbid OFP. Key Words: orofacial pain, vulvar vestibulitis syndrome, psychological distress
Abstract #25 RELIABILITY AND REPRODUCIBILITY OF NOVEL METHODOLOGY FOR ASSESSMENT OF PRESSURE PAIN SENSITIVITY IN THE PELVIC REGION Denniz Zolnoun, Eric Bair, Greg Essick, Richard Gracely, Jasmine Lewis and William Maixner Presented By: Denniz Zolnoun Objective: Vestibulodynia impairs the psychological, physical and reproductive health of nearly 1 in 10 women at some point in their lifetime. The aim of this investigation was 1) to establish reliable standardized methodologies for assessment of pain sensitivity in vulvar mucosa and pelvic musculature and 2) to relate these measures to patients clinical pain reports. Methods: 34 women with vestibulodynia and 21 pain free controls were recruited through at the UNCChapel Hill between March 2006 and August 2009. The participants underwent a nuanced vulvar mucosal and pelvic muscle pain sensitivity assessment, which consisted of a standardized approach to stimulation of precisely located vulvar mucosal and pelvic muscle sites. For some subjects the exam was repeated during the same session by a second examiner, or by one or two of the same examiners in a separate session approximately two weeks later. To assess the reliability of each instrument, Pearson correlations were calculated between each pair of measurements. The association between each measurement and vestibulodynia case status was evaluated using Cox proportional hazards models. A random effect for each subject was included in the models to account for repeated measurements. Results: Withinexaminer correlations were high (r=0.810.87) for both mucosal and muscle sites. However, betweenexaminer correlation on average was lower (r=0.110.58) for the mucosal sites, but within acceptable range for the respective muscle sites (r=0.580.85). On average mucosal and muscle measures were stable over a twoweek period, as evidenced by a robust correlation. However, the strength of this correlation varied across tested sites. The highest correlations were observed at the three lower mucosal sites (r=0.820.87). The correlations for the remaining three mucosal (r =0.550.66) and muscle sites (r=0.610.67) were lower.
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Overall, women with vestibulodynia showed significantly lower pressure pain detection thresholds compared to their painfree counterparts. This was particularly robust at the three sites on the lower vestibule (HR=1746), although the upper vestibule measurements were also strongly associated with vestibulodynia (HR=67). Similarly, compared to painfree participants, patients with vestibulodynia showed lower pelvic muscle pressure pain threshold and tolerance measurements. We observed a significant association between vestibulodynia case status and muscle threshold measures when measurements from all three sites were combined (HR=2.9, p=0.047). There was a similar pattern of association with respect to the muscle tolerance measures (HR=3.09, p=0.005). Conclusion: Our data support the feasibility of concurrent assessment of vulvar mucosa and underlying musculature in the pelvic region. Mucosal and muscle threshold measures remained highly stable over the two weeks study period, with high withinexaminer correlation. Both sets of measurements were also associated with vestibulodynia case status. Summary: A novel methodology for assessing pain in the pelvic region is shown to be reproducible. It is also associated with vestibulodynia case status. Key Words: vestibulodynia, sensory testing
Abstract #26 CATASTROPHIZING: A STRONG PREDICTOR OF PAIN AND TREATMENT OUTCOMES AMONG WOMEN WITH CHRONIC PELVIC PAIN Elisabeth Johnson, PhD, MSN, NP2; Caitlin Martin, BS1; Jane Leserman, PhD2; Denniz Zolnoun, MD, MPH2 1 Johns Hopkins; 2UNC Chapel Hill Presented By: Elisabeth Johnson (1690/3200) Objective: The objective of this study was to determine the predictors of pain improvement among women with chronic pelvic pain (CPP) Background: Chronic pelvic pain (CPP) in women causes significant disability and distress. Like other chronic pain conditions, psychosocial variables likely play as key a role in the development and maintenance of CPP as physiological ones. The purposes of this study were to determine the predictors of pain and to specifically examine to effect of catastrophizing on pain reports. Methods: Secondary analysis of baseline (n = 285) and 12month (n = 258) data collected from women presenting for CPP at a tertiary referral center was performed. Participants completed questionnaires assessing pain, mental health, and catastrophizing at entry and one year followup. The main outcome measure assessed was the interval change in pain report using the McGill Pain Questionnaire (MPQ). Results: Participants were predominantly middle aged (M = 34.85, SD = 10.36), married (67%), Caucasian (79%), and educated (M = 14.86, SD = 2.50). Baseline catastrophizing was a strong predictor of baseline pain (R2 = .34, p<.0001; = .40, p < .001). Adjusted for baseline pain, women with higher pain scores at oneyear were less likely to have a hysterectomy during the followup period (p<.0001), more likely to have been treated with narcotics at study entry (p = .04), and more likely to cope via catastrophizing at follow up (p<.0001) (R2 = .59, p<.0001; = .59, p < .001). Conclusions: These findings contribute to the existing body of literature by confirming the complex nature of CPP and suggest that psychological processes such as catastrophizing play a vital role in predicting pain improvement in women with CPP. Key Words: Chronic Pelvic Pain, Catastrophizing
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Summary (170/200): Future research will benefit from further exploration of the contribution of psychological processes to CPP and the application of research from other pain conditions to gynecologic pain disorders.
Abstract #27 BILATERAL ACCESSORY BREAST TISSUE OF VULVA: A CASE REPORT Ida Janelle Wagner, MD; Lynn Damitz, MD; Elisabeth Johnson, PhD, MSN, NP; Jasmine Lewis, BS; Denniz Zolnoun, MD, MPH UNC Chapel Hill Presented By: Elisabeth Johnson (2788/3200) Objective: To report a case of bilateral labial mass that presented in a woman during her second trimester of pregnancy Methods: Though extremely uncommon, vulvar breast tissue has been identified and reported in adolescent patients and during pregnancy. Supernumerary breast tissue is attributed to the failure of regression of remnant milk line during embryogenesis, which subsequently is stimulated during puberty or pregnancy. Though benign, lack of regression in size of the stimulated breast tissue often necessitates a surgical intervention. Our case is of a woman who presented with bilateral labial mass during second trimester of her first pregnancy. The masses progressively increased in size, particularly during lactation. At its maximum, it measured 8 cm in anterior posterior dimension within a pendulous sack of stretched skin down to perineal region (with patient in dorsal lithotomy position). Conservative management during pregnancy and postpartum allowed for significant reduction in size (down to 5 cm) and engorgement prior to surgery. The procedure to remove the redundant labial skin and underlying breast tissue highlights the application of a modified labioplasty approach to the vulvar region utilizing an inverted Uincision. In addition, using simple bed side sensory testing (a cotton swab), we were able to delineate the anatomical region innervated by dorsal clitoral nerve thus avoiding inadvertent surgical incision in areas associated with female sexual function. Results: The patient recovered well. Two months after her surgery, the patient reported that she had been sexually active without loss of any sensation and she was not experiencing any pain or discomfort. On exam her external genitalia appeared normal and very close inspection was required to identify any residual component of the surgery. Sensory mapping of the labia minora and clitoral area were completely unremarkable. Conclusions: In the current case, the proximity of the masses to the clitoral region necessitated care to preserve sensation of the dorsal clitoral nerve to insure the maintenance of sexual function. Detailed sensory mapping achieved by the stimulation of the skin with the soft end of a cotton swab in the areas innervated by the dorsal clitoral and perineal nerves preoperatively allowed for incisions to be made that would not cut across the sensory nerves. In gynecology, the tendency is to make a midline incision and then proceed with resection of superficial and centrally located vulvar masses. This approach can be detrimental to long term sexual function as the midline falls along the distribution of the dorsal clitoral nerve. Surgical scarring may further injure nerve endings and may result in abnormalities in arousal and sensation. In addition, care was given to maintain the anatomical asymmetry that was observed preoperatively. While the acknowledgement of naturally occurring asymmetry is appreciated in the plastic and general surgery literature, it is not well described in gynecology. This arises from the lack of the description of the normal variations of vulvar anatomy and the subsequent understanding of how these variations interact.
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Keywords: Supernumerary breast tissue, Summary (145/200): This case shows the importance of incision placement near the dorsal clitoral nerve and the need for further education on normal variations of vulvar anatomy in gyneclogy.
Abstract #28 DORSAL CLITORAL NERVE INJURY FOLLOWING TRANSOBTURATOR MIDURETHRAL SLING PLACEMENT Chailee Moss, BA; Elisabeth Johnson, PhD, MSN, NP; Jasmine Lewis, BS; Denniz Zolnoun, MD, MPH UNC Chapel Hill Presented By: Elisabeth Johnson (3194/3200) Objectives: To report a case of a woman with dorsal clitoral neuralgia after a transobturator sling procedure. Methods: A 51 year old woman presented with a 3year history of pain immediately following an anterior and posterior repair and transobturator sling placement for the treatment of stress urinary incontinence (SUI). She described the pain as a constant, leftsided pinching sensation localized to her clitoral region with radiation along her inner thigh that is exacerbated by movement and intercourse. Intermittently, she also experienced shooting pain down her posterior leg and ankle. An attempt at controlling her symptoms with ganglion impar block had lead to significant exacerbation, with resurgence of pinching sensation upon arousal, at which time patient was referred to our clinic. On abdominal examination, patient had pin prick hyperalgesia along the illioinguinal nerve on the left side with relative loss of acuity of sensation of gentle stroke with a cotton swab (as compared to the right side.) Downward traction on posterior vagina recreated her typical shooting clitoral painwhich extended upward on labia to the clitoris the left side, and followed by an achy after painwhich generalized to the lower abdomen bilaterally. Collectively these observations were suggestive of neuropathy along dorsal clitoral nerve. Results: 10 cc of 50:50 dilution of 1% lidocaine and 0.5% ropivacaine was injected at the perineal branch of pudendal nerve before it anatomically split into dorsal clitoral nerve. Subsequently 10 cc of the same dilution was injected into the region on the left side of the clitoris in a fanlike fashion. The distal block caused numbing and decreased intensity of the baseline irritation and perception of the clitoris. At her next visit, the patient reported 6 to 8 hours of complete pain relief following the nerve block and continued improvement with duloxetine use. The pain continued to be exacerbated by movement (particularly vibration associated with car rides and walking up hill). Her subjective evaluation of her overall improvement since the previous visit was 50%. A second nerve block was conducted with the use of an 80 cm nerve stimulator needle to help localize the lesion. The needle was primed with 0.5% ropivacaine and 1% lidocaine, and inserted into the perineal fascia set at 3 amperes. 2 cc of anesthetic were injected at the point of lesion confirmation. Anesthetic effect was confirmed with a repeat neurostimulation test. In addition, the entire left side of the vestibule (both the clitoral and vestibular branches) was blocked. On exam, consistent with previous suspicion that it was secondary to the dorsal clitoral nerve irritation, her muscle tenderness was resolved. The patient was instructed to use a vibrator to mobilize scar tissue, decrease nerve irritation, and treat potential muscle soreness caused in the distribution of her neuropathy.
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Conclusion: In cases where nerve compression is suspected to cause postoperative pain, early recognition would allow more prompt decompression and would decrease pain while preserving nerve function. Cases of postoperative neuralgia that are not attributed to compression may be managed expectantly with close followup, physical therapy, and antiinflammatory medications. Additionally, centrally acting agents such as duloxetine can be used to improve central sensitization problems in neuropathic pain, while local anesthetics may specifically address the peripheral component. This case is an example of how careful symptomatic management with attention to decreasing central sensitization may be used in the management of transobturator sling postoperative neuralgia, and affirms the vulnerability of the dorsal nerve of the clitoris to injury during sling placement. Key words: Transobturator sling, postoperative neuralgia (107/200) Summary: Sensory mapping and diagnostic nerve block may aid in identifying the source of post operative pain and subsequent treatment.
Absract #29 REDUCTION OF CHRONIC ABDOMINAL AND PELVIC PAIN, UROLOGICAL AND GI SYMPTOMS USING A WEARABLE DEVICE DELIVERING LOW FREQUENCY ULTRASOUND David Wiseman, BSc, PhD; MRPharmS1; Teena Petree, PT2 1 International Adhesions Society; 2Summit Physical Therapy, Dallas, TX Presented By: David Wiseman Objective: To assess the efficacy of Painshield (NanoVibronix Ltd., Nesher, Israel) a wearable device delivering lowfrequency, low intensity ultrasound in patients with pelvic and related pain. Methods: In this openlabel, prospective, experiential study, 16 women and 3 men (age 46, range 3362) with a history of chronic pelvic, urological or related pain or symptoms (15.3 years, range 133 years), received Painshield on prescription. Diagnoses included endometriosis (26%), adhesions (63%), bowel obstruction (42%), IBS (32%), Interstital Cystitis (32%) or other CPP (63%). Patients provided information about their symptoms before treatment and up to 51.4 days (range 1207) afterwards. Scoring was based on the Brief Pain Inventory, ShortForm McGill Questionnaire, and the International Pelvic Pain Societys form. Scores from before and after treatment were compared by t test comparison of rankings of levels (010) of each type of pain using the maximum score reported. Results: Often exceeding or approaching statistical significance, improvements in pain or related symptoms were noted (before treatment score v. after treatment score, N, p) for all symptoms which were pain before urination (6.1 v. 4.3, N=12, p=0.021); pain on urination (6.0 v. 2.0, N=7, p=0.001); urinary urgency (% of time) (100% v. 54%, N=6, p=0.06); urination frequency/day (21 v. 14, N=11); difficulty urinating (% of time) (100% vs 60%, N=8, p=0.08); Other chronic pelvic or abdominal pain (8.3 vs 5.9, N=12, p=0.042); dyspareunia (during) (7.8 v. 5.5, N=12); dyspareunia (after) (6.6 v. 4.3, N=8); dyschezia (7.7 v. 3.6; N=10, p=0.001); abdominal bloating (% of time) (83% vs 53%, N=10, p=0.049); rectal pain (9.3 v. 6.0, N=4); sacroiliac joint pain (8.5 v. 6.5, N=6, p=0.081); sitting tolerance (minutes) (36 v. 91 mins, N=12); other muscle/joint pain (7.4 v. 5.2, N=18, p=0.03). Patients often reported the onset of relief within hours or days after starting treatment and a reduced need for analgesic or other medication. Overall patients rated their response as Negative (2/19), Mild (4/19), Moderate (3/19) or Good (10/19). The two patients responding negatively reported a rapid onset (< 1 day) of pain and/or swelling which subsided from 1 to several days later. One patient responding well experienced some abdominal discomfort after using the device. Two of these patients reported similar reactions to conventional officebased ultrasound. Conclusion: Further evaluation of the utility of Painshield in this patient population is warranted.
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Summary: PainShield, a portable, wearable ultrasound device was found to reduce pelvic, urological pain and related symptoms in 19 patients presenting with longstanding and refractory symptoms. Keywords: Pain, pelvic, ultrasound, bladder, rectal We thank Nanovibronix for providing Painshield units at no cost. At the time of the study, neither author had a financial interest. Since concluding the study, the primary author's company has become a distributor for Painshield.
Abstract #30 COMPARISON OF OUTCOMES OF SPECIALIZED PELVIC PHYSICAL THERAPY BETWEEN PELVIC PAIN PATIENTS AND OTHERS REFERRED FOR PELVIC FLOOR REHABILITATION Karen Brandon, DSc PT WCS1; Ranjini Moses, DPT2 1 Kaiser Permanente Fontana, CA; 2Kaiser Permanente Fontana,CA Presented By: Karen Brandon Objective: To describe the utilization and efficacy of multimodal pelvic PT delivered by womens health specialty physical therapists in treatment of primary pelvic pain diagnoses in comparison with outcomes for other urogenital conditions that are seen in a typical womens health practice. Methods: We retrospectively reviewed 166 female patients, 15 85 years of age with complete data sets who were referred to pelvic PT between March 2006August 2009. Mean visits completed for all patients was 9. Frequency analyses were conducted to determine the primary diagnoses that were seen in volume. The outcomes were evaluated by patient survey at the completion of care into seven categories. Progress toward goals in three domains was reported for subjective data, objective findings, and functional self assessment and was cross tabulated with primary diagnoses to see the efficacy of the treatment across different patient populations. Results: Out of 166 patients, frequency of referral for pelvic pain (both acute and chronic and inclusive of sexual pain) was a total of 75 cases, 45% of the total referrals to the clinic. The second largest volume of referrals was stress urinary incontinence (16.9%), then mixed urinary incontinence (13.3%), then overactive bladder (OAB) dry (12%), fecal incontinence (8.4%), voiding dysfunction (2.4%), musculoskeletal obstetrics (1.2%) and OAB wet (.6%). Outcome measures demonstrated using a 7 item nominal scale with two investigator catagories for confounders such as No Infoif patient did not complete the survey or if patient was sent for a Evaluation Onlyto differentially diagnose musculoskeletal involvement. Patient polled at end of their care episode were asked if they felt their primary symptom complaint had been resolved and satisfied not warranting further medical management for this condition, reduced and satisfied not warranting further medical management for this condition, reduced and unsatisfied and interested in further medical management of this condition, primary symptom had been addressed and their diagnosis redefined to warrant further medical management of a related condition, or no impact, interested in further medical management of this condition. At the end of their care, 32.4% of pelvic pelvic pain patients reported reduced and satisfied, 16.2% were reduced and unsatisfied, 14.9% were resolved and satisfied, 14.9 were diagnosis redefined, and 14.9% had no information, and 4.1% reported no impact, with 2.7% evaluation only. In comparison the primary SUI patients reported they were reduced and satisfied by 35.7%, no information 25%, reduced and unsatisfied 21.4%, diagnosis redefined 7.1%, no impact 7.1%. The category with the third largest volume, mixed incontinence, demonstrated reduced and unsatisfied response of 36.4%, Resolved of 18.2%, reduced and satisfied 13.6%, No impact 13.6% no info 13.6% and redefined diagnosis 4.5% The highest reduced and satisfied percentage was in the anal incontinence group at 50%.
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Progress toward goals was measured by a likert type scale (goal met/partially met/not met) for three domains; Subjective goals, objective goals and functional goals. For goal progress, pelvic pain patients demonstrated 47.7% with 5075% improvement subjective report, 53.9% partial improvement of function, and 35.5% partial impairments reduced by discharge. As compared to the second highest volume, stress urinary incontinence patients who demonstrated 25% improvement in 5075% subjective report, 15.1% partial improvement in function, and 33.7% partial impairments reduced by discharge. Conclusions: The rate of referrals is consistent with findings that specialized services often have large referrals of complex cases that mainly consist of pelvic pain patients. In this study, we were evaluating the outcomes of pelvic PT for pelvic pain by patient reported satisfaction and also measured attainment of goals. When compared to outcomes for the other highest frequency of referrals for pelvic PT which include urinary incontinence, patients demonstrate higher attainment of subjective goals and changes in their functional measures though their objective measures improved at the same rate as other patient populations seen for pelvic PT. Summary: Pelvic Physical Therapy by a womens health specialist is highly utilized as a mode of treatment for pelvic pain diagnoses with musculoskeletal involvement, and in comparison with outcomes in other diagnosis categories it shows significance of positive changes in subjective, objective and functional domains.
Abstract #31 UROFLOW CHANGES IN A PAINFUL VOIDING DYSFUNCTION PATIENT WITH PELVIC FLOOR REHABILITATION AND ORGAN SPECIFIC VISCEROFASCIAL MANIPULATION Karen Brandon, DSc PT WCS1; Gail Wetlzer, PT, BID, EDO2 1 Kaiser Permanente Fontana, CA; 2Wetzler Integrative Physical Therapy Presented By: Karen Brandon Objective: Voiding dysfunction is a challenge to urogenital specialists especially in the absence of clinical findings that clearly define the etiology. Patients often undergo cystoscopy, urodynamics and pelvic exam and if dyssynergia is demonstrated or other factors indicate pelvic floor muscle involvement they may be referred to specialized pelvic physical therapy. Often once the pelvic floor muscle dysfunction is resolved, patients demonstrate improvements in their symptoms and voiding trials. However, if the muscle impairment is resolved but the patient continues to have dysfunction, there may be other soft tissue factors contributing to the patients persisting symptoms. This single case design investigated the integration of viscerofascial evaluation and treatment of a patient who had been referred to traditional specialized pelvic PT services and had not met her pain reduction and voiding goals. Case Study: 52 year old female dysfunctional voider, with difficulty emptying, as well as pelvic pain presents in pelvic physical therapy for pain, voiding disorder and urine loss from pelvic floor muscle incoordination. Symptoms gradually worsening over the last year, but history of abnormal voiding since hysterectomy 20 years prior. She also reports urgency severe and frequency of once every hour, bladder does not feel empty after urination and she has to strain to empty >50% of the time. Intake reveals history of sexual abuse/trauma as a child, three normal SVD, IBS, Fibromyalgia, and pulmonary nodule. Pain locations include Ribcage and low back and suprapubic area worse with full bladder and intercourse, better with emptying bladder. Main suprapubic pain was reported at 57/10 throughout the day.
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Pelvic PT findings included postural dysfunction of thoracic kyphosis, decreased lumbar lordosis pain with extension, poor breathing excursion and modified oxford strength of pelvic floor 2/5 with poor relaxation and descent and triggerpoints present in levator ani bilaterally and in rectus abdominus. She was treated with a series of nine manual therapy sessions intravaginally and extrapelvic treatments to normalize these impairement utilizing biofeedback, joint mobilization, postural retraining, neuromuscular reeducation and motor control. At the completion of the sixth visit she was reevaluated by her urologist for Uroflow study of emptying volume and rate. After the traditional pelvic physical therapy was completed she underwent organ specific viscerofascial assessment and it revealed mobility and motility restriction about the diaphragm, left lung, liver, right iliac vessels, intercostals, stinum, bladder and to a lesser extent restrictions involving the iliocecal sphincter, parietal peritoneum. The second series included 3 sessions of viscerofascial manipulation Results: After traditional pelvic PT she reported reduced frequency from hourly to 24 hours but continued slow stream and hesitancy. Void would take 1 hr, now only 10 minutes and intercourse painfree. Pain report went from initial 5/10 to now 02/10 suprapubic and before void with activity. Strength: modified oxford scale: from 2/5 to 3/5 , Mild PFM tightness right obturator internus and ilicococcygeus. Rib cage excursion 2cm to 4cm and limited trunk mobility T34 rib angle less than 90 degrees left ribcage depressed. After viscerofascial manipulation patient reported further improvement in emptying by single void and reduced time on toilet, as well as no need to strain to start or stop flow of urine. Uroflow data was collected prior to PT referral, post traditional PPT (tPPT) intervention and post visceral manipulation (VM) intervention. The findings demonstrated initially the patients Qmax was 4.9cc/min improved to 22.2 cc/min after tPPT, and even more to 30.3 cc/min after VM. Her Qave was initially 6.0 cc/min which improved to 7.9 cc/min with tPPT but then significantly increased to 15.9 cc/min after VM. All PVR were below 5cc at each testing. Conclusions: If traditional pelvic floor muscle and connective tissue rehabilitation have limited success, further evaluation utilizing visceral manipulation techniques and treatment strategies may demonstrate impairments in the viscerofascial system that can account for dysfunctional and painful voiding. These techniques may also be able to show improvement on urodynamics based on their ability to normalize the mobility about the entire urinary system and physiologic action of the bladder. Further studies are needed to look at imaging changes of the detrusor function before and after visceral manipulation so that the mechanisms of improvement can be better understood. Key Words: dysfunctional voiding, uroflow, visceral manipulation, physical therapy
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Abstract #32 QUALITY AND INTENSITY OF SENSATIONS EVOKED BY COTTON SWAB PALPATION OF THE VESTIBULE AMONG WOMEN WITH AND WITHOUT VESTIBULODYNIA Jasmine Lewis, Eric Bair, Richard Gracely and Denniz Zolnoun Presented By: Denniz Zolnoun Objective: The primary objective was to compare the quality and intensity of sensations evoked by cotton swab palpation of the vestibule among women with and without vestibulodynia. Methods: A total of 56 women underwent a structured sensory assessment of vulvar mucosa, including 35 vestibulodynia patients and 22 painfree controls. Six vestibular sites (three in upper and lower vestibule each) were palpated in a predetermined order with a cotton swab. The upper vestibular sites were labeled as 10,12,and 2,and the lower vestibular sites were labeled as 5,6,and 7corresponding to the positions of the sites on a standard clock face.The participants perceived sensation (cotton swab or misperception as pinprick) and intensity of the evoked pain sensations was determined at each site. The pain intensity was evaluated using a 010 visual analog scale (VAS). The association between examination site and vestibulodynia case status and each outcome variable were evaluated using mixed effects models. Case status and examination site were treated as fixed effects with a random effect for each subject. Results: Across all examination sites, vestibulodynia patients were more likely to report a pinprick sensation than healthy controls (OR=3.0, 95% CI=1.3, 7.1). The average intensity of the evoked sensations was similarly greater in the vestibulodynia patients (mean VAS difference=1.5, 95% CI=0.9, 2.2). The average VAS rating was also greater when participants reported a pinprick sensation (mean VAS difference=1.5, 95% CI=1.2, 1.8). The odds of reporting a pinprick sensation were higher at sites 6 (OR=3.9, 95% CI=1.5, 9.8) and 12 (OR=6.4, 95% CI=2.5, 16.3) compared to the baseline group (site 2). The odds of a pinprick sensation at the remaining sites did not differ significantly from the baseline. Similarly, the mean VAS ratings were significantly higher at sites 6 (mean VAS difference=1.5, 95% CI=1.0, 2.0) and 12 (mean VAS difference=0.7, 95% CI=0.2, 1.2) compared to the baseline, with no other sites showing significant differences from the baseline. A significant interaction was observed between case status and site 6 (mean VAS difference=1.7, 95% CI=0.7, 2.7), indicating that site 6 is significantly more sensitive among vestibulodynia cases than controls. No other significant interactions were observed. Conclusions: Women with vestibulodynia are significantly more likely to report a pinprick rather than a cotton swab sensation. Vestibulodynia cases also reported significantly higher VAS ratings than controls. Sites 6 and 12 were the most sensitive sites for both cases and controls. The mean VAS ratings were higher at both sites, as were the odds of a pinprick sensation. The difference between the VAS ratings of cases and controls was significantly larger at site 6, suggesting that cases are more sensitive more sensitive than controls at this site. Summary: The sensations evoked by cotton swab palpation of the vestibule vary depending on the examination site and vestibulodynia case status. Overall vestibulodynia patients show greater sensitivity than controls. Key Words: vestibulodynia; quantitative sensory assessment; mucosa
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Abstract #33 EFFICACY OF ACUPUNCTURE ON PAIN AND QUALITY OF LIFE IN WOMEN WITH A DIAGNOSIS OF CHRONIC PELVIC PAIN SECONDARY TO MYOFASCIAL SYNDROME ABDOMINAL Andria Souza, Master`s Degree Student2; Maria Gurian, Master`s Degree1; Manula Mximo, Master`s Degree Student1; Carolina Pazin, Master`s Degree Student1; Kalil Tawasha, Master`s Degree Student1; Ana Silva, Master`s Degree Student1; Patrcia Silva, Master`s Degree Student1; Karina Lopes, Master`s Degree Student1; Antnio Nogueira, MD, PhD1; Omero PoliNeto, MD, PhD1; Francisco Reis, MD, PhD1; Jos Zanardi, Master`s Degree Student1; Jlio RosaeSilva, MD, PhD1 1 University of Sao Paulo of Ribeirao Preto; 2University of Sao Paulo pf Ribeirao Preto Presented By: Andria Souza Chronic pelvic pain (CPP) is defined as nonmenstrual pain, not cyclical, lasting at least six months, interfering with daily activities from multifactorial etiological model, with a complex interaction between the gastrointestinal, genitourinary, nervous, endocrine and muscle skeletal, and requires medical or surgical treatment, considered a major health problem in women. Treatment strategies often result in failures, which is frustrating for the patient and the health professional therefore requires a multidisciplinary approach. As one of the musculoskeletal causes, the abdominal myofascial pain syndrome (AMPS) is characterized by intense pain and deep in the abdominal region originated from hypersensitive and tender points in muscles and / or fascia, called myofascial trigger points (MTrP). The treatment aims to stop the cycle of pain, abolish the MTrP, restore muscle flexibility and eliminate predisposing factors and perpetuation of pain. And among the various forms of existing treatments, acupuncture, which involves the application of needles at defined points of the body, called acupoints, has a therapeutic effect in various conditions, treating MTrP in myofascial pain, is well tolerated and has few adverse effects severe. Its neurobiological effects also act on the neurotransmitters related to pain and depression, describing the method as useful and appropriate in the treatment of chronic pain. Objective: To evaluate the effectiveness of acupuncture on pain and quality of life in women with a diagnosis of CPP secondary to SMFA. Methods: We evaluated 16 women diagnosed with AMPS submitted to the MTrP palpation, to evaluate pain we used a visual analog scale, McGill Pain Questionnaire, and Algometry Transcutaneous Neuromuscular Electrical Stimulation (TENS), and to assess the quality of life was used SF36 and Hospital Anxiety and Depression (HAD), after the needles were inserted into specific sites of pain and remained in situ for 25 minutes. 10 sessions were held, one session per week. Were then reevaluated 1 week e 1 month after treatment of acupuncture. Results: The median pain threshold was 4.165.98 before and 16.496.23 after (P = 0.93). In painful algometry was 2.28 0.99, 2.260.78 and 2.460.98 assessment, reassessment 1 week and 1 month (p = 0.87), respectively. As for VAS assessment, reassessment after 1 week and after 1 month was 5.682.64, 3.552.91 and 3.552.91, respectively (P = 0.10). In the evaluation of the McGill Pain Questionnaire, the results were 33.161853 assessment, 23:2421:48 reevaluation one week and 27.5020.93 reevaluation 1 month (P = 0.04). In evaluating the quality of life and anxiety and depression was pgreater than 0.05. Conclusion: There was no significant increase in threshold and aspects of quality of life assessed in the short term, showing that acupuncture treatment was not effective for women who participated in this study. Keywords: Acupuncture, Abdominal Myofascial Syndrome, Women's health, chronic pelvic pain.
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Abstract #34 ASSESSMENT OF SEXUAL FUNCTION, MOOD AND THRESHOLD OF PAIN IN WOMEN WITH CHRONIC PELVIC PAIN Ana Silva; Adriana Roma, MD; Kalil Tawasha, master's degree student; Andreia Souza, master's degree student; Maria Gurian, master's degree; Carolina Pazin, master's degree student; Manuela Maximo, master's degree student; Patricia Silva, master's degree student; Antonio Nogueira, MD, PhD; Omero Polineto, MD, PhD; Julio RosaSilva, MD, PhD University of Sao Paulo of Ribeirao Preto Presented By: Ana Silva Chronic pelvic pain (DPC) is defined as nonmenstrual pelvic pain or not cyclical, lasting at least six months. The etiology is unclear and often results from a complex interaction between systems and also influenced by psychological and sociocultural factors. Which can impair sexual function of women, even still it is not clear how chronic pain harms the sexual relationship. It is increasingly recognized the importance of sexual health for longevity, so the last ten years, women have resorted to medical care, most often in search of solutions to problems that interfere with their quality of life, especially those related to sexual function. Sexual function properly is an important factor in satisfaction and overall quality of life due to that the World Health Organisation (WHO) recognizes the sexual dysfunction as a public health problem and recommends its investigation to cause significant changes in quality of life. The most common female sexual dysfunctions are: lack of sexual desire, dyspareunia and orgasmic dysfunction. It is estimated that between 40 and 45% of women and 2030% of men have any complaints of sexual dysfunction. Objective: To assess sexual function, anxiety and depression and pain threshold in women with chronic pelvic pain, attended at the Ambulatory of Chronic Pelvic Pain HCFMRPUSPBrazil. Patients and Methods: This descriptive pilot study involved 20 women with chronic pelvic pain with a mean age 40.15 8.86 years. All women had stable marital status. Female Sexual Function Index (FSFI), Hospital Anxiety and Depression (HAD) and Visual Analogue Scale (VAS) were the psychometric instruments used. The pain thresholds were obtained by transcutaneous neuromuscular electrical stimulation (TENS). The software GraphPad Prism (5.0) were utilized by statistical analysis. It was considered =5%. Results: Pain intensity was on average 58.8cm [ranging: 0 to 90]. The pain threshold average was 16.1 [ranging: 11 to 23]. The mean score of depression group was 8.2 [3 to 13], and the cutoff>8 and the mean score of anxiety was 11.1 [ranging: 1 to 19], and the cutoff point>9. Regarding the FSFI scores, 55% of women had risk for developing sexual dysfunction, in other words, total score <26.6. The average scores for the FSFI domains were desire 3.4 [1.2 to 6.0], arousal 3.5 [0.0 to 5.4], lubrication 4.1 [0.0 to 6.0], orgasm 4.1 [0.0 to 6.0], satisfaction 4.3 [0.8 to 6.0] 2.4 and pain [0.0 to 6.0]. Conclusion: The results demonstrate that this population presents high risk scores for develop sexual dysfunction, anxiety and depression. Thus, the findings demonstrate the importance of a specific approach in the treatment of depression and sexual dysfunction in addition to clinical treatment, aiming at improving the quality of life of these women. We must also emphasize the interdisciplinary approach considering its physical manifestations, social, emotional, relational and sexual. Key words: chronic pelvic pain, sexual dysfunction, anxiety, depression, quality of life.
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Abstract #35 ANALYSIS OF PAIN MEASUREMENT IN WOMEN WITH CHRONIC PELVIC PAIN BEFORE AND AFTER TREATMENT Beatriz Gurian, master degree1; Andria Souza, Physiotherapist2; Manuela Maximo, Physiotherapist2; Carolina Pazin, Physiotherapist2; Ana Silva, Physiotherapist; Patricia Silva, Physiotherapist; Antnio Nogueira, MD, PhD3; Omero PoliNeto, MD, PhD3; Julio Rosa e Silva, MD, Master degree Student3; Jose Zanardi, MD, PhD3; Francisco Reis, MD, PhD3 1 Faculdade de Medicina de Ribeirao Preto Universidade de Sao Paulo; 2Faculdade de Medicina de Ribeirao Preto Universidade de Sao Paulo; 3Universidade de Sao Paulo Presented By: Beatriz Gurian Chronic pelvic pain (CPP) is a frequent complaint in gynecological practice, and although there is no consensus, is commonly defined as pain in the pelvic region persisted for at least six months. The etiological model is multifactorial, with complex interaction between the gastrointestinal, genitourinary, musculoskeletal, nervous and endocrine systems, influenced by sociocultural factors. The goal of therapeutic interventions is to relieve pain and return to activities of daily living, offering quality of life. According to the literature the best treatment for the CPP is through multidisciplinary approach. The pain can be evaluated when it is present, experimentally, that this is caused and / or inducible. The terms of pain measurement and evaluation are often used interchangeably, but many authors believe it is important to distinguish them. The measurement refers to the quantification of pain while the assessment is more related to an overall understanding of the pain experienced with various qualitative aspects. Therefore, it is important to measure more objectively the intensity of pain treatment to trace and verify the effectiveness of therapy. Objective: To measure the thresholds sensory, motor and painful, and evaluate the clinical severity of pain in women with CPP before and after treatment. Methods: were evaluated 51 women with CPP before starting treatment, with a mean age of 39.65 9.72 and index body mass of 27.2 4.95. The thresholds sensory, motor and pain were measured by means of transcutaneous electrical nerve stimulation and clinical pain intensity was measured by Visual Analogue Scale (VAS), Numerical Categorical Scale (NCS) and McGill Pain Questionnaire. The presence of anxiety and depression was assessed by the Hospital Anxiety and Depression. The same procedure was repeated six months after the first evaluation. Results: The median sensory thresholds before and after acupuncture was 03.09 0.72 and 3.66 1.57 respectively (P = 0.014) for the motor threshold, the values were 8.79 2.11 before and 9.90 2.3 after (P = 0.028) and pain threshold was 13.64 08.04 before and 17.22 4.16 after (P <0.0001). As for VAS before and after was 61.86 6.26 and 42.35 29.46 respectively (P = 0.0005). The result of NCS was 3.08 1:34 before and 1.82 1.23 after (p <0.001). In the evaluation of the McGill Pain Questionnaire, the results were 36.84 27.20 before and 19.29 16.78 after (P = 0.003). Conclusion: A significant increase in all aspects of the measurement evaluated, revealing that the treatments which were submitted were effective for women who participated in this study
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Abstract #36 PAIN ASSESSMENT IN PATIENTS WITH MYOFASCIAL PAIN SYNDROME UNDERGOING ABDOMINAL ACUPUNCTURE TREATMENT: A COMPARISON OF FOUR METHODS Andria Souza, Master`s Degree Student2;Beatriz Gurian, Master`s Degree1; Manuela Mximo, Master`s Degree Student1; Carolina Pazin, Master`s Degree Student1; Kalil Tawasha, Master`s Degree Student1; Ana Silva, Master`s Degree Student1; Aline Berno, Master`s Degree Student1; Karina Lopes, Master`s Degree Student1; Antnio Nogueira, MD, PhD1; Omero PoliNeto, MD, PhD1; Francisco Reis, MD, PhD1; Jos Zanardi, Master`s Degree Student1; Jlio RosaeSilva, MD, PhD1 1 University of Sao Paulo of Ribeirao Preto; 2University of Sao Paulo pf Ribeirao Preto Presented By: Andria Souza The abdominal myofascial pain syndrome (AMPS) is considered important in the genesis and perpetuation of chronic pelvic pain (CPP). It is characterized by intense pain and deep in the abdominal region originated from hypersensitive and tender points in muscles and / or fascia, called myofascial trigger points (MTrP). Several therapies are used to break the cycle of pain, abolish the MTrP, restore muscle flexibility and eliminate predisposing factors and perpetuation of pain, acupuncture among them. Pain is considered a multidimensional subjective event and, therefore, different instruments have been used to evaluate it and sensitive and reliable measures are necessary for the diagnosis and appropriate therapy. Objective: To evaluate and compare four methods of assessing pain in patients with AMPS submitted to acupuncture treatment. Methods: We evaluated 13 women with a mean age of 41.99.19, with CPP a secondary diagnosis of AMPS before starting treatment. The thresholds sensory, motor and pain were measured by means of transcutaneous electrical nerve stimulation (TENS), the sensory and pain thresholds were also evaluated by algometry and clinical pain intensity was measured by Visual Analogue Scale (VAS) and McGill Pain Questionnaire . After evaluation, underwent 10 sessions of acupuncture on points of local pain, and once a week and after reevaluation was performed using the same evaluation parameters. Results: In the evaluation of the McGill Pain Questionnaire, the results were 36.46 20:23 4:44 before and 5693 after treatment (p = 0.034). As for the VAS results shown before and after treatment 66.54 6.55 and 39.85 8.25 (p = 0.018), respectively. The median threshold by sensory TENS was 3.15 0.27 before after and 3.58 0.13 (p = 0.17), threshold engine 8.74 0.69 before and after 9:33 0.54 (p = 0.51) and pain threshold before and after 14:02 16.12 1.5 and 1.38 (p = 0.31), respectively. In evaluating algometry was analyzed and the MTrP and control points (CP), MTrP Sensory threshold was 1.51 0.21 before and 1.48 0.20 after treatment (p = 0.91) and pain threshold before and after MTrP of 2.26 0.24 and 2.23 0.26 (p = 0.94), respectively. Have the CP sensory threshold was 1.82 0.20 before and 2.4 0.18 after (p = 0.048) and pain threshold before and after CP of 1.86 0.2 and 2.50 0.3 (p = 0.08), respectively. Conclusion: It was observed that there was a statistically significant difference in the assessment of clinical pain, experimental pain to have the result of measurement was not significant, however, the sensory evaluation of the threshold through the algometer showed significance, as determined by the PC, and although not present significant difference, the threshold experimental TENS proved by the nearest level of significance, compared to algometer. Keywords: abdominal myofascial pain syndrome, chronic pelvic pain, pain measurement, Acupuncture.
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Abstract #37 ASSOCIATION OF BODY FAT AND BODY MASS INDEX TO MEASURE PAIN, ANXIETY AND DEPRESSION IN WOMEN WITH CHRONIC PELVIC PAIN Beatriz Gurian, master degree1; Andreia Souza, Physiotherapists2; Manuela Maximo, Physiotherapists2; Carolina Pazin, Physiotherapists2; Ana Silva, Physiotherapists2; Joyce Silva, Nuticionist2; Elizabete Flauzino, Physiotherapists2; Antonio Nogueira, MD; PhD2; Omero Poli Neto, MD, PhD2; Julio Rosa e Silva, MD, PhD2; Jose Zanardi, MD, Master Student2; Francisco Reis, MD, PhD2 1 Faculdade de Medicina de Ribeirao Preto Universidade de Sao Paulo; 2Faculdade de Medicina de Ribeirao Preto Universidade de Sao Paulo Presented By: Beatriz Gurian Chronic pelvic pain (CPP) is a debilitating and highly prevalent, with great impact on quality of life and significant costs to health services. The etiological model is multifactorial, there is interaction between the gastrointestinal, genitourinary, musculoskeletal, nervous and endocrine systems also influencing overweight and obesity. Studies show the prevalence of overweight and obesity in women was higher in the perimenopausal phase, probably due to metabolic changes inherent in this period, associated with physical inactivity, poor eating habits and also to genetic predisposition. Obesity is a chronic metabolic disease characterized by excess body fat (BF). Several methods for the evaluation of the excess being used more mass index (BMI). In some cases, BMI may not reflect the BF and its specific measure becomes important and can be assessed by bioelectrical impedance analysis (BIA) method of high speed information processing, noninvasive, convenient, reproducible and relatively inexpensive . From the physical point of view, obesity is associated not only with increased prevalence of some diseases, but also to increased levels of pain. It is very important to know and identify early problems that are related to the CPP including overweight and obesity. Objective: To analyze body fat associated with anthropometric markers in women with clinical and relate to the measurement of pain, anxiety and depression in the CPP. Methods: We evaluated 83 women with mean age of 40.67 10.20, weight of 69.75 14.66 and average height of 1.59 0.06, with a clinical diagnosis of CPP. For analysis of body composition was used weight, height and BMI, and BF was assessed by BIA. To assess experimental pain was used transcutaneous electrical nerve (TENS) and pain was assessed by clinical Categorical Numeric Scale (CNS) and Visual Analogue Scale (VAS). Results: For classification of BMI, were used cutoff points standardized by the World Health Organization, found that among women assessed 30% (n = 25) were obese, with a mean BMI of 33.78 2.98, 32.5% (n = 27) were overweight with average BMI of 27.56 1.50 and eutrophic accounted for 33.7% (n = 28) obtained an average BMI of 22.7 7.2 (p = 0.0001 .) As for the BF, the obese (n = 50) had a mean 36.71 7.49 (60.2%), overweight (n = 24) average of 32.19 4.30 (28.9%) and eutrophic (n = 1) averaged 28.96 7.04 (2.1 %) and below the average 9.6% (n = 8) with p = 0.0001. When analyzed anxiety and depression and pain measurement the value of p > 0.05. Conclusion: According to the percentage of body fat, we can appreciate that even though 28.9% normal weight (n = 24) have body fat percentage above the average, 60.2% (n = 50) is associated with risk obesity according to body fat percentage. However, when analyzing the measurement of pain and anxiety and depression, it was observed that there was no statistically significant association in our sample. Keywords: Body fat, BMI, chronic pelvic pain, pain
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Abstract #38 THE INFLUENCE OF HORMONES ON THE THRESHOLD EXOGENOUS SENSITIVE, MOTORS, AND PAINFUL HEALTHY WOMEN Manuela Maximo, Master's degree student, Patricia Silva, Master's degree student, Omero PoliNeto, MD, PhD, Thais Mangetti, PT student, Maria Gurian, Master's degree, Andreia Souza, Master's degree student, Ana Silva, Master's degree student, Carolina Pazin, Master's degree student, Kalil Tawasha, Master's degree student, Julio RosaeSilva, MD, PhD and Antonio Nogueira, MD, PhD University of Sao Paulo of Ribeiro Preto Presented By: Manuela Maximo The perception of pain is the result of a complex process. It is usually consequent to balance among the peripheral stimulus and descending modulation. Thus, numerous peripheral and central areas are fundamental to the painful experience lived. An important element to consider in situations of chronic pain is central sensitization. However, it is difficult to clinically diagnose it. One of the indirect ways to infer their presence is the measurement of pain thresholds. In general they were reduced at distant points of the affected area. Considering the peculiarities of the women with chronic pelvic pain in reproductive age, it is essential to plot thresholds curves for each population studied, considering not only the phase of the cycle, as well as serum levels of sex steroids and contraceptive use hormone. Although experimental pain does not reproduce accurately the pain clinic, pain measurement in an animal model may help the effectiveness of treatments and become one of the predictors of outcome. Objectives: To evaluate the experimental thresholds, sensory, motor and pain, by means of transcutaneous electrical nerve stimulation and pressure (algometry) in healthy volunteers without the use of any drugs and healthy volunteers users of injectable hormonal contraceptives (depot medroxyprogesterone acetate 150mg; 50mg of enanthate and norethisterone 5mg of estradiol valerate and monthly) and oral (levonorgestrel 0.15mg and ethinyl estradiol 0.03mg; and 0.10mg levonorgestrel and ethinyl estradiol 0.02 mg). Methods: A casecontrol study including 174 healthy women attending a primary care center linked to FMRPUSP. Seventy three women without the use of drugs [37 in the first phase of the cycle (group A1) and 36 in the second phase of the cycle (group A2)], 56 users of oral hormonal contraceptives [24 in use of levonorgestrel 0.10 mg + 0.02 mg ethinyl estradiol (group B1) and 32 in the use of levonorgestrel 0.15 mg + 0.03 mg ethinyl estradiol (Group B2)], and 45 users of injectable hormonal contraceptives [21 in depot medroxyprogesterone acetate use of quarterly 150mg (group C1) and 24 in use 50mg of norethisterone enanthate and 5 mg estradiol valerate monthly (group C2)]. The study was approved by the local Research Ethics Committee and all participants signed an informed consent. Sensory, motor and pain thresholds were measured by TENS in forearm and algometry were measured at forearm and abdominal wall (right and left side). The thresholds were measured by a trained examiner using three independent measurements. For purposes of statistical analysis we considered the average measurement. The pressure pain thresholds (algometry) was assessed with an pressure algometer DD500, model with digital traction and compression and measuring capacity is 5kg (Instrutherm Measuring Instruments Ltda, Brazil). The apparatus consists of a rubber disk 1 cm in diameter attached to the plunger of the pressure (force) gauge. The dial of the gauge is calibrated in kg cm2. Approximately 1kg cm2 s1 (time between measurements 2 minutes). Pain thresholds to electrical stimuli were obtained using a constant current device (961 Dualpex Quark neuromuscular stimulator). This device delivered a pulsed electric current at a fixed frequency of 50 Hz with a biphasic square waveform and a pulse duration of 200ms. Other materials included two new siliconcarbon electrodes measuring 3x2cm, 1ml of water soluble gel for each electrode (Measured with a syringe), hypoallergenic tape, the tape measure to correctly position the electrode, 70% alcohol, and cotton for disinfection of the appendage. The electrodes were coupled to the skin with 1 mL of water soluble gel for each
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electrode and were placed on the ventral side of the flexor muscles of the wrist and the fingers of the nondominant appendage. Their placement followed the longitudinal direction of the muscle fibers, with the first electrode being wellness coupled at a distance of 4 cm from the elbow joint interline and the second electrode affixed 4 cm from the first. During execution of the procedure, the subjects remained seated with their nondominant forearm in the supine position supported on the exam table. Local disinfection was performed using 70% alcohol, followed by coupling electrode. The device was turned on and the intensity was gradually increased by the examiner, 1mA increased 2 each second. The volunteer was instructed to report the first sensation of current flow, and identified that was the moment the sensory threshold. Later, the intensity continued to be Increased to identify (by visual inspection) the initial muscle contraction, which was the deemed the motor threshold. Finally, the intensity was incrementally increased until the first painful sensation was observed, which was the identified the pain threshold. Increase the intensity maintained the same rhythm and periodicity the deflagration threshold was sequential and constant. In other words, upon reaching the sensory threshold, the pulse amplitude indicated by the device was recorded (without stimulating that threshold), which was followed by increasing the intensity remaining until the thresholds were reached. The threshold values were within the limits of the technical specifications of the equipment and varied from 060mA. At the end of the sequence, there was an interval of 15 minutes so that the procedure repeated twice could be to obtain the mean threshold. All of these measurements were performed by the same examiner that was blind to all clinical data previously obtained. Age, anthropometric data such as body mass, weight, height and Beck depression scale were obtained. KruskalWallis test and Dunns post test to compare thresholds were utilized. It was considered = 5%. Results: no significant differences between groups of healthy women or users of hormonal contraceptives in sensory thresholds, motors and painful (electric and pressure). Data are presented for each threshold and respectively to the groups A1, A2, B1, B2, C1 and C2. Sensory threshold: 3.9 0.9 0.8 x 3.8 x 3.8 x 4.1 0.8 0.8 1.1 x 3.7 x 4.0 0.8; motor threshold: 8.5 1.6 1.9 x 9.3 x 8.2 x 9.1 1.4 1.8 1.5 x 8.6 x 9.1 2.1; pain threshold: 13.6 4.8 4.0 x 13.2 x 12.8 x 13.5 4.0 4.8 x 3.4 x 12.9 13.0 3.9; algometry forearm: 2.7 1.0 0.8 x 2.5 x 2.6 x 2.7 0.8 0.9 1.6 x 3.0 x 2.7 0.8; algometry right abdominal wall: 1.9 0.9 0.6 x 1.7 x 1.6 x 1.7 0.6 0.7 1.2 x 2.0 x 1.6 0.5; algometry left abdominal wall: 2.0 1.0 x 1.7 0.5 0.5 x 1.6 x 1.7 0.7 1.0 x 1.9 x 1.6 0.5. Discussion: Although there are published data suggesting that the cycle phase and serum sex steroids are important in determining the thresholds of pain, our preliminary results do not confirm this hypothesis, and show no interference of hormonal contraceptives on pain thresholds. These results emphasize that pain thresholds are defined by the complex interaction of several peculiarities of the subject beyond the cycle phases and levels of sex steroids. However, these results are important because they allow you to create a standard curve of pain thresholds for the healthy population and to propose cutoff points (cutoff) to define low thresholds and use them to identify clinical conditions in central sensitization of pain chronic, particularly in conditions of chronic pelvic pain. Key Words: chronic pelvic pain, pain threshold, central sensitization, hormonal contraceptives, sexual steroids.
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Abstract #39 PREDICTORS OF PERSISTENT PELVIC PAIN FOLLOWING HYSTERECTOMY J. Biba Nijjar, MD, MPH; Smorgick Noam, MD, MSC; Manar Abdelbegeed, MD; Nour AlHadidi; Ellen Davis; Sawsan AsSanie, MD, MPH University of Michigan Presented By: J. Biba Nijjar Study Objective: To determine the frequency of and factors associated with persistent pelvic pain after hysterectomy. Design: IRBapproved survey Setting: University hospital tertiary referral center Patients: All women who underwent hysterectomy from March 2001 to June 2010 for benign indications by faculty of the Division of Minimally Invasive Gynecologic Surgery Intervention: Mail or telephone survey to evaluate pelvic pain symptoms and comorbid pain syndromes prior to and after hysterectomy. Measurements and Main Results: 703 women underwent hysterectomy during the study period, contact information was available for 624 women, and 292 (47%) completed the survey. Indications for hysterectomy included abnormal bleeding (70.8%), uterine fibroids (61.2%), pelvic pain (54.1%), and/or endometriosis (21.2%). Most procedures were completed via a minimally invasive route (laparoscopy 75.4%, laparotomy 8.6%, vaginal 6.9%). 80.5% of women reported pelvic pain prior to hysterectomy with an average pain intensity of 6.5 2.1 on a 010 point scale. Among women who experienced pelvic pain prior to surgery, 16.6% reported persistent pelvic pain following hysterectomy and 11.0% reported that the pain was not improved at all. Persistent pelvic pain following hysterectomy was more common in women with a comorbid pain syndrome (OR 3.0, CI 1.46.5). Age, route of hysterectomy, and presence or severity of endometriosis were not associated with persistent pelvic pain. Conclusion: Pelvic pain is a common symptom prior to hysterectomy and persists in nearly 17% of women who undergo hysterectomy. The diagnosis of an additional chronic pain syndrome is associated with an increased likelihood of persistent pain. These findings may help guide women when considering hysterectomy for the treatment of pelvic pain.
Abstract #40 MEANINGS OF DIAGNOSIS FOR WOMEN WITH CHRONIC PELVIC PAIN Adriana Peterson Mariano Salata Romo, PhD; Ricardo Gorayeb, PhD; Ana Paula Moreira Silva; Gustavo Salata Romo, PhD; Omero Benedicto Poli Neto, PhD; Maria Beatriz Ferreira Gurian, Post Graduation; Andreia Moreira Souza, Post Graduation; Kalil Antonio Salotti Tawasha, Post Graduation; Antonio Alberto Nogueira, PhD Presented By: Ana Paula Moreira Silva Chronic Pelvic Pain (CPP) defined as continuous or recurrent pain in lower abdomen or pelvis lasting at least six months, severe enough to interfere with daily activities of women, requiring medical or surgical treatment. Its etiology is unclear and usually results from a complex interaction between the gastrointestinal system, urinary, gynecological, musculoskeletal, neurological, psychological and endocrinological, still influenced by sociocultural factors. Chronic pelvic pain is best managed with a multidisciplinary approach that can focus on complex and interactive components. Given the complexity of symptoms in this study we opted for a qualitative approach. Objective: to know the experience of women with CPP in relation to chronic pelvic pain.
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Methodology: how the data collection instrument was used in focus group interviews with eleven women. At the beginning of the interview, the researcher reported again the objectives of the study, all participants read and signed the consent form. The researcher used a research question (how to live with CPP) that served as the theme for conducting the group. The interview lasted one hour and thirty minutes, it was conducted by the researcher who placed himself as a facilitator and promoter of the conversation group, so that the opinions and ideas to surface without any claim to a consensus. This methodological approach allowed the interviewees to speak freely about the process of disease, as well as their everyday relationships, values and perceived changes after the onset of symptoms. For analysis of the speeches was the technique of content analysis proposed by Bardin. To better understand the data presented was a central theme category followed by their core meaning. The category and the meaning cores were constructed from the speech of womens. O research project was approved by the Ethics Committee of the institution. The themes addressed in the interview were: diagnosis, onset of pain, which worsens and that improvement, interpersonal and marital relationships, interference in daily activities, the association of pain with the emotional aspects and perspectives for the future. Thus we can see how these women need to be better heard, and how the association between mental and physical issues to be seen by professionals who attend them. Only a multiprofessional work can be successful in treating patients diseased by CPP because of the complexity of the problem. The approach taken by professionals from different areas, when properly structured, can minimize the problem of division of individual ill in isolated parts. This study also demonstrated the importance of psychological care, mainly related to the discovery of more effective strategies to live with the pain. Key words: lived experience; chronic pelvic pain,; qualitative methods, womens health
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Abstract #41 THE IMPACT OF CHRONIC PELVIC PAIN IN FEMALE SEXUAL FUNCTION Adriana Peterson Mariano Salata Romo, PhD; Ana Paula Moreira Silva; Ricardo Gorayeb, PhD; Gustavo Salata Romo, PhD; Maria Beatriz Ferreira Gurian, Post Graduate; Andrea Moreira Souza, Post Graduate; Omero Benedicto Poli Neto, PhD; Kalil Antonio Salotti Tawasha, Post Graduate; Antonio Alberto Nogueira, PhD Presented By: Ana Paula Moreira Silva The objective of the present study was to determine the prevalence of sexual dysfunction and depression of women with chronic pelvic pain (CPP). A crosssectional controlled study was conducted on 66 womens. 36 patients with CPP and 30 women without pain. Depression were evaluated by the Inventrio de Depresso de Beck (Beck) and sexual dysfunction was evaluated by the Female Sexual Function Index (FSFI) questionnaire. Data were analyzed statistically by the MannWhitney U test, the Fisher exact test, chisquare test, and Spearman correlation test. Regarding sociodemographic data were not detected significant differences in patient populations studied variables (age, education, number of children, income, salary and marital status) reflecting the homogeneity between the groups, thus increasing the reliability of data. To calculate the total score of sexual function, based on a cutoff of 26 points in the group of women with CPP 94.4% had high risk for sexual dysfunction. A comparison of scores of FSFI showed that sexual function domains in lubrication, orgasm and pain were significantly different from women without CPP. In this study correlations between the following items: Orgasm x age (r = 0, 01904); orgasm x number of children (r = 0, 00947); orgasm x IMC (r = 0, 00 955). Relationship x age (r = 0, 03,952) Income x Relationship (r = 0, 014,680); Relationship number of children (r = 0, 03 623) x Relationship Depression (r = 0, 16 091). Wish x age (r = 0, 45255); Desire x number of children (r = 0, 01824). Lubrication x Arousal (r = 0, 04198); Lubrication x IMC (r = 0, 01 608). Regarding the prevalence of depression found in this study was 38.9% in women with pain in women and 3.3% in the control group. Regarding sexual function, it was realized that these women have negative interference in relation to sexual functioning when compared to the control group. Thus, we can see that a specific approach related to sexuality is extremely important in the context of women with CPP. As for depression, there is clear association with DPC, thus, the interdisciplinary approach is crucial for solving this problem. Key Words: chronic pelvic pain, depression, sexual dysfunction,
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Abstract #42 PREVALENCE OF SEXUAL ABUSE IN WOMEN WITH CHRONIC PELVIC PAIN Kalil Antonio Salotti Tawasha, Post Graduate; Adriana Peterson Mariano Salata Romo, PhD; Carolina Pazin, Post Graduate; Manuela Menezes Mximo, Post Graduate; Ana Paula Moreira Silva, Post Graduate; Patricia Silveira Silva, Post Graduate; Antonio Alberto Nogueira, PhD; Maria Beatriz Ferreira Gurian, Post Graduate; Andreia Moreira Silva, Post Graduate; Omero Benedicto Poli Neto, PhD Presented By: Carolina Pazin Introduction: Chronic pelvic pain (CPP) is a clinical condition with high prevalence, associated with several comorbidities and impact marital, social and economic gloom. Its pathophysiology is not completely understood and, consequently, the therapeutic options are unsatisfactory, causing distress and dissatisfaction of women with, their neighbors and their own medical team that attends. Have been growing scientific evidence of a link between chronic pain and history of abuse and sexual violence and / or physical advance, but there is still a paucity of studies of patients with chronic pain exploring the possible impact of violence on the development of disease. Objective: To investigate the prevalence of sexual abuse in women with chronic pelvic pain. Methodology: Cross sectional pilot where 76 women were included, 60 had CPP and the other 16 women were in the control group. The instruments used were: Protocol of epidemiological and clinical data, Measurement Scale Hospital Anxiety and Depression (HAD) and the Childhood Trauma Questionnaire About (QUESI). The data were stored in a database created using the software Microsoft Excell 7.0. Statistical analysis is performed using GraphPad Prism and SPSS. The analyzes of the instruments were performed according to the criteria established by the authors. For comparative analysis will be used the nonparametric MannWhitney U. For comparative analysis of qualitative variables will be used Fisher's exact test or test between independent groups. For correlation between variables of the study will be used Spearman's test. Will be considered alpha <0.05. Results: The mean score of depression group was 7.95 with CPP [119], and the cutoff> 8 and the mean score of anxiety 9.11 [218], and the cutoff point> 9 for the control group the mean score of depression was 8.70 [118] and anxiety 8.64 [318]. Regarding scores QUESI significant difference in physical abuse between the groups, demonstrating that the group CPP higher prevalence of physical abuse when compared to the control group. Conclusion: The results are still preliminary, however realize that there is a strong tendency to have more changes in the group with CPP abuse in relationships when compared to the control group. The findings demonstrate the importance of a specific approach in dealing with women, aiming at an improved quality of life. We must also emphasize an interdisciplinary approach to considering the physical manifestations, social, emotional, relational and sexual. Key Words: chronic pelvic pain, sexual abuse, child neglect and mood disorders.
Abstract #43 THE RELATIONSHIP BETWEEN VAGINAL EXAM FINDINGS AND POSITIVE POTASSIUM CHLORIDE SENSITIVITY TESTING IN PATIENTS WITH SUSPECTED INTERSTITIAL CYSTITIS Diana Atashroo, MD; Michael Hibner, MD; Nita Desai, MD; Mario E. Castellanos, MD Arizona Center for Chronic Pelvic Pain Presented By: Diana Atashroo Objective: This study was designed to determine if pain on palpation of the anterior vaginal wall underlying the bladder was associated with positive potassium chloride (KCL) sensitivity testing, and thus a diagnosis of interstitial cystitis (IC).
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Methods: Using the CPT code J3480 for the Potassium Chloride (KCL) test, we identified 82 patients in our practice from January 2010 to June 2012 who had undergone KCL sensitivity testing for suspected interstitial cystitis. Every patient had a pelvic exam in the clinic. A positive KCL test was correlated with pelvic exam findings including anterior vaginal wall tenderness and pelvic floor tension myalgia (PFTM). Results: In this study, of the 82 patients, 37 (45%) had associated pain on anterior vaginal exam and a positive KCL test. However, 28 (34%) patients had positive findings on bladder exam, and negative KCL sensitivity. Only 7 (1%) patients had positive KCL testing despite negative anterior vaginal wall exam. Overall, using the anterior vaginal exam as a predictor of interstitial cystitis has a sensitivity of 84% and a specificity of 26%. The positive predictive value is 57% with a negative predictive value of 59% (95% confidence interval). Statistical analysis showed no clinical significance between a positive anterior vaginal exam and KCL testing (p =0.1878) using the Fishers exact test. There was, however, suggestion of clinical significance between pelvic floor exam findings and KCL sensitivity testing (p = 0.0786). Conclusion: Based on our study, positive anterior vaginal tenderness showed some correlation to a diagnosis of IC, but isnt predictive of IC and shouldnt be used solely to replace KCL sensitivity testing as a gold standard of making a diagnosis. Some clinical significance was seen between pelvic exam findings consistent with PFTM and a positive KCL test, warranting further research. Summary: Anterior vaginal wall tenderness does not predict positive KCL sensitivity testing, thus, cant replace the bladder test as the gold standard in diagnosing IC. A positive KCL test is more associated with the presence of PFTM. Keywords: potassium chloride test (KCL), interstitial cystitis (IC), anterior vaginal exam, pelvic floor exam, pelvic floor tension myalgia (PFTM)
Abstract #44 EXCURSION OF THE PUDENDAL NERVE AND CHANGE IN DISTANCE BETWEEN THE SACROSPINOUS AND SACROTUBEROUS LIGAMENTS Karen Brandon, PT2; Loretta Robertson, MD1; Mario Castellanos, MD1; Diana Atashroo, MD1; Andrea Chen, MD1; Michael Hibner, MD1 1 Arizona Center for Chronic Pelvic Pain; 2School of Allied Health, Loma Linda University Presented By: Karen Brandon Introduction: Pudendal nerve is the main sensory, motor and autonomic nerve of the rectum, perineum and external genitalia. Pudendal nerve entrapment causes significant neuropathic pain in the area of innervation and severely affects quality of life. This entrapment often occurs in the area where sacrospinous and sacrotuberous ligaments overlap and pudendal nerve travels in between the ligaments. Little is known about the dynamic relationship between those ligaments as well as the excursion of the nerve with movements of the lower extremity. The goal of this study was to examine those relationships. Materials and Methods: Two female cadavers were used. Sacrotuberous and sacrospinous ligaments were identified. Pudendal nerve was dissected out from the sacral plexus to the terminal branches (superior rectal, perineal and dorsal clitoral). All measurements were obtained using surgical tape measure. There were four anatomic landmarks, and distance was calculated between the ligaments as was the excursion of the nerve relative to the ischial spine. Measurements were obtained in lower extremity positions of neutral hip alignment, 90 degrees hip flexion, maximum hip flexion, end ranges of internal rotation, external rotation, adduction and abduction. Values are presented as means. Also pressure on the nerve was observed and palpated through the dissected window in gluteal muscle with use of vaginal retractor.
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Results: The average distance between the sacrospinous and sacrotuberous ligament was 10 mm in the neutral hip position. At 90 degree hip flexion it decreased to 9 mm but with maximum flexion it increased to 13 mm. With external rotation this distance was 8 mm, internal rotation 7 mm, adduction 8 mm and abduction 11 mm. In the neutral hip position pudendal nerve was 5 mm medial to the ischial spine. With 90degree flexion and maximum flexion it came within 1 mm medial of the ischial spine. In external rotation the nerve was 6 mm medial to the spine and internal rotation 1 mm lateral to the spine. In adduction it was 6 mm lateral to the spine and abduction 6 mm medial to the spine. All movements were observed only in the coronal plane of the nerve, and there was no axial excursion of pudendal nerve with hip movements. When deaver retractor was placed vaginally and pulled laterally at 90 degree angle to the axis of the vagina there was no pressure transmitted to pudendal nerve or any of its branches. There was a significant visible compression immediately caudad to the sacrospinous ligament when this retractor was rotated inwards (torqued). Conclusions: Changes observed in the distance between the ligaments may have implications on the mechanism of pudendal nerve entrapment, diagnosis, post operative instructions and physical therapy procedures. While majority of patients with pudendal nerve entrapment experience increased pain in squatting position there is a subgroup who experience pain relief. It is possible that patients who experience pain in this position have scarring or adhesion of the nerve attached to surrounding structures represented while patients who experience pain relief have compression on the nerve in the tight space between ligaments. Further studies with more precise distance and pressure measurements and development of ways to evaluate pudendal nerve dynamics in vivo are necessary. Summary: Pudendal nerve entrampent (PNE) is one of the causes of pudendal neralgia. Dynamic interation of the nerve and surrounding structures is crucial for understanding causes and potential treatments of PNE. This study examines the excursion of the nerve and size of intraligamentous space during movement of the hip. We have found that pudendal nerve moves only in the coronal plane and that intraligamentuous space is the largest with maximum hip flexion. Key words: pudendal nerve, nerve excursion, intraligamentous space
Abstract #45 COMMON MRI FINDINGS IN PATIENTS WITH SYMPTOMS OF PUDENDAL NEURALGIA. Andrea Chen; Olga Kalinkin, MD; Mario Castellanos, MD; Michael Hibner, MD Arizona Center for Chronic Pelvic Pain Presented By: Andrea Chen Objective: To evaluate the common findings on a pudendal protocol MRI used to evaluate patients with symptoms of pudendal neuralgia. Methods: From August 2010 to July 2012, patients who were referred to our institution (Arizona Center for Chronic Pelvic Pain, St. Josephs Hospital and Medical Center, Phoenix, Arizona) with symptoms of pudendal neuralgia were evaluated in our office. If the history and physical exam findings were indeed suggestive of pudendal neuralgia, patients were sent for an MRI pelvis with and without contrast at our Radiology department. The pudendal protocol consists of sections taken at an oblique angle parallel to the sacrum and then corresponding transverse sections. One hundred of these female patients were selected randomly and their MRI findings were reviewed and tabulated.
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Results: Out of the 100 patients, seven had completely normal findings. Twenty had an enlarged pudendal neurovascular bundle, with or without asymmetry. Eighteen patients had unilateral or bilateral Tarlovs cysts. Twentythree patients were noted to have subjectively prominent pelvic sidewall, parauterine, and/or paravaginal venous plexus. Twenty patients had abnormal findings of the pelvic floor muscles, usually involving concavity or atrophy and usually unilateral. Fiftyseven patients had abnormal findings along the lumbosacral vertebral discs, either a bulge or desiccation. Twentynine patients were found to have some abnormality of the pelvic bones, pelvic joints (including the hips and sacroiliac joint) or lumbosacral vertebral column. Six patients were noted to have an abnormality at the hamstring tendon insertion site. Three patients were noted to have an abnormality of the labrum of the acetabulum. Three patients were noted to have a thickened sacrotuberous or sacrospinous ligament. Conclusion: Although MRI findings did not always show an actual cause for or direct evidence of pudendal nerve entrapment, we did find many incidental findings or other possible etiologies for the patients symptoms, some of which are known to cause symptoms similar to pudendal neuralgia and others that will need further exploration. The findings involved many other systems, including musculoskeletal and neurovascular systems. These findings support our belief that all patients with symptoms suggestive of pudendal neuralgia should undergo an MRI of the pelvis using a pudendal protocol in order to better evaluate the etiology of patients pain and thus better guide our counseling and management decisions. Key words (limit 5): pudendal neuralgia, MRI protocol, Tarlovs cyst Summary (not to exceed 200 characters): All patients with symptoms suggestive of pudendal neuralgia should undergo an MRI pelvis with pudendal protocol to evaluate for other possible etiologies of their pelvic pain.
Abstract #46 EVIDENCE FOR CENTRAL SENSITIZATION IN BLADDER PAIN SYNDROME FROM THE ICEPAC TRIAL (INTERSTITIAL CYSTITIS: ELUCIDATION OF PSYCHOPHYSIOLOGIC AND AUTONOMIC CHARACTERISTICS) PRELIMINARY PSYCHOMETRIC FINDINGS Janata JW*1; Daneshgari F2; Buffington CAT3; Chelimsky G4; Louttit M5; Zhang D5; Chelimsky TC6 1 Case Western Reserve University School of Medicine Psychiatry, Cleveland, OH, USA; 2Case Medical Center and Case Western Reserve University Urology, Cleveland, OH, USA; 3Ohio State University School of Veterinary Science, USA; 4Medical College of Wisconsin Pediatrics, Milwaukee, WI, USA; 5Case Western Reserve University Neurology, Cleveland, OH, USA; 6Medical College of Wisconsin Neurology, Milwaukee, WI, USA Presented By: Thomas C. Chelimsky, MD Background: Interstitial cystitis (IC - Bladder Pain Syndrome), is characterized by pain in the bladder worse when full and better when empty along with urgency and frequency. Despite extensive research, the pathophysiology is unknown and there is no effective treatment. ICEPAC aims to evaluate psychophysiologic contributions to this disorder in general and to elucidate the role of central processing in particular. Methods: ICEPAC completed enrollment will include 76 women with IC, 76 women with myofascial pelvic pain disorder (MPP), 38 1st degree female relatives of IC subjects without pelvic pain, and 38 healthy age-matched women. Subjects complete comprehensive psychological measures of pain, function, catastrophizing, childhood trauma, PTSD, somatization, anxiety and stress. A subset of patients also undergo a Trier stress test, with assessment of the resulting catecholaminergic and hypothalamic-pituitary response.
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Abstracts
IPPS
Results: Initial recruitment has included 50 subjects: 22 with IC/MPP, 7 with MPP alone and 21 healthy controls. Ages ranged from 18 to 62. Compared to healthy controls, the pain groups show elevated levels of somatization, depression, anxiety, PTSD symptoms, pain catastrophizing and childhood trauma, and both groups show impairment of function. However, the IC/MPP group compared to the MPP group has significantly higher scores on childhood emotional abuse (mean=12.4 vs. 9.0), PTSD symptoms (13.3 vs. 5.1), and pain catastrophizing (28.0 vs. 16.6). Conclusion: These results are consistent with early exposure to trauma and subsequent central nervous system sensitization evidenced by PTSD symptoms and increased emotional processing of nociceptive input. These promising early findings require the confirmation that additional recruitment will provide. Evidence for autonomic signatures or correlates is pending continued recruitment. Keywords: Chronic pelvic pain, bladder pain syndrome, stress, psychometrics. Financial Support: NIDDK grant R01-DK083538 NIH NIDDK Interstitial Cystitis Elucidation of Psychophysiologic and Autonomic Characteristics (ICEPAC).
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Presentations Thursday, October 18, 2012
IPPS
8:05 a.m. 8:35 a.m. Introduction to the Physiology of Chronic Pain Thomas C. Chelimsky, MD 8:40 a.m. 9:00 a.m. Evaluation of the Chronic Pelvic Pain Patient Part I: Essential Elements of the History Kathryn M. Witzeman, MD 9:05 a.m. 9:25 a.m. Evaluation of the Chronic Pelvic Pain Patient Part II: Essential Elements of the Gynecologic Exam Ja Hyun Shin, MD 9:30 a.m. 9:50 a.m. Evaluation of the Chronic Pelvic Pain Patient Part III: Essential Elements of the Musculoskeletal Exam Elizabeth Dee Hartmann, PT, DPT 10:20 a.m. 11:00 a.m. Diagnosis and Treatment of Gynecologic Causes of Chronic Pelvic Pain Matthew T. Siedhoff, MD, MSCR 11:05 a.m. 11:35 a.m. Diagnosis and Treatment of Vulvar Pain Frank Tu, MD, MPH 11:40 a.m. 12:10 p.m. Diagnosis and Treatment of Abdominal and Pelvic Peripheral Neuropathies Mario Castellanos, MD
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Introduction to Chronic Pain Physiology

Thomas Chelimsky, MD Professor and Chair of Neurology, Medical College of Wisconsin IPPS Fall Meeting October 18, 2012
Disclosures
NIH support NIDDK R01-DK083538, ICEPAC (Interstitial Cystitis Elucidation of Psychophysiologic and Autonomic Characteristics) No financial disclosures, sadly.
Outline

Chronic vs Acute Pain

Intro: chronic is not long-lasting acute pain Case presentation: Lori Pain Signaling

Signal transduction (how does it start?) Signal transmission (how does it get to CNS?) Signal transfer (CNS handling of signal) Signal translation (meaning and reaction to it) Signal transformation (evolution over time)
What happened to Lori
Chronic pain is not just acute pain with a longer duration. Chronic pain refers to a continuous human state, akin to consciousness or depression. The use of acute pain to model our conceptualization of chronic pain has hampered progress in our understanding of chronic pain neurobiology because acute pain reflects a relatively briefer perceptual experience rather than an experiential state. Chronic pain = experiential state Acute pain = perceptual experience Recognition of the fundamental difference between these two conditions has fostered the emergence of a new understanding of the complexity of chronic pain neurobiology.
Acute vs Chronic Pain

Acute Pain
Physiology Experience Purpose and Outcome Neuronal Signal Unpleasant Perception
3 Types of Pain
Chronic Pain
Reinforcing Neuronal Network Mental State (akin to depression)
1) Physiologic (phone-line conversation)
Pain transmitted through normal neural pathways from injured tissue Pain generated by the nervous system in a pre-programmed response to injury Pain generated by an injured neural moiety
2) Adaptive Neural (phone-line alarm)
Action No Action Escape Danger Impedes Normal Human Function
3) Neuropathic (phone-line static)
Pain Terms
Pain Signaling (Trans5)

Hyperalgesia
Increase in pain level for all stimuli

Spontaneous pain Reduced pain threshold
Allodynia (non-painful stimulus induces pain)
Painful stimuli more painful
Sensitization
Corresponding neural phenomenon

Spontaneous activity Reduced threshold for neural response Increased responsiveness to effective stimuli
Case presentation Signal transduction (how does it start?) Signal transmission (how does it get to CNS?) Signal transfer (CNS handling of signal) Signal translation (meaning and reaction to it) Signal transformation (evolution over time)
Patient Case Important Questions

Patient Presentation

What is the diagnosis? Is this an acute or chronic pain syndrome? What is happening in muscles? What is happening in brain? What role are opiates playing? What is happening from a psychological perspective? Why so many co-morbidities?
Lori is a19 y.o. woman in first year college Severe progressive pelvic pain x 2 months

Urgency 14 x per day; frequency Pain with bladder full 7/10 Pain with bladder empty 6/10 Severe dyspareunia
Currently taking hydromorphone for pain What will examination show?
Patient Examination
Diagnosis

Normal

neurologic examination visual pelvic examination
Myofascial Pelvic Pain Syndrome
(aka Pelvic Floor Tension Myalgia etc) (aka Painful Bladder Syndrome etc.)
Severe abdominal tender points Bladder and uterus normal by palpation but both moderately tender. 8 to 10/10 pain on palpation of both levators, internal obliques and perineal body Severe adductor tender points at all 3 levels What is diagnosis?
Probably no Interstitial Cystitis
What are co-morbidities?
Case Co-Morbid History
Case Family History

Co-morbidities and family history

Migraine headaches since age 14, much worse since this started Irritable bowel for 6 months Fibromyalgia by examination Probable panic disorder and anxiety disorder. Unrefreshing sleep x 2 months, despite taking benzodiazepines and opiates for pain
Mother, sister, and 3 maternal aunts with migraine headaches Mother has IBS and fibromyalgia Sister, maternal aunt and 3 cousins with POTS One sister has pelvic pain (dx = endometriosis) One sister with generalized anxiety disorder.
What will family history show?
Is this acute pain or chronic pain?
What is the patients main question?

Science and Pontification
What will you do for my pain now? I am on hydromorphone and want a refill to keep me pain-free until you do whatever blocks and PT you need to do. What is the physician response?
There is something fascinating about science. One gets such wholesale returns of conjecture out of such a trifling investment of fact.
Mark Twain
Outline

3 Principles of Signal Transduction

Intro: chronic is not long-lasting acute pain Case presentation Signal transduction (how does it start?) Signal transmission (how does it get to CNS?) Signal transfer (CNS handling of signal) Signal translation (meaning and reaction to it) Signal transformation (evolution over time)
Activation: Transient Receptor Potentials (e.g TRPV1) play the major role Sensitization in positive feedback loop through inflammatory moities such as interleukins, NGF, CGRP etc which are also released by neurons Threshold for firing: K+ channel closure (eg TREK-1) reduces, while opening increases

Render active fibers more easily activated; Activate silent C-nociceptor fibers, esp bladder etc.
Heat Pain
NSC = Nonselective Cation Channel
Anchoring to Loris Problem

Her pain is now chronic pain. How did it start?

Transient receptor potentials V1 (TRPV1)

Capsaicin Agonist; Ruthenium Red Antagonist Partially responsible for heat pain and inflammatory pain Sensitized by bradykinin, NGF etc. Releases CGRP and substance P in periphery
K+ channels (KCNK2 or TREK-1 and KCNK4 or TRAAK) inhibited by heat (closure reduces threshold and increases function) Mechanical pain less well understood, involves acid-sensitive channels (ASICs) also Dubin and Patapoutian, J Clin Invest 2010
No injury reported Biochemical abnormality? Infectious process? Channelopathy? Central nervous system dysregulation?
Outline

Intro: chronic is not long-lasting acute pain Case presentation Signal transduction (how does it start?) Signal transmission (how does it get to CNS?) Signal transfer (CNS handling of signal) Signal translation (meaning and reaction to it) Signal transformation (evolution over time)
Signal Transmission
3 Principles of Signal Transmission

Population Coding AND Labeled Lines
Final signal at dorsal horn dictated by both labeled line and population coding Threshold and absolute maximum firing rate result from physio-biologic properties of sodium channels which dictate absolute refractory period Functional maximum firing rate dictated by accomodative currents reflecting mostly K+ and Cl- channels resulting in relative refractory period.
Labeled Lines

CH = Cool/Heat C2 = innocuous and noxious cold CHMC = noxious Heat/Mech/Cool
Conceptualize: like Morse code

Ma, 2010; Campero et al 2009
Sensory fiber diameters and conduction velocities

Fiber type Ia, Ib A beta A delta C Diameters Velocity mph* Vehicle (microns) (m/sec) 13-20 80 to 120 225 TGV 6 to 12 1 to 5 0.2 to 1.5 35 to 75 5 to 30 0.5 to 2 112 45 3 Porsche Caravan Walk
Ephaptic Transmission
Unmyelinated fibers shift within the fascicle to prevent firing Shifting is absent in regenerating nerve
Aguayo & Bray, 1976

* X 1 mile/1600 meters / 1 hr/3600 secs = 9/4 = factor of 2.25
Signal Transmission: Na+ Channel
Signal Transmission: channels
Channel subtypes and genes
9 Sodium channels

1.1 to 1.9, named after subunit 1.7, 1.8 and 1.9 are important in pain processing
IFM = isoleucinephenylalaninemethionine hydrophobic cluster
10 Ca++; 40 K+ Cl-, Mg++ uncatalogued
We will focus on just 2 channels

Raouf et al, 2010
N-type Voltage-gated Calcium Channel

Signal Transmission Pharmacology

Facilitation
Transmitters Glutamate / EAA Substance P, VIP CGRP, galanin, somatostatin Synaptic NGF Modulators Serotonin (2a, 3a) (Glial) CCK (+ on-cells) Opiates BDNF
Activated by NMDA receptor Ziconotide and Leconotide block the pore Pregabalin and gabapentin

Inhibition
Glycine GABA
Bind accessory 2 subunit May block channel trafficking into membrane Block thrombospondin binding and block synaptogenesis
Burgess and Williams, 2010
DNIC catecholamines (NE, 5-HT, DA) Cannabinoids Adenosine
Pain Signaling (Trans5)

Could she have a problem with signal transmission such as a channelopathy?
Sure she could Need to explain all the co-morbidities More parsimonious explanation is central dysfunction lets go on
Is it likely?

2 Principles of Signal Transfer
Signal Transfer / Gating Anatomy

All input to higher centers, i.e. cortex (pain and otherwise) is highly gated, and cannot gain access without high-level permissions (e.g. secure internal network).
Ascending (red) spinothalamic tract Descending (green) modulating system
Example - 2:1 cortex:retina projections to lateral geniculate
Gating is performed through a series of cascading brainstem nuclear switches with progressively less complex decision making tasks.
Pathway: Amygdala (CeA) projects to periaquaductal gray, locus ceruleus, rostroventral medulla, dorsal reticular nucleus, dorsal horn via dorsolateral funiculus. CeA neurons sensitized by glutamate (metabotropic receptor) in chronic pain Ossipov et al, 2010
Signal Transfer / Gating Function
Signal Transfer / Gating Pharmacology
Descending (green) modulating system (stress-induced analgesia)
DRt (dorsal reticular nucleus) coordinates the diffuse noxious inhibitory control (DNIC) modulation of pain Blocked by naloxone Requires convergent neurons in dorsal horn responsive to noxious and innocuous inputs. DNIC is non-functional in IBS, TMJ disorder, OA of knee, chronic pancreatitis, tension headache. ? Pelvic Pain? DNIC dysfunction predicts post-op pain.
Ossipov et al, 2010
Descending modulating system sites of drug action

PAG: opioids and NSAIDs RVM: Opioids and cannabinoids; Blocked by naloxone Dorsal Horn: Tricyclic agents, SNRIs, alpha-2 agonists, opioids.
Ossipov et al, 2010
Pain Signaling

Is her diffuse noxious inhibitory control (DNIC) working?
Probably not Probably not, just part of the picture
Does this account for all of her pain
3 Principles of Signal Translation Triangle of PFC, ACC, PAG

PFC: prefrontal cortex ACC: Anterior cingulate cortex PAG: periaqueaductal gray
Signal Translation: What about IC?

Hip OA: PFC, ACC, PAG
Clinical pain is recorded more anteriorly in IC Ascribe more negative meaning to perception In low back pain, sudden pain rises registered same as healthy controls, but on-going severe pain activates PFC and amygdala
(Baliki J Neurosci 2006)
The concept of nociceptive pain is challenged
RA: Medial PFC facilitates ONLY disease-relevant pain

(Schweinhardt, Neuroimage 2008) Activates hippocampus Inhibits lateral PFC-PAG
circuit in RA and IBS
ACC activation (to inhibit pain) fails in IBS and in FM.

(Mayer, Pain 2005)
Schweinhardt and Bushnell, 2010
Ossipov et al, 2010
Long-term consequences of pain
Reduction in gray matter volume

ACC, IC, PFC, thalamus Fibromyalgia, Osteoarthritis, CRPS, Migraine Reverses when pain goes away
Rat model of chronic pain

PFC atrophy Coincides with anxiety-like behavior Neuronal loss due to excitatory Amino Acids Loss of glial volume?
Schweinhardt and Bushnell, 2010
Cause ?

Now probably have failure of another central system: ACC activation of lateral PFC then PAG, which is why the descending system was failing. This is part of learned passivity which can occur very quickly in right setting, both in animals and in humans. Next question:
Should she be using opiates?
Pain Signaling

Principles of Signal Transformation

Neuronal pain signals induce glial inflammation at the synapse Glial inflammatory cytokines signal pain in neurons BDNF inverts dorsal horn GABA signal turning inhibition into activation of pain signals Opiates bind to TLR4 and activate glial proinflammatory pathways
Glial Function in Neuropathic (Sensitized) State

What are Toll-like Receptors (TLRs)?

Neuronal CGRP and SP remove Mg++ from NDMAR activating VGCC Neuronal ERK sensitizes NMDAR & AMPAR Glial ERK downregulates GLT1 and GLAST Glial ERK activates NF-k resulting in inflammatory factors TNF, PGE2, NO, IL-6, IL-1,, ATP which in turn activate TLRs
Receptors involved in innate immune response through recognition of microbial molecules Part of a family that includes all toll and interleukin-1 receptors Name toll derived from German: das ist toll meaning wild, when drosophila flies looked weird after mutation of the first gene in this group. 10 TLRs in humans; mostly in macrophages TLR4 most well-known as mediator of septic shock through binding of lipopolysaccharide (LPS)
Basically neuropathic pain is almost identical to the immunogenic state for glia which induce synaptic inflammatory state.
Opiates Bind to TLR4
Case Reconnect
Opioids cause release of pro-inflammatory cytokines through TLR4 (Hutchinson, 2007, 2008) Glial activation produces:

She has dysfunction of:

Opioid tolerance Reward seeking and addiction Respiratory depression
ACC to PFC to PAG Descending modulating system Now someone has stopped function of her glia in reducing chronic pain syndrome through TLR4 binding of opiates
Opioids enhance glial immunogenic state
One helpful thing: taper the opiates
Redirecting our thinking
Permissive Pain Network Hypothesis Supportive Clinical Observations
New proposal for pain thinking:

Incoming signal = information, not pain (Karen Berkley) Pain state = self-perpetuating signal interpretation with consequent changes in BOTH CNS and PNS Chet DeGroats elegant work showed that the exact same K+ channels that close in silent nociceptors in the bladder due to UTI are the ones that close due to spinal cord injury. This is a network, not dissectable signals. Both CNS and PNS can induced pain state, but need permission for activation of this network pattern.
Majority of interventions such as blocks, stimulators, and drugs, eventually stop working. The nervous system wants to get back to the pain state. We view at as bad but the brain views it as a protective armament, as good.
This is a testable hypothesis
The only evidence-based long-term effective treatment is based on the biopsychosocial model The nervous system in the chronic pain state will always circumvent every intervention done to it But it will not circumvent what it does to itself.
Clinical experience: Pain is not in our bodies, pain is not in the brain, pain is in our lives. Dennis Turk Scientific experience: virtually impossible to provide a cogent definition of a nociceptor. G.F. Gebhart Chronic pain is about a dynamic network that includes CNS, PNS, end-organ.
Part I: Essential Elements of the History in the Evaluation of a patient with Chronic Pelvic Pain
Kathy Witzeman, MD Assistant Professor, University of Colorado Director of the Pelvic Pain Clinic Department of OBGYN Denver Health Medical Center
Disclosures
I have no financial disclosures related to this presentation
Objectives
Identify potential barriers to obtaining an adequate history and how to overcome them Describe the potential contributing causes to chronic pain in the pelvis Identify ways to elicit essential patient history information that will help to determine contributing causes to their pain
Common Road blocks to diagnosis

Patient embarrassment Patient doesnt know what to tell their healthcare provider about their pain and other symptoms Physician or provider unaware of conditions, contributors or potential for treatment Provider preconceptions regarding pain Time constraints the evaluation takes time
How Pain Affects Women
How Chronic Pain Affects Self-Image
How a Patient with CPP Affects the Provider??

What is your first reaction when you see the Chief Complaint: Pelvic Pain??
CPP is Multifaceted
Irritable Bowel Syndrome
Painful Bladder Syndrome
Vulvodynia
Prolonged postsurgical or obstetrical damage

Endometriosis
Chronic Pelvic Pain
Pelvic Floor Myofascial pain
Abdominal Wall Myofascial Pain
A Systematic Approach to Taking the History:

Obtaining a complete and thorough history
Using a questionnaire will help gather information efficiently but does not replace taking a good history and spending time discussing in more detail what the woman has noted on the questionnaire If you dictate your notes, use a dictation template that includes all of the pertinent history points and just check off or take quick notes on the template to expedite the process
Meet Cristina
31 year old referred for evaluation of 15 year history of pelvic pain
History of Present Illness (HPI)

Let your patient tell their story (for 3-5min) Then focus in on key elements to elaborate on
Pain location(s), character and time line, how has it progressed
Pain scale rating (current, baseline, worst) Character of pain feeling of falling out, sharp, burning
History of Present Illness (HPI)

Other types of chronic pain they have
Low back pain, headaches, TMJ, knee pain
Prior Providers and Evaluations

Get records ahead if you can Pelvic infection testing, TVUS, CT Abd/Pelvis, MRIs, Colonoscopy, EGD, blood work Prior treatments medications, PT, massage, surgeries and their effect on the pain
Aggravating factors be specific

Related to menses, voiding urine or stool, lifting, sitting, walking, sexual intercourse
Alleviating factors be specific

Heat, cold, lying down, massage, prior medications tried, voiding, after bowel movement
Review of Systems
General: weight loss or gain, fatigue, poor sleep, fever, chills or sweats Urinary: frequency, dysuria, hematuria, urgency, incomplete voiding sensation, loss of urine either stress, urge or both, frequent bladder infections; kidney stones GI: nausea/vomiting +/-assoc with pain or meds; hematachezia, melena, dyschezia (pain with BM); change in frequency or consistency Reproductive/GU: vaginal dryness, dyspareunia, decreased lubrication; abnormal or foul-smelling vaginal discharge; cyclicity; hot flashes/night sweats; genital lesions; painful orgasm; inability to use tampons for how long;
Review of Systems cont.

Musculoskeletal: other focal or generalized pain or weakness Neurological: headaches/migraines describe; TMJ; h/o seizures; numbness or tingling; parasthesias (burning sensation); localized weakness Endocrine: thyroid sx; undiagnosed diabetes sx Psych/Sleep: sxs of depression, anxiety, PTSD, Panic Disorder, psychotic sxs; poor sleep both initiating and staying asleep Heme: blood clots, easy bruising CV/Pulmonary: palpitations, chest pain, respiratory difficulties
PMHx and PSHx

Ask specifically about Seizures, Asthma, CV problems, Fibromyalgia, Migraines, Depression, Anxiety, PTSD, IBS, Renal stones, DGD, arthritis, prior hospitalizations/MVAs/trauma especially back trauma List all surgeries with dates and any complications
Note specifically any surgery for pelvic pain (i.e. multiple laparoscopies results??)
OB and GYN History

List all pregnancies
years, mode of delivery, complications especially vaginal trauma macrosomic infants; also note D&Cs, TABs any relation to onset of pain? if still having menses then duration, flow, timing association with typical pain prior/current contraception HRT if menopausal h/o STIs, h/o cervical dysplasia known fibroids; ovarian cysts or other reproductive organ problems
Menarche and menstrual history
Sexual History
Review confidentiality reason for probing questions Onset of sexual activity, # of lifetime partners, time with current partner Single sex partner, Opposite sex partner, both? Pain with sexual intercourse; onset, introital, deep, or both; how long does it last; character Can orgasm be achieved, pain with or after orgasm Affect of pain on sexual relationships Use of lubrication, condoms, sexual props/toys
Social History
Who does pt live with married/children? Type of work if at all- specifically any repetitive motions? Financial/Social stressors? Education level Health Habits
Tobacco (amount/time period/thoughts of quitting) Drugs current/past/ type ETOH amount (CAGE) Exercise (type/frequency) Caffeine intake Dietary habits (fast food; vegan; well balanced, etc.)
Social History cont.

Coping Mechanisms who does pt talk with or get support from regarding pain and/or other life stressors (i.e. spouse/partner; clergy; other family; healthcare providers) How does partner react when shes in pain? (supportive; gets angry; tries to help; withdraws, etc.) How do they try to make themselves feel better when in pain? (i.e. try to relax; takes meds; heat; lies down; massage; nothing) Is the pain the most important problem or just one of many problems?
Psychiatric History
Known history of Affective disorders
Depression, Bipolar, Anxiety, PTSD, Panic disorder Treatment, current state, hospitalizations Screen if concerning or positive answers during Psych ROS and no prior diagnosis Use screening tools: Beck Depression Inventory, Edinburgh Postnatal Depression, Zung Depression Rating Scale, PHQ-9
Abuse History
Document childhood or adult history of physical, emotional or sexual abuse reported Ask these questions directly or patient is not likely to share information If positive history document type and timing of abuse if as child or as adult; any current abuse; has pt received treatment? Type/duration? Know your state laws and local resources regarding reporting abuse in the home
Family History
Ask specifically about pain disorders
migraines, painful bladder syndrome; irritable bowel syndrome; fibromyalgia; endometriosis; other pelvic pain; TMJ; vulvodynia; depression
Also review cancers/htn/dm/cad
Meds and Allergies

Current medications and dosing and consistency with taking them Past medications used for pain Drug and Latex Allergies Food Allergies (i.e. gluten, lactose, fructose) can lead to contributing GI distress
How do you put it all together?
Post Test - Question 1

What are potential barriers to identifying the possible contributing causes to your patients chronic pelvic pain? A. Provider unaware that a condition could contribute to this problem B. Not enough time C. Patient embarrassment D. A and B only E. All of the above
Post Test - Question 1

What are potential barriers to identifying the possible contributing causes to your patients chronic pelvic pain? A. Provider unaware that a condition could contribute to this problem B. Not enough time C. Patient embarrassment D. A and B only E. All of the above
Post Test Question 2

Which of the following is a likely a contributor or symptom of Cristinas pelvic pain problems:
A. Urinary frequency, urgency and sensation of incomplete voiding, and difficulty starting stream B. Difficulty falling and staying asleep C. Pelvic floor myalgias D. Chronic headaches and jaw pain E. Constipation F. A, C, and E G. All of the above
Post Test Question 2

Which of the following is a likely contributor or symptom of Cristinas pelvic pain problems:
A. Urinary frequency, urgency and sensation of incomplete voiding, and difficulty starting stream B. Difficulty falling and staying asleep C. Pelvic floor myalgias D. Chronic headaches and jaw pain E. Constipation F. A, C, and E G. All of the above
Thank you for your attention
Questions?
Objectives
International Pelvic Pain Society Basics Course October 18 2012 Chicago IL
Essential Elements of the Musculoskeletal Exam

Dee Hartmann, PT, DPT Dee Hartmann Physical Therapy Chicago IL healthyexp@gmail.com
Define differences between traditional physical therapy and womens health physical therapy Suggest assessment techniques that can be used on initial medical evaluation of men and women and why they are important Describe pelvic floor muscle mobility Suggest techniques to ease pain with digital assessment Suggest ways to locate appropriate therapist
2012 by Dee Hartmann, PT, DPT
Disclosures
Traditional Physical Therapy (PT)

Assessment

Intervention
Manual therapy Modalities Home exercise program
Gait Posture
Standing Sitting Sleeping
I have no disclosures, financial or otherwise

Muscle strength Muscle length Pelvic mobility testing
Frequency and duration

2-3x/week 4 weeks Reassessment
Womens Health Physical Therapists

Really do more than relaxation and surface EMG biofeedback for the pelvic floor muscles (PFM) Specifically trained
Internal assessment of the pelvis (anterior and
Difference Between the Two?

Traditional PT Assessment

Womens Health PT
All of Assessment
Pelvic function by history Bladder Bowel Sexual Assess system abnormalities Visceral system Fascial system Lymphatic system Musculoskeletal system Nervous system
In depth history Gait Posture

Standing Sitting Sleeping
posterior) in both females and males Assessment of the organs systems and their impact on the underlying pain (i.e. brain, fascia, GI tract, nerves, bladder)
Muscle strength Muscle length Pelvic mobility testing
Currently referred to as womens health PT

Should maybe be changed to pelvic health PT?
Difference Between the Two?

Traditional PT
Intervention
Manual therapy Modalities Home exercise program
Visceral? Fascial?
Reaches all areas of the body
What?
Womens Health PT
Intervention
Manual therapy Internal manual therapy Visceral, fascial, nerve, muscle, and lymphatic mobilization Diaphragmatic breathing Help with function (i.e. sex, GI) Modalities
Very gentle, hands-on therapy approach Assesses and treats all organ systems
Viscera, vascular, lymphatic, muscular, and nervous Head to toe, brain to the pelvis

2-3x/week 4 weeks Reassess
Home exercise programs
Goals
Discovering how the system abnormalities relate to

1-2x/week 10-12 weeks Reassess
the chronicity of pain

Treating with resulting release of tension, regaining
mobility, and restoration of function

Why bother?
Traditional physical therapy often falls short of eliminating chronic pelvic pain (CPP)
Not just the musculoskeletal system..
Fridays Schedule
8:10 a.m. 9:05 a.m.
An Update on the Pathogenesis and Treatment of Endometriosis

9:05 a.m. 9:45 a.m.
Innovative Injection Therapies for Pain Syndromes of Pelvic Floor Fascia

9:45 a.m. 10:25 a.m.
Have to get to the CAUSE of the problem

.and not just treat the SYMPTOMS Ever try to fill a bucket that has a hole in the
The Acute Anus

11:15 a.m. 11:35 a.m.

11:35 a.m. 11:55 a.m.
Vulvodynia
11:55 a.m. 12:15 p.m.
bottom?
Majority of my patient population have had traditional PT, typically more than once
Interstitial Cystitis
2:00 p.m. 2:40 p.m.
Visceral Pain Models

Visceral Assessments
Abdominal viscera
Extends from the
Impact of Abnormal Visceral Tension

Pelvic floor muscle tension Coccygeal pain, sacrococcygeal pain Sacroiliac (SIJ) dysfunction Dyspareunia Decreased lung capacity Urinary dysuria, urgency/frequency Diarrhea, constipation Low back pain Decreased trunk mobility General malaise Dysmenorrhea
respiratory diaphragm to the PFM Typically involved with CPP Palpate with a gentle hand for generalized abdominal tension
Abnormal Abdominal Visceral Tension

Signs of dysfunction
Tension anywhere throughout the abdominal cavity Pain with gentle pressure
Musculoskeletal Assessment
Psoas muscles
Hip flexor deep in the lower
abdominal cavity
Extends from the respiratory
Refer to appropriate PT
diaphragm, running below the inguinal ligament to insert on the lesser trochanter of the femur Underlies the kidneys, ascending/descending colons Adjacent to the descending portion of the duodenum
Psoas Assessment
Palpation
medial to ASIS superior to inguinal ligament
Impact of Abnormal Psoas Tension

Bladder dysfunction
Gentle sinking through the
tissues
Resist hip flexion and
assess tone of contracting muscle

Should feel the contraction
Chronic low back and sacroiliac (SIJ) pain Hip muscle imbalance PFM tension Difficulty coming from sit-to-stand without pain
but not bulkiness

Should not be painful
Abnormal Psoas Tension
Deep external rotators of the hip
5 small muscles
Oburator internus, externus Superior, inferior gemellus Quadratus femoris
Decreased ability to flex hip without pain Pain
Underlie the sciatic nerve Its not just a piriformis problem

2012 by Dee Hartmann, PT, DPT 2012 by Dee Hartmann, PT, DPT
Hip Rotator Assessment

2 step process
Locate deep rotators by
Impact of Abnormal Rotator Tension

cupping fingers around the greater trochanter fingers come in contact with the muscles Allow the hip to drop into external rotation Palpate for pain in both positions and with movement
Pelvic floor muscle tension Coccygeal pain, sacrococcygeal pain Sacroiliac (SIJ) dysfunction Sciatica Pudendal nerve irritation Dyspareunia Constipation
Abnormal Deep Rotator Tension
Decreased palpation space at medial trochanter Minimal mobility with attempted contraction Pain
The pelvic floor

Its more than just muscle accord to Delancey Includes the everything from the endopelvic fascia
on the cranial surface to the superficial PFM on the caudal end
Pelvic Floor Assessment

Includes the
Viscerauterus, tubes, bladder, urethra, and
Uracus Bladder, ureter (peritoneum)
Sacroiliac joint Uterus, fallopian tubes, Ovary (covered by peritoneum) Uterosacral ligament Pubocervical ligament Arcus tendineus Levator ani-Deep PF Iliococcygeus Pubococcygeus Puborectalis
rectum Fascial structuresuterosacral ligament, fascial support of the levator, arcus tendineus pelvic fascia, and pubocervical ligament Bony support structures PFM
Round ligaments
Superficial PF Ischiocavernosus Bulbospongiosus Superficial trans perineal Labia minora
Pelvic Floor Muscle Assessment

PFM
Extend from the sacrum/coccyx posteriorly to the pubic
PFM Action
ADD IN THE PRIMAL VIDEO
rim anteriorly
Generalized function
Support the pelvic viscera Provide assistance with continence for the urethra and bowel Contract and relax with orgasm Combine with the respiratory diaphragm, the abdominals, and the multifidus muscle to create core trunk support
Assessed rectally in men and vaginally and rectally in
women
Assessment of the PFM

Elevated PFM tension
Assessment of the PFM-Female

Be gentle and go slowly Place a gloved (non-latex), lubricated finger at the posterior fourchette If there is pain, before digital insertion, ask her to

will decrease the size of the openings (vaginal and rectal) Forcing a speculum into the vagina with elevated PFM tension will only cause increased spasm and pain, as will forced rectal digital insertion Be aware of vulvar sensitivity and PFM tension
Take a deep breath all the way down to my finger Try to contract, like holding back gas or urine, and then just let everything go Bring your hips up toward the ceiling and hold for 10 seconds. Come back down and let everything relax
If you need to use a speculum, consider using a pediatric size Please dont tell them to just relax because they have no clue what to relax Chances are, if theyre clenching their fists, theyre also clenching their pelvic floors, buttocks, adductors, teeth, and any thing else that they can possible hold tight
If PFM tension is present, there will be more space between the labia and the level of the PF muscle Once inside the vagina, the assessing digit goes off midline
If able, 2 digits can be inserted and bilateral
Assessment of the PFM-Male

If PFM tension is present, there will be more space between the external and internal anal sphincters Use same techniquesbreathing, contract/relax
Ask patient to bear down, like trying to pass gas before
Ask patient to squeeze, like trying to hold back gas and/or urine
With PFM tension (elevated PFM resting tone),
contracting is often quite difficult and minimal motion can be palpated The cue of holding back gas seems easier often times
insertion
Get a sense of motion and lift
Gently spread buttocks DONT say .just relax..
Assessment of the PFM-Male
Impact of Abnormal PFM Tension

Urinary and bowel dysfunction Difficulty with vaginal exams Inability to use tampons Pain
Clothing choices Biking Horseback riding
Once inside the rectum, the assessing digit goes off midline To assess PFM function, ask patient to squeeze, like trying to hold back gas
With PFM tension (elevated PFM resting tone),
Incontinence
Urgency Frequency
Constipation
Perceived constipation
contracting is often quite difficult and minimal motion can be palpated
Sexual dysfunction
Dyspareunia Apareunia and/or
Get a sense of motion and lift up and into the pelvis
vaginismus
Chronic vulvar pain

Abnormal PFM Tension
Assessment of Obturator Internus

Originates on medial
Decreased ability to fully contract or relax Minimal mobility with attempted contraction Pain
surface of obturator foramen Runs inferior and posterior to turn 120o Attaches to greater trochanter Function-helps to
laterally rotate extended
thigh
abduct flexed thigh steady the femoral head in
the acetabulum
Obturator Internus Assessment

Locate and palpate
On the vaginal sidewall Inferior to ischial spine
Impact of Abnormal Obturator Internus Tension

Pelvic floor muscle tension Coccygeal pain, sacrococcygeal pain Deep hip pain
Hip bursitis
Resist hip ER and assess tone of contracting muscle

Should feel the
Dyspareunia Obturator nerve compression
contraction but not bulkiness Should not be painful

Abnormal Obturator Tension
Urethra
Assessment of Pelvic Viscera Female

Feels like a pencil Palpation creates pain
Bulky feel to the muscle Pain with resisted palpation
and/or urgency
Bladder
Feels like a tennis ball Palpation creates pain
and/or urgency
Rectum
feels like a bumpy mass Palpation creates pain
and/or urgency
Assessment of Pelvic Viscera Male

Palpate rectally Urethra
Feels like a pencil Palpation creates pain
Impact of Abnormal Pelvic Visceral Tension

Pelvic floor muscle tension Coccygeal pain, sacrococcygeal pain Sacroiliac (SIJ) dysfunction Dyspareunia Dysmenorrhea
Urinary dysuria, urgency/frequency Diarrhea, constipation Low back pain Decreased trunk mobility General malaise
and/or urgency
Bladder
and/or urgency
Prostate
Abnormal Pelvic Visceral Tension
What will happen on my first visit?

History
Typical PMH + questions on physical history A lesson in pelvic anatomy and physiology
Complaints of urgency (urinary, fecal) Pain
Physical examination
Postural exam Assessment of abdominal and hip tension Overall assessment of systems
Externally Internally (no speculum with females)

How to Refer to PT
In the United States
www.womenshealthapta.org www.apta.org www.nva.org
How to find someone?

If you have PTs you refer to, call them Call your local PT offices Ask questions
Womens health PT? Experience in treating chronic pain? Extent of course work?
Outside of the US
www.ioptwh.org
Australia, Brazil, Canada, Denmark, Germany, Hong Kong, Ireland, Israel, Netherlands, New Zealand, Norway, Portugal, Slovenia, South Africa, Sweden, United Kingdom, and United States
Just like finding a qualified, experienced, compassionate physician, finding a good physical therapist may be equally as difficult
Thank you for your attention
Disclosures
I have no financial relationships to disclose
Diagnosis and treatment of gynecologic causes of chronic pelvic pain

Matthew Siedhoff, MD MSCR Division of Advanced Laparoscopy & Pelvic Pain University of North Carolina at Chapel Hill
Objectives
Discuss diagnosis and treatment of common gynecologic contributors to CPP:
Endometriosis Adenomyosis Adhesions Ovarian remnant syndrome Uterine retroversion
Gynecologic causes of CPP

Disclaimer #1
Not generally a Eureka! moment with chronic, as opposed to acute, pain The simple pain conditions wont be too challenging to identify and treat Majority of patients w CPP have centralized pain
Turn down the master volume Tune up the peripheral elements (focus of this talk)
Dysmenorrhea Healthy woman
Severe Dysmenorrhea Chronic pelvic pain

Disclaimer #2
The of chronic pelvic The source host where the disease pain in many women is not manifests is more important solely indisease the pelvis than the itself
Symptom vs diagnosis Treatment approach to symptom varies by what you believe is contributing to that symptom Example
Dyspareunia
Pelvic floor tension myalgia physical therapy Vestibulitis medications, vestibuloplasty Uterine retroversion position adjustments, uterine suspension Deeply infiltrating endometriosis surgical excision

Disclaimer #3
Surgery in CPP
Multifactorial approach to evaluating pain Be honest with patients about findings Focus on improvement rather than cure Delineate what may be helped by surgery and what isnt likely to be Value in negative findings in diagnostic surgery While surgery (including hysterectomy and removal of ovaries) can be helpful in some women, the treatment of chronic pelvic pain is NOT serial removal of organs
Endometriois
Benign condition in which endometrial glands and stroma are present outside the uterus ASRM Staging I - IV Deeply infiltrating: lesions extending >5mm below peritoneum or affecting other organs or ligaments Symptoms
No pathognomonic pain symptom Dysmenorrhea, non-cyclic pain, dyspareunia Infertility
Kennedy S, et al. ESHRE guideline for the diagnosis and treatment of endometriosis. Hum Reprod. 2005;20:26982704
Endometriosis
More common among women undergoing laparoscopy for CPP than women without pain Laparoscopic treatment is more effective than diagnostic surgery alone Stage of disease and symptom severity
Mild or no relationship for dysmenorrhea, noncyclic pelvic pain
Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Surv. 1993;48: 357-87 Sutton C, et al. Prospective, randomized, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril, 1994; 62: 696700 Abbott, J et al. Laparoscopic excision of endometriosis: a randomized, placebo-controlled trial. Fertil Steril, 2004; 82: 878-884 Porpora M, et al. Correlation between endometriosis and pelvic pain. J Am Assoc Gynecol Laparosc 1999;6:429-34 Milingos S, et al. Endometriosis in patients with chronic pelvic pain: is staging predictive of the efficacy of laparoscopic surgery in pain relief? Gynecol Obstet Invest 2006;62:48-54
Endometriosis
For mild disease, pelvic pain location likely not strongly correlated with surgical findings.
Hsu AL et al. Relating pelvic pain location to surgical findings of endometriosis. Obstet Gynecol. 2011;118(2):223-30
Endometriosis
Deeply infiltrating endometriosis
Dyspareunia and posterior culdesac disease Dyschezia and bowel disease Lower GU tract symptoms and bladder disease
Endometriois
Diagnosis
Laparoscopy Physical exam (advanced disease)
Uterine immobility Fixed adnexal mass (ovarian endometrioma) Uterosacral nodularity
Rectovaginal exam
Abdominal wall endometrioma

Vercellini P et al. Association be tween endometriosis stage, lesion type, patient characteristics and severity of pelvic pain symptoms: a multivariate analysis of over 1000 patients. Hum Reprod 2007;22:266-71. Gruppo Italiano per lo Studio dellEndometriosi. Relationship between stage, site and morphological characteristics of pelvic endometriosis and pain. Hum Reprod 2001;16:2668-71 Fauconnier A et al. Relation between pain symptoms and the anatomic location of deep infiltrating endometriosis. Fertil Steril 2002;78:719-26
CA 125 Transrectal ultrasound, contrast CT, MRI, etc.
Endometriois
Treatment
Medical
1st line treatment
NSAIDS OCs, cyclic or continuous Levonogestrel IUD (Mirena ) Progestins: norethindrone, medroxyprogesterone acetate Depression, loss of bone calcium
Endometriosis
Treatment
Medical
2nd line
GnRH agonists Relief of pain does not make the diagnosis of endometriosis Vasomotor sxs, vaginal dryness, bone loss Aromatase inhibitors Danazol Androgenic derivative which suppresses LH and FSH Anovulation, pseudomenopause Weight gain, hirsutism, acne, deepening voice
To move beyond these, strongly consider laparoscopy to both diagnose and treat the disease
Endometriosis
Treatment
Surgical
More effective than diagnostic surgery alone Excision vs ablation Presacral neurectomy
Randomized trial of 141 subjects to conservative treatment of endometriosis +/- PSN All subjects had a midline component to pain 80% vs 60% reported effective treatment of pain at 12 mos, maintained at 24 mos 5-15% risk constipation, urinary urgency Decreases dysmenorrhea, dyspareunia with central pain
Zullo F et al. Effectiveness of presacral neurectomy in women with severe dysmenorrhea caused by endometriosis who were treated with laparoscopic conservative surgery: a 1-year prospective randomized double-blind controlled trial. Am J Obstet Gynecol. 2003;189: 720721. Latthe PM et al. Surgical interruption of pelvic nerve pathways in dysmenorrhea: a systematic review of effectiveness. Acta Obstet Gynecol Scand. 2007;86(1):4-15
Adenomyosis
Ectopic endometrial glands and stroma within the myometrium
Adenomyoma is a nodule of adenomyosis Assoc w other pathology (fibroids, endometriosis)
Adenomyosis
Diagnosis
80% reported cases in 30s 40s 80-90% in parous women Symptoms
Incidental finding in up to 35% of women undergoing hysterectomy Heavy menstrual bleeding, intermenstrual bleeding, dysmenorrhea
Adenomyosis
Treatment
Medical
LNG-IUS Oral progestin GnRH agonists, aromatase inhibitors Controversy around use of OCs
Findings
Diffusely enlarged boggy uterus MRI superior to TVS in imaging diagnostics
Junctional zone > 12 mm
Brahgeto AM et al. Effectiveness of the levonorgestrel-releasing intrauterine system in the treatment of adenomyosis diagnosed and monitored by magnetic resonance imaging. Contraception. 2007;76(3):195 Lee NC et al. Confirmation of the preoperative diagnosis for hysterectomy. Am J Obstet Gynecol. 1984; 150: 283 Bird CC et al. The elusive adenomyosis of the uterus revisited. Am J Obstet Gyncol. 1972; 112: 582-593 Ascher et al. Adenomyosis: prospective comparison of MR imaging and transvaginal sonography. Radiology. 1994;190(3):803 Sheng J e tal . The LNG-IUS study on adenomyosis: a 3-year follow-up study on the efficacy and side effects of the use of levonorgestrel intrauterine system for the treatment of dysmenorrhea associated with adenomyosis. Contraception. 2009;79(3):189
Adenomyosis
Treatment
Surgical
Hysterectomy Hysteroscopic resection, ablation Laparoscopic excision of adenomyoma Uterine artery embolization
Ovarian Remnant Syndrome

Persistence of functional ovarian tissue inadvertently not removed at the time of intended extirpation of one or both ovaries Most often a complication of difficult oophorectomy
Endometriosis, PID, adhesions
Wood C. Surgical and medical treatment of adenomyosis. Hum Reprod Update. 1998;4(4):323 McCausland V, McCausland A. The response of adenomyosis to endometrial ablation/resection. Hum Reprod Update. 1998;4(4):350 Kim MD et al. Long-term results of uterine artery embolization for symptomatic adenomyosis. Am J Roentgenol. 2007;188(1):176
Presumed mechanism of pain: combination of dense adhesions and functional ovarian tissue leads to painful cyst formation

Diagnosis
Premenopausal, usually 30s-40s No vasomotor symptoms despite history of oophorectomy Cyclic pain in women w history of oophorectomy Physical exam: tender adnexum or adnexal mass Labs: FSH, LH, E, CA 125 Imaging: ultrasound, CT, MRI
Steege JF. Ovarian remnant syndrome. Obstet Gynecol. 1987; 70(1): 64-67 Pettit PD et al. Ovarian remnant syndrome: diagnostic dilemma and surgical challenge. Obstet Gynecol. 1988; 71(4): 580583

Treatment
Medical
GnRH agaonists, DMPA
Surgical excision
Meticulous dissection of pararectal, paravesical spaces, ureterolysis Divison of infundibulopelvic ligament at pelvic brim
Nezhat F et al. Operative laparoscopy for the treatment of ovarian remnant syndrome. Fertil Steril 1992; 57(5): 1003-1007
Adhesions
Controversial if a cause of chronic pain
Marginal higher incidence of adhesions in women w CPP vs no-CPP (25% vs 17%) No difference in incidence, site, or density of adhesions in women with infertility vs CPP RCT of adhesiolysis by laparotomy failed to show improvement in pelvic pain
Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Survey 1993: 48: 357-387 Rapkin AJ. Adhesions and pelvic pain: a retrospective study. Obstet Gynecol. 1986; 68:59-62. Peters AAW et al. A randomized clinic trial on the benefit of adhesiolysis in patients with intraperitoneal adhesions and chronic pelvic pain. Br J Obstet Gynaecol 1992: 99;: 59-62.
Adhesions
Diagnosis
No reliable predictors in symptom description History: prior abdominal surgery, PID, inflammatory bowel disease, perforated appendix, endometriosis Laparoscopy
Treatment
Laparoscopic adhesiolysis Putative benefit must be weighed against surgical risk
Steege JF et al. Resolution of chronic pelvic pain after laparoscopic lysis of adhesions. Am J Obstet Gyncol. 1991; 165: 278-283
Uterine Retroversion
Can be a factor in deep dyspareunia Associated with endometriosis Physical exam: tender, retroverted uterus Treatment
Position adjustment Uterine suspension
Halperin R et al. Long-term follow-up (5-20 years) after uterine ventrosuspension for chronic pelvic pain and deep dyspareunia. Gynecol Obstet Invest. 2003;55(4):216-9. Batioglu S et al. Laparoscopic plication and suspension of the round ligament for chronic pelvic pain and dyspareunia. J Am Assoc Gynecol Laparosc. 2000 Nov;7(4):547-51 Carter JE. Carter-Thomason uterine suspension and positioning by ligament investment, fixation and truncation. J Reprod Med. 1999 May;44(5):417-22
Hysterectomy
600,000 annually in the US 10% done for pelvic pain as primary indication
Hysterectomy
1249 women evaluated 6 and 24 mos after hysterectomy for quality of life, impact of depression and pain on outcomes Not surprisingly, women without pain or depression had highest function levels Even among women w/ pain and depression, pelvic pain decreased from 97% to 19%; reduction by half in limited physical and social function Women w/ depression only had improvement in impaired mental health: 85% down to 33% Dyspareunia decreased in all groups Newer RCT data suggesting improved quality of life in TLH over TAH durable to 4 years out from surgery!
Hartmann KE et al. Quality of life and sexual function after hysterectomy in women with preoperative pain and depression. Obstet Gynecol. 2004 Oct;104(4):701-9 Nieboer TE et al. Quality of life after laparoscopic and abdominal hysterectomy: a randomized controlled trial. Obstet Gynecol. 2012 Jan;119:8591
Question #1
Which of the following is FALSE in regards to endometriosis?
(a) There is little or no relationship between stage of disease and severity of symptoms (b) Deeply infiltrating endometriosis can be detected on physical exam (c) Improvement of symptoms with GnRH agonist treatment is diagnostic for endometriosis (d) There is added benefit to excision of endometriosis with presacral neurectomy for patients with a midline component of pain
Question #2
Which of the following is FALSE in regards to adenomyosis?
(a) LNG-IUS can be an effective treatment for the symptoms of adenomyosis (b) The third decade is the most common age when women are diagnosed with adenomyosis (c) Adenomyosis is sometimes incidentally diagnosed in hysterectomy specimens (d) Adenomyosis is more common in parous women
Disclaimer
No financial disclosures
Diagnosis and Treatment of Vulvar Pain

Denniz Zolnoun , MD, MPH Department of Obstetrics & Gynecology University of North Carolina-Chapel Hill
2012 IPPS Annual Fall Meeting on Chronic Pelvic Pain
Whose Story is it?

30 yr old post partum patient 65 yr post operative patient vulvar pain 70 yr old women with vulvar burning 55 yr old women with vulvar pain 4 yr old with itching 35 yr old with itching and burning 45 yr old with vulvar pain following treatment for breast cancer 55 yr old with vulvar pain and rawness following radiation for colorectal cancer
Symptom based-Assessment
Skin
Partner Affective
Pain
Nerve
Muscle
Objectives
Provide guidance on in trenches symptoms based assessment and treatment of women with vulvar complaint Competency in symptoms based management of itch and scratch-burning (regardless of etiology
What is your diagnosis?
Clinical Exam: Where is 2,4,6,8, and 10?
Clinical Exam: Vestibulodynia
The cotton swab is used to test for pain locations on the vulva. Testing starts at the thighs and moves medially to the vestibule. The vestibule is tested at the 2:00, 4:00, 6:00, 8:00, and 10:00 positions. Each time the vestibule is touched if pain is present, the patient is asked to quantify the pain as mild, moderate, or severe.
(From Haefner, HK. Critique of new gynecologic surgical procedures: surgery for vulvar vestibulitis. Clin Obstet Gynecol 2000;43:689700. Reprinted with permission from Lippincott Williams &Wilkins.)
Manner of Examination
Objective Punctate/static allodynia Dynamic allodynia
Itch & Scratch

Step 1: Abort Perpetuation & Maintenance Step 2: Identify Etiology? If possible
Tools
Cold (e.g. frozen bag of peas, handheld shower) Pressure Rest (anxiolytic, sedation at night)
Biopsy? Diagnosis?
Baseline
1- month later
5- months later
Disclaimer
Basic Skin Care
Disclosures
Diagnosis and Treatment of Abdominal and Pelvic Peripheral Neuropathies

Mario Castellanos, MD St Josephs Hospital and Medical Center Creighton University School of Medicine Phoenix, Arizona
None
Objectives
To identify neuropathic pain as a cause of pelvic pain Develop strategies for diagnosis Understand treatment options for peripheral neuropathies Review clinical cases
Abdominal and pelvic neuralgia
Lateral cutaneous branch of iliohypogastric nerve Iliohypogastric nerve
Femoral branch of genitofemoral nerve Genital branch of genitofemoral nerve Lateral femoral cutaneous nerve
Inferior rectal nerve Posterior femoral cutaneous nerve
Femoral nerve
Clitoral/perineal nerves Cutaneous branch of obturator nerve
Discrimination between visceral and somatic pain Visceral

Internal pain Dull/vague Hard to pinpoint
Types of neuropathic pain

Dysesthetic pain Nerve trunk pain
Somatic
Surface pain Intense / sharp Easier to locate

Dysesthetic pain Affects skin and subcutaneous structures Constant or intermittent Described as searing, burning, or icy-cold May have a temporal pattern of worsening at periods of rest or bedtime

Nerve trunk pain Deep-seated, sharp, knifelike proximal pain along nerve roots or trunks Mediated by spontaneous impulses arising from nervi nervorum Improves with rest or optimal position but is aggravated by movement May develop muscle tenderness and pain
Etiology
Blunt Trauma Falls Car accidents Pelvic fractures Obstetrical Prolonged second stage of labor Positioning Traumatic Delivery Surgery Incisions Compression from retractors Stretching from positioning Suture ligature Radiation Therapy Fibrosis Medical conditions
Physical Examination
Cotton Swab Test
Trigger points
Jarrell, J. Demonstration of cutaneous allodynia in association with chronic pelvic pain. J Vis Exp. 2009 Jun 23;(28).
Pain Threshold Test

Devices that objectively measure when pain is experienced at certain pressures or temperatures Device is tested first at a reference point Measurements are taken across the abdomen and pelvis
Reliability of bedside testing
John Jarrell,1 Maria Adele Giamberardino,2 Magali Robert,1 and Maryam Nasr-Esfahani1 Bedside Testing for Chronic Pelvic Pain: Discriminating Visceral from Somatic Pain. Pain Research and Treatment. Volume 2011 (2011)
Peripheral nerve blocks
Diagnostic Treatment of Pain
Diagnostic Testing
Basic principles of nerve blocks

Pain must be present
Patients must have pain at the time of the injection
Materials
Local anesthetic
Lidocaine 1 2% with epinephrine Bupivacaine 0.5% with epinephrine
Evaluated for technical success

Anatomical position, diffusion of solution, and achieved analgesia
Sodium Bicarbonate 8.4% (10:1 ratio) Three to five milliliters, to minimize spread Image guidance (ultrasound, CT-scan, etc)
Interpretation
Relief of symptoms, the specificity of the block, and the possibility of placebo effect
Rigaud, J, Riant, T, Delavierre, D, Sibert, L, Labat, J-J. Progrs en urologie : journal de lAssociation franaise d'urologie et de la Socit franaise d'urologie. 2010;20(12):1072-83.
Ultrasound guided ilioinguinal nerve block
Post block technical evaluation

Analgesic effect in the distribution of the target nerve
Cotton swab Alcohol swab (cold sensation)
Check for diffusion

spread to other nerves may complicate the interpretation
Negative blocks should be repeated before concluding absence of efficacy
Post block patient evaluation

Evaluate patients at 30 minutes Have patients try to reproduce their pain
Ex: sitting, bending down, stretching
Visual analogue scale or numerical pain scale

Obtain before and after the procedure 50% improvement can be considered a positive outcome
Treatment
Medical management
Goals
Reduce the pain experience Improve allodynia and hyperalgesia
Medical management: First line

Drug Gabapentin Pregabalin Tricyclics Amitriptyline Duloxetine Venlafaxine 5% Lidocaine Patch Dose Range 300-1200mg PO TID 150-600mg PO (BID or TID) 75-150mg PO daily 30-60mg PO BID 75-150mg PO BID 1-3 patches / 12 h
Mechanism
Decreases peripheral nerve activity Acts on the central nervous system
Medical management: First line

Drug Gabapentin Pregabalin Tricyclics Amitriptyline Duloxetine Venlafaxine 5% Lidocaine Patch Adverse effects Drowsiness, dizziness, fatigue, difficulty concentrating Same Anticholinergic effects, weight gain, orthostasis Nausea, anorexia, insomnia, dizziness, fatigue Hypertension, sexual dysfunction Skin Reactions
Medical management: Second line

Durg Tramadol Opioids Dose Adverse effect 50-100mg PO QID Drowsiness, constipation, dizziness, seizures, dependency Varied Constipation, sedation, nausea, substance abuse
Physical therapy
Recommended when concomitant musculoskeletal dysfunction is present Muscle spasms may be contributing to nerve dysfunction Manual techniques, patient education, and neuromuscular reeducation may help resolve contributions of muscular component of pain May be an adjunct to help in diagnosis
Corticosteroids
Peripheral nerve blocks with corticosteroid
Triamcinolone (Kenalog) 40mg
Mechanism
Enhances anesthetic affect Reduces spontaneous ectopic discharges
Up to 70% of patients obtain long term pain relief Block may be repeated if / when pain returns
Corticosteroids: Adverse effects

Risk of nerve injury (1:10,000) Rebound pain
Experienced for 3-5 days after injection
Neurolysis / Surgical decompression
Intravascular injection Risk of steroids
When patient require more than 3 injections a year, consider neurolysis of surgical decompression of entrapped nerves.
Neurolysis: Chemoablation
Image guided nerve injection with:
Absolute alcohol Phenol 5-6%
Chemoablation: Adverse effects

Non-target tissue necrosis Neuritis up to 10% Neuroma formation at site of injection Anesthesia dolorosa
Destroys myelin sheaths and causes axonal edema Patients will initially have pain in the distribution of the nerve with treatment effects within 12 to 24 hours Some studies show 1-2 years efficacy Duration of pain relief is dependent on nerve regeneration
Radiofrequency neurolysis
Utilizes alternating electrical current at 250khz for thermocoagulation Generates frictional heat by molecular movement Helps identify nerve by replicating pain at higher frequency and lower voltage prior to neurolysis
Radiofrequency neurolysis: Outcomes

About 70% of patients obtained relief of pain Longer lasting effect than a nerve block
Kastler, A., Aubry, S., Piccand, V., Hadjidekov, G., Tiberghien, F., & Kastler, B. (2012). Radiofrequency neurolysis versus local nerve infiltration in 42 patients with refractory chronic inguinal neuralgia. Pain physician, 15(3), 237-44.
Cryoablation
Utilizes cold (-60 C) for ablation Prevents neuroma formation
Axons and myelin sheaths are lysed, but epineurium and perineurium remain intact
Radiofrequency vs cryoablation: Adverse effects

Neuroma formation: Radiofrequency > cryoablation Non-target tissue injury: Radiofrequency > cryoablation Shorter acting: Cryoablation
Effects are immediate (RF may take up to a week)
Surgical
Neurectomy
Surgical resection of the nerve
Treatment algorithm
Neuropathic pain
Adhesiolysis
Surgical decompression of the nerve
Medication / Physical therapy
Nerve Blocks
At least 70% effective in improving pain

Repeat Nerve Block Infiltration with Corticosteroids
Other pathology Visceral Myofacial
Repeat Blocks 6 weeks apart
Surgical Management: Ablation Neurectomy Decompression
Choosing a surgical management

Procedure Ablation Neurectomy Decompression Motor + Sensory + + Regeneration +/+
Causes of treatment failure

Involvement of other peripheral nerves or wrong diagnosis Regeneration / neuroma formation Incomplete decompression Central Sensitization
Case 1
35 year old woman presents with right flank pain and right groin pain for several years. She has a history of nephrolithiasis and has been seen by her urologist who performed an extensive work up without any evidence of stones. Further history reveals that pain started after a c-section. She has generalized burning in the RLQ and is unable to lean up against a counter secondary to pain.
Clinical cases
Exam shows tenderness of the right aspect of her prior suprapubic transverse incision.
Case 1
Which of the following nerves is affected?
A. Iliohypogastric B. Genitofemoral C. Lateral femoral cutaneous
Iliohypogastric nerve
Originates from L1 ventral ramus Sensory:
Posterior lateral glute Suprapubic skin
D. Pudendal E. F. Posterior femoral cutaneous Obturator
Motor:
Transverse abdominus Internal oblique
Iliohypogastric nerve: Surgical cause
Iliohypogastric chemoablation
Transection, entrapment, crush injury, neuroma formation
Case 2
40 year old presents with right labial and groin pain. She has been treated for vulvodynia for the past 5 years without much relief. She is unable to wear underwear due to irritation. Careful history reveals that pain started after emergency placement of a IVC filter Exam shows hyperalgesia of the right labium majus and anterior thigh
Case 2
A. Ilioinguinal B. Genitofemoral C. Lateral femoral cutaneous
Genitofemoral neuralgia
Originates from L1-L2 ventral nerve roots Divides into genital and femoral branches Sensory:
Labium majus / Scrotum Anteromedial thigh
Genitofemoral neuralgia: Surgical causes

Compression from aberrant IVC filter placement Injury at inguinal ligament.
Motor:
Cremaster
Genitofemoral Nerve
I V C
Genitofemoral neuralgia: CT guided block
Genitofemoral neuralgia: Ultrasound guided block of the genital branch
Genitofemoral neuralgia: Neurectomy (robotic approach)
Case 3
55 year old underwent vaginal hysterectomy for prolapse. Immediately after surgery, she developed severe pain to her right vulva and rectum. She was managed expectantly, but after 6 months she had no improvement of her post op pain. Review of the operative report shows that she had concurrently undergone Prolift mesh placement. On vaginal examination she has tenderness at the right ischial spine and along the right obturator internus muscle.
Case 3
Pudendal neuralgia
Arises from S2-4 ventral nerve roots Sensory
Rectum Perineum Scrotum / Vulva Penis / Clitoris
Motor
Sphincters (anal, urethral) Muscles of the urogenital triangle
Autonomic
Pudendal neuralgia: Mechanism of injury
Pudendal Neuralgia: Proximity of Prolift trocar to nerve
Sacrospinous lig.
Pudendal nerve
Proximity for Prolift trocar to rectal nerve
Pudendal neuralgia: Neurolysis
Case 4
30 year old woman presents with bilateral vulvar pain. She has been treated for yeast and lichen sclerosis for several years without any improvement. Her history reveals that it began a few days after sitting on a hard bleacher for several hours. She has burning in the gluteal creases and posterior thighs bilaterally. Exam shows tenderness at bilateral ischial spines and levator ani muscle spasms and tenderness.
Case 4
Posterior femoral cutaneous nerve

Emerges from S1-4 Sensory:
Inferior buttocks Lateral perineum Proximal medial thigh Labia majora Clitoris
Posterior femoral cutaneous nerve
Often confused with the pudendal nerve
Posterior femoral cutaneous nerve: Ultrasound guided block
Case 5
27 year old woman with chronic pelvic pain after the birth of her son. Pain is mostly left pelvis and worse with physical activity. She was treated for pelvic congestion syndrome and underwent hysterectomy without any improvement. History shows that she delivered a 10lb infant and had a prolonged second stage of labor. Adduction of her thighs is uncomfortable and causes pain in bilateral inner thighs. Exam shows hyperalgesia of bilateral medial thighs.
Case 5
Obturator nerve
Emerges form L2-4 Sensory
Medial thigh
Motor
Pectineus Abductor longus/brevis Gracillis
Obturator neuralgia: Ultrasound guided block
Obturator neuralgia: Surgical decompression
Thank You
Presentations Thursday, October 18, 2012
IPPS
1:20 p.m. 1:50 p.m. Diagnosis and Treatment of Urologic Causes of Chronic Pelvic Pain Barry K. Jarnagin, MD 1:55 p.m. 2:35 p.m. Diagnosis and Treatment of Musculoskeletal Causes of Chronic Pelvic Pain Brandi Kirk, PT, BCB-PMD Colleen Fitzgerald, MD 2:40 p.m. 3:10 p.m. Diagnosis and Treatment of Functional Bowel Disorders Alain Watier, MD 3:40 p.m. 4:20 p.m. Medical and Behavioral Therapies for Chronic Pain Devon M. Shuchman, MD 4:25 p.m. 5:00 p.m. Psychological Aspects of Living with Chronic Pelvic Pain: Evaluation and Treatment of Comorbid Anxiety and Depression Sarah M. Fox, MD
Page 78
CPP and Bladder Health Conditions Significantly Impact Quality of Life (QOL) Diagnosis and Treatment of Urologic Causes of Chronic Pelvic Pain
Barry Jarnagin, MD Medical Director Center for Pelvic Health
OAB,1 IC/CPPS,2 and UTI3 have a significant negative impact on many aspects of QOL as assessed by the SF-36, including
Physical functioning General health Vitality Social functioning Mental functioning
CPPS = chronic pelvic pain syndrome; IC = interstitial cystitis; OAB = overactive bladder; UTI = urinary tract infection. 1. Abrams P et al. Am J of Managed Care. 2000;S580-S590. 2. Rothrock NE et al. J Urol. 2002;167:1763-1767. 3. Ellis AK et al. J Am Board Fam Pract. 2000;13:392-397.
CPP Substantially Impacts Quality of Life

100 80 % Patients 60 40
CPP Is a Significant and Common Disorder in Women

Magnitude of CPP
>9 million women in the United States1 20% of women had pelvic pain >1 year in duration2
88%
82% 58%
56% 47% 26%
CPP accounts for

10% of referrals for OB/Gyn visits3 Over 40% of laparoscopies4 18% of hysterectomies5
20 0
Pain During/After Intercourse Impacted Energy Reduced Activity Interfered With Felt Mood Downhearted and Blue Stayed in Bed
Patients with CPP have significantly lower general health scores compared with patients without CPP 1 CPP is associated with painful intercourse 1. Mathias SD et al. Obstet Gynecol. 1996;87:321-327. 2. Jamieson DJ, Steege JF. Obstet Gynecol. 1996;87:55-58. (dyspareunia) 3. Reiter RC. Clin Obstet Gynecol. 1990;33:130-136.
4. Howard FM. Obstet Gynecol Surv. 1993;48:357-387. 5. Carlson KJ et al. Obstet Gynecol. 1994;83:556-565.
Effect of CPP
Mathias SD et al. Obstet Gynecol. 1996;87:321-327.
The Pelvic Theatre

There is more in the pelvis than gynecologic organs Need to see and examine the entire pelvis Consider all systems
Majority of Women With CPP Have No Obvious Etiology

39% Confirmed Diagnosis
Source of CPP in Female Patients1

Visceral Sources of Pelvic Pain2
12% 20% 31% 37% Gastrointestinal Urinary Reproductive Musculoskeletal/Other
61% Undefined Etiology
Reproductive causes are the source of CPP in only 20% of patients1

Mathias SD et al. Obstet Gynecol. 1996;87:321-327. 1. Zondervan KT et al. Br J Obstet Gynaecol. 1999;106:1156-1161. 2. Howard FM. Obstet Gynecol. 2003:101:594-611.
Chronic Pelvic Pain Is Characterized by Overlapping Disease Conditions

IC Can Appear Concurrently With Endometriosis Two Studies* Confirm the Overlap Between
IC and Endometriosis1,2
Diagnosis IC Endometriosis Study 1: Chung et al1 (n=60) 90% 80% 70% Study 2: Chung et al2 (n=111) 89% 75% 65%
Endometriosis
Chronic Pelvic Pain Overlapping Disease Conditions
Vulvodynia
GI Disorders
Pelvic Infection and Adhesions
Both
In a separate study, Clemons et al determined that 38% of women scheduled to undergo laparoscopy for CPP had IC3 Consider the bladder as the source of pain, even when endometriosis is confirmed 1
Recurrent UTI
*At a regional Pelvic Pain Center. 1. Chung MK et al. J Soc Laparoendosc Surg. 2002;6:311-314. 2. Chung MK et al. J Soc Laparoendosc Surg. In press. 3. Clemons JL et al. Obstet Gynecol. 2002;100:337-341.
Vulvodynia May Be Concurrent With IC: Summary of 3 Studies

Study 1: 2405 individuals with IC were surveyed 10.9% were diagnosed with concurrent vulvodynia Study 2: 428 women with vulvodynia 11% were also diagnosed with IC
In the Past, IC Was Often Diagnosed Late in Disease Continuum

Average time between development of symptoms and diagnosis is 5 years1 See at least Significant suffering 5 physicians and reduced QOL3 before diagnosis2
Development of IC Symptoms
May have unnecessary hysterectomy4
1. Driscoll A, Teichman JMH. J Urol. 2001;166:2118-2120. 2. Metts JF. Am Fam Physician. 2001;64:1199-1206. 3. Held PJ et al. In: Interstitial Cystitis. Springer-Verlag; 1990:29-48. 4. Carlson KJ et al. Obstet Gynecol. 1994;83:556-565. 5. Messing EM, Stamey TA. Urology. 1978;12:381-392.
Diagnosis of IC 2-7 years1,5
Study 3: 46 women with IC or vulvodynia

24% had both conditions
1. Alagiri M et al. Urology. 1997;49(suppl 5A):52-57. 2. Gordon AS et al. J Sex and 1990;35:873-876. Marital Ther. 2003;29(s):45-58. 3. McCormack WM. J Reprod Med.
Spectrum of IC Symptom Severity OverTime

IC symptoms range from mild to severe and may be attributed to other conditions in the early stages
Endometriosis/ Vulvodynia Misdiagnosis Chronic Pelvic Pain (CPP) Advanced CPP Syndrome
Evaluation
Consider all potential causes of pain Thorough History Thorough Exam --examine vulva, vagina, pelvic muscles, bladder, rectum, pelvic organs Assess the emotional/psychological needs Supplemental labs as needed Testing as neededultrasound, cystoscopy, awake pain mapping, traditional laparoscopy
Increasing Severity
UTI Misdiagnosis
Urge/Freq Failed OAB Tx
Urethral Syndrome
NIDDK IC
Advanced IC
NIDDK = National Institute of Diabetes and Digestive and Kidney Diseases. Adapted from Butrick CW. Clin Obstet Gynecol. 2003;46:811-823.
Goals of Therapy
Develop an individualized treatment plan for the particular patient Treatment plan must address all of patients causes of pain Multidisciplinary approach to address all areas contributing to pain
Pharmacologic Therapy for IC Symptoms

Treatment ELMIRON* plus dietary guidelines Dose 100 mg tid Indication Treatment of pain related to IC
Optional Adjunctive Treatment Amitriptyline (Elavil) 10 mg-25 mg qhs Moderate/severe anxiety; depression associated with chronic physical disease Management of allergic conditions and histamine-mediated reactions Symptomatic relief of anxiety and tension
Hydroxyzine (Atarax)
10 mg-25 mg qhs or 25 mg qam and qhs
*ELMIRON is the only FDA-approved oral drug for the relief of bladder pain or discomfort associated with IC. Atarax (hydroxyzine hydrochloride) is a registered trademark of Pfizer. Elavil (amitriptyline HCl) is a registered trademark of Astra Zeneca. ELMIRON [prescribing information]. Raritan, NJ: Ortho-McNeil Pharmaceutical, Inc; 2004.
Pharmacologic Therapyother adjuvant considerations

Gapapentin Lyrica Gabapentin and lidocaine ointment NSAIDsPO, patches, creams GNRH Agonist Hormonal considerations Holistic considerationsfish oil, hyaluronic acid, Chondroitin, other
Intravesical Instillations Have Been Reported to Aid in Acute Pain Relief of IC

Optional Adjunctive Therapy: Intravesical instillation along with oral therapy 1 At initial visit to aid in acute pain relief or to treat flares
A variety of intravesical cocktails are used
Examples Parsons2 40,000 IU heparin sulfate, 8 cc 1% or 2% lidocaine and 3 cc 8.4% sodium bicarbonate suspended in a volume of 15 cc total fluid2 20,000 IU heparin sulfate, 30 cc of a 1:1 0.5% bupivacaine and 2% lidocaine jelly, 40 mg triamcinolone, and 80 mg gentamycin1
Moldwin, Sant1
1. Moldwin RM, Sant GR. Clin Obstet Gynecol. 2002;45:259-272. 2. Parsons CL. Urology. 2005;65:45-48.
Behavioral Therapy for CPP/IC

Stress reduction1 Warm sitz baths and tub Bladder training2 Practice scheduled voiding pattern Perform pelvic floor relaxation exercises Utilize support groups, such as the Interstitial Cystitis Association, for resources and information1,2 Psychological counseling may help patients manage quality of life issues associated with chronic pain2 Avoid foods that exacerbate symptoms1,2
1. Selo-Ojeme DO, Onwude JL. J Obstet Gynaecol. 2004;24:216-225. 2. Dell JR, Parsons, CL. J Reprod Med. 2004;49:243-252.
Supplemental Treatment Options

Physical therapy Bladder training1 Practice scheduled voiding pattern Perform pelvic floor muscle relaxation exercises, other Lifestyle modifications Dietary adjustments2s Stress reduction2 Utilize support groups1,2
1. Dell JR, Parsons CL. J Reprod Med. 2004;49(suppl):243-252. 2. Selo-Ojeme DO, Onwude JL. J Obstet Gynaecol. 2004;24:216-225.
baths1,2
Dietary Guidelines for Interstitial Cystitis

Food Category Fruits Vegetables Milk/Dairy Carbohydrates/Grains Meats/Fish Permitted Foods Blueberries, melons other than cantaloupe, and pears Potatoes, homegrown tomatoes, and vegetables other than those listed on the right White chocolate, cottage cheese, American cheese, milk Pasta, rice, and breads other than those listed on the right Poultry, fish, and meats other than those listed on the right Foods to Avoid or Use Cautiously All other fruits and juices made from them Fava beans, lima beans, onions, rhubarb, tofu, and store-bought tomatoes Aged cheeses, sour cream, yogurt, chocolate Rye and sourdough breads Aged, canned, cured, processed, and smoked meats and fish; anchovies; caviar; chicken livers; corned beef; and meats that contain nitrates or nitrites Most other nuts Alcoholic beverages; beer and wine; carbonated drinks; coffee, tea, and cranberry juice Mayonnaise, ketchup, mustard, miso, spicy foods (especially Chinese, Mexican, Indian, and Thai foods) Benzyl alcohol; citric acid; monosodium glutamate; aspartame; saccharin; and foods containing preservatives, artificial ingredients/colors
Therapy continued
Begin multidisciplinary therapy
Medication Trigger point injections PT Counseling Surgery as indicated
Nuts Beverages
Almonds, cashews, and pine nuts Bottled or spring water; decaffeinated, acid-free coffee and tea; some herbal teas Garlic and seasonings other than those listed on the right
Seasonings
Preservatives and Additives
Adapted from the Interstitial Cystitis Association. Treatment options, IC and diet. Available at: http://www.ichelp.org/treatmentandselfhelp/ICanddiet.html. Accessed January 26, 2004.
Therapy continued
Reevaluate after institution of therapy
Whats working? Whats not?
Therapy continued
Continue to reassess Continue to adjust Begin to withdraw therapies as patient responds Educate patient that she can have recurrence
Adjust therapy based on progression Add additional therapy as needed Add additional therapists as needed
Interventional radiologyCT guided injections Pain specialistsother injections Other specialists
How I See It
Need to understand all causes of pts pain Evaluate all the organ systems in the pelvisThe Pelvic Theatre ConceptStage the CPP Develop treatment regimen that addresses every aspect of pts pain
Conceptual Staging for CPP

Stage 1--duration>6 months in <1year organ system(s) affected-1 Stage 2--duration>6 months<2 years organ systems affected-2 Stage 3--duration>6 months<5 years organ systems affected-3 Stage 4--duration>5 years organ systems affected>3
Conceptual Staging of CPP

Pre-CPPan in situ stage duration>1 month<6 months organ system affected-1 Organ Systems Considered Bladder Psychiatric Reproductive Nervous system GI Epidermal/skin Musculoskeletal
Conceptual Staging of CPP Summary

CPP in situ/pre CPP-<6 months Stage 1-< 1 year/1organ Stage 2-<2 years/2 organs Stage 3-<5 years/3 organs Stage 4->5 years/> 3 organs Hypothesis--Treatmentthe higher the stage, the more intensive treatment required to resolve the pain
Goals of Therapy
Address underlying pathology(s) of CPP Set expectations
Time to response
Goals of Therapy
Develop an individualized treatment plan for the particular patient Treatment plan must address all of patients causes of pain Multidisciplinary approach to address all areas contributing to pain
Establish long-term treatment plan

Lifestyle change
Collaborative Effort
Surgical Options
Cystoscopy Awake Pain Mapping Laparoscopy
Excision of endometriosis Appendectomy Lysis of Adhesions
MD and NP
Evaluate the patient Develop the treatment plan Medications as indicated Office treatments as indicated
Trigger point injections
Physical Therapist
Pelvic Floor PT
Patient
Psychiatric Nurse Practitioner

Counseling Assist in medication therapy
Interstim Other
Gastroenterologists Interventional radiology Pain specialty Neurology Rheumatologist Accupuncturist Dietician Massage therapist
Summary
CPP is a common condition that affects millions of women CPP is a multiorgan, multisystem disease CPP is a complex disorder CPP requires a multidisciplinary approach to adequately address all of the conditions that contribute to the syndrome
Summary
Therapy may include medical therapy, physical therapy, surgical therapy Therapy requires a team approach Urologic causes are an important component of CPP If all of the causes of the pain are addressed, most women can achieve improved quality of life with proper therapy
Dont Lose..
Thank you
Questions??
sight of the big picture
Objectives
Describe the role of Pelvic Physical Therapy in the treatment of chronic pelvic pain. Describe different treatment techniques offered by pelvic physical therapists for treatment of chronic pelvic pain.
Brandi Kirk, PT, BCB-PMD

Faculty Herman & Wallace Pelvic Rehabilitation Institute Teaching Assistant for the Barral Institute Former Board Member Chicagoland Pelvic Floor Research Consortium
List appropriate sources in order to locate pelvic physical therapists. Describe how to evaluate a pelvic physical therapists skill-set in order to choose the appropriate therapist for your patient.
Why Physical Therapy?

PTs are experts on neuromuscular and musculoskeletal
functions
Pelvic Physical Therapists Treatment Misconceptions

Biofeedback Stretch muscles Massage muscles Kegels Strengthening
Sub-specialties in visceral mobilizations, fascial releases,
internal vaginal/anal techniques International Pelvic Pain Society (www.pelvicpain.org) Herman and Wallace Pelvic Rehabilitation Institute (www.hermanwallace.com) Barral Institute (www.barralinstitute.com) Section on Womens Health of the APTA (www.womenshealthapta.org) Chicagoland Pelvic Floor Research Consortium (www.cpfrc.com)
Pelvic Physical Therapists Treatment Realities

Visceral System Fascial System Lymphatic System Musculoskeletal System Nervous System
Visceral Treatments
Visceral Manipulation
Science of Osteopathic Medicine Created by Jean-Pierre Barral, DO Over 35 years of clinical experience / authored 15 books Gail Wetzler, RPT,BI-D, EDO currently doing research/
speaker at IPPS
Organ specific fascial mobilization Not only the pelvic floor but organs above the pelvic floor www.barralinstitute.com
Visceral Treatments
Manual therapy consisting of gentle, specifically placed
Visceral Treatments
Mobility: movement of viscera in response to external
forces that encourage normal mobility and tone of viscera and connective tissues. Tissues that surround the organ lose normal motion when inflamed, healing: inelastic granular tissue replaces normal fibers=localized drying out of tissues=restrictions can cause pain=body hugs the restriction Inflammation causing factors: infections, trauma, repetitious movement, diet, environmental toxins, stress
forces, each organ needs to be able to glide and slide in relationship to all other tissues without any restrictions Indirect Techniques: moving the viscera into ease or putting slack into the system (Induction:towards restriction) Direct Techniques: moving the viscera into tension/stretch (away from restriction)
(Gail Wetzler will describe this in greater detail during her presentation at IPPS)
Visceral Treatments
Sacrorectalgenitalpubo Fascia
Visceral Treatments
Posterior Parietal Peritoneum
Visceral Treatments
Uterosacral Ligament Mobilization
Fascia Treatments
Visceral Manipulation: Organ Specific Fascial
Mobilization
Myofascial Release Connective Tissue Manipulation
Fascia Treatments
Myofascial Release
Techniques created by John F.
Fascia Treatments
Myofascial Release
Hip Distraction Lumbosacral Decompression
Barnes, PT Release restrictions in deeper layers of fascia Stretch cross-links Change viscosity of ground substance Multi-directional www.myofascialrelease.com
Fascia Treatments
Reflexive Connective Tissue Manipulation
Musculoskeletal problems influence visceral symptoms
Fascia Treatments
Connective Tissue Manipulation: Adjusted CTM Techniques
One hand Use tips of fingers Lead with tip of thumb Keep thumb parallel to tissue Use other 4 fingers to stabilize tissue Areas to utilize Medial to the ischial tuberosities, ST/SS ligaments, perineum, scrotum
* Provided by Stephanie Prendergast, PT
and vice versa through the facilitated segment theory
Treating one structure may decrease the altered level of
activity in other structures sharing the same segmental nerve supply This is done through skin stimulation via the somatoautonomic reflex Increase muscle tone occurs segmentally to visceral disorders
*Provided by Stephanie Prendergast, PT
Fascia Treatments
Connective Tissue Manipulation: Adjusted CTM Techniques
Thumb and index finger Use tips of fingers Very gentle Areas to utilize Vulvar tissues
Lymphatic Treatments
Manual Lymph Drainage
Specific gentle manual techniques Promotes movement of lymph fluid towards
lymph nodes Utilize if patient is in too much pain for deeper techniques Utilize after any technique that increases inflammation
* Provided by Stephanie Prendergast, PT * Provided by Debora Hickman, DPT, WCS
Lymphatic Treatments
Manual Lymph Drainage
Musculoskeletal Treatments
Strain-Counterstrain/Positional Release Internal vaginal/rectal releases Contract-Relax Stretch Thiele Massage Trigger Point releases Intramuscular Manual Therapy/Dry Needling
* Provided by Debora Hickman, DPT, WCS
Positional Release / Strain-Counterstrain
Based on the work of Lawrence Jones, DO Relief of pain by reduction and arrest of
Pelvic diaphragm (posterior release)
ongoing inappropriate proprioceptor activity

Treatment brings maximal shortening to the
proprioceptor reporting strain so well, it cannot continue to report tension The false strain message is stopped and with it the irritation and pain www.jiscs.com
Obturator Internus
Internal Vaginal Releases
Internal Rectal Releases
Internal Vaginal Releases: Obturator Internus
Intramuscular Manual Therapy / Dry Needling
Involves the use of a very thin filament needle into the
Intramuscular Manual Therapy / Dry Needling
Ishiocavernosus
muscle into the area of a palpable Trigger Point The goal is to achieve a local twitch response to release muscle tension and pain. If the muscles are normal, it does not hurt. If not it feels like a muscle spasm.
* Provided by Dawn Sandalcidi, PT, RCMT
* Provided by Dawn Sandalcidi, PT,RCMT
Stretch surrounding musculature Sacroiliac mobilization Sacroiliac stabilization Numerous Lumbar spine treatments Numerous Thoracic spine treatments
Nervous System Treatments

Nerve Mobilization / Flossing
CNS and PNS form a continuous tract via connective tissue, neuronal electrical activity, and chemical neurotransmitters NS is an elastic structure that moves and is vulnerable to unwanted fixation Changes in one area have repercussions in another
* Provided by Stephanie Prendergast, PT

Nerve Mobilization / Flossing PN
Dorsal Branches Perineal Branches

Characteristics of Central Sensitization
Pain persisting beyond 3 months Pain is unpredictable, not closely tied to mechanical or
biomechanical influence
Catastrophizing, fear and avoidance, thinking about the
area or activity may trigger pain

Pain is modulated by mood or social context Pain is spreading or does not follow a particular
distribution
*Provided by Stephanie Prendergast, PT
* Provided by Sandy Hilton, PT

Central Sensitization
Graded Imagery Graded Exposure (dilators for example) Must identify and reduce fear to limit cortically driven
Summary
Muscles do not spasm for no reason Find the primary issue and treat Interview your physical therapists Short nails or long nails???!!!
pain responses Educate the patient in the biology of pain, the neuroimmune influences and threat reduction. Studies show this is effective (Lorimer Moseley will describe this in greater detail during his presentation at IPPS)
* Provided by Sandy Hilton, PT
Questions?
Brandi Kirk, PT, BCB-PMD
Kirk Center for Healthy Living www.kc4hl.com brandi@kc4hl.com (815) 838-0529 16618 W. 159th Street Lockport, IL 60441 and 5716 W. 95th Street OakLawn, IL 60453
Thank You!
DIAGNOSIS AND TREATMENT OF IRRITABLE BOWEL SYNDROME

INTERNATIONAL PELVIC PAIN SOCIETY BASICS COURSE
INTRODUCTION
ROME III CRITERIA

Recurrent abdominal pain or discomfort at least 3 days / month in the last 3 months associated with two or more of the following: 1. Improvement with defecation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool
Irritable bowel syndrome (IBS) is a functional G-I disorder (FGID) characterized by abdominal pain or disconfort associated with changes in bowel habit and features of disordered defecation
Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC Fuctional Bowel Disorders. Gastroenterology 2006;130(5):1480-1491
BOWEL HABIT SUBTYPE CLASSIFICATION
Constipation (IBS-C) (20%) Diarrhea (IBS-D) (30%) Mixed IBS Constipation and diarrhea the same day (IBS-M) Alternant IBS (50%) Patient initially with constipation that develop diarrhea with time (IBS-A) Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin
F, Spiller RC Fuctional Bowel Disorders Gastroenterology 2006;130(5):1480-1491
The prevalence of IBS ranges from 7% to 15% of the population IBS is more prevalent in women. Subtypes of IBS are also differing as a function of gender, with men less likely than women to have IBS-C Young adult patients are more commonly diagnosed with IBS than those over the age of 50 years
70%do not seek health care for their symptoms. IBS patients accounts for 12% of all visits to primary care physicians and comprise the chief diagnosis group visiting gastroenterologists. They represent > 3.6 millions physician office visits
Comorbid symptoms or disorders are common in patients with IBS particularly those with severe symptoms and in those attending referral practices Psychiatric comorbidity in patients with IBS has been estimated to be about 48-60%. It may reach 70% in those attending tertiary care referral centers The burden of illness of IBS is significant
Predictors for health care seeking include severe symptoms (mainly pain) and psychological variables (anxiety, depression, abuse, illness behavior, somatic attribution and health concerns )
There is a great economic burden associated with IBS owing to substantial direct health-care costs and indirect costs. These patients have more missed workdays, and have lower work productivity 1.4 billions dollars are spent in direct health care costs and $205 million in indirect costs, such as loss of work productivity IBS has a marked negative impact on patients health-related quality of life (HRQOL) that is correlated with symptom severity. Only 35% of these patients described themselves as having good health
Patients with IBS use more health-care services than the general population, even for non-GI symptoms
They undergo more surgical procedures compared with individuals without IBS. (cholecystectomy, appendicectomy, hysterectomy, back surgery)
Drossman Douglas A., Chang, Lin Clinical Symposia: Irritable Bowel Syndrome Not yet published Khan, S., Chang, Lin Diagnosis and management of IBS Nat. Rev. Gastroenterol. Hepatol. 2010;7:565-581
PATHOPHYSIOLOGY OF IBS
IBS is best considered as an interaction between biological and psychosocial factors that lead to a disturbance in brain-gut interactions associated with altered GI motility, hyperalgesia, alterations in mucosal immune function and the microflora environment, and autonomic and hormonal abnormalities.
Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC Fuctional Bowel Disordersw. Gastroenterology 2006;130(5):1480-1491 Drossman DA. The functional gastrointestinal) disorders and the Rome III process. Gastroenterology 2006;130(5):1377-1390
Genetic susceptibility Early environmental exposures that include infection or family modeling of ilness Abnormal GI motility Visceral hypersensitivity Infection / inflammation / altered mucosal immune function (post-infectious IBS) Dysregulation of the brain-gut axis Abnormal permeability of the intestinal mucosa The importance of food !!!! The role of microbiota !!!!
The hallmark symptom of IBS is abdominal pain
DIAGNOSIS OF IBS
CLINICAL SYMPTOMS
The diagnosis of IBS is based on the association of abdominal pain with altered bowel habits, that is, diarrhea and/or constipation Pain is typically worse with eating, associated with a change in stool consistency, and improved by bowel movements 70% of IBS patients attribute their symptoms to adverse food reactions
Hard or loose stools, urgency, straining, bloating (96%), a sensation of incomplete evacuation, mucus in the stool are reported symptoms Patients with IBS have a greater prevalence of non G-I symptoms including headache, fatigue, myalgias dyspareunia, urinary frequency or other urinary symptoms, dizziness and psychological symptoms IBS may overlap fith fibromyalagia, chronic pelvic pain disorders and chronic fatigue syndrome
The association of IBS symptoms with menstruation and other gynecological features may make the diagnosis more complex
Long history with relapsing and remitting course Exacerbations triggered by life events and difficult life situations
OTHER CLINICAL FEATURES SUPPORTING THE DX OF IBS
Variability of symptoms Association with symptoms in other organ systems Coexistence of anxiety and depression Distress that seems out of proportion to the nature of the symptom
Symptoms that are exacerbated by eating Conviction of the patient that the disease is caused by popular concerns e.g. allery, pollution, candidiasis, food toxicity
COMORBIDITIES AND IBS
SEXUAL DYSFUNCTION IN IBS

43% have sexual dysfunction 83% of women have vaginal and abdominal pains during intercourse 36% of women and 28% of man have decreased libido 16% of women and 4% of men have dyspareunia Related to the severity of IBS not to psychological problems
IBS AND OTHER MEDICAL CONDITIONS

TEMPEROMANDIBULAR JOINT DISORDER CHRONIC FATIQUE SYNDROME CHRONIC PELVIC PAIN FIBROMYALGIA BLADDER PAIN SYNDROME VULVODYNIA TENSION HEADACHE SOMATOFORM DISORDERS MAJOR DEPRESSION ANXIETY SUBSTANCE ABUSE
Vestibulitis/CPP/urethral obstruction/IBS /constipation CPP/dyspareunia/urological problems/IBS IBS/Dyspareunia/Urethral problems/CPP Urethral syndrome/dyspareunia/IBS/ abdominal pain Fibromyalgia/IBS/vestibulitis/IC Penismus/anismus/IBS IC/headache/FM/IBS/depression/vulvodynia
WHAT IS THE LINK ?
CENTRAL SENSITIZATION
PELVIC ORGAN CROSS-SENSITIZATION
FIBROMYALGIA PTSD
IBS
IC CRPS
ALARM SIGNS OF IBS
VULVODYNIA CHRONIC PROSTATITIS ?
New onset of symptoms at 50 years or older Unintentional weight loss Nocturnal diarrhea Anemia Bloody stools Family history of colon cancer, celiac disease or IBD Acute onset Signs of infection (Fever)
DIAGNOSTIC TESTING
IBS is not a Dx of exclusion. There are no specific diagnostic tests, and the diagnosis is based on clinial symptoms that are evaluated in light of the Rome III criteria The psychosocial interview is an essential part of history taking in the clinical assessment of a patient with IBS Routine diagnostic testing should not be performed for patients with typical IBS symptoms without alarm features Full blood count in patients who are older at first presentation (>50 years)
Full blood count, ESR and C-reactive protein in patients with recent IBS-D The prevalence of biopsy-proven celiac disease is increased fourfold in individuals with IBS symptoms. Routine serologic screening for celiac disease in patients with IBS-D and IBS-M should be done Colonoscopy is not recommended in patients with IBS who do not have alarm signs. Routine screening colonoscopy over the age of 50 years should be done
Sitzmark study for colonic inertia, and anorectal manometry may be useful in dyssynergic constipation in an IBS patient Colonic imaging in individuals under the age of 50 years with typical IBS symptoms and no alarm features should not be done Random biopsy samples should be taken to rule out microscopic colitis in IBS-D patients Lactose breath testing may be done if suspicion is still high after a dietary exclusion trial
Breath testing for small intestinal bacterial overgrowth in patient with IBS is not recommanded owing to insufficient data. Cases of severe diarrhea, especially when it causes awakening during sleep should be tested
Spiller, R. et al. Guidelines on the irritable bowel syndrome: mechanisms and practical management; Gut 2007;56:1770-1798 Khan S., Chang, Lin. Diagnosis and management of IBS Nature Reviews. Gastroenterology & Hepatology 2010;7:565-581 Cash BD, Schoenfeld P, Chey WD. The utility of diagnostic tests in irritable bowel syndrome patients: A systematic review. Am J Gastroenterol 2002 Nov;97(11):2812-2819
BRAIN IMAGING AND IBS
GOLDEN STRANDARD TEST
Instead of testing regions of interest research has evolved toward network-driven hypotheses. Entire functional networks are examined
Structure of the cingulate cortex. The anterior region of the mid cingulate cortex (MCC, shown in green) is a subregion called the anterior mid cingulate cortex ofthe ACC (aMCC); it has a variety of other names including the caudal ACC, the dorsal ACC (dACC), or cognitive division of the ACC (ACC-CD). pACC, anterior perigenual ACC; rACC, rostral ACC.
Brain activation by rectal pain during stress: reduction by amitriptyline Orange and yellow pixels indicate brain regions with reduced pain related activation by amitriptyline The perigenual anterior cingulate cortex (white circles) and the left posterior parietal cortex (blue circles) had significant reductions by amitriptyline.
The core regions of the homeostatic afferent (A) and emotional arousal (B) networks
Tillisch K. et al. Gastroenterology 2011;140:407-411
MODULATION OF THE BRAIN-GUT AXIS AFTER 4-WEEK INTERVENTION WITH A PROBIOTIC FERMENTED DAIRY PRODUCT
Kirsten Tillisch # 589
Consomption of this probiotic was associated with modulations of brain activity. Affects brain regions concerned with the central processing of afferent signals from the gut Reduces the impact of the brain regions involved in emotional arousal of the central processing of gut afferent signals
Drossman DA et al. Gastroenterology 2003;124:754-761 DDW 2012
The brains ability to continually adapt to new information and experiences by changing its structure, function, or chemistry. Such changes have been shown to occur in response to chronic pain; now, research shows that relief of pain can reverse structural and functionnal changes and restore normal brain function
NEUROPLASTICITY
MANAGEMENT OF IBS
PHYSICIAN-PATIENT RELATIONSHIP
ESTABLISH A TRUSTING RAPPORT
PHYSICIAN PATIENT RELATIONSHIP
A balanced biopsychosocial history should be part of a comprehensive evaluation of severity
ESTABLISH A NEGOCIATED AND EFFECTIVE PLAN OF CARE
Drossman Douglas A., Chang, Lin Clinical Symposia: Irritable Bowel Syndrome Not yet published
Figure 1 Graduated treatment approach for IBS
Permission obtained from D. Drossman, Rome Foundation Khan, S. & Chang, L. (2010) Diagnosis and management of IBS Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2010.137
DIETARY MODIFICATIONS
Page 2
70% of patients with IBS believe that diet has a role in symptom exacerbation Lifestyle changes that patients felt improved their symptoms
Eating small meals (69%) Avoiding fatty foods (64%) Increasing fiber intake (58%) Avoiding milk products (54%) Avoiding carbohydrates (43%) Avoiding caffeine (41%) Avoiding alcohol (27%) Avoiding high-protein foods (meats) (21%)
Distinction between food allergy vs food intolerance No gold standard diagnostic test for food allergy exists
Park, M. I., Camilleri, M. Is there a role of food allergy in irritable bowel syndrome and functional dyspepsia ? A systematic review. Neurogastroenterol. Motil. 2006;18:595-607 Brandt, L. J. et al. An evidence-based position statement on the management of irritable bowel syndrome. Am. J. Gastroenterol 2009;104 (Suppl. 1) :S1-S35
HELP
Celiac disease markers may be able to identify patients with IBS-D who will respond to a glutenfree diet Patients with IBS have a higher prevalence of lactose maldigestion and symptoms of subjective lactose intolerance compared with healthy controls Evidence is also increasing of an association between IBS symptoms and fructose intolerance (FODMAP exclusion diet)
PHARMACOLOGICAL TREATMENTS OF IBS
WE ARE TREATING THE SYMPTOMS NOT THE DISEASE
PLACEBO EFFECTS
PIAI MILO PAGE HEEFNA MYREN LONGSTRETH FIELDING FIELDING PRIFINIUM DOMPRIDONE DICYCLOMINE DSIPRAMINE TRIMIPRAMINE PSYLLIUM TIMODOL TRIMEBUTINE 50% 34% 54% 60% 67% 40% 59% 50%
TREATMENT OPTIONS FOR IBS-C
Table 3 Treatment options for IBS-C
Khan, S. & Chang, L. (2010) Diagnosis and management of IBS Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2010.137
Page 2
CONSTIPATION IS A GUT DISORDER
CONTROLLED EXPIRATION
BIOFEEDBACK
TREATMENT OPTIONS FOR IBS-D
ANISMUS + BFB
Table 4 Treatment options for IBS-D
TREATMENT OF ABDOMINAL PAIN

Khan, S. & Chang, L. (2010) Diagnosis and management of IBS Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2010.137
BILE ACID SEQUESTRANTS
Page 2
ANTISPASMODICS ANTISPASMODICS The ACG IBS Task Force recommend the use of certain antispasmodics (hyoscine, cimetropium, pinaverium) for short-term relief of abdominal pain/discomfort in IBS but acknowledge that long-term efficacy data and data on safety are not available
In clinical practice, antispasmodics can be particularly helpful for postprandial symptoms if taken at least 30 min before meals They may cause dry mouth, constipation, urinary retention and visual disturbances
Brandt, L. et al. An evidence-based position statement on the management of irritable bowel syndrome. Am. J. Gastroenterol. 2009;104 (Suppl. 1): S1-S35
ANTIDEPRESSANTS Antidepressants are used for their effects on: The central modulation of visceral afferent input Slowing of GI tract Decreased primary afferent nerve fiber firing Treatment of comorbid psychological conditions (Anxiety and depression)
ANTIDEPRESSANTS Tricyclic antidepressants (TCAs)
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin-norepinephrine reuptake inhibitors (SNRIs)
If single-medication treatments are not successful, one should consider intensifying the treatment by using combination of treatments to achieve synergistics effects. This concept of augmentation is the use of two or more treatments that function upon different receptor sites or areas of the brain to enhance the therapeutic effect
PSYCHOLOGICAL BEHAVIORAL INTERVENTIONS
Drossman, DA Abuse, Trauma, and GI illness: Is there a link ? The American Journal of Gastroenterology Volume 106/ January 2011:14-25
Cognitive behavioral therapy (CBT) Dynamic psychotherapy Stress management methods and relaxation Hypnotherapy Stress management
Brandt, L.J. et al. An evidence-based position statement on the management of irritable bowel syncrome. Am. J. Gastroenterol 2009;104 (Suppl.1): S1-S35
HYPNOSIS AND IBS
ABUSE, TRAUMA AND GI ILLNESS: IS THERE A LINK ?
MEDITATION AND IRRITABLE BOWEL SYNSROME
Drossman DA. Abuse, Trauma, and GI illness: Is there a link ? The American Journal of Gastroenterology Volume 106 / January 2011 / 14-25
IBS: 40% CPP: 48%-56% Obstetrics

(Increased incidence of perineal tears and miscarriages)
Sexual pain Urology

(Enuresis, urinary retention, dyssynergia..)
Chronic bladder pain

(IC)
Chronic pelvic pain syndrome in man

(chronic prostatism)
THE PHENOMENA EXISTS
WHAT CAN WE OFFER THESE PATIENTS

ABUSED MEN: PTSD: 12.2% ABUSED WOMEN: PTSD: 26.5% RAPE: PTSD: 50% NATURAL CATASTROPHE: PTSD: 5% PHYSICAL / SEXUAL ABUSE: # 1 CAUSE OF PTSD IN WOMEN
COMPLEMENTARY AND ALTERNATIVE MEDICINE
50%
Chinese herbal therapy Some herbal therapies may have benefit in IBS, but poor quality of study design, questionable purity of these compounds and concern over serious adverse effects limit their use
ACUPUNCTURE AND IBS
Liu, J. P. , Yang, M. .Liu, Y. X. , Wei, M. L. , Grimsgaard, S. Herbal medicines for treatment of irritable bowel syndrome. Cochrane Database of Systematic Revieus, Issue 1. Art. No. : CD004116. Doi: 10.1002/14651858. CD004116.pub2(2006)
Self-help group The dedication of such organizations is unquestionable and the quality of the information they provide is high. Many patients are helped by joining such groups.
PROGNOSIS
www.iffgd.org
Remissions and recurrences..

Once the Dx of IBS is established, it rarely needs to be revised and the incidence of new significant Dx is extremely low. In fact, the chance of remaining free of serious disease in IBS is excellent. Factors that have been shown to worsen prognosis include more prominent psychological symptoms, a longer history of illness, and previous adominal surgery
Lembo T, Fulletton S, Diehl D. et al. Symptoms duration in patients with IBS. Am J Gastroenterol 1996;91:898-905
WHERE ARE WE STANDING NOW !!!!!
WE SHOULD STOP TREATING JUST THE ORGAN (SPECIFIC END-ORGAN CONCEPT) WE MUST INTEGRATE THE PAIN SYNDROME
PERIPHERAL ORGANIC ETIOLOGY OF SYMPTOMS DOES EXIST Gut permeability.. Microbiota..

A MORE INTEGRATED PSYCHO-SOCIONEUROBIOLOGICAL APPROACH IS MANDATORY
Alain Watier md LMCC FRCP Professeur titulaire Gastroentrologie Rducation prinale (Lyon) Unit de Pelvi-Prinologie Facult de Mdecine et des sciences de la Sant Universit de Sherbrooke 580 Bowen Sud Sherbrooke, Qubec, Canada J1G2E8 - 819-346-1110 a.watier@videotron.ca
Chronic pain Medical and Behavioral Therapies for Chronic Pain

Devon Shuchman, MS, MD October 18th, 2012 IPPS Annual Meeting - Basics Course
Pain that has persisted for a time frame that exceeds expected healing time
What kind of pain is it?

Nociceptive Superficial Deep somatic Visceral Neuropathic Peripheral Central
Approaching treatment
Complete assessment Multidisciplinary Care Associated issues
Common descriptors:
Sore Dull Tender Throbbing Aching Burning Tingling Numbing
Medical Therapies
Medication Skilled therapies Manual Medicine Interventional Procedures
MEDICAL THERAPIES
Opioid Medication
Effects: Intended Unintended Receptors: Delta, Kappa, Mu, Epsilon Location: CNS GI Peripheral sensory neurons
Opioid Medication
Morphine Hydrocodone Oxycodone Hydromorphone Fentanyl Methadone Buprenorphine Route of Administration: Short acting Long acting Oral Sublingual Duragesic Intravenous Intrathecal
Non-opioid Medication
NSAIDs Acetaminophen Neuromodulators Antidepressants (TCA) Antidepressants (SNRI) Antispasmodics Adjunct Other
Skilled Therapies: PT
Rehabilitative approach
Restoration of movement and function
Exacerbation is not failure

Self-management takes daily effort
Goal Setting Domains

Physical
Social Functional Goals must be personally relevant, interesting, measurable, and achievable
Skilled Therapies: OT
activity patterns time use goal fulfillment changes in routines habits roles skills
Manual Medicine
Soft tissue work Mobilization/manipulation Strain-Counterstrain Muscle Energy Technique HVLA
Interventional Pain Management

Careful patient selection Chronic pain is not acute pain Potential for centralized pain
Interventional Pain Managment

Injection/procedural therapy
Neuromodulation
BEHAVIORAL THERAPIES
Behavioral Therapies
Relaxation therapy Education Addressing the typical history for a patient pelvic pain Cognitive behavior therapy Acceptance therapy Values modification
Vlaeyens Cognitive-Behavioral Model of Post-Injury Pain Disability
Cognitive-Behavioral Treatment
Challenging maladaptive cognitive structures and processes Homework Self-management 4 common components Education Skills acquisition Cognitive and behavioral rehearsal Generalization and maintenance
Cognitive-Behavioral Treatment
Exposure therapy Relaxation therapy Increased engagement with pleasurable activities Distraction activities
Cognitive-Behavioral Treatment Values Social support Co-existing diagnoses

Co-existing diagnoses
Depression Anxiety PTSD Personality disorders
Post-traumatic Stress Symptoms/Disorder
Post-traumatic Stress Symptoms/Disorder

History of accident/injury/trauma PTSD more likely if a physical injury and/or pain results
Biofeedback
Reduce pain by enhancing a sense of perceived control over variables related to pain Electromyography (EMG) Thermal Neurofeedback or electroencephalography (EEG)

Pain Catastrophizing
Negative mental set Characterization of pain Perceived lack of control Expectation of continued uncontrollable pain
I wonder whether something serious may happen. I kept thinking I cant stand this much longer, I want to get out. Its terrible and its never going to get any better. I worry all the time about whether it will end.
Pain Catastrophizing
Predicts depression Associated with:
pain intensity perceived disability affective distress employment status
Pain-Related Fear and Kinesiophobia

Signal of harm Activity Avoidance The pain I usually experience is a signal that damage is being done. If I exercise, I could make my pain problem worse. Something is wrong with my body which prevents much movement or exercise. My accident has put my body at risk for the rest of my life.
Predicts disability Decreased catastrophizing associated with:

reduced disability reduced depression reduced pain intensity
Acceptance of Pain
Acceptance mediates the relationship between pain catastrophizing and depression, anxiety and avoidance Acceptance and values-based action associated with several positive pain-related outcomes
Medical therapies Medication Skilled therapies Manual medicine Interventional
Recap
Behavioral therapies Co-existing diagnoses Kinesiophobia Catastrophizing CBT Biofeedback Acceptance
Thank you!
Disclosures
I have no financial interests to disclose
Managing Anxiety and Depression in the Pelvic Pain Patient

Sarah D. Fox, M.D. 10/18/12
o me n & nf a nt s
Objectives
Review diagnosis and implications of chronic anxiety and depression in pain patients Review pharmacologic options for treating anxiety and depression Review non-pharmacologic options for treating anxiety and depression
Anxiety
Generalized Anxiety Disorder

Lifetime prevalence is 4-8% in a general population Twice as common in women 70-90% of patients have co-morbid psychiatric diagnoses (lifetime rates):
Social phobia 34% Specific phobia 35% Panic disorder 24% Major depression 62%
GAD Pathophysiology
Risk factors:
Stressful life events History of childhood traumatic events Family history plays a modest role
Involves changes in neurophysiology:

Decreased amygdala connectivity Involvement with neurotransmitters, GABA, serotonin and cholecystokinin
Hettema JM. J Nerv Ment Dis 2001 Etkin A Arch Gen Psychiatry 2009
31% of women with CPP report symptom-related anxiety

Wittchen HU. Arch Gen Psychiatry 1994 Zondervan KT Br J Gen Pract 2001
GAD Diagnosis
DSM IV Criteria
Excessive anxiety and worry occurring more days than not for at least 6 months, out of proportion to likelihood of feared event Worry is pervasive and difficult to control Associated with 3 symptoms
Restlessness or feeling keyed up or on edge Easily fatigued Difficulty concentrating, mind going blank Irritability Muscle tension Sleep disturbances
Algorithm for Diagnosis of Anxiety Disorders

Significant anxietyrelated symptoms and impaired functions
yes
Also moderate/severe depression?
Treat depression
No
Predominant symptom focus
Trauma history/flashbacks
Obsessions or compulsions
Uncontrollable worry about several areas
Intermittent panic or anxiety attacks and avoidance
Anxiety, worry or physical symptoms cause clinically significant distress or impairment in social, occupational or other areas of function.
Diagnostic and Statistical Manual of Mental Disorders, 4 th Edition, Primary Care Version
Check for posttraumatic stress disorder
Check for obsessive compulsive disorder
Check for generalized anxiety disorder
Fear of social scrutiny
Discreet object or situation
Uncued or spontaneous
Check for social phobia
Check for specific phobia
Check for panic disorder
From Tyrer P Lancet 2006
GAD 2 for Screening

Over the last 2 weeks, how often have you been bothered by the following problems? Not at all Several days 1 More than half the days 2 Nearly every day 3
Non-medical Treatments for Generalized Anxiety Disorder

Cognitive Behavioral Therapy (CBT)
Components of treatment Computer based CBT
1. Feeling nervous, anxious or on edge 2. Not being able to stop or control worrying
Psychodynamic therapy Mindfulness Meditation Acceptance and Commitment Therapy (ACT) Exercise
Score of 3 or more should have additional evaluation

From Kroenke K Ann Intern Med 2007
Cognitive Behavioral Therapy

People with GAD engage in overestimations and catastrophizing and have limited confidence in problem solving GAD is associated with avoidance behaviors:
Excessive preparation Checking behaviors Procrastination
Symptoms of GAD that CBT Addresses

Excessive and uncontrollable worry Physical symptoms: muscle tension, vigilence, restlessness, poor sleep, poor concentration Behavioral symptoms: excessive preparation, procrastination, poor decision making
CBT addresses cognitive, behavioral and physiological features of GAD

Evidence based thinking reduces overestimations and catastrophizing Behavioral practices can reduce excessive checking and procrastination Repeated exposure to catastrophic images can reduce emotional and autonomic responses
Specific CBT Techniques

Education Self-monitoring Relaxation training Cognitive restructuring Imagery exposure Exposure to anxiety-provoking situations Relapse prevention
CBT Efficacy
Meta-analysis of 65 RCTs with 7739 participants showed CBT to be better than placebo CBT is more effective than non-directive supportive therapy and psychodynamic therapy Treatment effects last for 6-12 months Head to head trials with pharmacotherapy have mixed results, but seem to have similar effects
Mitte K Psychol Bull 2005
CBT: Predictors of Worse Outcome

Interpersonal difficulties Poor physical health High baseline levels of neuroticism Mixed results in patients with co-morbid psychiatric diagnoses
Does help with co-morbid depression
Psychodynamic Therapy
Traditional therapy
Focus on core conflictual relationship themes Emphasis on a positive therapeutic approach
Limited data on efficacy for GAD

1 trial compared to CBT, both groups showed improvement, but CBT had greater improvement
Durham RC Behav Cog Psychother 1999
Mindfulness Based Stress Reduction

Standardized program developed in 1979 by Jon Kabat Zinn to introduce eastern meditative practice to western medicine: Removes religion and mysticism Training in:
Mind-body awareness in relation to health Decreased stress reactivity Improved coping
Mindfulness Meditation and GAD

Meta-analysis of 4 studies showed modest reduction in GAD symptoms with Mindfulness Meditation Limited by small studies and 2 with poor design MBCT may be more effective for anxiety
8 week program
2 hour sessions weekly 1 day silent retreat Daily homework 30 min per day
Bohlmeijer E. J Psychosom Res 2010
Pharmacotherapy for GAD

First-line medications:
Selective serotonin reuptake inhibitors (SSRI) Serotonin-norepinephirine reuptake inhibitors (SNRI)
SSRIs and GAD

Little data on which SSRI is best
Supported by RCTs: paroxetine, sertraline, citalopram and escitalopram Not supported by data: Fluoxetine, fluvoxamine
Second-line medications:
Tricyclic antidepressants (TCA) Benzodiazepines Buspirone Pregabalin
Most trials show response rates of 60-70%

Paroxetine RCT 566 patients followed for 8 weeks with 20 or 40 mg doses.
Greater reduction in anxiety symptoms with both doses compared to placebo
Rickels K. Am J Psychiatry 2003
SNRIs and Anxiety

Typically more expensive than SSRIs
Only generic is venlafaxine
Scale: 0=none, 1+=slight, 2+=low, 3+=moderate, 4+=high, ND=inadequate data
Also efficacious in managing comorbid depression and some chronic pain syndromes Venlafaxine (75-150mg/day) and duloxetine both reduce emotional and autonomic symptoms of GAD
From uptodate.com: pharmacotherapy for generalized anxiety disorder
Second Line Agents

Tricyclic Antidepressants:
Efficacious but more potential side effects Have a neurolytic effect for pain
Benzodiazepines:
Efficacious but concern for dependence and tolerance, especially for chronic treatment
Relatively contraindicated with a history of substance abuse Discontinue if rapid tolerance, increase of dose against medical advice or withdrawal symptoms between doses
Should be used as an adjunct to other antidepressant therapy may counter initial anxiety associated with SSRI/SNRI therapy
Second Line Agents

Buspirone: blocks 5HT1A serotonin receptors
Similar efficacy to oxazepam (benzodiazepine) Low risk for dependency Takes 4+ weeks for effect Titrate dose to 10-60mg/day
Summary of GAD
Anxiety is commonly seen in patients with chronic pain Use GAD2 to screen for anxiety Non-pharmalogic treatment seems to be as efficacious as pharmacologic treatment CBT is best studied non-pharmalogic treatment Multimodal treatment with CBT, exercise and medication may be most effective approach
Pregabalin
Better than placebo for GAD Not FDA approved for anxiety Also acts as a neurolytic
Depression
Depression and Public Health

Estimated cost annually of $83 billion Non-psychiatric physicians miss the diagnosis half the time
Chronic pain patients have 30-87% risk of depression
Depression worsens pain:
Decreased serotonin and norepinephrine activity Increased transmission of pain signals to cortex
Patients with chronic pain and depression are at increased risk for suicidal ideation and completion.
Risk is increased with a central (abdominal or pelvic) pain process Risk is increased with insomnia
Donohue JM. Pharmacoeconomics 2007; Cepoiu M. J Gen Intern Med 2008; Hitchcock J Pain Symptom Manage 1994
Depressive Syndromes (DSM IV)

Major depression
5 symptoms present most days for minimum of 2 weeks
Major Depression
5 or more of the following symptoms present most of the day on most days for at least 2 weeks
Depressed mood Loss of interest or pleasure in most activities Insomnia or hypersomnia Change in appetite or weight Psychomotor retardation or agitation Low energy Poor concentration Thoughts of worthlessness or guilt Recurrent thoughts about death or suicide
Dysthymic disorder
depressed mood for at least 2 years with 2 symptoms present. Symptom free periods may not exceed 2 months Doesnt meet criteria for major depression in the first 2 years
Adjustment disorder with depressed mood

In response to an identifiable stressor Doesnt meet criteria for other depressive syndrome Symptoms resolve 6 months after stressor ends
Remember SIG: E CAPS

Sleep, interest, guilt, energy, concentration, appetite, psychomotor, suicide
Minor depression
2-4 symptoms present on most days for at least 2 weeks
Screening for Depression
Other Diagnostic Considerations

Screen for bipolar disease Consider medications and drugs which can cause depression Assess suicide risk in all patients with chronic pain. Query family history of mood disorders or other psychiatric diagnoses. When to refer:
Severe depression with suicidal ideation Depression that has not responded to initial treatment Symptoms of psychosis or mania Patients for whom the diagnosis is uncertain
Scoring: score of 3 requires further evaluation
Kroenke K. Med Care 2003
Educate about Depression

Pain leads to depression or the blues Depressed mood effects spinal cord function More pain signals get to the brain Leads to more pain and worsened mood Vicious cycle needs to be broken in as many places as possible, so we focus on mood as well as pain.
Treatment of Depression
Psychotherapy Pharmacotherapy St. Johns wort Exercise Mindfulness Meditation Cognitive Behavioral Therapy
Pain
Depression
norepi & serotonin
Psychotherapy
Meta-analysis of psychotherapy vs. medication with similar results in managing mild-moderate depression May be used alone or in combination with medication If no response to psychotherapy alone after 12 weeks, medication should be started
Pharmacotherapy vs Psychotherapy
91 patients with major depression randomized to problem solving or amitriptyline
At 12 weeks, 60% of problem solving group and 52% of medication group had resolution of symptoms Unclear which patients will benefit from which intervention
For severe symptoms combination therapy is better than either intervention alone
Mynors-Wallis LM BMJ 1995 Thase ME Arch Gebn Psychiatry 1997
Schulberg HC. Gen Hosp Psychiatry 2002
Pharmacotherapy for Depression: How to Choose?

First-line agents:
SSRIs
Better tolerated, may lead to greater treatment compliance
SNRIs
Well tolerated but more costly
Aminoketone antidepressant
Buproprion - norepi-dopamine reuptake inhibitor
Second-line agents:
Tricyclic antidepressants MAO inhibitors
Augmentation agents:
Antipsychotics Mood stabilizers Anxiolytics
Per American College of Physicians Guidelines, 2008
Pharmacotherapy for Depression

Start at a low dose and titrate up slowly Assess patient 1-2 weeks after starting therapy then every 2-4 weeks until stable
Status of depression and therapeutic response Suicidal ideation Adverse effects
St. Johns Wort for Depression

Several meta-analyses report that St. johns wort is more effective than placebo and equally effective as TCAs for mild depression Concern for medication interactions:
Reduces warfarin effect May interfere with anesthesia May reduce contraceptive efficacy Should not be used with SSRI or SNRI due to concern for serotonin syndrome
Hammerness P. Psychosomatics 2003
Consider modification of therapy after 6-8 weeks Continue therapy for 4-9 months after an adequate clinical response to prevent relapse
Qaseem A. Ann Intern Med 2008
Exercise
Cochrane review found exercise to improve symptoms moderately
Most studies are observational and of poor quality Efficacy is comparable to psychotherapy Should not be used alone in severe depression
Mindfulness Meditation
Meta-analysis of 6 RCTs showed a small effect of meditation on reduction of depression
Most studies used a wait list control 1 study used a support group control
Use of Mindfulness Based Cognitive Therapy (MBCT) may be more promising for depression
MBSR was developed to manage chronic illness, not specifically for depression Multicenter trial of MBCT vs usual treatment in patients recovered from recurrent depression 40% more patients remained in remission in MBCT group over 60 weeks of follow up Patients with MBCT had fewer hospital admissions for depression
Bohlmeijer J Psychosomatic Research 2010 Teasdale JD J Consult Clin Psychol 2000
Patients who exercise have lower rates of relapse

156 subjects randomized to exercise, SSRI or both At 6 months after completion of treatment, exerciser alone were more likely to be categorized as improved or resolved
Mead GE Cochrane Database Syst Rev 2008 Babyak M Psychosom Med 2000
Cognitive Behavioral Therapy for Depression

Meta-analysis of 15 RCTs found CBT to have a moderate effect on depression
Requires typically fewer sessions than classic psychotherapy May be more acceptable to patients who are not interested in therapy
GAD2 PHQ2
Conclusions
Use brief screens for anxiety and depression in all patients Use multimodal treatments
Medications Psychotherapy, MBSR or CBT Exercise
Refer for patients with severe symptoms or nonresponsive to treatment

Nieuwsma JA Intl J Psych Med 2012
References
Wittchen HU et al. DSM-III-R generalized anxiety disorder in the National Comorbidity Survey. Arch Gen Pysciatry 1994; 51:355 Zondervan KT et al. The community prevalence of chronic pelvic pain in women and associated illness behaviour. Br J Gen Pract 2001;51(468):541 Hettema JM et al. A population based twin study of generalized anxiety disorder in men and women. J Nerv Ment Dis 2001; 189:413 Etkin A et al. Disrupted amygdalar subregion functional connectivity and evidence of a compensatory network in generalized anxiety disorder. Arch Gen Psychiatry 2009: 66:1361 Tyrer P et al. Generalized anxiety disorder. Lancet 2006; 368: 2156 Kroenke K et al. Anxiety disorders in primary care: prevalence, impairment , comorbidity and detection. Ann Intern Med 2007; 146:317 Mitte K. Meta-analysis of cognitive behavioral treatments for generalized anxiety disorder: a comparison with pharmacotherapy. Psychol Bull 2005; 131:785 Durham RC et al. One year follow up of cognitive therapy, analytic psychotherapy and anxiety management training for generalized anxiety disorder: symptom change, medication usage and attitudes to treatment. Behav Cog Psychother 1999; 27:19 Bohlmeijer E. et al. The effects of mindfulness based stress reduction therapy on mental health of adults with chronic medical disease: a meta-analysis. J Psychosom Res 2010; 68(6):539 Rickels K et al. Paroxetine treatment of generalized anxiety disorder: a double blind placebo controlled study. Am J Psychiatry 2003; 160:749 Donohue JM et al. Reducing the societal burden of depression: a review of economic costs, quality of care and effects of treatment. Pharmacoeconomics 2007; 25:7
References
Cepoiu M et al. Recognition of depression by non-psychiatric physicians a systematic literature review and meta-analysis. J Gen Intern Med 2008 23:25 Hitchcock LS et al. The experience of chronic non-malignant pain. J Pain Symptom Manage 1994;9:312 Kroenke K et al. The Patient Health Questionairre-2: validity of a 2 item depression screener. Med Care 2003; 41:1284 Schulberg HC et al. The effectiveness of psychotherapy in treating depressive disorders in primary care practice: clinical and cost perspectives. Gen Hosp Psychiatry 2002; 24:203 Mynors-Wallis LM et al. Randomised controlled trial comparing problem solving treatment with amitriptyline and placebo for major depression in primary care. BMJ 1995; 310:441 Thase ME et al. Treatment of major depression with psychotherapy or psychotherapypharmacotherapy combinations. Arch Gebn Psychiatry 1997; 54:1009 Qaseem A et al. Using second generation antidepressants to treat depressive disorders: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2008; 149:725 Hammerness P et al. St. Johns Wort: A systematic review of adverse effects and drug interactions for the consultation psychiatrist. Psychosomatics 2003; 44(4):271 Mead GE et al. Exercise for depression. Cochrane Database Syst Rev 2008 Babyak M et al. Exercise treatment for major depression: maintenance of therapeutic benefit at 10 months. Psychosom Med 2000; 62(5):633 Teasdale JD et al. Prevention of relapse/recurrence in major depression by mindfulness-based cognitive therapy. J Consult Clin Psychol 2000; 68:615 Nieuwsma JA et al. Brief psychotherapy for depression: a systematic review and meta-analysis. Intl J Psych Med 2012; 43(2):129
Presentations Friday, October 19, 2012
IPPS
8:10 a.m. 9:05 a.m. James E. Carter Memorial Lecture: An Update on the Pathogenesis and Treatment of Endometriosis Erkut Attar, MD 9:05 a.m. 9:45 a.m. Innovative Injection Therapies for Pain Syndromes of Pelvic Floor Fascia Hal Blatman, MD 9:45 a.m. 10:25 a.m. The Acute Anus Dana Hayden, MD, MPH 11:15 a.m. 11:35 a.m. Irritable Bowel Syndrome Alain Watier, MD 11:35 a.m. 11:55 a.m. Vulvodynia Andrea Rapkin, MD 11:55 a.m. 12:15 p.m. Interstitial Cystitis Nel E. Gerig, MD 2:00 p.m. 2:40 p.m. Visceral Pain Models Kevin Hellman, PhD 2:40 p.m. 3:10 p.m. Vulvar Pain Mechanisms Melissa Farmer, PhD
Page 79
The INTERNATIONAL Society

2012 Annual Meeting October 18-20 The Palmer Hilton Chicago, IL
1
Chair, Integrative Medicine Consortium Past President, American Holistic Medical Association
Author: Winners Guide to Pain Relief Medical Director: Blatman Pain Clinic
Holistic Comprehensive Pain Care Wellness and Rehabilitation
www.blatmanpainclinic.com
Objectives
Learn the complexity of muscles and fascia that cause pelvic pain Analyze physical findings and history to determine which muscles are involved in a pain pattern Explore the benefit and potential of PRP injection for treatment of pelvic pain
3
Pelvic Floor Pain Diagnoses

Vulvodynia Dyspareunia Interstitial Cystitis Prostatitis Clitoral pain (anterior division of pudendal nerve?) Pelvic floor myalgia Penis pain 4 Others
Pelvic Floor Pain Causes

Pudendal nerve (neuritis, neuralgia) Bladder mucosa injury Childhood or adult trauma
Muscle
Myofascial Pain
Trigger points
Fascia
Sexual, fracture pelvis, childbirth

Mind/body/spirit (abuse/trauma issues) Muscle and fascia (myofascial pain)
5
Trigger points
Ligaments
Trigger points
Entheses
Attachment where tendons, ligaments, and

muscle meet bone
Myofascial Pain
There is no pain sensation that can be described that cannot come from muscle and fascia
Sharp, dull, burning, numbness, tingling,

radiating, stabbing, cramping....
Referral pain patterns can be complex All sensations can occur at the same time 7 The sensations can be difficult to describe
Hip Adductor
Piriformis Rectus abdominus Gluteus Minimus
Gluteus maximus
Gluteus Medius
11
Hamstring Hip adductor
How Do TrPs Cause a Pain Pattern?

The pain patients feel is the total of the CNS/ANS input from the orchestra of TrPs in the body How patients feel depends on:
Pelvic pain
How loudly the orchestra plays Which solo artist stands up to sing
How does this cause my pain?

This depends on
What they have done in the past 3 days that

has ticked off their muscles
What the weather is going to do tomorrow How well they slept last night How much stress they are under What they have eaten in the past 4 months
Focus of Hyperirritability in a muscle or its fascia that causes pain Refers pain at rest Refers pain with motion that stretches or loads that muscle Always tender, usually will refer pain with direct compression Weakens and prevents full lengthening of the muscle Can evoke autonomic phenomena
Does not cause pain during normal activity Usually causes pain when palpated May persist for years after recovery Causes restriction of motion Causes weakness without atrophy Predisposes person to acute attacks of pain:
T.P.s re-activated with:

over stretching chilling overuse
The Ticket out of this Pain is Two Pieces:

#1 -- all these knots in the orchestra need to be made #2 -- whatever it takes to get patients body healthy enough that it can help with piece #1
First Steps
Correct perpetuating factors Stretch involved musculature to full and normal resting length
24
INACTIVATE TRIGGER POINTS

Ischemic compression (Accupressure)
1 to 2 minutes
Dry needling Trigger Point Injection (local anesthetic) Photon Therapy
Why inactivate trigger points?
What if the Enthesis Is Injured?
Where tendon, ligament Or muscle Inserts into Bone
How do we heal?......Ankle sprain
Healing From Injury
Every time the muscle/fascia fibers pull on the attachment, the weakened fibers perpetuate firing of the trigger points and continued pain
27
Ligaments tear Inflammatory mediators released Blood vessels become incompetent

Leak fluid and WBCs Ankle swells WBCs release enzymes, debride injured ligaments
3 days later fibroblasts migrate to area and work to

rebuild the injured ligaments
28
Medications Block Healing

NSAIDs (and perhaps ice) in the first 3-4 days stop this process of healing
Why Ligaments/Fascia Do Not Heal on Their Own

Poor blood supply Smoking, stress, medication, lack of sleep, poor nutrition Incomplete healing is common 50-60% of pre-injury tensile strength is considered return to normal
30
Dont hurt or swell as much Dont heal as much

Digestive enzymes have also been shown to decrease inflammation and pain from athletic activity
29
Induce/Augment Healing
In order to re-start or re-run the bodys healing program, you have to cause a new injury The best way to make a controlled injury is to poke the tissue with a needle The injury is small, and there is just a little step backwards for a larger step forward in healing
31
Prolotherapy
Poke the ligament with a needle, create a small and new injury to make the bodys healing mechanism start again--even acupuncture bone pecking Injection of Novocaine/Dextrose --hyperosmolar solution
Local tissue cells lose fluid, augment inflammatory cascade Fibroblasts migrate to area and rebuild tissue
Acupuncture needles work Hyperosmolar solution works better PRP (platelet rich plasma) works best--4 week healing reaction--like prolotherapy on anabolic 32 steroids
Most Powerful Are: latelet ich lasma and Stem Cells

What is latelet ich lasma? PRP is a normal blood clot with an
enhanced concentration of platelets (4-7x)
Platelet Rich Plasma

Extracted from your own blood
Contains growth factors

Injection into tendon/ligament/joint will accelerate healing Very good for
33
Partial tendon tears Rheumatoid arthritis Osteoarthritis Ligament injuries Muscle injuries Enthesis and fascia injuries
34
Normal Platelet Count
Platelet Concentrate (PRP)
35
36
Why Concentrate Platelets?

Source of Growth Factors
Activated Platelets Release Growth Factor Proteins into the Surrounding Tissue
Platelet Derive Growth Factor

PDGFaa, PDGFbb, PDGFab
Vascular Endothelial Growth Factor

VEGF
Epidermal growth Factor

EGF
The Measure of Available Platelets Relates to the Measure of Growth Factors at the Wound Site
37 38
SmartPReP 2 Concentrate System Delivering a Concentration of Augologous Proteins to the Healing site can Improve the Healing Response and Result of Treatment
39
APC-20 Kit Provides 3-4 ml of PRP from 20 cc blood APC-30 Kit Provides 4-5 ml of PRP from 30 cc blood APC-60 Kit Provides 10 ml of PRP from 60 cc of blood
40
Isolation of Growth Factors in 15 Minutes
Fascia--Common Denominator
Trigger point work Acupuncture Osteopathic therapy Craniosacral therapy Rolfing Myofascial release
Load Blood
Process
Deliver
41 42
Anatomy Trains
Fascia is contiguous throughout the body Fascia lines can be traced in the body
Quic kT ime and a dec o mpr ess o r ar e needed t o see t his p ic t ure .
43
44
Fascia
There are 10x as many sensory receptors in fascia as in muscle
Ligaments
Mostly arranged in series with muscles, not parallel
Golgi tendon organs-measure stretch Paciniform endings-measure pressure Ruffini ending-inform CNS about shear forces
The body and fascia net is a single connected unity in which the muscles and 45 bones float
Tense a muscle, ligaments automatically tense

to stabilize the joint
Function through the full range of motion of the joint, not just at full extension
46
Nerve Endings
Arranged according to the forces that commonly apply in that location in that individual
Fascia
More innervated than muscle Proprioception and kinesthesia are primarily fascial, not muscular
Not according to genetic plan Not according to anatomical division we call a

muscle
No representation of a deltoid muscle inside your movement brain Sensors in and near skin are more active in 47 joint detecting and regulating movement than the ligament receptors
48
Forms of Fascia
Fascia and Muscle
49
50
Prolotherapy
There are three trigger point zones in a muscle
Fascia as a System
Origin Belly Insertion

Prolotherapy at enthesis is also a trigger point injection--relieving the controversy Tendon weakness perpetuates trigger point in the muscle, increases fragility 52
51
When a trigger point is inactivated, the pain pattern may shift to that of an earlier TrP and that muscle must also be treated If the original TrP in pain pattern is inactivated first, patient may recover without further treatment
Pain patterns evolve backwards in time as the patient heals.
53
Put it Together for Treatment

Myofascial pain
Bus is driven in many patients by the

adductors
Other major muscles/ligaments include:
Pelvic floor Sacrotuberous ligament Hamstring origin from ischial tuberosity Rectus abdominus External/internal rotators of hip Gluteals
55
56
Note from PT
57
58
Comorbid Conditions
Women with vulvodynia are 2-3x more likely to have comorbid chronic condition
Fibromyalgia Interstitial cystitis Irritable bowel syndrome

Pelvic pain
Obstetrics and Gynecology July 2012
59
Put it Together for Treatment

Trigger point injections to loosen muscle and fascia Prolotherapy injections to restore strength to tendon, fascia, enthesis PRP injections
62 61
Suboptimal Results
Mostly diet related Smoking (75% decrease healing) Nutrients are necessary for healing (C, Zinc) There is a strict
Contact and Advanced Training

www.blatmanpainclinic.com hblatman@iac.net Series of Five CME Weekend intensive hands-on seminars
Head, Neck, TMJ Chest, Upper back, Shoulder, Upper Extremity Abdomen, Lower back, Pelvis, Hip, Lower extremity Put it all together and Fascia Advanced techniques
Comprehensive Pain Treatment
DO NOT EAT LIST

63
Myofascial trigger point injections Prolotherapy Nutrition therapy Compounding pharmacy
64
www.blatmanpainclinic.com
Anorectal pain- the colorectal surgeons perspective

Objectives
The Acute Anus

what causes a pain in the butt?
Dana M. Hayden, MD, MPH Division of Colon and Rectal Surgery Loyola University Medical Center Maywood, IL
Why this is so important? Frequent and infrequent causes of anorectal pain

Fissures Abscesses and fistulas Hemorrhoids Pilonidal disease STDs Prolapse Anorectal tumors Pelvic pain syndromes
Anorectal conditions
Extremely common reason for PCP visit Difficult diagnosis Low sensitivity for the correct diagnosis for primary care physicians, general surgeons, family physicians and gynecologists Delay in treatment, detrimental for patients
Quality of life Morbidity and mortality if cancer misdiagnosed or unrecognized
Anorectal Disease in Managed Care DCR 1996; 39:1193-1198

100 consecutive referrals for anorectal symptoms Correct dx made by 53% PCPs, 53% gen surgeons Delay to diagnosis or treatment in 25%
of these, 60% had an adverse outcome, complications
Of 19 patients initially evaluated by gen surgeons

4 had the wrong operation 5 were untreated because of incorrect diagnosis 3 were correctly diagnosed but not treated correctly Only 2 were diagnosed and treated appropriately
Anorectal Disease in Managed Care DCR 1996; 39:1193-1198

Hemorrhoids
sensitivity 73%, PPV 58%
Conclusions
PCPs tend to over attribute anorectal symptoms to hemorrhoids Most abscesses are easy to detect by PCPs Low sensitivity for detecting fissures is worrisome, delays could affect quality of life Low sensitivity for fistulas could lead to persistent septic symptoms
Fissures
Abscesses
Fistulas
Pain is the hallmark symptom

Constant
Abscess Thrombosed external hemorrhoids Cancer Warts
Intermittent
Fissure Levator ani syndrome
Anal Fissures - Causes

Trauma is the initiator
Hard, large stool, diarrhea, trauma
Pain leads to internal anal sphincter hypertonicity Ischemia is the perpetuator Terminal branches of inferior rectal artery pass through internal anal sphincter Decreased mucosal blood supply to posterior anal canal
Increased internal sphincter pressure exceeds arteriolar pressure, decreasing blood flow to fissure, preventing healing
Anal Fissures
Severe, intermittent anal pain associated with bowel movements, exacerbated with sitting
Anal Fissures
Men: 99% posterior, 1% anterior Women: 90% posterior, 10% anterior Beware- lateral locations, multiple fissures
may be Crohns, infection, cancer
Physical Findings
Chronicity
Exposed sphincter muscle at base Hypertrophic anal papilla or sentinel pile
Physical Findings
Hemorrhoids
Constant pain only when external and thrombosed
Symptomatic, enlarged hemorrhoids

Increased pressure through arterio-venous shunt at level of hemorrhoids
Hemorrhoidal arteries Portal veins Systemic veins
Hemorrhoids
Internal
Bleed Prolapse Discharge Pain is NOT a feature
External
Nuisance Difficulty with hygiene Pain with thrombosis
Constipation, chronic straining, heavy lifting, pregnancy, cirrhosis
Hemorrhoids
Endoscopic evaluation
What a pain
Anal Abscesses, Fistulas

Constant perianal pain, not related to bowel movements
Perirectal abscesses
Majority occur spontaneously in health individuals Risk factors include diabetes, Crohns disease, previous perianal surgery, immunosuppression Peaks in 30s, more common in males
Abscesses
Described by the anatomic location
Perianal (40%, most common) Ischiorectal (20%) Intersphincteric (20%, most commonly associated with fistula Supralevator
Etiology of Fistulas
Majority result from the drainage, either spontaneous or surgical, of cryptoglandular abscesses Can be a manifestation of Crohns disease Can result from anorectal trauma, including surgery
External fistula openings
Fistula
Intersphincteric 1. Results from the drainage of a perianal abscess 2. Do not involve the external anal sphincter
Fistula
Transsphincteric 1. Results from the drainage of a perirectal abscess 2. Involves varying amount of the external sphincter
Anatomy
Extrasphincteric 1. Results from rectal trauma 2. Most commonly is a rectovaginal fistula from obstetric trauma
Rectovaginal Fistulas
Fistulas from Crohns
Pilonidal Disease
Constant pericoccygeal pain when infected
Pilonidal sinus
Acquired subcutaneous chronic infection secondary to hair implantation Some theories support congenital etiology Mostly commonly in hirsute, white males; not always Most under 40 which may support sex hormone association May be foreign body reaction
STDs associated with proctitis

Chlamydia
commonly associated with fissure
Gonorrhea
STDs
Severe pain or discomfort, can be constant or intermittent
Symptoms include bleeding, urgency, mucous discharge, abdominal pain, rectal pain
STDs associated with perianal ulcer

Chlamydia
herpetiform vesicle followed 1-2 weeks later by groin lymphadenopathy
Chancre (primary syphilis)
Syphilis
painless ulcer at anal margin (chancre) may cause discomfort, difficult defecation, urgency confused with fissure but will have groin lymphadenopathy
Herpes
painful blisters open sores preceded by tingling burning in perineum, buttocks or legs
Granuloma inguinale (Donovanosis)

cauliflower growth with associated pustules and papules
Anal condyloma lata (secondary syphilis)
Donovanosis
Perianal Herpes
Anal Warts
Constant perianal discomfort unrelated to bowel movements
Human Papilloma Virus

Double-stranded circular DNA virus coding for 8 proteins Over 90 subtypes identified Types 16,18,45,56 implicated in malignancy Infects epithelial and mucosal cells
Clinical Presentation: Condyloma Acuminatum

Superficial cauliflower-like wart lesion Can cause pain, itching, bleeding, 2 bacterial infection Incubation period averages 3 months Incidence 500,000 to 1 million new cases/yr Immunosuppressed, DM, pregnancy, trauma, multiple sexual partners
Genital wart on penis, scrotum, or anus 5% involve urethra
Genital wart on vulva, vagina, or anus Can occur on cervix
Clinical Presentation: Giant Condyloma Acuminatum

A.K.A Buschke and Loewenstein tumor Large exophytic mass May progress to verrucous carcinoma Local invasion of dermis w/ inflammatory infiltrate
Rectal prolapse
Discomfort but may infrequently cause severe pain if incarcerated
Rectal prolapse
Still poorly understood Mostly in older females, but found in both sexes and all ages Chronic straining Abnormal intestinal motility Associated with tenesmus, discomfort, bleeding, mucous discharge Although infrequent, can cause severe pain if becomes incarcerated or strangulated
Solitary rectal ulcer syndrome

Variety of complaints
Constipation, diarrhea, passage of mucous, tenesmus, rectal bleeding, proctalgia fugax
Occurs mainly in women with long history of bowel management problems Unclear etiology, associated with pre-prolapse and rectal prolapse but also thought associated with local trauma from fecal impaction/manual disimpaction Endoscopic exam: ulcer with hyperemic edges and induration or exophytic lesions
Anorectal Tumors
Constant anal pain with sphincter involvement Ominous clinical feature
Variety of anorectal tumors

Low rectal adenocarcinomas Anal cancer (epidermoid): squamous cell cancer anal canal, margin and perianal skin Rarer lesions
Anal melanoma Pagets and Bowens disease
Anal cancer
Bleeding, discharge, palpable lump, pain with defecation, soiling or incontinence Symptoms often attributed to benign conditions, diagnosis is usually delayed Majority of patients with sphincter involvement at diagnosis, 1/3 with lymph node metastasis
Pain may be associated with sphincter or pelvic wall involvement (poor prognostic sign)
Fissure associated with constipating lesion Post-radiation proctitis or stricture
Anal cancer
Anal cancer associated with HPV
Presacral tumors
Rare cause of rectal pain, pelvic pressure and change in bowel movements
Presacral or retrorectal tumors

Very rare Developmental or acquired Inflammatory, non-neoplastic, benign, malignant or metastatic Symptoms depend on size and location Rectal pain, pelvic pressure, change in bowel habits, buttock or back pain, perianal numbness, muscle weakness, difficulty voiding, constipation
Large variety of presacral lesions

Developmental lesions
Germ cell tumors, tail gut or duplications cysts, anterior sacral meningocele
Inflammatory lesions
Abscess (most common), postpartum hematoma
Neoplastic (benign or malignant)

Chordoma, bony tumors (osteochondroma, chondrosarcoma, Ewings), neurogenic tumors
Metastatic tumors (lymphoma, myeloma, adenocarcinoma)
Sacrococcygeal teratoma
CT scan of presacral mass
Posterior excision of presacral tumor
Pelvic pain syndromes

Severe intermittent rectal pain
Levator Ani Syndrome

Diagnosis of exclusion
Patient will require extensive work-up for organic etiology of pain
Levator Ani Syndrome

Diagnosis made by digital rectal exam
Pluck the levator muscle like a harp string to
reproduce pain
Fleeting, intermittent deep rectal pain Worsened by sitting, better with walking, laying down May cause pain with ejaculation or dyspareunia Pain may radiate to coccyx, buttocks, legs Can wake people up from a deep sleep
Frustrating problem to treat Can use botulinum toxin injection, biofeedback
Proctalgia fugax
Levator syndrome variant Short-lived rectal pain Awakens patient from sleep Usually abates spontaneously Occurs infrequently, every 1-2 months
Coccygodynia
Organic origin, different from levator syndrome Pain may follow trauma, pelvic fracture, arthritis Pain can be triggered by transanal digitation of coccyx Only type of pelvic pain syndrome that improves after coccygectomy
In conclusion
There are lots causes of anorectal pain Thorough history and physical exam are key to diagnosis Appropriate imaging is a good adjunct If the story and exam do not make sense
Dig Deeper!
Must exclude organic causes Believe the patient...respect the pain!
HIGHLIGHTS IN IBS
Irritable bowel syndrome (IBS) is a functional G-I disorder (FGID) characterized by abdominal pain or disconfort associated with changes in bowel habit and features of disordered defecation
Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC Functional Bowel Disorders. Gastroenterology 2006;130(5):1480-1491
IBS is best considered as an interaction between biological and psychosocial factors that lead to a disturbance in brain-gut interactions associated with altered GI motility, hyperalgesia, alterations in mucosal immune function and the microflora environment, and autonomic and hormonal abnormalities.
Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC Functional Bowel Disordersw. Gastroenterology 2006;130(5):1480-1491 Drossman DA. The functional gastrointestinal) disorders and the Rome III process. Gastroenterology 2006;130(5):1377-1390
Genetic susceptibility Early environmental exposures that include infection or family modeling of ilness Abnormal GI motility Visceral hypersensitivity Infection / inflammation / altered immune activation
Dysregulation of the brain-gut axis Autonomic dysfunction Altered mucosal permeability Psychosocial distress The importance of food !!!! The role of microbiota !!!! At present, treatment of IBS is largely empiric, based upon a patients predominant symptoms rather than underlyng physiology. It is likely that the inherently hererogeneous pathogenesis of IBS accounts for the modest clinical benefit of currently available medical therapies.
HELP
WE ARE TREATING THE SYMPTOMS NOT THE DISEASE
INTESTINAL PERMEABILITY AND IBS
All disease begin in the gut (Hippocrate) Zonulin and tight junctions Leaky gut syndrome (Bacterial toxins, ischemia, autoimmune disorders, Rx, infections) Abnormal passage of Ag Stimulation of immune system Secretor-motor response Affects sensory afferents ( Explains pain) Increases visceral hypersensibility
What may trigger increased permeability ??? Food Microbiota Bile acids Stress Genetic Allergic reactions Luminal factors (proteases)
Increased permeability in IBS-D
EFFICACY OF AMYTRIPTLINE IN IMPROVING INTESTINAL PERMEABILITY AND QoL IN PATIENTS WITH IBS
Amytriptiline is effective in improving QoL and intestinal permeability in patients with IBS
Giovanni Gigante et al. # Sa1422
GUT MICROBIOME AND IBS
The gut microbiome plays a critical role in normal GI tract, ENS & CNS development & function Perturbations in the gut microbiome have been associated with IBS Acute gastroenteritis Post-infectious IBS SIBO Dysbiosis
Agents that influence the gut microbiome offer benefits to some patients with IBS Diet Probiotics Antibiotics
Gastroenterol Clin North Am 2011;40:141-162 Am J Gastroenterol 2009;104:1033-1049 Dig Dis Sci 2006;51:1297-1301 N Engl J Med 2011;364:22-32 Gastroenterology 2008;134:P-255 (T1390) Am J Gastroenterol 2006;101:326-333
THE GUT MICROBIOME IN HEALTH AND GI DISORDERS

Bacteria exceed the # of host somatic cells by > one order of magnitude
Gut bacterial population +/- 100 trillion 500-1000 different species of bacteria 50% of fecal biomass is from bacteria
QUANTITATIVE AND QUALITATIVE DIFFERENCES : IS THE COLONIC MICRIOBIOME DIFFERENT IN IBS COMPARED TO HEALTHY INDIVIDUALS ?
Microflora exerts important effects on:

Structure, physiology, biochemistry, immunology, maturation of vasculature, and gene expression Bidirectional effects on gut neuromotor function Role in C. diff. Colitis, IBD, SIBO, IBS. Diverticular disease ? Differences in microflora reported in IBS vs controls
DIFFERENCES IN GUT MICROFLORA BETWEEN HEALTH AND IBS

There is extensive variability in flora amongst IBS patients and control General observations from IBS patients:
Fewer lactobacillus, Bifidobacteria , coliforms Greater instability of microbiota
Quantitative PCR suggest:

Decreased Lactobacillus sp in IBS-D Increased Veillonella sp in IBS-C Considerable overlap between IBS and controls
SMALL BOWEL BACTERIAL OVERGROWTH AND IBS FACT OR FICTION ?
Using 16S ribosomal RNA gene coding and sequencing of 3753 clones and follow-up PCR:
Differences in Coprococcus, Colinsella, Coprobacillus found between IBS/controls
BREATH TESTING & IBS: METAANALYSIS OF AGE + SEX-MATCHED CASE CONTROL STUDIES
6 Studies Different types of breath test 4 positive / 2 negative
PI-IBS: 10% (Campylobacter/Salmonellose) 3 months post Campylobacter, 67% of patients have an increases in E. Coli in their small bowel Breath testing in IBS 37% of IBS patients have bacterial overgrowth 66% patients PI-IBS have bacterial overgrowth
DDW 2012
Clin Gastroenterol Hepatol 2009;7:1279-1286 Expert Opin Investig Drugs 2009;18:349-358
MANIPULATE THE MICROBIOTA WITH ANTIBIOTICS
The efficacy and safety of Rifaximin for the Irritable bowel syndrome: A systematic review And meta-analysis
S.B. Menees, M. Maneerattannaporn, H.M. Kim, W.D. Chey Am J Gastroenterol 2012;107:28-35
Rifaximin more efficacious than placebo for global IBS symptom improvement NNT: 10.2 Rifaximin significantly more likely to improve bloating than placebo NNT: 10.1 The modest therapeutic gain was similar to that yielded by other currently available therapies for IBS (Tegaserod, Lubiprostone, alosetron)
Older patients and females demonstrated higher response rates Most common adverse events: headache, upper respiratory infection, nausea, nasopharyngitis, diarrhea, abdominal pain
ANTIOBIOTICS FOR IBS: THE WAY FORWARD

Reasons for symptoms improvement unclear
- Location ? Composition ? Genetics ?
ANTIOBIOTICS FOR IBS: THE WAY FORWARD

Potential consequences of repeated widespread antibiotic use ?
Optimal diagnostic test for SIBO unclear

- Breath test results may not predict response to antiotics
Optimal antibiotic therapy unclear Benefits appear transient

- How can we increase the durability of response? - How best to treat recurrent symptoms
DIETARY INTERVENTION
HOW CAN FOOD CAUSE GI SYMPTOMS

The forgotten factor: 2/3 of IBS patients increases their symptoms by eating
By increasing the gastro-colonic reflex By changing colonic sensation

Duodenal lipid infusion changes colonic sensation
By changing the microbiota By increasing endotoxin activity

Changes mucosal permeability, changes microbiota
Avoid excess ( chocolate, caffeine, sorbitol, junk food Soluble fibers helps constipation Food elimination reduces IBS symptoms Very low CHO diet (55% CHO vs 5% CHO) 100% amelioration !!! Gluten free diet
Gluten causes symptoms in IBS patients without celiac disease Gluten free diet in IBS patients reduces fatigue
By increasing fermentation By increasing production of gaz Psychological factors Food allergies Food intolerance
Elimination diet in allergic /intolerance

Importance of challenge and re-challenge
Free lactose diet (36% are intolerant)
FODMAPs
Food choice as a key management strategy for functional gastrointestinal symptoms Peter R. Gibson Susan J. Shepherd Am J Gastroenterol 2012;107:657-666
Fermentable oligo-, di-, monosaccharides and polyols

Fruits with fructose exceeding glucose
Apple, pears, vatermelon
Fructan containing vegetables

Onions, leaks, asparagus, artichokes
Wheat based products

Bread, pasta, cereal, cake, biscuits
FODMAPs
Fermentable oligo-, di-, monosaccharides and Polyols
Sorbitol and lactose containing foods Raffinose containing foods
Legumes, lentils, cabbage, brussels spouts Decreases breath hydrogen production Decreases fermentation Decreases IBS symptoms Clin Gastro Hepatol 2008;8:765
PROBIOTICS AND IBS
Probiotics are nonharmful pathogens that improve the balance of intestinal microflora and can positively influence digestive health Mostly Lactobacillus and Bifidobacteria More often used in IBS-D May reduce flatulence, bloating and abdominal pain, disconfort and bowel habit difficulty Usually no significant adverse events
MODE OF ACTIONS OF PROBIOTICS

Binding to epithelial cells and inhibition of pathogen binding Antiinflammatory effect ( IL10 /IL-12) Enhance barrier function and prevent bacterial translocation May target the neuromuscular apparatus and improve muscle function May reduce fermentation Alteration in mucosal response to stress May affect neurotransmission and modulate visceral perception
More rigorous studies are needed before a conclusion is reached about the role of this type of therapy in the treatment of IBS Heterogeneity of studies Subobtimal study design Inadequate number of subjects Different doses and vehicles Inadequate length
PROBIOTICS FOR IBS: A SYSTEMATIC REVIEW

48 probiotics in IBS citations retrieved 21 probiotic studies assessed 16 RTCs included Improvement in IBS symptoms B. Infantis 35624 (2 RTCs studies) Decreases abdominal disconfort and bloating Bifidobacterium animalis DN 173 010 for IBS-D
DDW 2012
MODULATION OF THE BRAIN-GUT AXIS AFTER 4-WEEK INTERVENTION WITH A PROBIOTIC FERMENTED DAIRY PRODUCT
Kirsten Tillisch # 589
Consomption of this probiotic was associated with modulations of brain activity. Affects brain regions concerned with the central processing of afferent signals from the gut Reduces the impact of the brain regions involved in emotional arousal of the central processing of gut afferent signals
NON COELIAC GLUTEN HYPERSENSITIVITY

DDW 2012
3.6% of celiac patients also have IBS Less than 1% of patients with IBS have celiac disease Gluten causes symptoms in IBS patients without celiac disease 7% of IBS patients avec antibodies to gliadin. These patients will respond to a gluten free diet Non celiac gluten hypesensitivity: 10% of population 36% of patients with food intolerance get better on a gluten free diet Significant decreases of fatigue, exhaustion, amelioration of sleep in patients with IBS put on a gluten free diet
TREATMENT OF IBS
MIND AND BODY MEDICINE
HYPNOSIS AND IBS
HYPNOTHERAPY FOR FUNCTIONAL GASTROINTESTINAL DISORDERS: A REVIEW Vivien Miller Peter J. Whorwell
Intl Journal of Clinical and Experimental hypnosis: 57(3):279-292, 2009
GUT FOCUSED HYPNOSIS
GUT-DIRECTED HYPNOTHERAPY
Decreases the primary symptoms of IBS: abdominal pain and distension Improves bowel habits Decreases extracolonic symptoms Beneficial effects can last for many years Improves QoL Decreases anxiety Decreases depression Improves work attitude 60% to 70% chance of substantial reduction of symptoms
Reduces anxiety and depression Improves cognitive function Improves Gut motility Visceral sensitivity Gastric emptying Gastrocolonic response to lipid infusion Modulates the activity of the anterior cingulate cortex where the emotional content of pain is is processed
HYPNOTHERAPY FOR IBS: AN AUDIT OF 1OOO PATIENTS

Symptom severity score Total non-colonic score Illness impact score HAD anxiety score HAD depression score
Vivien Miller, Peter J. Whorwell
DDW 2012
OPERATOR DEPENDANT
MEDITATION AND IRRITABLE BOWEL SYNSROME
MINDFULNESS MEDITATION
Ellen Flynn MD Sarah Fox MD
IPPS Chicago Ocober 2011
Mindfulness training reduces the severity of IBS in women: Results of a randomized controlled trial
Gaylord S.A, Palsson O.S., Garland E.L., Faurot K. R., Cobie R. S., Mann J. D. Frey W., Leniek K.,Whitehead W.E.
American Journal of Gastroenterology Volume 106, Sept 2011, 1678-1688
Greater reductions in IBS symptoms severity after training and at 3-month follow-up Changes in QoL, psychological distress, and visceral anxiety were not significantly different between groups immediately after treatment, but evidenced significantly greater improvements at 3-month follow-up in the group of MT Mindfulness scores increased significantly more in the MT after after treatment, confirming effective learning of mindfulness skills
ACUPUNCTURE AND IBS
Acupuncture for irritable bowel syndrome: Systematic review and meta-analysis

Cochrane study in 2006: inconclusive result
Eric Manheimer, L.Susan Wieland, Ke Cheng, Shih Min Li, Xueyon Shen Brian M. Berman, Lixing Lao Am J Gastroenterol 2012; 107: 835-837
Lim, B. et al. Acupuncture for treatment of irritable bowel syndrome. Cochrane Database of Systematic Reviews. Issue 4. Art. No. : CD05111. Doi: 10.1002/14651858. CD0055111.pub2 (2006) Khan S, Chang l. Diagnosis and management of IBS Nat. Rev. Gastroenterol. Hepatoogy. 2010;7:565-581
Acupuncture for treatment of irritable bowel syndrome

Manheimer E, Wieland LS, Cheng K et al. Cochrane Database Syst Rev 2012;(5):CD005111
No statistically significant differences between acupuncture and sham acupuncture on the outcomes of symptom severity or QoL Participants receiving acupuncture reported a greater improvement that participants receiving pharmacological therapies Participants receiving adjuvant acupuncture were more likely to have reported improvement than those treated with another Chinese medicine treatment alone or those treated with psychotherapy alone
Alain Watier md LMCC FRCP Professeur titulaire Gastroentrologie Rducation prinale (Lyon) Unit de Pelvi-Prinologie Facult de Mdecine et des sciences de la Sant Universit de Sherbrooke 580 Bowen Sud Sherbrooke, Qubec, Canada J1G2E8 - 819-346-1110 a.watier@videotron.ca
Practical Diagnosis and Management of Vulvodynia for the Consultant
Andrea J. Rapkin, MD Professor, Department of Obstetrics and Gynecology UCLA David Geffen School of Medicine Los Angeles, California
Disclosure: consultant for Bayer Pharma
Objectives
Describe the differential diagnosis and multidisciplinary management of vestibulodynia and generalized vulvodynia Identify and manage vulvar lichen sclerosis and lichen planus Characterize peripheral neuropathies and formulate management plan
Vulvodynia is not a disease

Vulvodynia is set of symptoms not an identifiable entity with one cause Are there definite subtypes? Is there tissue damage or is it neurogenic? Peripheral and central sensitization?
ISSVD Terminology (symptom based) *

PVD: Sharp/burning pain when pressure applied to vulvar vestibule. Vestibulodynia is usually provoked only, but may be unprovoked or both Physical findings : allodynia +/- erythema Generalized VD: pain not limited to the vestibule, but often most severe in the region of the vestibule Physical findings: none or hyperalgesia; +/allodynia of the vestibule
* J Reprod Med 2004
Etiology: elusive and likely multifactorial

-Peripheral neuro-inflammation or neuropathic -Myofascial abnormalities -Psychological changes and deterioration of sexual functioning -Altered central sensory processing plays a role in development or maintenance
8-16 % of women suffer with Vulvar Pain

PVD is the most common form of vulvodynia GVD is a rule out diagnosis and few studies have been published Prevalence studies often do not distinguish location of pain Population based survey: ~65% had only provoked pain, 20% only unprovoked, 14 % had both (Reed B et al Am J Ob Gyn 2012)
See also: Arnold L et al . Am J ObGyn 2007, Harlow B et al. J Womens Health 2009, Reed B et al .ObGyn 2006
How to take a 1 hour history in 15 minutes Be quiet and listen to the patient. She is trying to tell you what is wrong Sir William
Osler
Prior to visit: ask patient to complete a detailed pain questionnaire Circumstances surrounding onset of pain: stress , trauma, new activities, Severity (VAS) and meaning of pain Aggravating and alleviating factors Include validated questionnaires for other medically unexplained pain disorders, trauma, and psychosexual functioning See www.pelvicpain.org or create your own form
UCLA Pelvic Pain Questionnaire available on request)
WET MOUNT: Look for infectious, inflammatory, hormonal etiologies Close visual inspection +/- colposcope Saline and KOH wet mount and pH of vaginal secretions Estrogenization, WBCs , hyphae, clue, trich Fungal culture for resistant yeast subtypes
Rule out: Candida, Desquamative Inflammatory Vagingitis (DIV), lichen planus, estrogen deficiency
Saline prep of vaginal secretions with estrogen deficiency, atrophy, desquamative inflammatory vaginitis or lichen planus
Treat with estrogen if atrophy is suspected. Biopsy for definitive diagnosis of LP.
Vulvar vestibule assesssment
Gently palpate 10, 2, 4, 6 oclock positions and peri-urethral with cotton swab
Neurologic exam of inguinal, vulvar and gluteal area for allodynia and hyperalgesia (or decased sensation) to light touch with cotton swab and to pin prick
Taken from the National Vulvodynia Registry GYN examination
Pelvic floor muscle evaluation

Tone Strength Increased sensitivity/pain with single digit pressure Trigger points
Taken from the National Vulvodynia Registry GYN examination
Intrapelvic muscles
Sarton J. Jol Sex Med 2010
Pubo-coccygeus Ilio-coccygeus Ischio-coccygeus
Obturator internus
Piriformis
Vestibulodynia
Diagnosis: vestibular tenderness with positive cotton swab test and varying degrees of erythema
Rule out: lichen sclerosis, lichen planus, allergy/dermatitis, candida, tight hymen, granuloma fissuratum, estrogen deficiency, vaginismus
Vestibulodynia: What is the role of estrogen and testosterone? OCPS are one of the risk facators for vestibulodynia, especially low -dose, long term, or before age 17
PVD and any evidence for possible hormonal deficiency on history or exam: Atrophic appearing vestibule, flattened ruggations, presence of parabasal or intermediate cells on each HPF of saline wet mount Consider discontinuing OCPS in favor of barrier or LNG IUD Initiate topical treatment: Estradiol =/Testosterone
(Estradiol .03% /Testosterone 0.1 % bid x 6 months)
If Pain is not localized to the vestibule Generalized vulvodynia (GVD): NIH consensus conference 2003: Complex regional pain syndrome like fibromyalgia and IC may be part of a continuum with severe PVD and not a separate disorder
GVD or vulvar dysaesthesia

Determine if there is an underlying or comorbid diagnosis:
referred visceral or muscular pain, peripheral neuropathy, dermatosis, dermatitis, allergy, anxiety, rarely sacral tumor
Patients presenting with Generalized Vulvodynia

68 y/o w 3 year history of severe generalized vulvodynia, urinary urgency, frequency, supra-pubic pain, constipation 45 y/o w 5 year history of severe right sided vulvar pain labia majora and minora 60 y/o w new onset incapacitating vulvar and clitoral pain and severe anxiety disorder 38 y/o with severe vulvar pain s/p vaginal birth
Peripheral Neuropathy Presenting as Vulvodynia

Genito-femoral Ilio-inguinal Inferior cluneal Obturator Pudendal Sciatic -Injury, entrapment in tight muscles or trigger points Perform a diagnostic nerve block
Pelvic floor muscles

One finger digital exam of :
Bulbocavernosis Pubo-coccygeus Ilio-coccygeus Ischio-coccygeus Obturator internus Piriformis
Piriformis Syndrome
SX: pain tingling nunbness of buttocks, back of leg Dx: clinical exam, MRI, nerve conduction studies Rx: PT, nerve blocks, botox
Referred pain from other structures innervated by Sacral 2-4

Urethral or bladder inflammation/pain can refer pain to vulva Gynecologic procedures can lead to vulvar pain Pelvic floor muscle trigger points can present as vulvar pain Rectosigmoid pathology or procedures can lead to vulvar pain
Innervations of Pelvic Viscera
Trigger Points: Viscero-somatic hyperalgesia

Pelvic visceral stimulation can lead to the generation of trigger points in pelvic floor muscles
Pain Modulating Factors

Depression / Anxiety / Stress Catastrophizing/ loss of control/ somatization Pain behavior reinforcement Family role/ expectations Physical / sexual / emotional trauma / PTSD Mechanical factors: de-conditioning, posture, obesity, re-injury Poor sleep Genetic predisposition
Tailored treatment of neuropathic pain: were not there yet

Mechanism based approach We dont know the molecular mechanisms involved producing neuropathic pain in an individual patient
Future goal will be to characterize patients at baseline based on symptoms and quantitative sensory testing
Topicals: good tolerability and few systemic side effects/ Combine in versabase or lipoderm Gabapentin 6% qd to qid: calcium channel blocker Lidocaine 2-5%: Na+ channel blocker NSAIDS : aspirin 5%, ketoprofen 6% Clonidine 0.1% tid : activated inhibitory g protein coupled to TRPV-1 pos nociceptors Amitriptyline 1-3 %: Na+ channel blocker Diltiazem 2%: muscle relaxation of anal
Myofascial Pain and Pelvic Floor Dysfunction

Myofascial pain is the most common type of chronic pain Primary: injury, dysbehaviors Secondary: following painful or inflammatory insult such as infection, surgery, birth, etc IC/BPS: 59% - 85% have pelvic floor findings Vulvodynia: 85% Chronic pelvic pain syndrome: >50%
What does a Physical Therapist look for?

Examines all muscles between ribs and knees Myofascial trigger points: hyper-irritable spots within a taught band of muscle or fascia (Rectus abdominus, obturator internus, piriformis, gluteal muscles, quadratus lumborum, adductors) -Responds to manual therapy, dry needling, trigger point injections Connective tissue restrictions Muscle hypertonicity & pelvic floor dysfunction
Physical therapists perspective

Restore normal motor function and decrease negative psychological impact of pain Approaches vary: manual therapy techniques, directed exercises, strengthen core muscles, instruction in gait and posture
Hartmann D. Dermatologic Therapy 2010
Physical therapy for vulvar pain

sEMG biofeedback training for 16 weeks reduced vulvar pain by 83%, intercourse in 22/28 subjects1
Physical therapy: complete or great improvement for 51.4%, a moderate improvement for 20.0% with significant decrease in pain during intercourse and increase in intercourse frequency, sexual desire, and arousal.2
1.Glazer H. J Repro Med 2005. 2. Bergeron S. J Sex and Marital Ther 2002.
Pharmacological muscle relaxation

Diazepam1 or cyclobenzaprine vaginal suppositories: 5-10 mg up to tid Botulinum toxin A: 100 units in 10 cc 0.NS2 Trigger point injections: 0.25% marcaine
1. Rogalski MJ, Kellogg-Spadt S, Hoffmann AR, Fariello JY, Whitmore KE Retrospective chart review of vaginal diazepam suppository use in high-tone pelvic floor dysfunction. Int Urogynecol J. 2010 Jul;21(7):895-9. 2. Jarvis SK, Abbott JA, Lenart MB, Steensma A, Pilot study of botulinum toxin type A in the treatment of chronic pelvic pain associated with spasm of the levator ani muscles. Aust N Z J Obstet Gynaecol. 2004 44: 46-50.
Treatment of Vestibulodynia
Tricyclic antidepressants: 50-150 mg HS1 Topical lidocaine 5% HS1 Topical gabapentin 6%2 or oral gabapentin Cognitive Behavioral Therapy or Biofeedback3 Pelvic floor physical therapy4 Local anesthetic nerve blocks5,6 Vestibulectomy3
1. Foster D, et al . Obstet Gynecol. 2010;116:583-9 2. Boardman L, et al. Obstet Gynecol. 2008 ;112:579-85 3. Bergeron S, et al. Pain 2001;91:297-306 4. Bergeron S, et al. J Sex Marital Ther. 2002;28:183-92 5. Rapkin A, et al . Am J Obstet Gyncol 2008;198:41 6. McDonald J and Rapkin A. J Sex Med 2012: in press.
Enoxaparin RCT for PVD

40 mg sc abdominal wall self administered x 3 mos : N=40 LMW Heparin with anti-heparinase activity 3 months post injection : 75% had more than 20 % pain reduction vs. 27% with placebo. 7/20 vs 3/20 had almost no pain with intercourse E group with improvement had decreased intraepithelial free nerve endings May increase bleeding and bruising
Farajun Y, Zarfati D, Abramov l, Livoff A, Bornstein J. OBGYN 2012
There were significant reductions in ovarall pain, dyspareunia, and depression as assessed by McGill (Sensory and Affective), open ended subjective questions, and Beck Depression Inventory comparing baseline ( visit 1 ) and post study (visit 6). No significant changes on FSFI.
Pudendal nerve block using Iowa trumpet
Computed tomography-guided pudendal block for treatment of pelvic pain due to pudendal neuropathy. .
McDonald JS, Spigos DG. Obstet Gynecol.2000
Boney landmarks for caudal block
Lower apex of triangle is the sacral ligament between the sacral cornua
Vulvar Dermatoses: vulvar pain, pruritis and dyspareunia

Contact dermatitis and Lichen Simplex Chronicus: Frequently misdiagnosed as vulvodynia History, careful exam, wet mount r/o vaginitis, fugal culture, biopsy Vulvar care; avoid self medication, allergens, scratching, over cleansing Topical med.high potency corticosteroids for at least 1 month, Antihistamines, +/- low dose TCA
Rodriguez M and Leclair C Benign vulvar dermatoses. Obstet Gynecol Surv 2012:55-63.
Lichen Simplex Chronicus

Also called eczema or atopic dermatitis Skin changes are caused by rubbing or scratching Itching is the predominant symptom but pain may also be present
Lichen Sclerosus: itching, vulvar pain, dyspareunia
Chronic inflammatory autoimmune disorder (associated with lichen planus, pernicious anemia, alopecia areata, autoimmune thyroid disease Average age 51 years ; 1/70 women; Extra-genital in 11%, 4-6% chance of squamous cell carcinoma Biopsy for diagnosis
Treatment of Lichen Sclerosus

Ultrapotent steroid ointment: clobetasol 0.05%; BID for 1 month then tailor : QD for 1 month then 3x per week for 3 months then 1-2 x per week, prn. Tacrolimus (macrolide immunosupressant 0.1 % ointment : ) Frequent follow-up visits Estradiol and Testosterone for vestibule? Dilators: order from vaginismus.com Treatment is successful in over 80% Surgery needed for less than 0.5%
Surgery for intractable scarring

Problem of Koebernisation (isomorphic response to trauma) Buried clitoris with decreased sensation or retention pseudocyst Midline fusion: Urethral outlet obstruction Introital stenosis and dyspareunia
Surgical Approaches
Release of adhesions with laser or diathermy Perineoplasty, V-Y or double Z plasty Ultrapotent topical steroid 2 weeks before and resuming with healing Vaginal dilators
Goldstein A and Burrows L. Surgical treatment of clitoral phimosis caused by lichen sclerosus Am J Obstet Gynecol,2007 Gurumurthy M et al. Surgical Management of complications of Vulvar Lichen Sclerosus Euro J Obstet Gynecol and Reprod Biol 2012
Lichen Planus : Pain, burning, post coital bleeding

Progressive, erosive autoimmune inflammatory process affecting 1-2% of population Erosions (74%), redness (66%) scarring (63%), lacy changes (56%) Vestibule, vagina, gingiva Abnormal vaginal discharge Rule out: Crohns, Lichen Sclerosus, or atrophy
Saline prep of vaginal secretions with immature cells and WBCs
Treat with estrogen if atrophy is suspected. Biopsy for definitive diagnosis.
Lichen planus: treatment

Vulva: Super and mid potent corticosteroid ointments Vagina: Clobetasol 0.05% cream, hydrocortisone suppositories 25 mg Systemic therapy with dermatologist Tacrolimus ointment 0.1% or intravaginal preparation Prophylaxis for candida with weekly fluconazole Dilators and physical therapy
Vulvar Granuloma Fissuratum:

Dyspareunia with post coital bleeding and severe pain of posterior fourchette
Goldstein A . J Sexual Medicine 2011; 8: 2984-2987
Vulvar Granuloma Fissuratum

Etiology: atrophy (menopause, low dose OCPs) , dermatoses, VIN, hypertonic pelvic floor muscles, poorly healed episiotomy Diagnosis: Visual exam, biopsy, wet mount, pelvic floor muscle evaluation Targeted treatment : Pharmacological , dilators, physical therapy, sexual therapy
J Sexual Medicine 2011; 8: 2984-2987
Pudendal nerve entrapment

Only the operative finding of nerve entrapment and post operative pain relief can confirm the diagnosis!
Pudendal neuropathy is one of the most common causes of perineal pain

Vulvar, perineal and/or buttock pain Pain accentuated by sitting
Over-diagnosis or under-diagnosis?
WHAT CAUSES PUDENDALNEUROPATHY?

INJURY REPITITIOUS WORKOUTS, PREGNANCY
AND DELIVERY, PELVIC FLOOR SURGERY,

CHRONIC CONSTIPATION
MUSCLE FIBROSIS (POST INJURY)

INFLAMMATION ? Herpes, other agents
PUDENDAL NEUROPATHY
PudendalNerve
PudendalNeuropathy
Pudendal Neuropathy Involving the Perforating Cutaneous Nerve After Cystocele Repair With Graft.
Bohrer J, Chen C , Walters, M Obstetrics & Gynecology. . 2008;112:496-498
Diagnosis is clinical
No pathognomonic imaging, laboratory, or electrophysiology criteria
PNML testing is not useful for sensory lesions
Nantes criteria for Pudendal neuralgia

Essential criteria Complementary diagnostic criteria Exclusion criteria
Labat, J et al Neurology and Urodynamics 2007;
Essential criteria
Pain in the territory of pudendal nerve: Superficial or deeper in anorectal, vulvovaginal, and distal urethral region Pain mostly while sitting: may become continuous over time Pain does not wake patient at night Pain without sensory deficit Relief by diagnostic pudendal nerve block
Complementary diagnostic criteria

Burning, shooting, stabbing pain, numbness Allodynia or hyperalgesia in PN territory Rectal or vaginal foreign body sensation Worsening of pain during the day Predominantly unilateral pain Pain triggered by defecation Exquisite tenderness on palpation of ischial spine
Exclusion Criteria
Exclusively coccygeal, gluteal, pubic, or hypogastric pain Pruritis: dermatologic lesion Exclusively paroxysmal pain Imaging abnormalities account for the pain
Associated signs that do not exclude the diagnosis Buttock pain on sitting Referred sciatic pain Pain referred to medial aspect of thigh Suprapubic pain Urinary frequency and or pain on a full bladder Dyspareunia is not typical but pain can be increased after intercourse
Management of nerve compression

Neural blockade 0.25% bupivocaine with 25 gauge needle or Iowa trumpet With or without steroids (depomedrol 40 mg) Repeat without steroids every 2-4 weeks CT guided transgluteal or Transvaginal injection medial to ischial spine NO CONTROLLED TRIALS
Pharmacological therapy
TCAs: nortriptyline, desimipramine, amitriptyline (10-25 mg hs titrate to effect or 150 mg) SNRIs: duloxetine (30 mg to 60 mg bid) venlafaxine (37.5 mg qd or bid to 225 mg) Anticonvulsants: gabapentin (300 mg hs to 600-900 mg tid), pregabalin ( 75 mg qd to 300 mg bid), topiramate (50 mg to 100 mg bid) Topical- 5% lidocaine ; compounded
Pudendal nerve neuromodulation
Effective in some patients affected by CPP and the effect persists over time. A positive screening phase and a positive response to gabapentin or pregabalin showed to be predictors of a successful response. Multiple localizations of pelvic pain and pain occurred after stapler surgery seem to be negative factors for the success of the treatment.
Pulsed radiofrequency (PRF)

PRF delivers an electromagnetic field, which modifies neuro-cellular function with minimal cellular destruction. PRF of the pudendal nerve has promise as a potential treatment of PN that is refractory to conservative therapy.
Rhame EE, Levey KA, Gharibo CG. .Pain Physician. 2009 May-Jun;12(3):633-8. Successful treatment of refractory pudendal neuralgia with pulsed radiofrequency.
Indications for Surgery

Diagnosis of pudendal neuropathy by Nantes criteria Failure of conservative treatment
Surgical Exploration and Release

Divide Sacrotuberous ligament Explore proximal nerve Incise Alcocks Canal Section Sacrospinous ligament Transpose pudendal nerve
Courtesy of Charles Popeney, Van Ansell, Ken Renney Fort Bend Neurology Foundation Surgical Hospital Houston Orthopedic Sports Medicine Associate
Pudendal decompression surgery

Robert R et al. 1993: 67 % improved, with good relief in 16% and some relief in 58% of 40 patients with 6 month to 7 yrs of follow-up Robert R et al. 1998: good results in 70% of 170 patients. Maullion et al 1999: 3 out of 12 patients cured; 1 slightly improved, rest- no change. 3 who were cured had at least 2 weeks of pain relief after nerve blocks Filler A. 2009: 87% had excellent outcomes most within 4 weeks, some continued to improve up to 12 months post op. Noted 4 common patterns of impingement
One RCT of surgical decompression

*Positive temporary response to blocks at the ischial spine and in Alcock's canal. -Surgery (n=16) and control (n=16) groups. -At 3 months: 50% of the surgery group reported improvement in pain vs. 6.2% of the control group (p=.02) -At 12 months: 71.4% of the surgery group vs 13.3% of the control group were improved At 4 years: 8 remained improved - No complications were encountered.
Robert R et al. Eur Urol 2005
Multiplatform Management
Pharmacological: NSAIDs, ? Narcotics with contract Local anesthetics TCAs, SNRIs, SSRIs, Anticonvulsants, muscle relaxants, Botox Hormonal modulation where indicated Physical therapy Cognitive behavioral therapy / Mindfulness Surgery Neuromodulation
Form a multidisciplinary TEAM
THANK YOU
Biologically-Relevant Time Scales
Vulvar Pain Mechanisms

Melissa A. Farmer, Ph.D. Northwestern University Feinberg School of Medicine Department of Physiology Chicago, IL, USA
Post-phallic imagery vaginal engorgement response: 5 seconds Full vaginal engorgement with sexual arousal: 13 minutes Maximum perception of vaginal fullness: 2 and 5 sec post-insertion Re-consolidation of a learned fear memory: 24 hours Peripheral nerve sprouting after an inflammatory insult: 3 days Measurable changes in cerebral blood flow: 5-7 sec Measurable changes in white matter (axonal) microstructure: days-weeks
Nervous System
Genitourinary
Muskuloskeletal (pelvic floor)
Cutaneous / Subcutaneous
Pain Systems (IASP Axis II)
Traditional static measures of vulvar touch and pain perception provide limited information
Nonpainful Vulvar Pressure Painful Vulvar Pressure
More naturalistic static measures of fullness induced by vaginal distension

Nonpainful Vaginal Fullness Nonpainful vs. Painful Vaginal Fullness
Controls PVD
Controls PVD
PVD Controls
PVD Controls
Farmer et al., In Preparation
How do you measure dynamic perception?

(t) = 1/ (T ) Translation: Your continuous perception can be predicted if you know: (1) rate of change for the perception (2) stimulus threshold at which a perception begins
Dynamic perception of vaginal distension

6.00E+01
5.00E+01
4.00E+01
3.00E+01
2.00E+01
1.00E+01
0.00E+00
100
VAS
Touch Onset
Offset
50
PVDs feel touch more slowly than controls
10
Pain Onset
Time (min)
100
PVDs begin to feel pain with less pressure than controls PVDs begin to feel fullness with lesser volumes than controls
VAS
Distension Onset
50
Time (min)
Brain Regions Recruited in Pain

from 224 studies
www.neurosynth.org
CPPS patients show a unique pattern of brain activity during spontaneous pelvic pain
Insula
Thalamus
Dorsolateral Prefrontal Cortex
Posterior Parietal Cortex
(Apkarian et al., 2005)
Farmer et al., J Urology 2011
Task-related anterior insula activity correlates with ongoing CPPS pain
Regional gray matter density correlates with CPPS pain intensity and duration
Anterior Insula
Anterior Cingulate Cortex

Farmer et al., J Urology 2011 Farmer et al., J Urology 2011
How long does it take brain gray matter to reflect the presence of chronic pain? It depends
A
Diffusion Tensor MR-Imaging enables studying properties of human brain white matter
B C C
Fractional Anisotropy (FA)
Isotropic Diffusion
Anisotropic Diffusion
FA = 0.0 FA = 0.0
0 FA = 0.4 0 FA = 0.4
FA = 0.7 FA = 0.7
FA maps are generated for each subjects brain
Chronic Back Pain: 10 years
CRPS:
(Complex Regional Pain Syndrome)
Knee Osteoarthritis: ?
2.5 years
Group average FA skeletons represent white matter common to all subjects
Regional mean diffusivity* differentiated between UCPPS, IBS, and Controls
Cluster 1
Cluster 2
Cluster 3
Cluster 4
*One-way ANOVA using FSLs Randomise (a permutation method), controlling for sex, age, and site.
Farmer et al. (MAPP), In Preparation
Farmer et al. (MAPP), In Preparation
Regional white matter properties are associated with condition-specific symptom profiles
3e-3
Disrupted global white-gray matter relationships across chronic pain conditions

UCPPS IBS Brain Skeletal FA
Gray Matter Volume (cc)
Cluster 1
Mean Diffusivity
2e-3 r = 0.12 r = -0.21 1e-3 r = -0.42 0 0 5 10 15 20 25 r = -0.46
Pain Symptoms
3e-3
10 15 Depression
20

Farmer et al., 2011

Geha et al., 2008
Cluster 2
Mean Diffusivity
CPPS
2e-3 r = 0.10 1e-3 r = -0.37 0 0 5 10 15 20 25 0 5 10 15 20 r = -0.23
IC
IBS
r = -0.39
Pain Symptoms
Depression
550
600
650
700
750
550
600
650
700
750
Mentors and Contributors
Acknowledgements
National Vulvodynia Association
National Institute of Neurological Disorders and Stroke (F31NS062611)* A. Vania Apkarian Jeffrey S. Mogil Yitzchak M. Binik James G. Pfaus
Canadian Institutes of Health Research
Undergraduates: Leigh MacIntyre Zarah Milagrosa Halley Crismann Lindsey Chan Julian Becher Ally Leja Martha Monterrosa Jose Lao Emilie Boucher Allison Graham
Stephanie Boyer
Alfredo Ribeiro-da-Silva
Gary J. Bennett
Anna M. Taylor
* This research does not necessarily reflect the official views of the NINDS or NIH
Presentations Friday, October 19, 2012
IPPS
3:55 p.m. 4:25 p.m. Dyspareunia in Women with Cancer Stacy T. Lindau, MD, MAPP 4:25 p.m. 4:55 p.m. Neurobiology of Complex Painful Dysautonomias Thomas C. Chelimsky, MD
Page 80
Funding/Support
Dyspareunia in Women with Cancer

Stacy Tessler Lindau, MD, MAPP
Associate Professor Depts. of Ob/Gyn and Medicine-Geriatrics The University of Chicago October, 2012
NIH/NIA 1K23AG032870-01A1 NIH/NIA 5P30 AG 012857 University of Chicago Comprehensive Cancer Center University of Chicago Medicine, Dept. of Obstetrics and Gynecology, Section of Gynecology Oncology
ST Lindau, 02/2012 10/2012
ST Lindau, 02/2012
Objectives
1 Understand the etiology of dyspareunia in women with cancer 2 Become familiar with the clinical presentations of dyspareunia in women with cancer
Tamoxifen (nolvadex)
AstraZeneca Pharmaceuticals LP
Arimidex (anastrozole)
AstraZeneca Pharmaceuticals LP Physicians Total Care, Inc.
Estradiol
Aromasin (exemestane)
Pharmacia and Upjohn Company Physicians Total Care, Inc. Roxanne Lab, Inc.
Femara (letrozole)
Novartis Pharmaceuticals Physicians Total Care, Inc.
http://pubchem.ncbi.nlm.nih.gov/ The PubChem Project, National Center for Biotechnology Information ST Lindau, 02/2012 10/2012
Sexual Activity* and Breast Cancer Prevalence among Older Females

Prevalence estimates and stated reasons for use of tamoxifen and raloxifene, NHIS 2010 Tamoxifen*
Reason for Use Prevention of a primary tumor Prevention of a recurrence or secondary tumor Osteoporosis Treatment No. of women using tamoxifen
(95% CI)
Raloxifene**
%
(95% CI)
No. of women using raloxifene

(95% CI)
%
(95% CI)
20,598
(518 - 114,864)
0.03
(0.001 - 0.15)
96,890
(41,277 - 192,391)
0.21
(0.03-0.17)
277,621
(168,988 - 429,690)
0.36
(0.22 0.56)
14,854
(1,738 54,292)
0.03
(0.004-0.12)
N/A
N/A
287,100
(180,417 433, 391)
0.63
(0.40-0.96)
*Weighted estimate from a sample of 32 women aged 35-79 who report using tamoxifen of a total sample of 9,906 ** Weighted estimate from a sample of 46 women aged 50-79 who report using raloxifene of a total sample size of 5,959
Adapted from: Waters, Erika A.; McNeel, Timothy S.; Stevens, Worta McCaskill; and Freedman, Andrew N., "Use of tamoxifen and raloxifene for breast cancer chemoprevention in 2010" (2012). Cancer Prevention Faculty Publications. Paper 6. http://digitalcommons.wustl.edu/canpre_pubs/6
Lindau et al. A study of Sexuality and Health among Older Adults in the US. NEJM 2007;357(8):762-774. ST Lindau, 02/2012 10/2012 SEER Cancer Statistics Review. US Prevalence Estimates 1975-2009 (www.seer.cancer.gov)
Hormonal Therapies
Chemotherapies Antimetabolites Taxanes Topoisomerase Inhibitors Alkaloids Nucleoside Analogs CFU Paclitaxel Docetaxal Doxorubicin CMF
Biological Therapies
Class
Selective Estrogen Receptor Modulators
Non-steroidal Aromatase Inhibitors
Steroidal Aromatase Inhibitors
Estrogen Receptor Modulators
Biologics
Example Drugs
Tamoxifen
Anastrozole/ Letrozole
Exemestane
Fulvestrant
Trasutzumab (Herceptin)
Lapatinib
Bevacizumab
Use Hormone Receptor Positive Early Stage Mestastic Breast Cancer Pre-menopausal Peri-menopausal Post-menopausal Sexual Side Effects Vaginal Dryness Vaginal Discharge Vaginal Bleeding Endometrial Bleeding Vaginitis Dyspareunia Vulvar changes Urogenital atrophy Hot flashes Decreased libido ++ +++ +++ ++ + ++ + + +++ ++ ++ +++ ++ ++ +++ +++ ++ +++ ++ ++ +++ +++ + + + + + + + + + x (skin changes) x (skin changes) +++ ++ ++ +++ ++ ++ + + + + + + + + + + + + + + + + + + + + + + + Her2(+) Disease + + + + Her2(+) Disease
Clinical cases will be presented, slides not included in consideration of patient confidentiality
Lindau ST, Sandbo S, Goldfarb S, Dickler M. from J.P. Mulhall et al. (eds.). Cancer and Sexual Health, Current Clinical Urology, 2011.
ST Lindau, 02/2012 10/2012
Common Gynecologic Diagnostic and Therapeutic Procedures

Diagnostics
Vulvar biopsy Bacterial, fungal, viral cultures Urinary incontinence evaluation Imaging (rare) Hormonal evaluation (rare Pregnancy testing (rare)
Evidence-Generating, Regional Care Model

Oncology Multi-institution clinical program for region Across cancer continuum Sleep, nutrition, urogyn, urology, GI, psycho-oncology, oncofertility, derm, pathology, reconstruction, AIM Multi-site, national research program
Gynecologic Therapies Sex and body education Hormonal therapy

Topical
Mechanical therapy
Moisturizer and/or lubricant therapy Vaginal dilator therapy Vibrator therapy Pelvic floor training Condoms, interim contraception Anesthesia, analgesia
General Ob/Gyn
Female Cancer Patient
Specialized Gyn Care and Research
Anti-inflammatory and ID treatment

ST Lindau, 02/2012 10/2012
Psych, CST
PT
Pt ed, research
For more information contact:

Director, Stacy Lindau, MD, MAPP
Seeking partners for multi-site clinical research network slindau@uchicago.edu
To join the Scientific Network

Emily Abramsohn, MPH, Coordinator
(773) 834-4832
eabramsohn@babies.bsd.uchicago.edu
Program Website
http://www.uchospitals.edu/PRISM
Lindau ST, Sandbo S, Goldfarb S, Dickler M. from J.P. Mulhall et al. (eds.). Cancer and Sexual Health, Current Clinical Urology, 2011.
ST Lindau, 02/2012 10/2012
ST Lindau, 02/2012 10/2012
Disclosures
Neurobiology of Functional Pain and Autonomic Disorders

October 19, 2012 International Pelvic Pain Society Meeting Thomas Chelimsky, MD Professor and Chair of Neurology Medical College of Wisconsin
NIH support NIDDK R01-DK083538, ICEPAC (Interstitial Cystitis Elucidation of Psychophysiologic and Autonomic Characteristics) No financial disclosures, sadly.
Outline
The Spectrum of Autonomic Disorders What are Functional Pain and Autonomic Disorders? Assessing the Autonomic Nervous System
Structure Function
FPADs as a loaded gun: Thoughts of a very young investigator
Functional Pain and Autonomic Disorders as models to understand brain-body networks
History
Case Autonomic Lab 1st Patient 1993 Traditional View of Autonomic Disorders Tom directed a CARF-accredited Pain Center 1994-2004 on the side. Gisela Started Pediatric GI/Motility/ANS Fellowship 1995 Index Case Published 1999 Inter-disciplinary Pediatric Autonomic Clinic 2006
ACUTE VS CHRONIC PAIN

Acute Pain
Physiology Experience Purpose and Outcome Neuronal Signal Unpleasant Perception
Chronic Pain
Reinforcing Neuronal Network Mental State (akin to depression)
Abdominal Pain as the Presenting Symptom of Autonomic Dysfunction: A Pediatric Patient Report
Action No Action Escape Danger Impedes Normal Human Function
Dysautonomia Types
Structural: a well-defined change in ANS structure produces disease - examples:
Multiple system atrophy Diabetic autonomic neuropathy Baroreflex failure due to neck radiation

Structural Dysautonomias
Central Nervous System
Multiple system atrophy Lewy body disease Myelopathies, traumatic & demyelinating Strokes
Functional: a change in ANS function is involved in disease production, but is (1) less well-defined; (2) a link in a pathogenic chain, not primary:
Postural tachycardia syndrome Irritable bowel syndrome Syncope Interstitial Cystitis?
Peripheral Nervous System

Pure autonomic failure Autonomic neuropathy
Diabetes Immunologic (Sjogrens) Metabolic/Mitochondrial
Dysautonomia
Disease-Based
(Primary)
Peripheral
Central
Pure Autonomic Failure MSA
n = 88
n = 49
n = 68
Small Fiber Neuropathy
LBD
Diabetes
Immune
Genetic
Metabolic
Inflammatory
Mitochondrial
Dysautonomia
Disease-Based
(Primary)
Syndromic
(Secondary)
Moving towards Pelvic Pain Studies

2005 Dr. Tony Buffington came for a visit and talked about his cats. They had feline interstitial cystitis
Migraine
Peripheral
Central
Pure Autonomic Failure MSA Postural Tachycardia
Small Fiber Neuropathy
LBD
Functional GI Disorders
2007 We applied for an ICA grant together, and got $30k, enough to hire our first research assistant, who did some epidemiologic work on IC. 2008 MAPP RFA comes out. Gettysburg vacation tinted 2009 ICEPAC Interstitial Cystitis Evaluation of Psychophysiologic and Autonomic Characteristics Funded by NIH NIDDK.
Diabetes
Immune
Complex Regional Pain
Fibromyalgia
Genetic
Metabolic
Inflammatory
Mitochondrial
Patient Presentation
Lori is a19 y.o. woman in first year college Severe progressive pelvic pain x 2 months
Urgency 14 x per day; frequency Pain with bladder full 7/10 Pain with bladder empty 6/10 Severe dyspareunia
Patient Examination
Normal
neurologic examination visual pelvic examination
Severe abdominal tender points Bladder and uterus normal by palpation but both moderately tender. 8 to 10/10 pain on palpation of both levators, internal obliques and peroneal body Severe adductor tender points at all 3 levels What is diagnosis?
Currently taking hydromorphone for pain What will examination show?
Diagnosis
Myofascial Pelvic Pain Syndrome
(aka Pelvic Floor Tension Myalgia etc)
Case Co-Morbid History

Co-morbidities and family history
Migraine headaches since age 14, much worse since this started Irritable bowel for 6 months Fibromyalgia by examination Probable panic disorder and anxiety disorder. Unrefreshing sleep x 2 months, despite taking benzodiazepines and opiates for pain
Probably no Interstitial Cystitis

(aka Painful Bladder Syndrome etc.)
What are co-morbidities?
What will family history show?
Case Family History

Mother, sister, and 3 maternal aunts with migraine headaches Mother has IBS and fibromyalgia Sister, maternal aunt and 3 cousins with POTS One sister has pelvic pain (dx = endometriosis) One sister with generalized anxiety disorder.
What is the patients main question?

What will you do for my pain now? I am on hydromorphone and want a refill to keep me pain-free until you do whatever blocks and PT you need to do. What is the medical response?
Is this acute pain or chronic pain?
What is the doctors main answer?

Consider how many places in your body have pain. The problem is not in your pelvis, or it would not be associated with so many other painful areas in your body. Your pain filter is broken. It can be fixed, but it takes work. There is no magic drug. But there are bad drugs and hydrocodone is one of them. They keep the filter open.

Functional Dysautonomias
Non-painful
Syncope Postural Tachycardia Syndrome (POTS) Chronic Fatigue Syndrome Cyclic Vomiting Syndrome
Painful
Functional Dyspepsia Functional Abdominal Pain Abdominal Migraine Migraine Headache Irritable Bowel Syndrome (IBS) Interstitial Cystitis Complex Regional Pain Syndrome (CRPS) Raynauds Syndrome Fibromyalgia Myofascial Pelvic Pain
Classification Principles
Structural Patient Presentation Minimizes Complaints Family often argues patient is much worse than they admit Many Clearcut Cardiovascular reflexes impaired Orthostatic Hypotension Brainstem Pass-through Impaired few sensations reach cortex Functional Overwhelming number of complaints with great details. Heartsink Few Nebulous Cardiovascular reflexes preserved Postural Tachycadia Brainstem Filter impaired all sensations reach cortex
Why Diagnose Dysautonomia?

Diagnosis
Differential diagnosis of peripheral and central differ.
Prognosis
Primary dysautonomias (MSA, DM) more serious than secondary (POTS) 5-year mortality of diabetics with autonomic neuropathy 50% (Ewing, 1980)
Examination Findings Putative Pathology Autonomic Testing Tilt Table Testing Theory of Fundamental Physiology
Autonomic Testing Why?

Mainly assess efferent autonomic function of different branches
Heart Rate/Air Flow
Cardiac Parasympathetic Cardiac Sympathetic Vasomotor Sympathetic
Arterial Venous
110
Cardiac Response to Deep Breathing

Airflow Heart Rate 90
Localizes lesion in the neuraxis

Post-ganglionic Sudomotor Axon Reflex Thermoregulatory Sweat Test
70
50
Differentiates Structural and Functional Dysautonomias
30 30 36 48 57 Time 66 72 81 89
Cardiac Response to the Valsalva Maneuver

200
Tilt Table testing

Orthostatic Hypotension Structural Poor prognosis Gradual sustained sBP>20 dBP>10 3 Postural Tachycardia Functional Good Prognosis HR>30 in 10 no BP Reflex Syncope Functional Sudden BP HR
Systolic BP
180 160 140
Diastolic BP Heart Rate
Phase I
Phase IV
mmHg/Bpm
Phase II
120 100 80 60 40 20 0 0 3 6 9 12 15
Phase III
Associated Dysauton. Definition BP / HR Pattern Physiology
18
21
24
27
30
Seconds
CV reflexes
Arterial denervation impacts diastole Usually abnormal
Venous return impact systole Usually normal
Brainstem threshold Usually nl
Axon Reflex Sweat Test
Thermoregulatory Sweat Test
Autonomic Tests of Sweating

Axon reflex testing (QSART - Low, 1983)
Tests the post-ganglionic segment only
Loris results
Deep Breathing Response: 24 bpm (Nl > 16 bpm) Valsalva Ratio: 2.10 (Nl > 1.65) Tilt Table Test: Postural Tachycardia Syndrome 45 bpm increase in heart rate, no reflex syncope Axon Reflex Test: Reduced in the foot and calf, normal in the hand and forearm. Conclusion: Mild autonomic neuropathy accompanied by postural tachycardia syndrome (POTS)
Thermoregulatory sweat test (Fealey, 1989)

Checks the entire system
Test QSART PNS Abnormal CNS Normal
TST
Hands & Feet
Inverted
Confirms Functional, not Structural Disorder; Sympathetic denervation and hyper-function
Plan
Pelvic Floor Therapy and Conditioning Program Very difficult opiate taper (hard to convince her) Started doxepin 50 hs and Lyrica 50 bid Intensive cognitive behavioral therapy After 3 months, she was back in college functioning at baseline.
Management of all functional autonomic disorders

Taper Opiates Taper Benzodiazepines Start Exercise Program with PT for conditioning Achieve Excellent Sleep
Tricyclic agents such as doxepin or amitriptyline
Consider anticonvulsant Cognitive Behavior Therapy with Psychologist Her case: Pelvic floor PT
ODYSA Survey Instrument

Assesses for 12 autonomic disorders
Orthostatic intolerance Reflex syncope Cyclic vomiting syndrome Interstitial cystitis Raynauds syndrome Complex regional pain Irritable bowel Functional dyspepsia Functional abdominal pain Migraine headache Fibromyalgia Chronic fatigue syndrome
Clustering of Functional Disorders

Syndrome # of P t s OI Syncope CVS IC Group 1 IC Group 2 Raynauds CRPS IBS FD Migraine FM CFS Controls 566 122 9 20 30 72 130 306 132 355 205 18 30 OI Syncope 74 (13) -2 (22) 2 (10) 7 (23) 13 (18) 15 (12) 42 (14) 15 (11) 44 (12) 28 (14) 4 (22) 0 (0) Number (%) with symptoms of another syndrome CVS 4 (1) 2 (2) -0 (0) 0 (0) 1 (1) 0 (0) 0 (0) 0 (0) 4 (1) 1 (0.5) 0 (0) 1 (3) IC 34 (6) 10 (8) 0 (0) --3 (4) 22 (17) 28 (9) 7 (5) 27 (8) 23 (11) 6 (33) 0 (0) RS 46 (8) 13 (11) 1 (11) 1 (5) 2 (7) -18 (14) 32 (10) 15 (11) 29 (8) 30 (15) 4 (22) 1 (3) CRPS 95 (17) 15 (12) 0 (0) 5 (25) 14 (47) 18 (25) -63 (21) 22 (17) 63 (18) 76 (37) 9 (50) 1 (3) IBS 190 (34) 42 (34) 0 (0) 11 (55) 18 (60) 32 (44) 63 (49) -51 (39) 120 (34) 101 (49) 9 (50) 6 (20) FD 89 (16) 15 (12) 0 (0) 5 (25) 6 (20) 15 (21) 22 (17) 51 (17) -53 (15) 41 (20) 0 (0) 0 (0) MHA 200 (35) 44 (36) 4 (44) 11 (55) 18 (60) 29 (40) 63 (49) 120 (39) 53 (40) -100 (49) 13 (72) 13 (43) FM 150 (27) 28 (23) 1 (11) 9 (45) 15 (50) 30 (42) 76 (59) 101 (33) 41 (31) 100 (28) -18 (100) 2 (7) CFS 16 (3) 4 (3) 0 (0) 1 (5) 4 (13) 4 (6) 9 (7) 9 (3) 0 (0) 13 (4) 18 (9) -0 (0) Mean Added -74 (61) 4 (44) 8 (40) 27 (90) 46 (64) 95 (73) 190 (62) 89 (67) 200 (56) 150 (73) 16 (89) 2 (7) 1.6 2.0 1.3 2.7 3.7 2.7 2.9 2.1 2.2 1.8 2.8 4.4 1.0
Is Chronic Pain Associated with Autonomic Dysfunction?

25
20
15
Score
10
0
to le ra nc e Va so Se m c re oto to r m oto rD is ord er G as tro pa re Au s is to no m ic D ia rrh ea
F NA f) (re PN f) (re
on s ti pa tio n
In
ys fu nc tio n
rth os ta ti c
om oto
L NM
is ord er
Sy nc op e
f) (re
Bla dd er D
Pu p ill
Sle ep
Co-morbidities of Interstitial Cystitis

IC by physician Number of subjects Age Gender (% females) Dizziness or other orthostatic symptoms >2x/week Fainting > 3 x/lifetime Symptoms suggestive of CVS (1) Fingers turn white in cold Isolated extremity pain Symptoms suggestive of IBS (2) Symptoms suggestive of dyspepsia (3) > 50 HA/lifetime 5-50 HA/lifetime HA lasting> 4 hours with at least one of : throbbing, photo/phonophobia, unilateral Chronic pains (non-HA) for > 6 months Unexplained fatigue > 6 month Delayed onset of sleep > 30 min. Sleepiness during daytime (need to force myself to stay awake) Does not feel refreshed in am Snoring or stopping breathing at night Complains of awakening before needed in am Symptoms concerning for iC 26 47 +/-16 years 92% 32% 24% 8% 32% 36% 44% 40% 52% 36% 60% 57% 52% 52% 56% 84% 40% 80% IC by NIDDK criteria based on self reported symptoms 58 39.6 +/- 17 79% 74% 45% 3% 46% 51% 27% 43% 64% 14% 64% 91% 53% 69% 60% 67% 43% 83% P between both IC groups Control group IC by MD vs control IC NIDDK vs controls 48 31 +/-14 77% 18% 2% 4% 14% 12% 12% 6% 54% 25% 47% 31% 2% 27% 23% 27% 18% 41% 0%
Co-morbidities of Functional Gi Disorders in kids

100 90
< 0.01 0.06 0.4 0.2 0.1 0.2 0.7 0.3 0.03 0.7 < 0.01 0.8 0.09 0.6 0.2 0.7 0.5
0.2 < 0.01 0.5 0.09 0.02 < 0.01 < 0.01 0.7 0.4 0.4 0.03 < 0.01 0.05 < 0.01 < 0.01 0.06 < 0.01
< 0.01 < 0.01 0.8 < 0.01 < 0.01 < 0.01 < 0.01 0.3 0.1 0.1 < 0.01 < 0.01 < 0.01 < 0.01 < 0.01 < 0.01 < 0.01
p = 0.21
80
70
60
p = 0.77
50
p = 0.07
40
30
20
p = 0.04 p = 0.04
p = 0.37
p=1 p = 0.16
10
p = 0.01
Night Waking Difficulty with m orning waking Ins om nia OSA ESS Ins ufficient s leep Poor Sleep hygiene School abs ence Shifting of s leep wake s chedule
Functional Disorders %
Organic GI illness %
p value
Frequency Analysis Normal
Frequency Analysis Fibromyalgia
Staud, 2008
Current Speculation (Feeling Free since no Data)

What is the fundamental defect? The toggle switch concept (completely on or completely off)
Sleep Void Respiration ? Stress -> heightened sensitivity
Switch remains in on position Where? ? Locus coeruleus or raphe area?
Current hypothesis
FPAD life-cycle Hypothetical 7 stage FPAD evolution 1. Genetic or Epigenetic Vulnerability 2. Early Life Stress - Rats limited bedding 3. Pre-symptomatic State 4. Later Triggering Stress - Rats sleep deprivation 5. Single FPAD Development Stage 6. Multiple Evolving FPADs 7. FPAD Recovery
Functional Pain Recovery Center The Future

An interdisciplinary diagnostic and treatment core for the most poorly serviced and poorly understood disorders in medicine: Functional Pain Disorders. The common core feature of these disorders is a predisposition to central afferent sensitization, aberrant autonomic efferent responses, and a reduced threshold to activating the stress response.
Presentations Saturday, October 20, 2012
IPPS
8:00 a.m. 8:55 a.m. C. Paul Perry Memorial Lecture: Rethinking Pelvic Pain Lessons From Two Decades of Explaining Pain Lorimer Moseley, PhD, B.App.Sc.(Phty)(hons) 8:55 a.m. 9:35 a.m. Simultaneous Pelvic Floor Physical Therapy and Functional Brain Imaging: Applications to Mind-Body Interactions in Chronic Pain Daniel Kirages, DPT, OCS, FAAOMPT Jason Kutch, PhD 9:35 a.m. 10:15 a.m. Optimizing Organ-Related Pelvic Pain: Making a Difference With Visceral Manipulation Gail Wetzler, RPT, CVMI 11:00 a.m. 11:40 a.m. Opioids: Part of a Polymoidal Pain Treatment: Which Patent, Which Drug, and Patient Monitoring Robert L. Barkin, PharmD 11:40 a.m. 12:10 p.m. Hysterectomy Differential Diagnosis Joseph M. Maurice, MD 1:40 p.m. 2:20 p.m. The Management of Chronic Pelvic Pain: Neuromodulation and Other Novel Techniques Kenneth Peters, MD 2:20 p.m. 3:00 p.m. Nutritional Considerations in Treating Patients With Pain Geeta Maker-Clark, MD
Page 81
C Paul Perry Memorial Lecture, IPPS 2012 Chicago
Is nociception sufficient or necessary for pain? If so, we should see no change in pain without change in nociception.
Rethinking pelvic pain. Reflections on two decades of Explaining Pain.

BodyinMind.org
Pain
C fibres
And no change in nociception without a change in pain.

A fibres
Very cold (-20C) stimulus associated with a red or a blue light
Visual cue = safe
Visual cue = danger
10
Pain
Pain 5
C fibres
This is a change in pain without a change in nociception.
Red light
Blue light
A fibres
Moseley & Arntz 2007 PAIN
Visual cue = safe
Visual cue = danger
Credible evidence of danger danger
Visual cue = safe
Visual cue = danger
Credible evidence of danger danger
Pain-free trauma
Pain
This is pain without nociception.
Pain
C fibres
C fibres
This is nociception without pain.
A fibres
A fibres
Experimental studies
Are the participants normal?
Pain
Is the stimulus normal? Is anything normal?
C fibres
A fibres
Visual experience depends on the evaluation of sensory input
The same thing applies to pain Complex reasoning mechanisms based on experience, context, environmentMEANING
How dangerous is this really?
Nociception & pain.

Nociception is activity in high threshold primary fibres (C and A) & their projections. Pain is an emergent conscious experience that serves to evoke a behavioural protective response.
Some nonsense terms:

Pain stimulus Pain receptor Pain pathway Descending pain control
Nociception & pain.

Modulators of nociception
Sensory stimuli
Nociception & pain.

Spinal nociceptor Normal Sensitised
Sensory stimuli
Where?
Primary nociceptors in tissue In tissue (peripheral sensitisation) In dorsal horn (central sensitisation) In brain (cortical sensitisation) In dorsal horn
Where?
Primary nociceptors in tissue In tissue (peripheral sensitisation) In dorsal horn (central sensitisation) In brain (cortical sensitisation) In dorsal horn
Immune mediators (cytokines)
Sensitivity of primary nociceptors Sensitivity of spinal nociceptors
Sensitivity of supraspinal networks
Primary nociceptor
Descending modulation
NOT heat sensitive Mechanically sensitive
Nociception & pain - targets.

Sensory stimuli
Where?
Primary nociceptors in tissue In tissue
Modulators of pain
Nociception
Where?
Brain
Modulators of pain: 1. Nociception
In dorsal horn (central sensitisation) In brain (cortical sensitisation) In dorsal horn
Anything relevant Brain to the need to protect body tissue (mood & meaning context, Immune sensitivity consequences etc)
Endocrine sensitivity
2. Anything relevant to the need to protect body tissue (mood & meaning context, consequences etc)
Related tags share neurones

Pelvic pain.

Pelvic pain, its MY pelvis

Pelvic pain, its my pelvis, sex.

Pelvic pain, its my pelvis, sex, beliefs about sex
Pain
Beliefs Knowledge, logic Other sensory cues Social context Anticipated consequences Family media
previous history
culture
GP
work
physiotherapist education
activity self-efficacy
access
Beliefs Knowledge, logic Other sensory cues Social context Anticipated consequences Family
media
previous history
culture
GP
work
access
Pain
Relay 2: The thalamus
Its not that dangerous
exposure
Relay 1: The dorsal horn
exposure
Danger
Beliefs Knowledge, logic Other sensory cues Social context Anticipated consequences Family
media
previous history
culture
GP
work
access
Pain
Relay 2: The thalamus
Its MORE dangerous than that!
exposure
Body percept 1 Motor/SMA/prem 1/2 Sensory otor PPC Frontal Visual Frontal Vestibular Auditory Insula & operculum Body ownership The pain matrix
+
Relay 1: The dorsal horn
Danger
Moreaux et al 2011 Neuroimage
Body percept 1 Motor/SMA/prem 1/2 Sensory otor PPC Frontal Visual Frontal Vestibular Auditory Insula & operculum Body ownership The The salience pain matrix matrix Body protection & regulation
Inhibition = precision.
Primary somatosensory cortex (S1)
DISinhibition = IMprecision.
Primary somatosensory cortex (S1)
- + -- - - Inhibitory intracortical neurons
- + -- - - Inhibitory intracortical neurons
+
Thalamus Tactile input
+
Thalamus Tactile input
Normal
Representation of the pinky Representation of the thumb
Imprecision within cortical body matrix multiple system dysfunction
Perceived Blood flow size Motor Inflammation Tactile Meaning Ownership

Maihofner et al 2003 Neurology 61 1707-15
Pain
100
* **
1.2 Posttask swelling (aff/unaff)
B
Min. Mag. Clear Ctrl
* *
Peak pain (100 mm VAS)
Ctrl Clear Mag. Min.
0.8
0 Recovery time (minutes)
20
40 Change in pain (100 mm VAS)
Control
Clear
Magnified
Minified
Control 0 M R 0 10 20 Trial time (minutes)
Clear
Magnified
Minified
Moseley et al 2008 Current Biology
Moseley et al 2008 Current Biology
The rubber hand illusion
The rubber hand illusion
Ctl 10 Vividness of RHI 0
RHI
Ctl
Moseley et al 2008 PNAS 105(35), 13169-73
0 Foot temperature -1
60 s
0 Hand temperature -1
The key: Pain is an output related to perceived threat to body tissue

Nociception Other cues Beliefs Logic Knowledge Previous exposure Social context Culture Expectation Meaning, mood & biological advantage
Barnsley et al. 2012 Current Biology 21:R945-6.
consciousness
Concerted behavioural response
Understanding this helps.

Nociception Other cues Beliefs Logic Knowledge Previous exposure Social context Culture Expectation Meaning, mood & biological advantage
Therapeutic targets
1 2 3
Metaphors & stories Get under the conceptual radar Randomised controlled trial
Gallagher et al 2012 Clin J Pain
1. Understand pain
Decrease catastrophising Increase pain-related knowledge Increase participation in subsequent intervention
Therapeutic targets
1
2 3
Metaphors & stories Get under the conceptual radar Explain pain biology
Reconceptualise pain
Therapeutic targets
1
2 3 1. Understand pain 2. Identify & defuse all threats
1. Understand pain
Randomised controlled trials
Moseley et al., 2004 Clin J Pain Moseley 2004 Euro J Pain Moseley 2005 Aus J Physioth Moseley 2006 J Man Manip Ther Meeus et al., 2007 Clin Rheumatol Meeus et al., 2010 Arch Phys Med Rehab Ryan et al., 2010 Man Ther Van Oosterjick et al., 2011 J Rehab Res Develop Louw et al., 2012 In press
Systematic reviews/meta-an.
Clarke et al., 2011 Man Ther Louw et al., 2012 Arch Phys Med Rehab
Truly biopsycho social Graded exposure
Cognitive behavioural principles

Coping skills Continual and conservative
Decrease pain & disability Increase participation in subsequent intervention
Therapeutic targets
1 2 3 2. Identify & defuse all threats 3 1. Understand pain 1 2
Therapeutic targets
1. Understand pain 2. Identify & defuse all threats
3. Normalise the cortical body matrix

Graded motor imagery Randomised controlled trials and Meta-analyses Decrease pain & disability
Moseley 2004 Pain Moseley 2005 Neurology Moseley 2006 Pain Bowering et al., 2012 J Pain Daly & Bialocerkowski 2009 Euro J Pain Goebel et al., 2012 Euro J Pain
3. Normalise the cortical body matrix

Graded motor imagery
Tactile discrimination training
RCTs & replicated case series Decrease pain & disability

Flor et al., 2001 The Lancet Moseley et al., 2008 Pain Wand et al., 2011 Clin J Pain
Summary.
Nociception is neither sufficient nor necessary for pain Pain is an emergent property of the human Nociception refers to activity in nociceptors and their projections Pain relates to implicit evaluation of Pain threat to body tissue and serves to protect Understanding this helps Targets for treatment are: Meaning, exposure and the cortical body matrix
bodyinmind.org
LECTURE OBJECTIVES
Simultaneous Pelvic Floor Physical Therapy and Functional Brain Imaging

Applications to Mind-Body Interactions in Chronic Pain
Daniel Kirages, DPT, OCS, FAAOMPT Jason Kutch, PhD
1. Appreciate heterogeneity in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) treatment outcomes, but recognize consistent clinical patterns. 2. Understand the need to apply new technology to better classify CP/CPPS patients. 3. Visualize the neural correlates of pelvic pain that arise in CP/CPPS patients but not controls.
HAVE YOU SEEN THESE PATIENTS?
PATIENT 1 PRESENTATION 30 year old male Main Complaint / Problem List: anal pain (2-6/10) perineal pain (2-6/10) suprapubic ache - pressure feeling (2-4/10) Onset: 3 years ago Gradual rectal pain with bowel movements Dx: fissure / levator ani syndrome (Botox infection) Aggravating Factors: - ejaculation / sitting / stress related activities Other factors: clinical depression Dx in 2001(Paxil) NIH-CPSI Score: 11+0+11 = 22
PATIENT 2 PRESENTATION 23 year old male Main Complaint / Problem List: painful and difficult bowel movements suprapubic discomfort (1-5/10) anal pain (3-8/10) 1 hour urination intervals during awake hours interrupted flow of urination at times Onset: 2 years ago (worst last 2 months) Gradual anal pain from difficult bowel movement Hemorrhoid removal and fissure repair (no change) Aggravating Factors: - bowel movement / ejaculation / sitting / urine holding NIH-CPSI Score: 8+6+8 = 22
PATIENT 3 PRESENTATION 41 year old male Main Complaint / Problem List: tip of penis burning and itching (0-6/10) rectal burning and itching (2-6/10) lower abdominal pain (1-4/10) nocturia x 3 incomplete urination 10 drops stuck Onset: 9 months ago Golf trunk rotational injury followed 3 days later with pain/burning in perineum and penis Aggravating Factors: - ejaculation / sitting / squatting / carrying baby / anxiety NIH-CPSI Score: 8+1+7 = 16
WHAT WILL A PHYSICAL THERAPIST DO?
WHAT WILL A PHYSICAL THERAPIST DO? A typical interventional skill set will include:
Perform an examination to look for body structure and function deficits in: Mobility Flexibility Power Motor coordination
Manual therapy Joint mobilization (lumbar spine, sacro-iliac joint, hip, thoracic spine) Soft tissue mobilization (trigger point release, skin rolling, etc.) Neuromuscular reeducation Pelvic floor awareness training Respiration training (relaxation, autonomic nervous system adjustment) Biofeedback / down-training Therapeutic exercise Stretching General activity walking program Patient education / counseling Condition / behavioral modification / fear reduction / positive thinking
These deficits may be specific pain generators or contributing factors leading to pain from other tissues
PATIENT 1 OUTCOME
PATIENT 2 OUTCOME
Total number of PT visits: 31 by me over 2 year span Multiple others in New York, Wash DC, San Francisco Numerous MD TrP injections and dry needling visits Multiple supplements and pollens taken Trends during PT sessions: Significant flare after internal STM (lasts 10 days) Tender to touch anywhere in external perineum Identifiable specific TrP in suprapubic region Internal STM globally painful not specific Outcome: Unable to determine improvement with flares Suprapubic ache resolved Anal pain worse with internal STM Perineal pain no noticeable change overall
Total number of PT visits: 23 over 9 months No other interventions from other providers Trends during PT sessions: Symptom free post-PT session for 4-5 hours R internal anal canal is worst spot (7 oclock supine) Internal and external STM described as burning Outcome: 70% improved painful and difficult bowel movements suprapubic discomfort (0-2/10) anal pain now pinching (0-5/10) Interrupted urine flow only after ejaculation 2-3 hour urination intervals normalized
PATIENT 3 OUTCOME
THESE PATIENTS ARE NOT ALONE CP/CPPS Relaxation / Physical Therapy Outcome Data
Total number of PT visits: 19 over 6 months Trends during PT sessions: Worry about hemorrhoids was abolished quickly Suprapubic symptoms improved quickly over 7 visits Tolerated each session well without flares Outcome: 95% improved No bowel movement issues No urine drops stuck Ejaculation usually fine 3 weeks ago in penis (3/10) Holding and rocking baby without pain Random, fleeting pressure in R ischial tuberosity
Anderson et al., 2005
A CENTRAL QUESTION IN CP/CPPS RESEARCH
TYPICAL CP/CPPS TIMECOURSE: SNAPSHOT OF MECHANISM?
Kutch et al., In Review
STAGING CP/CPPS PATIENTS You could be treating: A chronic end-organ disease
STAGING CP/CPPS PATIENTS You could be treating: An entrenched central pain syndrome
STAGING CP/CPPS PATIENTS You could be treating: A patient that is transitioning over time End-Organ Disease Central Pain Syndrome
HYPOTHESIS
1) It is important to estimate the stage of your patient.

Time (weeks to months)
2) Staging should use objective measures, not only patient report. 3) The patient stage can help determine treatment.
WHAT WOULD WE DO IF WE KNEW DISEASE STAGE?
GOAL: OBJECTIVELY STRATIFY PATIENTS PRIOR TO TREATMENT
End-Organ Disease
Central Pain Syndrome
MANUAL THERAPY
NEUROMUSCULAR REEDUCATION
THERAPEUTIC EXERCISE
PATIENT EDUCATION/ COUNSELING

BACKGROUND: FUNCTIONAL IMAGING IN CP/CPPS PATIENTS Suggested by Allsop et al. 2011. First studied by Farmer et al. 2011.
BACKGROUND: FUNCTIONAL IMAGING IN CP/CPPS PATIENTS
Main limitation of previous research: no comparison of functional imaging data to unaffected controls. Previous neuroscience research has identified the right anterior insula as a center of interoceptive awareness (i.e. evaluation of your internal body state) (Critchley et al., 2004). Right anterior insula activation could be due to the task, and would appear in participants even if they did not have chronic pelvic pain.
Farmer et al. 2011
Two findings: 1) Fluctuations in spontaneous pain (left) and 2) Correlated fluctuations in right anterior insula activity (right)
CP/CPPS PAIN FLUCTUATES, BUT NOT DURING A FMRI RUN (~ 10 MIN)
THE FMRI APPROACH TO CP/CPPS AT USC
fMRI scanner Pelvic floor physical therapist CP/CPPS patient or unaffected control participant (has keypad to continuously rate pain)
Farmer et al. 2011
CP/CPPS patients with large pain fluctuations are informative, but are not expected to be typical.
Feedback to therapist: instructions, and pain rating from participant
CONSIOUS PAIN DID NOT FLUCTUATE, BUT BRAIN ACTIVITY DID Right anterior insula exhibited spontaneous low-frequency activity fluctuations
ACTIVITY FLUCTUATIONS WERE SCATTERED ACROSS CORTEX, AND SPECIFIC TO CP/CPPS PATIENTS RATING PAIN
Patient 1
NETWORKS FOR PAIN DIFFERENT AMONG CP/CPPS PATIENTS
HYPOTHESIS: MERGING OF RESTING STATE AND PAIN RATING NETWORKS IN CP/CPPS PATIENTS (Part 1) Fransson 2005: Resting state in controls CP/CPPS Patient 1
HYPOTHESIS: MERGING OF RESTING STATE AND PAIN RATING NETWORKS IN CP/CPPS PATIENTS (Part 2)
ACTIVITY OSCILLATIONS FROM END-ORGAN DISEASE? Next step: model end-organ disease with painful palpation in controls Healthy Control Healthy brain Healthy pelvis Palpated by therapist To simulate healthy brain with end-organ disease Suggests CP/CPPS is end-organ or central pain disorder
End-organ if brain looks like patient in spontaneous pain
Hypothesis: In CP/CPPS patients, pain rating appears so natural that it can be done using resting state networks in the brain. For controls, thinking about pelvic discomfort is an explicit task. Related clinical question: Is encouraging a CP/CPPS patient to think about their pain (i.e. through a journal) a good thing, or does it reinforce the pathological merging of pain rating and resting state?
Central pain if brain does not look like patient in spontaneous pain
CONTROLS WITH ACUTE PAIN FROM PALPATION Z=-14 R Control 1 Brain activity of controls experiencing acute pelvic pain from palpation does not look like CP/CPPS patients experiencing spontaneous pain. Hypothesis: CP/CPPS in some patients is a central pain syndrome. Control 3 Z=10 Z=42
SUMMARY
1) The physical therapy toolbox is effective for some CP/CPPS patients, but not all. Could treatment help more patients if interventions were matched to objective staging? 2) fMRI is a promising approach for non-invasive objective staging of CP/CPPS patients. fMRI indicates that some CP/CPPS patients may be suffering from a central pain syndrome. 3) More studies of CP/CPPS patients and unaffected controls are needed to examine the utility of fMRI for screening. Please contact us if you would like to collaborate.
Control 2
INTERNATIONAL PELVIC PAIN SOCIETY
Making A Difference With Visceral Manipulation
Gail Wetzler, PT, EDO, BI-D Private Practice, Newport Beach, Calif. Physical Therapy Consultant, UCI, Center of Integrative
Medicine
Optimizing Treatment Of Organ-Related Pelvic Pain
Director of Curriculum and Research Coordinator for the Barral
Institute
Developer of Visceral Gynecological Curriculum for the APTA Currently in Doctorate program at Rosalind Franklin University,
Chicago
Objectives
1. Describe the basic premise and clinical reasoning for visceral
Goal of Conference
New information and
manipulation.
2. Explain the visceral concept of internal anatomical
relationships and how pelvic pain can be driven from these specific areas in the body.
3. Identify how organ specific fascial mobilization/manipulation
new treatment techniques for chronic pelvic pain

Perhaps these patients
can enhance our treatments for pelvic pain.

4. Introduce you to some of the studies related to these deeper
fascial-organ relationships.
may have a viscerogenic cause to their pelvic pain experience
Foundation of Visceral Manipulation is based

In the science and
Pioneering Therapist of Visceral Studies

Jean Pierre Barral, a
practice of manual therapy In the interaction between anatomy and physiology of the whole body In the philosophy that homeostasis is a constant balance
physical therapist and osteopath Curiosity Initial studies/LBP US before and after kidney mobility 23/25 increased ROM 21 maintained post 1m (Visceral Manipulation I text)
Basic Premise of VM
Hypothesis: An organ is good health has physiologic
Basic Premise of VM
Motion is influenced
motion Motion is influenced by: CNS gross movement is the consummation of numerous small movements ANS has a direct or indirect impact on the viscera Diaphragm- primary driver of visceral mobility Cardiac wave motion of blood (from the left ventricle) is propagated via the arterial bed to the most distant organ Peristaltic contractile waves of the hollow organs
by: Motility Inherent motion of the viscera themselves Sliding surfaces ie. peritoneum/serous fluid System of attachment mesenteric, omental, irregular c.t. and ligaments Turgor and intracavity pressure
Organ Motion
Mobility Motility
Understanding the deeper anatomy through dissection

Lung Disease Hospital
.dysfunctional biomechanics in living subjects...followed patterns of stress in the tissues of cadavers
Introduced him to how
the visceral system may have a potential to promote lines of tension within the body
Lines of tension within the body

He found that the fascial
Visceral Fascial Inter-relationships

Understanding
envelope layers of the organs had a functional relationship with the M/S system
It is best to follow the
anatomical continuity is important
tissues for they often may be better guides than our own reasoning JPB
Visceral Fascial Inter-relationships

Fascia regulates matrix
How pelvic pain can be driven from these anatomical relationships Parietal Peritoneum
tension in response to dynamic physiological processes
Peritoneal possibilities for pelvic pain
Endopelvic Fascia and Pelvic Organs
Dissection of female pelvic organs
Vascular considerations such as pelvic congestion syndrome or reflex vascular spasm
Neurologic considerations for ANS impairment, nerve entrapment, pudendal neuralgia
Development of Clinical Reasoning

Hypothesis Oriented:
Viscera in good health has physiologic motion Data Collection: _Trial techniques based on gathering of significant , differing or conflicting findings _Use of Fluoroscopy and US _Collaborated with manual therapy colleagues _Observations lead to contributing factors of precaution/contraindications
Development of Clinical Reasoning

Managing Interventions:
Purposed Mechanism
Clinical application as to how organ tissues can respond to
_Identified how a visceral restriction improved nonoptimal biomechanics in organs and their related connections _Observed how input and output pain mechanisms were affected by organ related treatments
(Butler,2000,Galea, 2002)
mechanical load (mechanotransduction)

The extracellular matrix senses physical forces and can convert
external mechanical signals into internal biochemical reactions (maintained by fibrocytes)

Fibrocytes can further transform into myofibroblasts with
contractile properties to be able to alter tissue tension

Cell-cell communication in which stimulus in one location leads
to a distant cell registering a new signal

Effector cell response mechanical loading stimulates protein
_ Observed how pain and disability have more than physical and sensory dimensions
(Merskey and Bogduk, 1994)
synthesis at the cell level, promoting tissue repair and remodeling (Fascial Research III, Chaitow, Findley, Schleip)
The Role of Fascia as a body wide communication system

New imaging methods
Peritoneal Adhesions
confirm the connectivity of organs and tissues

Bove and Chapelle, 2011
Better understanding how
cells respond to forces

Can local manual treatments
affect the fibrotic process early on in its development?
Hypothesis: An anatomically based visceral mobilization treatment could manually lyse and prevent surgically induced adhesions Design: Cecal and abdominal wall abrasion was used to induce adhesions in 3 groups of 10 rats. Results: Adhesion severity and number of adhesions were significantly lower in the preventive group. Conclusions: VM may have a role in the prevention and treatment of post-operative adhesions
The importance of fascia in the context of a sensory organ

Fascia research has
What we began to notice.

Motion of internal organs
discovered its important proprioceptive and nociceptive functions which have implications for (pelvic) pain and dysfunction.
Findley, Schleip, Chaitow, Huijing April 2012
Staubesand (1997) and
Schleip (2003) found mylinated and unmylinated fibers of autonomic origin in fascia
seemed to send a pattern of stimulus to the CNS and used it for communication with other systems (2006 study) As changes began to occur more interactions occurred in the overall well being of the person In chronic pain patterns, look for a shift in words, movement or function further away from the where pain may be (dysfunctional patterns of adaptation)
Autonomic, Hypothalamic, Limbic and Pituitary Influences

Lack of organ mobility or
Neurobiology of Emotions
Emotional systems utilize
motility seemed to influence the function of neuronal pathways.

Thermoregulation Hormone Secretion Blood Pressure Appetite and Hunger Immunomodulation ANS Communication Emotions
somatic and visceral information for appraisals of events to facilitate the regulation of internal balance.
Neuropeptides are abundant
along the gustatory-visceral axis ( Brain and Cognition, Swanson, Schulkin, Thompson and Rosen, Elsevier, 2002)
ThusThe purpose of organ related treatment

To facilitate proprioceptive
Treatment techniques.
Law of precision and least
communication for internal mechanisms toward better health

To enhance O/N/V/M/S
force
Rhythm and amplitude Each organ moves in
particular directions along a particular axis

Evaluation process to find
mobility via the fascial connections

To influence the general
primary dysfunction (driver)

Restrictions (adhesions,
metabolism (regain motility)

Assist tissue repair (pain,
inflammation) and adaptation processes (position, ROM)
fixations, ptosis or viscerospasm) need to be localized Specific, gentle forces provides a stimulus to which the body responds
Specificity of Organ Related Pelvic Pain Sphincter functions - requires
Indications for Pelvic Organ Specific Fascial Mobilization

Pelvic organs first interpret disorder as pressure
good organ mechanics

Respond to hormonal
influences - more then the other organs Pelvic organs - move with breathing also Biomechanics of these organs - influence biomechanics of the pelvis Most stressed tissues - m/s dysfunction, intestinal problems, emotional holding, forces of gravity, pregnancy, delivery, menses, # of surgeries and easier access to infection
If the pressure is not resolved, then symptoms may occur.. Intermittent pain, pelvic floor spasm, constipation,urinary frequency If it continues changes in organ tissue viscosity and loss of elasticity begin to occur This contributes to inflammation (irritated tissues) Cystitis, IBS, dysmenorrhea, prostatitis, ovarian cysts Fibrositynerve entrapments,vasocontrictions, intertubal adhesions and chronic pain Laxietyprolapse, incontinence or celes
Examples.
Endometriosis uterus/tube pressure system dysfunction,fluid
Examples.
Cystitis/Prostatitis/Ovarian Cysts/Dysmenorrhea decrease
flow pattern, mechanics of tubes, uteral position and restore the homeostasis of endometrial tissues (motility). Versions of uterus, ptosis, prolapse induced pain cervix should be the most stable part of the uteral anatomy. Menses, pregnancy, menopausal, hormonal challenge its position. Increase precision in fascial releases of associated organs and specific to the broad, round and uterosacral ligaments. Reflex vascular spasm with deviations in endopelvic fascia. Release hypogastric, pelvic, sacral plexuses and pudendal nerve from potential fascial compression. Celes prevention with intracavity pressure balance, release restrictions and chain of fascial links to help restore connective tissue integrity. (History of difficult deliveries, suction/forceps encourage ptosis of kidneys) Nerve pain related to the 5 nerves posterior to the kidneys.
local inflammatory responses, increase circulatory flow and motility, motility, motility. (Cell forces in tissues, Curtis, 2005)
Dyspareunia/Vestibulodynia chronic pelviperineal pain is
significantly reduced when PFM show a decrease in resting tone and improved mobility. VM helps when muscular sources of pain do not resolve due to internal fascial patterns, vascular congestion, deeper nerve entrapments and the co-existing driver of hip muscle tension via bladder/acetabular ligament relations Irritable Bowel Syndrome Pelvic organs are connected functionally through shared common nerve pathways with the bowels. IBS is also associated with sleep deprivation and depression which is associated with lower levels of serotonin. According to Michael Gershon, chair of cell biology at Columbia Univ., the gut functions as our second brain the enteric nervous system.. Manufactures more than 30 neurotransmitters, including serotonin
Patient Examples and Goals
Clinical Expertise
Books
14 books relating to the visceral system 2 on the nervous system 2 on the vascular/lymphatic system 1 on general diagnosis for the manual therapist
2006 Pilot Study

Dr. Daniel Amen
Patient with C/O of anxiety and stomach pain
Neuroscientist, psychiatrist, expert on brain/behavior, who pioneered the use of brain imaging Purpose to prove or disprove organ related treatment may have an effect on the brain In other words, do the brain and viscera communicate 8 people SPECT Scan look directly at cerebral blood flow and brain activity (metabolism)
Patient with C/O of chronic pelvic pain
Outcomes of 2006 pilot study

Day 1 Spect Scan pre-evaluation of brain Day 2 Visceral treatment Post scan done within 30 minutes of treatment Meanwhile we compiled our data and made predictions Tests and measures read by Dr. Amen Outcomes: All 8 had cerebellar symmetry changes
(Indicating an increase in proprioceptive communication) 6/8 Better balance in overall surface scan (Calming of overactive area, metabolic changes) Conclusion: Visceral Manipulation may have some effect on proprioceptive and overactive areas in the brain. Further studies are needed to look at functional scans so that the mechanism of change can be better understood.
May 2012 Kidney/Brain Study

J of Neuroscience Univ. of Pittsburgh Cerebral cortex contain
Chronic Pelvic Pain

36 women with chronic
output neurons that indirectly influence kidney function Area 1 adds precision and organ-specific regulation to descending visceromotor commands Area 2 adds anticipatory processing essential for allostatic regulation (higher brain centers generate autonomic activity)
pelvic pain, S/I joint dysf, tenderness, pelvic torsion and loss of motor control Pain perception via VAS Comparison of VM vs Joint Manipulation Post 1 mo. VM group able to maintain a greater reduction in pain intensity (32%), S/I dysf (11%) and greater correction of torsion (22%) Primary organ/ ligament was the uterosacral (surrounding plexuses) Primary means of pelvic stability is the position of the sacrum
Urodynamic changes in patients with painful voiding dysfunction

Karen Brandon, DScPT,
Collaboration and advancing care.. together

Curiosity and
WCS
Dept of Ob/Gyn, Kaiser
Dedication
Sharing knowledge Techniques based on
Hospital Urodynamic changes in a painful voiding dysfunction patient

years of clinical experience
Qmax 22.2 (pre) 30.3(post) Qave 7.9 (pre) 15.9(post)
After viscero-fascial
techniques, patient reported improvement by single void, reduced time on the toilet and no strain or pain
Interest and Growth of Visceral Techniques
Interest and Growth of Visceral Techniques
Next Step for Organ Related Pain and Dysfunction

Further Collaboration More precise and
Who will benefit.

Patient Medication resistant cases
objective measures RTUS, HRV, fMRI Expand our knowledge of effective integrative strategies
Non-surgical candidates Poly traumas, deeper scar tissue formation Patients with complex interactions between multiple body systems (gastroenterological, urological etc) Therapist.. Increased knowledge Better screening and palpation skills Increased potential for objective findings Increased strategy for treatment MD Another opportunity to help your patients Help with differential diagnosing in regards to organ or fascial contribution to pelvic pain
A final thought.
Pelvic Pain Can it be driven by
Thank You for the opportunity to share new ideas and perhaps make a difference in someones life!
organs and related deeper fascia? Can the complexity be associated with tissues further away from the pelvis?. Ignore or Explore?
References
Amen, Daniel G. MD, Change Your Brain Change Your Life,
References
Lederman, Eyal, The Science and Practice of Manual Therapy,
Three Rivers Press, 1998.

Barral, Jean-Pierre, Mercier, Pierre, Visceral Manipulation,
Elsevier, 2005
Lee, Diane, Lee, Linda-Joy, The Pelvic Girdle, Elsevier, 2011 Mullin, Gerard E., Integrative Gastroenterology, Oxford
Eastland Press, Incorporated, 1988 Barral, Jean-Pierre, Pierre, Urogenital Manipulation, Eastland Press, Incorporated, 1993 Cavallaro-Goodman, Catherine, Snyder-Kelly, Teresa E, Differential Diagnosis for Physical Therapists, Saunders, 2013 Finet, Georges, DO, Williame, Christian, DO, Treating Visceral Dysfunction, Stillness Pres, LLC, 2000 Greenman, Philip E., Principles of Manual Medicine, Williams & Wilkins, 1996
University Press Inc., 2011

Stecco, Luigi, Stecco, Carla, Fascial Manipulation, Piccin Nuova
Libraria S.p.A, Padova, 2009

Stone, Caroline, Visceral and Obstetric Osteopathy, Churchill
Livingstone, Elsevier, 2007
References
Bove, J, Chapelle, S, Visceral Mobilization can lyse and
References
Hartman, D, Chronic vulvar pain from a physical therapy
prevent peritoneal adhesions in a rat modelJ Bodywork and Movement Therapies (JBWMT), Feb 2011 Curtis, A, Cell Forces in Tissues, Medical Engineering Physics, Elsevier, April, 2005 Dusi,J, France, D, George, S, Phelps, A, Somers, D, Assessing Physical Therapy Outcomes for Women with Urinary Incontinence, JWH, Aug 2012 Findley, T, Chaitow, L, Schleip, R, Introduction to Fascial Research, Fascial Research III, Kiener, Munich 2012 Grimaldi, M, Painful Perineum in all its forms. Contribution of manual medicine and osteopathy. Clinical Study, J Gynecol Obstet Biol Reprod (Paris) Sept, 2008
perspective, Dermatol Ther, Wiley Periodicals, Inc, Sept 2010
Hurley, D, Your backup brain, Psychology Today, Nov 2011 Levinthal DJ, Strick, PL, The motor cortex communicaates with
the kidney, J Neurosci, May 2012
Neville,C, Fitzgerald, C, Mallinson, T, Badillo, S, Hynes, C,
Tu, F, A preliminary report of musculoskeletal dysfunction in female chronic pelvic pain: A blinded study of examination findings, (JBWMT), Jan 2012 Simmonds, N, Miller, P, Gemmell, H, A theoretical framework for the role of fascia in manual therapy, JBWMT, Aug 2010 Tettambel, M, Using integrative therapies to treat women with chronic pelvic pain, J Am Osteopath Assoc, Nov 2007
References
Tozzi, P, Bongiorno, D, Vitturini, C, Low back pain and kidney
mobility, Fascia Research III, Mar, 2012

Wetzler, G, Barral, JP, The impact of the uterus on pain and
function of the female pelvic girdle, Surg Radiol Anat, Scientific Congress, June 2011
OPIOIDS: PART OF A POLYMOIDAL PAIN TREATMENT: WHICH PATIENT, WHICH DRUG AND WHY?, AND THE USE OF PATIENT MONITORING
Robert L. Barkin, PharmD, MBA, FCP, DAAPM, DACFE, DACFM Clinical Pharmacologist at the Pain Centers of Skokie & Evanston Hospitals of North Shore & University Health System Department of Anesthesiology Professor Rush University Medical College Faculty of: Anesthesiology, Family Medicine, Pharmacology
THE COMPLETE ARTICLE ENTITLED PHARMACOLOGY OF OPIOIDS IN THE

TREATMENT OF CHRONIC PAIN SYNDROMES CAN BE VIEWED AT THE WEBSITE BELOW
http://www.painphysicianjournal.com/2011/july/2 011;14;E343-E360.pdf
Hysterectomy for Chronic Pelvic Pain
Joseph M. Maurice, MD, FACOG Director, Division of Gynecology Director, Minimally Invasive Gynecologic Surgery Associate Residency Program Director Associate Medical Student Clerkship Director Assistant Professor Department of Obstetrics and Gynecology Rush University Medical Center
Disclosures
Intuitive Surgical Ethicon Karl Storz Covidien
Objectives
Review the definition of chronic pain, and how its applied to chronic pelvic pain Review diagnostic modalities used by Gynecologists to address chronic pelvic pain Discuss appropriateness of hysterectomy for chronic pelvic pain
What is Chronic Pain?

Pain that has persisted beyond the normal tissue healing time
Usually more than 3 months
Hardt J, Jacobsen C, Goldberg J, Nickel R, Buchwald D. Prevalence of chronic pain in a representative sample in the United States. Pain Med. 2008;9(7):803.
Chronic Pain
Variations of this definition may encompass the types of pain:
Nociceptive pain: perception on nociceptive input (e.g., nerve fiber sensitive to a noxious stimulus)
Visceral: arises from viscera mediated by stretch receptors
Poorly localized (e.g., appendicitis cholecystitis)
Nociceptive Pain:
Musculoskeletal (e.g., hamstring strain) Inflammatory (e.g., arthropathies) Mechanical/compressive (e.g., low back or neck pain)
Somatic: arises from injury to body tissues

Well localized (e.g., postoperative pain)
Neuropathic Pain
Neuropathic Pain
Abnormal neural activity secondary to disease, injury or dysfunction of the nervous system Persists without ongoing disease
Neuropathic Pain
Categories:
Sympathetically mediated pain: arising from a peripheral nerve lesion and associated with autonomic changes (complex regional pain syndrome) Peripheral neuropathic pain: damage to a peripheral nerve without autonomic change (post-herpetic neuralgia) Central pain: pain from abnormal central nervous system activity (phantom limb pain) Mononeuropathy: only one nerve is affected
What about Chronic Pelvic Pain?
Chronic Pelvic Pain
The prevalence of chronic pelvic pain (CPP) in women is 3.8%.
Zondervan KT, Yudlin PL, Vessey MP, Dawes MG, Barlow DH, Kennedy SH. Prevalence and incidence in primary care of chronic pelvic pain in women: Evidence from a national general practice database. Br J Obstet Gynaecol 1999;106:1149-55.
Chronic Pelvic Pain
Definition?
Estimating its prevalence is problematic due to the difficulty in standardizing a definition for CPP.
Some studies, though estimate the prevalence to be much greater.
Mathias SD, Kuppermann M, Liberman RF, Lipschutz RC, Steege JF. Chronic pelvic pain: prevalence, healthrelated quality of life, and economic correlates. Obstet Gynecol 1996;87:321 7.
Chronic Pelvic Pain
No definitive definition of CPP exists, and current descriptions are unwieldy.
ACOG Practice Bulletin No. 51 Chronic Pelvic Pain. Obstet Gynecol 2004;103:589-605.
Chronic Pelvic Pain

The American College of Obstetricians and Gynecologists proposes the definition CPP as:
non cyclic pain of 6 or more months duration that localizes to the:
anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back or buttocks
Chronic Pelvic Pain
Diagnosis
is of sufficient severity to cause functional disability or lead to medical care requiring treatment.
ACOG Practice Bulletin No. 51 Chronic Pelvic Pain. Obstet Gynecol 2004;103:589-605.
Chronic Pelvic Pain

When evaluating a patient for CPP, two basic aspects are important to consider:
Duration Location of the pain.
Chronic Pelvic Pain

Objective analysis of a patients symptoms helps focus the practitioners attention on specific causes. Administering standardized patient questionnaires allows a thorough evaluation of the pain symptoms.
The International Pelvic Pain Society: Pelvic pain assessment form. April 2008
Willliams RE, Hartmann KE, Steege JF. Documenting the current Definitions of Chronic Pelvic Pain: Implications for Research. Obstet Gynecol 2004;103:686-691.
Visual Analog Scale
Visual Analog Scale

Use of visual analog scale is also helpful to objectively describe pain, but
The scale is limited, as it does not address severity and timing of the symptoms.
Chronic Pelvic Pain

Any clinical assessment should embrace the multifactorial nature of the condition and include evaluations:
Gastrointestinal Urologic Musculoskeletal Neurologic Psychiatric causes
Multiple diagnoses can cause CPP

Further complicating the diagnostic investigation is the fact that CPP may encompass more than one disorder:
Endometriosis Painful bladder syndrome.
Physical examination is important
Dont for get the Physical Therapists!!!

Consultation with pelvic physical therapists may help focus the diagnosis, as physician physical examinations of the pelvic floor are often cursory.
Laboratory analysis is limited in its usefulness
Chronic Pelvic Pain
Radiologic studies may be helpful to elucidate abnormalities in pelvic organs.
Treatment
Chronic Pelvic Pain

The diagnosis of CPP is unwieldy, and therefore
Chronic Pelvic Pain
Gynecologic Causes the effectiveness of treatment varied and subject to failure
Chronic Pelvic Pain

Commonly sited gynecologic causes of CPP:
endometriosis leiomyoma adenomyosis pelvic congestion syndrome adhesions
Chronic Pelvic Pain
When to go to the Operating Room?
Chronic Pelvic Pain

A multidisciplinary approach including:
cognitive behavioral therapy, physical therapy and analgesic therapy
May be equally or more effective for the treatment of CPP than surgical treatment such as hysterectomy
Lamvu G. Role of hysterectomy in the treatment of chronic pelvic pain. Obstet Gynecol 2011;117:1175-8.
Chronic Pelvic Pain
When is it appropriate to perform a hysterectomy for CPP?
Chronic Pelvic Pain
Chronic Pelvic Pain

The greatest success at treating patients with CPP with hysterectomy is:
the presence or of a gynecologic cause.
Laparoscopy is an important diagnostic tool prior to hysterectomy:

gynecologic v. non-gynecologic cause.
Chronic Pelvic Pain

Hysterectomy for disease confined to the uterus can lead to symptom improvement in over three-quarters of patients.
Stovall TG, Ling FW, Crawford. Hysterectomy for chronic pelvic pain of presumed uterine etiology. Obstet Gynecol 1990;75(4):676-9
Chronic Pelvic Pain

What about endometriosis?
Endometriosis
When considering a diagnosis of endometriosis:
biopsy proven disease is critical.
Chronic Pelvic Pain
Chronic Pelvic Pain

The question of the usefulness of oophorectomy at the time of hysterectomy further complicates the therapeutic decision making process. Caution is warranted.
Oophorectomy?
Chronic Pelvic Pain

The potential benefits of pain relief may not outweigh the resultant harms of an early oophorectomy at the time of hysterectomy for CPP
Chronic Pelvic Pain
Oophorectomy for Endometriosis
Lamvu G. Role of hysterectomy in the treatment of chronic pelvic pain. Obstet Gynecol 2011;117:1175-8
Oophorectomy for Endometriosis

Removal of normal ovaries at definitive surgery for endometriosis-associated pain should be decided on a case by case basis with full discussion of risks Recommend a conservative approach with normal ovaries, but excision of all visible disease should be undertaken at the time of hysterectomy
Falcone T, Lebovic D. Clinical Management of Endometriosis. . Obstet Gynecol 2011; 118(3):691-705
Pelvic Congestion Syndrome

Bilateral oophorectomy combined with hysterectomy is an effective treatment for intractable pelvic pain associated with pelvic venous congestion which has failed to respond to medical treatment.
Oophorectomy for Pelvic Congestion Syndrome
Beard RW, Kennedy RG, Gangar KF, Stones, RW, RogersV, Reginald, PW, Anderson M. Bilateral oophorectomy and hysterectomy in the treatment of intractable pelvic pain associated with pelvic congestion. BJOG 1991;98:988-92
Non-gynecologic causes of CPP

Non-gynecologic causes of chronic pelvic pain
are less likely to be ameliorated by hysterectomy than those performed for a gynecologic cause
Sixty premenopausal women Median age: 29 Laparoscopy: normal findings
Baker PN, Symonds EM. The resolution of chronic pelvic pain after normal laparoscopy findings. Am J Obstet Gynecol 1992;166:835-6
All 60 patients attended 6-week follow-up:
All patients were assured postoperatively that no gynecologic abnormalities had been noted Asked to follow-up in 6 weeks and 6 months
22% pain free 40% pain had diminished 38% pain was unchanged or worse
57 patients attended the 6-month follow-up:

58% pain free 39% pain had diminished 4% pain was unchanged or worse
Non-gynecologic causes of CPP

Interestingly, for those patients a nongynecologic cause of CPP, laparoscopy itself, can help with the symptoms of CPP in patients with no identifiable etiology.
Conclusion
Conclusion
Hysterectomy is more effective at treating CPP when an identifiable gynecologic etiology exists
Conclusion
Diagnostic laparoscopy prior to consideration of hysterectomy is an important step in the patient work-up in patients without an identifiable cause.
Conclusion
Patients without an identifiable gynecologic etiology at laparoscopy or with other diagnostic tools are less likely to benefit from hysterectomy
Conclusion
Coordination of care with a multidisciplinary approach, especially with the diagnostic and therapeutic regimens of pelvic physical therapists is warranted prior to any surgical intervention.
Question
Chronic pelvic pain secondary to pelvic congestion syndrome is a controversial topic. Prior to performing a hysterectomy and oophorectomy for this condition, what therapies should be considered? 1. Attempt at medical management 2. A thorough evaluation and treatment by a pelvic physical therapist 3. After selective ligation of congested pelvic vessels 4. All of the above
Thank you
Consultant
Medtronic EM Kinetics Uroplasty AMS Taris Biomedical
Kenneth M. Peters, MD
Professor and Chairman of Urology Oakland University William Beaumont School of Medicine Royal Oak, Michigan
Review the literature regarding neuromodulation for pelvic pain Discuss the challenges associated with evaluating and managing pelvic pain Thinking outside the bladder and implementing a multimodal approach to treating pelvic pain
Utilizes mild electrical pulses to the nerves associated with voiding function. Over 100,000 implants have been performed worldwide.
Placement of a sacral electrode was initially a complex surgery requiring large incisions and hospitalization Advances in technology have made this a minimally-invasive procedure
Peters KM. Atlas Urol Clin. 2004;12:275-291.
Skin nick to place electrode Percutaneous extension lead 1 cm buttock incision to connect percutaneous extension lead
Peters KM. Atlas Urol Clin. 2004;12:275-291.
Fowlers syndrome (retention, decreased sensation)
Normal
fill bladder
Deactivations present with an empty bladder and no SNM With full bladder or after SNM
more activation less deactivation
SNM
More nearly normal

Courtesy of Clare Fowler, MD
Dasgupta R, Critchley HD, et al. J. Urol, 2005. 174, 2268
Courtesy of Clare Fowler, MD
Dasgupta R, Critchley HD, et al. J. Urol, 2005. 174, 2268
SNM for Intractable Pelvic Pain

Maher, et al 15 women
73% improved pain, freq, nocturia, urgency 87% with at least 50% decrease in pain 47% with 50% decrease in frequency Improved QOL general , social health, bodily pain
Maher CF, Carey MP, Dwyer PL, Schluter PL (2001) Percutaneous sacral nerve root neuromodulation for intractable interstitial cystitis. J Urol 165:884886

Bajewski and Al-Zahrani
78 patients , single center, all with glomerulations/ulcers 46 patients (59%) went onto IPG implantation Long term success 72% (GRA improved 80%), avg f/u 62 mos Explantation rate of 28%
Poor outcome, pain
Revision rate of 53%

Pain, loss of efficacy, battery depletion
Bajewski JB, Al-Zahrani AA. BJUI 2010; 107:1258-6
Rackley, Vasavada
82% yield from stage I to stage II 13/20 (65%) who kept device maintained efficacy 13/27 (48%) tested had long term success
Rackley R, Vasavada S, Daneshagani F, Murphy D, Hijaz A, Vaze A (2005). Neuromodulation for interstitial cystitis. Urology/AUAAbstracts
Chai, et al
APF and EGFs are elevated in urine of pts with IC/PBS Levels normalized after SNS trial
Chai TC, Zhang C, Warren JW, Keay S (2000) Percutaneous sacral third nerve root neurostimulation improves symptoms and normalizes urinary HB-EGF levels and antiproliferative activity in patients with interstitial cysitits. Urology 55:643 Int Urogynecol J (2010) 21:15531558 1557

Powell and Kreder
32 women, 7 men with IC/PBS 22/39 went onto IPG implantation 19/22 long term success, avg f/u 60 mos 50% re-operation rate
Loss of efficacy, battery depletion, foot movement, device malfunction
Powell CR, Kreder KJ: J Urol 2010; 183:173-176.

SNS has been shown to lessen intractable pelvic pain in IC/PBS patients
Re-establish PF muscle awareness, decreases pelvic floor hypertonus
Fariello JY, Whitmore K (2010) Sacral neuromodulation stimulation for IC/PBS, chronic pelvic pain, and sexual dysfunction. Int Urogynecol J . 21:1553-1558
Peters, et al
21 patients, failed 6 previous treatments 36% decrease in narcotic use 95% with moderate/marked improvement in pain 25% narcotic free
Peters KM, Konstandt D (2004) Sacral neuromodulation decreases narcotic requirements in refractory interstitial cystitis. BJU Int 93:777779
SNS for men with CPPS

voiding dysfunction and prostatitis pain in 3/3 men
Hellstrom WJ, Schmidt RA, Lue TF, Tanagho EA (1987) Neuromuscular dysfunction in non-bacterial prostatitis. Urology 30:183188
Seigel, et al: multicenter trial of 10 pts

SNS decreased pain from 9.7 to 4.4 on VAS Improved QOL at 19 months f/u
Siegel S, Paszkiewicz E, Kirkpatrick C, Hinkel B, Oleson K (2001) Sacral nerve stimulation in patients with intractable pelvic pain. J Urol 166:17421745

Comiter
17 patients, 14 months follow-up Statistically significant improvement in freq, voided volume, average pain (5.8 to 1.6 on VAS) 87% of Stage IIs sustained improvement
Continue other multi-modal therapy
Comiter CV (2003) Sacral neuromodulation for the symptomatic treatment of refractory interstitial cystitis: a prospective study. J Urol 169(4):13691373
Pudendal Neuromodulation
Pudendal nerve: peripheral nerve composed mainly of afferent sensory fibers from S1-S3.
S2 - 61%, S3 - 36%
Huang JC, Neurosurgery 41: 411-15, 1997.
Major contributor to bladder afferent regulation

Therefore attractive neuromodulation target
Pudendal nerve entrapment

Voiding dysfunction, OAB
Beco J, BMC Surg 4:15, 2004 Popency C, Neurourol Urodyn 25:820-7, 2007.
Martellucci et al
27 patients, 37 month follow-up; mean pain duration 51 months VAS 8.1 to 2.3
Martellucci et al. Sacral Nerve Modulation in the treatment of chronic pelvic pain. Int J Colorectal Dis. 2012 Jul;27(7):921-6
Pudendal nerve stim vs Sacral nerve stim

Pudendal nerve preferred by patients More efficacious Salvages sacral failures
Peters KM, BJU Int 100: 835-9, 2007.
Stimulation of the 3rd sacral nerve has been shown to be effective in treating voiding dysfunction The pudendal nerve is a distal branch of S2, S3, and S4 The potential benefit of pudendal nerve stimulation is increased afferent stimulation through the sacral nerve roots
Subjects with urgency, frequency, or urge incontinence were tested Baseline CMG 15 minute pudendal stimulation Repeat CMG
Peters KM et al. Neurourol Urodyn. 2005;24:643-647.
FSF increased 98% p <0.001 pre-stim 102cc (range 21-191) post-stim 202cc (range 93-384) N=22 MCC increased 66% p <0.001 pre-stim 203cc (range 76-358) post-stim 336cc (range 127-552)
30 subjects with voiding dysfunction refractory to multiple therapies 48 years (26-70) Pudendal or sacral nerve stimulation in a blindedrandomized fashion, each for 7 days Successful placement of sacral and pudendal leads in all subjects Time to lead placement
Sacral: 25.9 min Pudendal: 23.7 min
(P=0.57)
Peters KM et al. Neurourol Urodyn. 2005:24:643-647.
24/30 (80%) responded and had a permanent generator placed

19/24 (79.2%) pudendal implant 5/24 (20.8%) sacral implant 6 explants due to poor response to either lead
Overall improvement
Sacral 44%
Pudendal 59%
p-value 0.05
The order in which the leads were stimulated had no impact on the final lead implanted, confirming appropriateness of the crossover design
On a 7-point scale: Markedly-worse, Moderately-worse, Mildly-worse, Same, Mildly-improved, Moderatelyimproved, Markedly-improved Pudendal > Sacral
Pelvic pain (p=0.0024) Urgency (p=0.005) Frequency (p=0.007) Bowel function (p=0.049)
22 subjects
Baseline
Voids/24 hr Mean voided Volume (cc) Smallest voided Volume (cc)
Sacral
Pudendal
p-value
Retrospective chart review from November 2003 to June 2008 of patients with pudendal electrode
24.1 81.8 24.8
13.9 152.8 42.8
12.8 158.0 60.9
0.001 0.001 0.012

Peters KM, et al. Neurourol Urodyn. 2010 Sep;29(7):1267-71
67 patients had a pudendal lead placed 80.6% female, 19.4% male Mean age: 54.5 years Primary diagnosis Interstitial cystitis/PBS: 26 patients Urgency/Frequency or urge incont: 29 patients Urinary Retention: 9 patients Pelvic pain: 2 patients Tethered sacral cord: 1 patient Pudendal neuropathy 3 patients Mean follow-up 32.3 months
Peters KM, et al. Neurourol Urodyn. 2010 Sep;29(7):1267-71
P<.001
90% of patients who failed SNS Responded to PNS
P<.002
P<.002
P<.001
ns
Percutaneous Tibial Nerve Stimulation

Peripheral mixed sensory-motor nerve
Originates from spinal roots L4-S3 Contributes directly to sensory and motor control of bladder and PF
Alternative to sacral Stimulates S2, S3, and S4 More desired than sacral Salvages >90% of sacral failures No multicenter pivotal trial
? Depolarization of somatic sacral and lumbar afferents

Provides central inhibition of preganglionic bladder motor neurons through direct route in the sacral cord
Amarenco G, J Urol 169:2210, 2003
A needle electrode inserted near the medial malleolus to stimulate the tibial nerve.
PTNS in patients with IC/PBS

Zhao J, et al: (2008) Posterior tibial nerve stimulation twice a week in patients with interstitial cystitis. Urology 71:1080-4
18 females, avg 60 yrs old Prospective, open study

30 minutes PTNS, 2x per week, 5 weeks Statistically significant improvements in:
ICPI, ICSI, SF-36 health status transition
Percutaneous Posterior Tibial Nerve Stimulation in Patients with Chronic Pelvic Pain: A Preliminary StudySoo Woong Kima, Jae-Seung Paicka, Ja Hyeon Kub Urologia Internationalis 2007;78:58-62 Methods: 15 patients (10 women and 5 men, mean age 60.0 years, range 41-78) with CPP were enrolled in prospective clinical trial. 12 weekly outpatient treatment sessions, each lasting 30 min. Results: After 12 weeks of PTNS, 9 (60%) and 3 patients (30%) had an improvement of >50% and 25-50% in the VAS score for pain, respectively. Mean VAS for pain changed from 8.1at baseline to 4.1 after 12 weeks of treatment (p < 0.01) Mean VAS for urgency changed from 4.5 at baseline to 2.7 after 12 weeks of treatment (p < 0.05). There was no statistically significant difference in the number of voids and bladder volumes
No change in:
pain, freq, voided vol, nocturia, SF-36 physical/mental health
8/18 some effect 0/18 significant effect
Effects of percutaneous tibial nerve stimulation therapy on chronic pelvic pain. Gokyildiz S, Kizilkaya Beji N, Yalcin O, Istek A., Gynecol Obstet Invest. 2012;73(2):99-105 Methods: 12 patients in active treatment and 12 in control group 12 weekly outpatient treatment sessions, each lasting 30 min. Controls standard therapy Results: Pain intensity and interval decreased significantly in PTNS group Improved dyspareunia Improved quality of life
Efficacy of posterior tibial nerve stimulation in category IIIB chronic prostatitis/chronic pelvic pain: a Sham-Controlled Comparative Study Kabay S, Kabay SC, Yucel M, Ozden H., Urol Int. 2009;83(1):338 Methods: 89 patients, 45 PTNS and 44 Sham 12 weekly outpatient treatment sessions active vs sham Results: NIH-CPPSI, VAS pain scores and urgency improved in the active treatment group No changes were seen in the Sham treated group
Multiple studies suggest that neuromodulation can improve the symptoms of chronic pelvic pain There is a need for well-designed, prospective, sham-controlled trials of neuromodulation techniques to manage the symptoms of IC and chronic pelvic pain
1 out of 9 women in the U.S has CPP
More than 1,000,000 of these women have been told they have IC
1943
Ulcerative IC is defined as symptoms of urinary frequency and/or urgency and pelvic pain with documentation of an ulcerative lesion in the bladder on cystoscopic evaluation. (only in 5-10% of the IC cases) 1. Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology of lower urinary tract
function report from the Standardisation Sub-Committee of the International Continence Society, Am J ObstetGynecol 2002; 187:116126.
1970
Non ulcerative IC/PBS as defined by the International Continence Society (ICS) is the complaint of suprapubic pain related to bladder filling accompanied by other symptoms, such as increased daytime and nighttime frequency in the absence of proven urinary infection or other obvious pathology.
Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology of lower urinary tract function report from the Standardisation Sub-Committee of the International Continence Society, Am J ObstetGynecol 2002; 187:116126.
syndrome (sndrm) n. 1. A group of symptoms that collectively indicate or characterize a disease, psychological disorder, or other abnormal condition.
by Melynn and from www.art4ic.com.-reproduced with permission
Became clear that IC may not be a disease of the bladder Rather the bladder is an innocent bystander is a larger pelvic/systemic process 20 years of clinical trials sponsored by industry and the NIH has shown no response over placebo when therapy is directed toward the bladder in IC/BPS To improve symptoms of IC you must be an astute clinician and think outside the bladder
Approximately 70%-90% of patients with IC have pelvic floor dysfunction1 Levatorani muscle myalgia can be a source of chronic pelvic pain.
1. Peters et al. Urology. 2007 Jul;70(1):16-8
Shortened PFD/Trigger points Weak Pelvic Floor Muscles
More Frequency, Urgency, Pain
Increased PFD needed to suppress Urgency/Frequency
Slow relaxation Hesitant Painful Voiding

Source: UPPCRN PT Protocol V 1.0 Sept 2006
Office Evaluation of Abuse: (n=87)
1 out of 6 women were either sexually or 4 physically abused during their childhood. Beaumonts mailed survey study (2005) found that 36.9% of women with IC reported being abused vs. 22.4% of the controls. This was a significant difference (p=0.001).
4
55% of these women had been abused physically, sexually or emotionally. Mean number of years from onset of abuse to IC diagnosis = 24.4 years. Abuse is more common in women with IC who have levator pain than those without levator pain (55% vs 36.9%). The pelvic floor may be a significant source of pain in women with IC.
The Commonwealth Fund Survey-1998
The bladder may be an innocent bystander in a bigger process The pelvic floor is crucial in normal voiding and bowel function Pelvic floor dysfunction may be the cause of many of the symptoms of the IC syndrome Triggers for development of PFD may exist
Randomized Multicenter Pilot Trial Shows Benefit of Manual Physical Therapies in the Treatment of Chronic Pelvic Pain
MP FitzGerald,1 RU Anderson,2 CK Payne,2 JPotts,3 KM Peters,4 JQ Clemens, 5 L Cen6 ,S Chuai6, JR Landis6
J Urol. 2009 Aug;182(2):570-80. Epub 2009 Jun 17.
GTM
Number Randomized 24 5 (21%)
MPT
23 13 (57%)
Total
47 18 (38%)
Total (p=0.03)
Responders
Should be performed by a physical therapist specially trained in pelvic floor dysfunction related to these symptoms. Involves internal and external therapy Biofeedback
Similar findings in f/u study of 81 women: 59% PT vs 26% massage Very successful in improving symptoms pelvic pain, dyspareunia, urgency, frequency
J Urol. 2009 Aug;182(2):570-80. Epub 2009 Jun 17.
Urologists Physical Therapists
NP/PA/Nurses Psychologists
Nutritionists
Patient
Integrative Med Gynecologists/ Primary Care Pain Clinics
Rheumatologists
Evaluate whole patient Identify pain triggers Prioritize problems Engage your colleagues Be open minded Mind-body connection Provide encouragement Provide support
Guided Imagery Cognitive behavioral therapy Stress Reduction Increase water intake (dilute the urine) Dietary modifications Yoga/meditation
Intravaginal Valium
Crystal Wand for Trigger Points Injection of Marcaine and Kenalog into Trigger Points Vaginal Dilators
Emu Oil for Vulvodynia
So, exactly what is IC? PBS? BPS?

Guided Imagery Reiki Therapy
Accupuncture
68 years later.. We still dont know!!

What if the reason that 20 years of bladder directed therapy has not found an effective treatment is that the bladder is not the problem in most patients (ulcers excluded)?
1943
What if IC starts as PFD that is triggered from certain events such as abuse, pelvic surgery, UTI, stress etc. The inability to relax the pelvic floor results in voiding dysfunction, urgency, frequency, hesitation, dyspareunia, nerve upregulation, bowel dysfunction etc?
What if we train our clinicians to evaluate the pelvic floor? What if PFD is found in 70-90% of patients with IC What if we train physical therapists in directed myofascial release and make this treatment accessible to our patients? What if we add cognitive behavioral therapy, stress reduction, psychological support and coping skills? What if we use muscle relaxants rather than narcotics? What if we use neuromodulation techniques to treat the urgency/frequency/ pain associated with IC What if we inject botox in the levators rather than the bladder? What if we not ignore things such as sexual dysfunction? What if we engage our integrative medicine clinicians?
I believe that we will do more to advance the treatment of men and women with pelvic pain, urgency and frequency than we have in the past 20 years It is time to think outside of the bladder!
Where do we go from here?

Welcome to Beaumonts Womens Urology Center
At the Beaumont Womens Urology Center

one will find: Expert clinicians (urologist, urogynecologist, nurse practitioner) to address urologic symptoms, incontinence, pelvic and genital pain, and sexual function concerns. An eco-friendly healthcare environment We also promote health and optimal quality of life through the following services:
Womens Urology Center-Waiting Room
Womens Urology Center-Physical Therapy Specialized pelvic floor physical therapy performed by female therapists that are specifically trained to treat pelvic floor dysfunction, chronic pelvic pain, vulvodynia, voiding dysfunction and incontinence
Womens Urology Center-Physical Therapy Room
Womens Urology Center-Integrative Medicine Medical massage, Reiki, accupuncture, and guided imagery are offered in the Womens Urology Center to improve health and healing.
Womens Urology Center

We strongly believe in the mind-body connection, and are pleased to offer these Integrative Medicine therapies to enhance your health and well-being.
Womens Urology Center Exam Room
Womens Urology Center-Psychological services A psychologist specializing in womens issues is available for patient appointments She is involved in general counseling, cognitive behavioral therapy and sexual counseling
Womens Urology Center-Innovation New therapies are being offered through our research program in the Womens Urology Center. We have a close association with our anesthesia pain service to provide nerve blocks and spinal cord stimulators
Womens Urology Center

Urinary frequency Leaking/incontinence Unexplained pelvic pain Post-cancer vaginal dryness Urinary urgency
Interstitial cystitis Vulvar pain Pain with intercourse
Objectives
To understand the connection between the diet and
inflammation/pain
To understand the role that omega 3 fatty acids play in
inflammation pathways
To be able to discuss specific nutritional
recommendations for patients with pelvic pain

Geeta Maker-Clark, MD Coordinator of Integrative Medical Education Clinical Assistant Professor Pritzker School of Medicine, University of Chicago NorthShore University Health System
Idea
While it is true that many people simply can't afford to
Consider food thy medicine and medicine thy food

Hippocrates
pay more for food, either in money or time or both, many more of us can. After all, just in the last decade or two we've somehow found the time in the day to spend several hours on the internet and the money in the budget not only to pay for broadband service, but to cover a second phone bill and a new monthly bill for television, formerly free. For the majority of Americans, spending more for better food is less a matter of ability than priority. Michael Pollan, In Defense of Food: An Eater's Manifesto
Pelvic pain/IC/PBS
Pain is usually complex- neuropathic, nociceptive and
Inflammation
CVD Neurodegenerative dz Cancer
visceral aspects
Delay in symptom onset and diagnosis is long, severe
symptoms that require multimodal long term therapy

Diet must be a part of the treatment strategy
Forrest, Mishell. Vol 54 Jour Repro Med, Jan 2009
inflammation
Redness Warmth Swelling Pain Self limited Sophisticated weaponry, powerful on cellular level
Chronic inflammation
Fatigue Depression Pre-diabetes Chronic pain
One way?
Treating all chronic diseases with one strategy
Inflammation
People taking NSAID medications had protective
effect on dementia
Same hormones that are increased in inflammation
are up regulated in cancer states, cell turnover is quicker and more likely to mutate
Pro inflammatory pressures

Stress Environmental toxins: cigarette smoke, pesticides,
Pain and Inflammation

Pro inflammatory cytokines produced at the site of
parabens from cosmetics, additives/chemicals Genetic predisposition Nutrition- diets high in meat and milk products increase PGE2, PGF2, and TXA2
nerve injury may be involved with sensitization of nociceptors and hyperalgesia

Inflammation and oxidative stress play a significant
role in persistent pain conditions

Reducing inflammatory mediators through diet can be
an effective therapy
Tall, Raja, Clin J Pain, vol 20, Jan 2004
Cytokines and diet

Cytokine activity is suppressed through manipulation
Nutritional medicine
Are there general guidelines for a healthful lifestyle? Can diet be the primary treatment strategy for disease? Can diet be part of the treatment plan for chronic
of dietary fats, protein and micronutrients
pain?
Grimble RF. Nutrition and cytokine action, Nutr Res Rev 1990:3:193-210
How does nutrition impact?

CHOICES! Variety Fresh Reducing processed foods Eliminating fast food (trans fat) Higher quantity fruits and vegetables Distribution of calories (dont eliminate any of the
THE STANDARD (NORTH) AMERICAN DIET (SAD DIET)

nutrients!)40-50 carbs, 20-30 fat,,30-40 protein

Omega -3
Unhealthy fats Unhealthy carbohydratess Irregular eating Increasing portion size combined with Physical inactivity
Eating for health and eating for pleasure are not mutually exclusive
Criteria for Choosing Diet

1. 2. 3. 4. 5. 6.
Recent Food Technologies

Hydrogenated fats Chemical farming methods Processed grains Food additives (color, preservatives) Solvent and high temperature extraction processes
Maintain healthy weight Must be enjoyable to be sustainable Vitamins, Minerals, Phytochemicals, and EFAs for optimizing function and preventing disease Favorable effect on lipids (cholesterol) Non-Inflammatory Affordable
For more information

Documentaries: Food, Inc King Corn The Future of Food Books: In Defense of Food-Pollan Animal,Vegetable, Miracle-Kingsolver
MACRONUTRIENTS
1. Protein 2. Carbohydrate 3. Fat
PROTEIN
HEALTHY PROTEIN SOURCES

Soy Other legumes (lentils, beans, etc) Nuts Fish (issues around sustainable harvesting and
ANIMAL PROTEIN
Issue of modern farming methods (hormones, antibiotics, confined spaces, grain fed) Meat and Dairy major source of saturated fat Higher consumption of animal protein associated with vascular disease and certain cancers Range-fed organic meats and dairy likely much more healthful
environmental toxins, particularly mercury)
How much protein should we consume?

There is little hard science to guide us Deficiency is not a concern for most in our culture
Take Home message on Protein

Eat more protein from fish and vegetable sources; eat less
(even vegetarian diets) 10 20% of calories or 8 grams of protein per 20 pounds of body weight generally recommended In Nurses Health Study, higher protein diets increased wrist fractures in women
red meat and dairy

Poultry if preferred is best free-range organic (skin off) Omega 3 rich eggs Good plant sources of protein include soy, other legumes,
nuts, nut butters, whole grains Soy is highly digestible
CARBOHYDRATES
CARBOHYDRATES
Provide most of the calories in most diets The bodys preferred fuel source Exert the greatest effect on glucose control Are central to issues in weight control Are often demonized in low carbohydrate diets (ie
Atkins Diet)
GLYCEMIC INDEX
The older notion of dividing carbohydrates into simple
(vs complex) is now felt to be less useful in making healthy choices

Currently, the most useful and increasingly validated
way to categorize carbohydrates (for health promotion) is the Glycemic Index (David Jenkins, University of Toronto, 1981)
GLYCEMIC INDEX - GI
The glycemic index of a food is the area under the
GLYCEMIC INDEX - GI
Blood glucose is measured every 15 minutes for 2 hours and plotted against time. The average area under the curve for a group of volunteers is the Glycemic Index of that food. Glucose or white bread is used as index and is assigned an arbitrary value of 100. All other foods assigned GI relative to this
glucose-time curve (above the fasting glucose level) after 50 gm carbohydrate of the food in question is ingested.
GLYCEMIC LOAD - GL
Walter Willet (Harvard), 1997 GI x Quantity of food eaten Lower GI carbs can be high GL if you eat enough, especially if the food is predominantly carbohydrate (ie basmati rice and pasta) High GI carb-dense foods will have even higher GL (so bread, sticky rice, and potato are very high GL if quantities not lowered)
Half of the carbohydrates in the North American diet come from: bread, soft drinks, cakes, cookies, donuts, quick breads, sugars, syrups, jams, white potatoes, breakfast cereals and milk
Willett, W. Eat Drink and be Healthy, 2002, p. 87
Influences on the GI of foods

Amount of processing (increases surface area) Fiber content (decreases GI) Fat content (many fat-free diet foods are high GI and contribute to obesity) and protein slow stomach emptying and lower GI
Influences on the GI of foods

Low GI diets are linked to

Lemon and vinegar lower GI Type of starch contained: amylose ( i.e. basmati rice) vs amylopectin (i.e. sticky rice) Amylose lower GI than amylopectin Al dente pasta lower GI than well-done
Better weight control (better than low fat, likely safer than low-carb) Diabetes prevention, improved glycemic control More favorable lipid profiles (high GI/GL diets linked to higher triglycerides and lower HDL) Lower heart attack rates (Nurses Health Study) Earlier satiety (demonstrated in well-designed feeding studies)
GI feeding study
Two groups fed iso-caloric meals (breakfast and lunch) Meals differed only in GI Subjects free to graze for five hours after meals 81% greater intake of calories in high GI group
GL and Inflammation
244 healthy women CRP (serum marker of inflammation) measured and
food frequency questionnaires administered

Lowest and highest quintiles of dietary GL (controlled
for confounders)
Median CRP was 1.4 and 3.8 resp
FATS
Fats to avoid/reduce
Hydrogenated/trans fats (increase LDL and lower HDL - worse than saturated, and highly correlated with CAD) Deep fried foods (commercial deep frying fats are often very unhealthful, ie oxidized and trans fats) Saturated fats (key sources are meat and dairy) - increase LDL and HDL (thus likely not as bad as trans) and are associated with insulin resistance - 7 Countries Study and others since have shown strong correlation between saturated fat intake and CAD
Hydrogenated oils represent a huge disaster. They are one of the worst things ever to happen in our food supply
- Walter Willett, MD
FATS TO EMPHASIZE
Monounsaturates (olive oil, avocado, nuts) decrease
LDL and BP, anti-oxidant flavonoids in olive oil

Essential fatty acids (especially omega three) Omega six fatty acids are essential but are consumed
in excess in the North American diet (meat, poultry, vegetable oils)
OMEGA THREE FATS

Omega threes are critical to cell membrane function, modulation of inflammation, healthy brain function, arrythmia protection, among many other functions Prospective trials show supplementation decreases NSAID use in RA and decreases sudden death in prevention of MI Healthiest diets are rich in omega three fats
OMEGA THREE FATS

PLANT SOURCES generally provide alphalinolenic acid (ALA) and include walnuts, flax seeds, pumpkin seeds, hemp seeds, purslane, others - ALA converted to DHA and EPA in body Not converted very well by every individual, usually only 20%
OMEGA THREE FATS

ANIMAL SOURCES provide EPA and DHA and include salmon, herring, mackerel, sardines, and many other fish (avoid farmed salmon and large fish that concentrate toxins)
Desired ratio: 4:1
Diet induced pro-inflammatory state

increase tissue concentration of arachidonic acid by: Consuming foods in rich in linoleic acid-seed oils,
grains, vegetable oils (found in many processed foods)

Consuming AA-containing animal products: beef,
chicken, dairy
Consuming minimal amounts of foods rich in
linolenic acid: green leafy vegetables, fish and fish oil
Imbalance
NSAIDS may offer symptomatic relief from pain and
Benefits of fish oil

Less pain and inflammation Cardiovascular health
inflammation, but cannot influence the pro inflammatory state created by unbalanced ratio of omega 6 to omega 3
Protects from sudden cardiac death in those with known CVS disease Lowers triglycerides and increases HDL(good cholesterol) Slows the buildup of atherosclerotic plaques Lowers blood pressure
Less Depression and psychosis Reduces breast, colon, and prostate cancer
Ongoing studies: Possible benefits of fish oil

Dysmenorrhea (painful menstruation) ADHD

Foods that contain good fats Omega-3
Inattention Hyperactivity Impulsivity
Asthma Eczema Inflammatory bowel disease When taken by pregnant or breastfeeding mothers may decrease infants BMI
Foods that contain bad fat Omega-6 and 9

Margarine Chips Cookies Cakes Biscuits Salad dressings Chocolate bars Crackers
Omega 3-how much?

2000-3000 mg daily for Supplementation often
patients with chronic inflammation Above 6000 mg can interfere with bleeding time. =3 servings of wild caught cold water fish/week
necessary
Keep in freezer to avoid
after taste
THE MEDITERRANEAN DIET
MEDITERRANEAN DIET
High in fruits, vegetables, whole grains, legumes,
MEDITERRANEAN DIET (contd)

Red wine with dinner Moderate use of yogurt and cheese A health-promoting diet which is delicious and dramatically reduces heart disease, cancer incidence, and systemic inflammatory markers
nuts, seeds
High in fish, low in meat and dairy Olive oil is principle fat
Fruits and Vegetables are:

Nutrient dense Rich in fiber Rich in protective phytochemicals (usually the
Fruits and Vegetables are:

colored pigment)
Rich in vitamins and minerals Protective against heart disease, cancer, obesity,
hypertension, stroke, eye diseases, diverticular disease
Low in calories Rich in visually appealing color Rich in flavor Low in the food chain (leading to less accumulation of biotoxins) Chemically complex with hundreds of identified and many as yet unidentified health-promoting plant chemicals
Eat a RAINBOW of fruits and vegetables

Orange Beta Carotene Green Glucosinolates Yellow/Green Lutein Red Lycopene Purple Anthocyanins White/Green Allyl Sulfides
Anti oxidants
Bioflavonoids exert an inhibitory effect on eicosanoid
synthesis
Animal products do not contain anti oxidants and
phytochemicals, fruits and vegetables contain appreciable amounts
Havsteen B. Flavonoids class of products of high pharmacologic potency. Biochem Pharmacol 1983;32:1141-8
ANTI-INFLAMMATORY DIET
Evidence scattered in basic science, observational studies and RCTs of components Collateral benefit - this eating plan is also generally best for overall health and disease prevention Significant benefit in significant numbers of patients reported by nutritionally-oriented practitioners
INFLAMMATORY CONDITIONS: ANTI-INFLAMMATORY DIET

Emphasize fruits, vegetables, Omega 3 fats and MUFA (olive oil, canola), low GI carbs, nuts, seeds. Limit meat and dairy, processed foods, additives. Identify sensitivities : dairy, wheat etc. Reduce ratio of omega 6 (pro-inflammatory) to omega 3 (inflammation modulating) essential fatty acids (Okinawa 4:1, typical N America diet 20-40:1)
Components of Optimum Diet

8-10 rainbow assorted fruits and vegetables per day (excluding potatoes) Minimal trans and hydrogenated and saturated fat (minimal red meat and dairy, minimal processed foods), low in added salt Red wine with dinner if preferred, green tea Organic, locally grown where possible Consider a multivitamin
Eat a RAINBOW of fruits and vegetables

Orange Beta Carotene Green Glucosinolates Yellow/Green Lutein Red Lycopene Purple Anthocyanins White/Green Allyl Sulfides
Tart cherries
Anti oxidant activity is related directly to anthocyanin
recommendation
Montmorency cherry juice concentrate 2 tbsp / day Can drink more, but high amounts (6-8 ounces) can
content in berries
Cyanidin from tart cherry extract, showed better anti
inflammatory activity than aspirin

Isolated compounds from cherries shown COX-1 and 2
cause diarrhea
High calorie, no fiber
inhibition activity comparable to ibuprofen and naproxen

Wang,Cao, Strasburg. J Nat prod 1999:62:294-296
Soy
soy is safe and nutritious when eaten in relatively
soy
One cup of soymilk =four to 10 grams of soy protein,
whole and unrefined forms in reasonable amounts

one to two daily servings a cup of soymilk, a half cup of tofu, tempeh or green
soybeans (edamame) or roasted soy nuts

Soymilk provides all the benefits of cow's milk,
20 to 40 mg of isoflavones, plant chemicals that may act like estrogen but probably account for soy's protective effect against hormonally driven cancers (especially when soy is part of the diet from early childhood)
Japanese women have 1/5th the amount of breast
without the milk protein (casein), and milk sugar (lactose), which can cause digestive distress if you lack the enzyme that breaks it down.
cancer compared to Western countries
soy
Soymilk is fortified with calcium, shake it up! many soy crops are heavily treated with pesticides,
Soy
Unsaturated, high in linoleic acid and ALA, high in
vitamin E, iron zinc, calcium and B vitamins.

Isoflavones- part of a class of phytochemicals called
always buy organic soy products, non GMO soy

avoiding brands of soymilk that contain the thickening
flavonoids- similar to estrogen

Consumption of soy protein has been shown to have
agent carrageenan, a seaweed derivative, which is harmful to the intestinal tract
antioxidant effects in vivo in humans, as well as reduces amount of TNF-alpha put out by macrophages
soy
High amounts of omega 3 fatty acid ALA, which is
Cruciferous veggies
Broccoli, Brussels sprouts, cabbage, turnip greens and
converted to EPA.
EPA acts a substrate for cyclooxygenase in place of AA,
kale
rich in antioxidants which help protect against both
cancer and heart disease

Population studies have shown that people who eat
and can suppress production of the eicosanoid inflammatory mediators

Recs: 1-2 servings per day
broccoli and other cruciferous vegetables have lower rates of cancer than those who don't.
cruciferous
indole-3 carbinol (I-3-C), or the carotenoid pigments
Dark green leafy veggies

good sources of many vitamins A, C, K and folate)
these vegetables contain may be the secret ingredient

Other possibilities include vitamin C or sulforaphane,
minerals ( iron and calcium) and fiber.

dietary fat needed to absorb some of the vitamins
a compound thought to increase production of an anti-tumor enzyme . Most likely, the cancer-protective effects of broccoli and its relatives result from a synergistic interaction of these and other components of the vegetables
found in dark green vegetables. Add a bit of oil (such as olive or canola oil) or salad dressing to your dark green vegetables
Dark greens
Arugula Broccoli Collard Greens Dandelion Greens Kale Mustard Greens Romaine Lettuce. Spinach Swiss Chard
Berries
High in fiber Rich in many phytochemicals, some known and others
unknown
Recent study Dr. Christine Sardo at OSU: cancer-causing chemical N-
nitrosomethylbenzylamine given three times a week for five weeks to rats. After 20 additional weeks, rats that ate a diet consisting of ten percent black raspberries showed reductions in oral, esophageal and colon cancers of about 50 percent compared to rats that did not eat berries.
berries
The berries prevented the entire spectrum of tumors
mushrooms
from being initiated and promoted- Dr. Sardo

Fine to go with the standard berries available, acai and
We are more closely related to mushrooms than any other plants, shared DNA Used liberally in traditional chinese medicine
goji berries have a lot of vitamin C but dont deserve the prices they garner
Mushrooms
Shiitake: eritadenine, which encourages body tissues to absorb
mushrooms
Maitake: This delicious Japanese mushroom is also called "hen of the
cholesterol and lower the amount circulating in the blood. Shiitakes also have antiviral and anticancer effects.
Cordyceps: A Chinese mushroom used as a tonic and
restorative. It is also known for improving athletic performance. You can buy whole, dried cordyceps in health food stores and add them to soups and stews, or drink tea made from powdered cordyceps.. For health maintenance, take it once or twice a week.
Enoki: Slender white mushrooms that need only brief cooking
woods" because it grows in big clusters that resemble the fluffed tail feathers of a nesting hen. You should be able to find it dried or fresh in Japanese markets, gourmet foods stores, or upscale supermarkets. Maitake has anticancer, antiviral, and immune-system enhancing effects and may also help control both high blood pressure and blood sugar levels.
Reishi: Strictly a medicinal mushroom, not a culinary one, reishi is
and have a very mild taste. They are good in soups and salads. Enoki mushrooms have significant anti-cancer and immuneenhancing effects.
woody, hard, and bitter. Like maitake and other related mushrooms species, reishi can improve immune function and inhibit the growth of some malignant tumors. It also shows significant anti-inflammatory effects, reduces allergic responsiveness, and protects the liver. You can buy dried, ground mushrooms and use them to make tea if you don't mind the bitterness. Otherwise, buy reishi tablets, liquid extracts or capsules, which are available in health food stores and follow the recommended dosage. Take reishi every day for at least two months to see what it can do for you.
tea
Black, white, green and oolong Green tea has highest level of antioxidant When buying fresh organic green tea, the first quality
tea
All true tea comes from the same plant, Camellia
sinensis.
The differences between types of tea result from
to look for is color - the tea leaves should be a dark, rich green. The scent the leaves give off when you hold a small amount in your hand is your best clue to freshness and flavor.
different methods of processing the leaves.
tea
Green tea, the tea leaves are steamed, rolled and dried, a method
that preserves the content of polyphenols, that confer the wellknown health benefits of tea.
Black tea, the leaves undergo a process of oxidation that changes
Resveratrol- red wine?

Resveratrol- an antioxidant found in
the color and flavor and reduces the content of polyphenols.

Oolong is intermediate between green and black tea - in color,
flavor and polyphenol content.

White tea- imported from one region of China. This is the least
red wine and in the skin of grapes, prevents the negative health effects of weight gain in mice - enlarged livers, high insulin levels and diabetes and reduced the risk of death by 31 percent.
Recommendation that red wine is good for you, came
processed form, with an even greater antioxidant activity than green tea. It produces a very pale infusion with a very delicate taste.
from this study primarily
Red wine
If you drink, drink red wine If you dont, dont start Resveratrol found in the darker berries Cranberries, blackberries, grapes, blueberries,
turmeric
(Curcuma longa) major ingredient in Indian curries, and makes American is a culinary spice mustard yellow that spans cultures.
raspberries
Turmeric
One of the most comprehensive summaries of
turmeric
Arthritis: Turmeric contains more than two dozen
turmeric studies to date ethnobotanist James A. Duke, PhD., in the October, 2007 issue of Alternative & Complementary Therapies
Reviewing some 700 studies, Duke concluded that
turmeric appears to outperform many pharmaceuticals in its effects against several chronic, debilitating diseases, and does so with virtually no adverse side effects.
anti-inflammatory compounds, including six different COX-2-inhibitors (the COX-2 enzyme promotes pain, swelling and inflammation; inhibitors selectively block that enzyme). curcumin - the component in turmeric most often cited for its healthful effects - is a multifaceted antiinflammatory agent, curcumin has demonstrated positive changes in arthritic symptoms.
turmeric
Cancer: Duke found more than 200 citations for
Chocolate
Beneficial cardiovascular effects of flavonoids are
turmeric and cancer and more than 700 for curcumin and cancer. curcumin and/or turmeric were effective in animal models in prevention and/or treatment of colon cancer, mammary cancer, prostate cancer, esophageal cancer, and oral cancer.
The effectiveness of the herb against these cancers
attributed to their ability to improve endothelial function, by activation of the nitric oxide (NO) synthase system
Natural antioxidant properties ability to decrease blood clotting by inhibiting platelet
compared favorably with that reported for pharmaceuticals
activation and aggregation
chocolate
Flavanols found in cocoa bean, higher concentrations in dark chocolate. Milk impairs absorption.
Lifestyle changes to reduce inflammation

Exercise Lose weight if you are overweight (eat
calories to maintain a healthy weight)

Floss your teeth Eat lower glycemic foods/more fiber
Highest concentration of flavanols are in chocolate in comparison to other foods
Eat more fish/nuts/seeds and anti inflammatory foods Eat less meat Stop smoking
Tips on returning to a simple healthy diet

1. EAT LARGE AMOUNTS OF FRESH, LOCALLY AND ORGANICALLY GROWN PRODUCE
5. REDUCE AND LIMIT DAIRY CONSUMPTION 6. LIMIT GRAINS. USE ONLY WHOLE AND/OR SPROUTED GRAINS 7. USE RAW HONEY AS PRIMARY SWEETENER IF NEEDED
2. EAT AT LEAST ONE HANDFUL OF UNSALTED NUTS AND SEEDS EACH DAY 8. AVOID ALL CHEMICAL ADDITIVES (PRESERVATIVES, SWEETENERS, FLAVORINGS, ETC) 3. REDUCE AND RESTRICT ANIMAL PROTEIN SOURCES TO GRASS FED AND/OR WILD 9. AVOID COOKING FOODS AT TEMPERATURES GREATER THAN 350 F 4. GET OUTSIDE AND MOVE. DAILY SUNLIGHT EXPOSURE OR TAKE VITAMIN D 10. SEARCH FOR WILD EDIBLES AND HEIRLOOM VARIETIES OF ALL PLANTS AS OFTEN AS POSSIBLE
Patient handouts
Video on the effect of emotions on pain Anti inflammation diet, glycemic index and load,
Questions
1. Which of the following foods are high in omega-3
fatty acids? a. walnuts b. salmon c. chocolate d. Blueberries e. all of the above f. a and b
protein alternatives to meat, breathing exercises

All available at: http://www.fammed.wisc.edu/integrative/modules
questions
2. Which foods are considered anti-inflammatory? a. Tart cherries b. Turmeric c. Dark green leafy vegetables d. Grass-fed beef e. a,b and c
If you remember only one slide

Eat Food Not too much Mostly plants
Michael Pollan - In Defense of Food
Presentations Saturday, October 20, 2012
IPPS
3:30 p.m. 4:10 p.m. Medical Management of Sexual Dysfunction/Pelvic Pain Susan Kellogg-Spadtt, CRNP, PhD 4:10 p.m. 4:40 p.m. Leveraging the Intersection Between Sexuality and Chronic Pelvic Pain in Treatment Design Heather Howard, MBA, PhD, ACS
Page 82
Sexual Pain in Women: History, Assessment and Management

Susan Kellogg PhDCRNP Director: Sexual Medicine The Pelvic & Sexual Health Institute of Philadelphia Professor: OBGYN Drexel University College of Medicine Professor: Human Sexuality Widener University E-mail: Phillypelvic@aol.com
At the completion of the presentation, participants should be able to: Identify 3 possible contributing factors to the onset of sexual pain in women. Explain the touch test technique as it relates to the physical assessment for provoked vestibulodynia .
Describe the interdisciplinary management of the woman with sexual pain.
1.
Develop a timeline of the dyspareunia. Has intercourse always been painful? Has tampon use always been painful? Did the pain start acutely or gradually? Is the pain only during intercourse or is there pain without provocation? Since the pain began, have there been episodes of completely pain free sex?
Determine the location of the pain Is the pain upon penetration? Is the pain inside the vagina? Is there pain with deep thrusting? Are there any positions that are more/less painful? Is there pain with clitoral stimulation? Is there post-coital pain?
Elicit symptoms Burning, rawness, cutting, tearing, searing, aching, dull, throbbing, tearing, dryness, pruritus ? Is there urinary hesitancy, urgency, frequency, incomplete emptying? Is there constipation, rectal fissure?
Did the pain start while on hormonal contraception? Allergic reaction to creams, soaps, spermicides? Positive cultures? Previous vulvar biopsy? Is the pain different when using a condom? Is there bleeding during/after sex? Is there tearing during sex? Are there oral lesions?
Visual inspection of the vulva. Vulvoscopy with biopsy if indicated Cotton swab test Vaginal exam with a pediatric/pederson speculum- insert without touching the vestibule. Examination of pelvic floor muscles Palpation of the urethra and bladder
Visually inspect the vulva
Begin by touching the labia majora, interlabial sulci and minora Touch lateral to Harts line and then just medial Harts Line Touch the vestibule at Skenes and Bartholins ostia as well as at 12 and 6 oclock vestibule Can use a 1-5 or 1-10 scoring system for pain May use algesiometry for research purposes
Erythema Lichenification Fissures, erosions, ulcerations Scarring & architectural changes Atrophy Hypo/hyperpigmentation Evidence of VIN
Vulvar biopsy- Only if there skin changessend to a dermatopathologist with a differential diagnosis.
Microscopy: wet mount, KOH, pH Cultures for speciation and sensitivity Serum: estradiol, total and free testosterone, SHBG, (HSV2, GC, chlamydia-not routine) Perineometry, biothesiometry, bladder scan Cystoscopy- ONLY IF THE BLADDER IS TENDER
*PFM are an integral support system with several fx *PFM work with large postural groups to maintain skeletal position *PFM superficial and deep PFM provide local front, middle, rear support *PFM enhance FSR (muscles place pressure on deep dorsal clit. vein =preventing venous escape; facilitate sensation during intercourse) PFM can contribute to FSD if they are either HYPO- or HYPERTONIC
Travell JG & Simons DG. Myofascial Pain and Dysfunction. Chapt 6: Pelvic Floor Muscles.1992.Baltimore, Williams & Witkins/ Rosenbaum TY, Role of PT in FSD, Current Sexual Health Reports,2008 Graziottin A: Female Sexual Dysfunction.: Evidence Based Physiology for the Pelvic Floor: Bridging Research and Clinical practice. Eds K Bo et al. Oxford, Elsevier2005.
Associated with: low back pain, holding urine, excessive strengthening, sacroiliac joint dysfunction, piriformis syndrome, hip pain/labral tears.
Iliococcygeus Pubococcygeus
Puborectalis
Obturator Internus
Insert one finger through the hymenal ring then:
1. 2. 3. 4. 5. 6.
Palpate the superficial and deep PFM For each muscle ask is this pressure or pain? Are there trigger points? Is there hypertonicity? Have them squeeze- is there weakness? Can they relax the muscles? Palpate the urethra and bladder- it should cause urgency but not burning or pain.
Increased tone= decrease oxygenated blood flow = increased lactic acid in PFM Symptoms: vulvar pain, burning, tenderness, introital dyspareunia, urinary symptoms, constipation, fissures PE=erythema, Trps, poor sustained contraction or full relaxation Vaginismus =used in the past but term may be removed from the new DSM V. Treatment: pelvic floor physical therapy (www.womenshealthapta.org, NVA.org).
27 year old woman presents c/o 6 year 6 yr. history: pain upon penetration. Gradual onset of pain after 1 year of pain free sex + PVD / PFM Hypertonus on exam
QTIP TESTING SUGGESTS: PVD= Provoked Vestibulodynia Formerly= Vulvar Vestibulitis
Treatment: Stop hormonal contraceptives then use: estradiol 0.01 to 0.02% and testosterone 0.05% - 0.1% in compounded base BID to the vestibule. Expect 50% improvement by 12 weeks.
Women report onset of symptoms after severe or recurrent candidiasis or allergic reaction1,2 Polymorphism in genes coding for IL-1ra, IL-1b 2,3 Decreased INF-a3 Elevated TNF, IL-1b, IL-6, IL-8, Heparanse3 Increased mast cells in mucosa4 Proliferation of C-afferent nociceptor4
s LJ, Goldstein AT. Vulvodynia. J Sex Med 2008;5:5-15.
1. 2. 3. 4.
Harlow BL Ann Epidemiol. 2009 Nov;19(11):771-77 Witkin SS Am J Obstet Gynecol. 2002 Mar;186(3):361-4. Foster Am J Obstet Gynecol. 2007 Apr;196(4):346.e1-8 Bornstein J Int J Gynecol Pathol. 2008 Jan;27(1):136-41.
TCAs/ anticonvulsants - Amitriptyline 25-150mg -Gabapentin/Neurontin 100-900mg -Pregablin/ Lyrica 50-300mg
*Montelukast 10mg / d x 2.5 yrs.

.Kamdar N et al. JRM 2007 52(10)912-6.
*Cromolyn cream
(Nyirgesy et al, 2001)
*Traumeel subdermal injections (Feloney,

Kellogg-Spadt et al, 2005)
*CBT,ST
(Rosen, Kellogg-Spadt 2004)
1 hr before sleep
Butrick CW. 2009. Obstet Clin N America 36;707-722.
Manual Therapy Techniques

Myofascial Release Soft Tissue Mobilization Muscle Energy Techniques Stretching Strengthening
Internal pelvic floor muscle RX
Deposits of fibrous tissue or crosslinks are a natural response to soft tissue strain or injury. When they form in the fascia or muscle they distort anatomy and cause decreased mobility and function. Manual therapy restores function by interrupting crosslinks and allowing fascia/ muscle to move freely.
Herman, H. Physical therapy for female sexual dysfunction. In Womens Sexual Function and Dysfunction (eds) I Goldstein et al , 2005, Iondon, Taylor Francis Travell JG & Simons DG. Myofascial Pain and Dysfunction. Chapt 6: Pelvic Floor Muscles.1992.Baltimore, Williams & Witkins
Post-Internal
Pelvic Floor Pelvic Floor
Abdominals
Abdominals
Fitzgerald,MP et al.2009;J Urol. (8) pp570-580 Multicenter trial; 48 F/M CPPS/HTPFD subjects General therapeutic massage protocol vsMyofascial PT with internal massage x10w PRIMARY END POINT:Global Assessment Response 57% MPT vs. 21% GTM mod-marked improvement Improvement sexual function (p 0.002 FSFI total) and in pain (p 0.005 VAS) Most common AE : Pain 52% MPT vs. 21% GTM
Butrick CW. 2009. Obstet Clin N America 36;707-722.
1 hr before sleep -Myorelaxant drugs: -mataxolone/Skelaxin -cyclobenzaprine/Flexeril -tizanadine/Zanaflex -diazepam suppositories 5-10mg -
??UNILATERAL PAIN WITH SITTING

Compression of pudendal nerve at sacrotuberous / sacrospinous ligaments and Alcocks Canal
Branch Of Pudendal Nerve
Sacrospinous Ligament
Alcocks Canal
Sacrotuberous Ligament
Acetabular labral tear

Patients may present with groin pain, difficulty w prolonged sitting and dyspareunia. Although this clinical condition may be present with or without a history of trauma or athleticism; HCPs should always question the presence of a labral tear and should order further diagnostic tools including MRIs and UTZ.
GOAL=Restore function via multidisciplinary team

*Maintain strong postural and PFM muscles *Restore tissue integrity and reduce inflammation
*Employ adjuvant therapies, as necessary

acupuncture, mindfulness,TrP injections, intravaginal suppositories, botox, CBT, sex therapy, topical creams, steroids. THANK YOU FOR YOUR KIND ATTENTION!!
Objectives
Leveraging the Intersection between Sexuality & CPP in Treatment Design

International Pelvic Pain Societys Annual Meeting: Chicago October 20, 2012
Intersection between Sexuality & CPP Leveraging intersection in treatment of CPP Approaches for Sexual Adjustment
Heather S Howard, PhD, MPH
The Center for Sexual Health and Rehabilitation San Francisco, California 415.683.3231, Dr@HeatherHoward.com www.SexualRehab.com
Copyright 2012 H. Howard. All rights reserved. Copyright 2012 H. Howard. All rights reserved.
Context
Objectives
Perspective

Intersection between Sexuality & CPP

Sexologist & Mind-body health facilitator Specialty: Pelvic, Sexual, Chronic Pain Patient Sex Counseling: Education & Skills Training Attitude-aware, patient-centered & collaborative Adjustment & coping (despite improvements) Source: Association between sex & pain
Known Proposals Importance of sexuality to patients
Clinical Approach

Client Concern

Source of Approach: Hx & Methodology

Copyright 2012 H. Howard. All rights reserved.
Intersection Sexuality & CPP Known
Intersection Sexuality & CPP Proposals
Sexual concerns common with CPP

More sexual problems than any other type of chronic pain

(Collett, Cordle, Stewart, & Jagger, 1998)
Unknown: Causation and direction of relationship
CPP affects structures involved in sexual pleasure Sexual problems often unresolved when pain improves (if pain improves)
Sexual adjustment support should be offered in addition to pain management Team member responsible for SHA Sexual patterns may contribute to pain Sexual response may provide pain management benefits
(Bergeron et al., 2001; Goldfinger, Pukall, Gentilcore-Saulnier, McLean & Chamberlain, 2009)
Sexuality important component of relationships and quality of life (Tripoli et al., 2011)
Intersection Sexuality & CPP Importance

Why is sexuality important to your clients?

Linked to identity Quality of life Source of connection and communication with self and others Source of pleasure or pain
(Howard, 2008)
A guy's penis is gold, so when that thing is hurting or dysfunctional, you're reduced to less than human. It might be clich, but sometimes guys think with their dicks. That happens to be true, that everything starts there and when that becomes a vulnerable point, you've got some issues to deal with. It's completely emasculating. Overall, having orgasms and sex improves the conditions of your life. I still do get anxious and have fear and get depressed, but it helps with thinking I'm more normal, more of a woman. When I was single again and dating, it was much harder: Phobia sets in. Your mind starts to wander and you get fearful and you wonder if each person will have compassion. It deters you from getting into a relationship or fucking. Theres fear of embarrassment.
(Howard, 2008)

Objectives

It strained the relationshipits hard to be a couple without intimacy....My partner viewed it as "my problem, but I corrected him: its our problem"I couldn't care less [about intercourse].... Pelvic pain has taken away an important part of my life; its had a major negative impact on my sex life with my husband for most of my marriage. Now, when I'm not comfortable, I know I won't be able to climax, but with a partner it involves his ego and becomes about a sense of accomplishment.
(Howard, 2008)
Intersection between Sexuality & CPP Leveraging intersection in treatment of CPP

Theory Benefits Methods Perception matters
Leveraging Intersection Theory: Mechanisms
Leveraging Intersection Potential Benefits
Intr. sexual response improves pain mgt.?

Genital stimulation raises pain threshold Positive emotions modulate pain Flood CNS with pleasure messages (gate control) Recalibrate brains perception of pleasure & pain using shared neural pathway Improve muscle pliability with warmth from orgasmic contractions Follow TP release by full range of motion lasting Retrain high-tone pelvic muscles using movement & while engaged in task Release and circulate trapped energy (trauma) Orgasm optimal state for re-education
Leveraging pains location in sexual organs by addressing sexuality could improve:

Empowerment Match patient experience Outlook: focus on pleasure (not pain) Quality of Life Integration of care / embodiment Intimate Relationship Partner Support Adherence to Exercises Pelvic & CNS Physiology (form follows function)
Re-education
Leveraging Intersection Methods Learned
Patients using sexuality to manage pain
Patient 2
When I masturbate, I do self-internal massage. It creates blood flow and tingling. With a rabbit [vibrator], it does that. I either turn off the clitoral stimulator or move it aside or angle it above or below my clit. I feel the vibration in my entire pelvic area. I never move the stimulation directly on my clit to orgasm; general vibe stimulation is enough.With internal massage, the sides provide the most pleasure before climax; a circular motion is good because it hits those areas. When orgasming, I hold tight and my muscles clench the base of the rabbit. Cradling underneath, I release the deeper muscles when I tighten the outer muscles. I use muscle control, pulling everything up, sucking in and cradling my deeper muscles. Having something inside (a rabbit or a partner) helps. It's the sensation of holding and pulling, not thrusting. Feels like everything can be soft inside because it's protected from the outside. Without something inside, I have no gauge of what muscles I'm using.
My method: orgasm-release Patient 1

Orgasm changes the way pain feels; I can have an orgasm first and often intercourse is easier. I have used orgasm with a large partner and it helped.
Patient 3
I have invented several home-exercises involving vibration. I regularly use an external clitoral vibrator for pleasure, but when I use internal vibrators, I never expect any pleasure. Inserting anything kinda feels like getting kicked in the stomach. Actually, more like what Ive heard guys describe being kicked in the balls feels like. Fun fun fun. I start small and go slow. I also experience other types of pain in the pelvic floor region, usually resulting from different stimuli. Most stimuli cause an intense burning in the urethra. I also often experience sharp bitting sensations, similar to a cut. I can usually manipulate my mind around these forms of pain better than the gut-jarring pain of being penetrated. By focusing either further away or closer to the pain, I can vary the degree I have to feel pain. In this way, I can orgasm even while feeling pain, because if I focus correctly and after many, many months of conscious practice I can get the pain to complement the pleasure. I have a much easier time being aroused and orgasming when there is no pain however. I dont think it adds to sexual experiences, I think I am just minimizing how much it takes away.
Patient 3 continued
The first vibrating penetrative tool I used was a dilator set which had an inexpensive built-in vibration mode. Unfortunately, the low setting was hardly that, so my use of the vibration was infrequent given the increased pain. Later on I used the We-vibe, which is nice because its vibrations can be highly controlled and I dont have to hold the vibrator in place. However, I actually experience no pleasure because the clitoral stimulation is too mild in comparison to the vaginal pain. I have also used a small anal dildo with a texture in-between that of beads and a cylinder in an attempt to loosen the rectal muscles, which are also in bad shape. I have never used anything that vibrates anally. I usually settle down for 20-60 minutes in bed. I use a heating pad to both help keep myself warm and in the hopes of improving circulation and reducing pain. I usually select a good movie or book with an engaging plot and characters and often a mildly erotic plot (e.g. includes sex scenes, but more like Phantom of the Opera than Girls Gone Wild).
Patient 3 continued
I found that this works well because I can (1) be mentally engaged and thus not bored during the process, (2) aroused enough to actually feel mildly like engaging in anything remotely sexual, and (3) experience enough increased lubrication generation and blood flow to ease the pain a bit.I have also found that orgasming right beforehand can often help insertion. After I give myself ten to twenty minutes to get into the story, I insert whatever I am inserting using lube. It will take me a while to work it all the way in, and I will usually spend a good five minutes or more moving it around, in and out, etc. Finally I will either leave it be if I feel like it is stretching on its own or hurting too much to move or turn on a low vibrating function.After a while, when I either dont feel anymore pain or when the uncomfortableness becomes too much, I take whatever it is out and finish my movie or book. I often finish off by masturbating / masturbating again. I have personally found that orgasming after is a good way to prevent negative mental associations with the gentiles being formed.
Close relationship between pleasure/ pain
Patient 4
Mentally I might go back and forth between pain and pleasure and I haven't shared that with a partner.
Patient 5
In the early days of vaginismus, I created pleasure out of it, like I was a virgin and he was hitting a wall.I used that pain/ pleasure feeling as foreplay, and then the popping open was like I was a virgin. But the type of pain has changed in nature because I'm dryer and now it feels like sandpaper, so combined with the tightness, I havent gotten that part to feel good.
Patient 6
Even upon arousal, even like here [pointing to the perineum on a diagram], I feel sort of soreness. So its almost how I know that Im aroused....I feel a bulging in my perineum, pressure. It doesn't really feel good; it's kind of sore. This sensation usually leads to intercourse, it's a precursor. I know sex is just so painful for me throughout my whole life, before [my current partner], and I just dont understand if I ever knew what it was, what an orgasm was supposed to feel like...the thing is, I dont know if what I was experiencing was just intense pain or intense pleasure.
Patient 7
Sometimes the pain gets you off a little bitin a weird way. Pain in the past could be a stimulant, pain can be a turn -on; I had some pain with internal stimulation towards the bladder. It was gspot pleasure and latching onto the pleasure overrides the irritation. But the orgasm wasn't as good and I had an increase in pain afterwards. But now it's a process of relaxing in the pain, and eventually there's no pain. I have confidence that I will have an orgasm. I don't have intercourse when I'm in pain (I'm not being stupid) and am having massage now all over and more, which helps more. Arousal takes over and it's a relaxed arousal and it takes more time to build. My three stages of arousal are:
Patient 7 continued
1. Pre: it feels good, there's foreplay, I'm not building up yet; 2. Build: I'm building, not ready to come yet, but confident I will. This stage lasts longer, I'm more relaxed, less tense; 3. Orgasm: I come. I have had pain with urgency or a sharp pain on my right, but the urgency has subsided, the pain subsided and I'm not as distracted. I could experience pain in the future and being aware of what helps now can help get me through a flare in the future.
Patients re-wiring nervous system
Patient 8
I had no vaginal intercourse for over a decade. The pain was overwhelming, and creative sex took a different direction (I was always creative, but this increased). I learned to do anal, learned to orgasm easily from that. I could erogenize other parts of my body, like my ears, my nipples and my toes. My lover did this unintentionally. He touched one place that was erogenous (in my case, my clit), then he touched two places simultaneously, like my nipples and my clit, to re-wire my brain. Then he would only touch my nipples in a certain way. At first, that would send a message to my clit, and now it doesnt do thatits its own sensation. Now I can have vaginal intercourse sometimes, but my range is expanded.
Leveraging Intersection Perception Important
Patients re-wiring nervous system
Are we treating pain or improving sex?

Patient 9
Umm, I think that for a long time, something that I kind of evolved into was sort of having small orgasms from him sucking my breasts, because it was something where he didnt have to touch my vagina or vulva. So I think I kind of evolved into that, and we still enjoy that and its definitely part of our intercourse. I had a little orgasm before intercourse through breast stimulation, after trigger point release. There was no pain during that. In the past there was pain, but there was simultaneous vaginal touching and there was no vaginal touch this time.
Impacts visualization Impacts adherence Impacts outcomes
Objectives

Sexual Adjustment Education & Skills Needed

Intersection between Sexuality & CPP Leveraging intersection in treatment of CPP Approaches for Sexual Adjustment

Education & Skills Needed Solutions Additional Resources
Learning Body (Anat & Phys, Pleasure/ Pain Mapping) Learning Comfortable Activities (incl. sexual ergonomics) Developing Sexual Skills/ Competence Developing Sexual Confidence Developing Trust of Body and Partner Becoming Embodied Remaining Present Managing Inner Dialogue Building Sacred Space Setting Boundaries Developing Appropriate Sexual Self Learning to Navigate & Stimulate Body & Partner Working Through Fear / Loss of Control Improving Verbal and Nonverbal Communication Recalibrating Brains Assessment of Pain
Sexual Adjustment Solutions: Approach

Sexual Adjustment Solutions: Modalities Used

Focus on pleasure Build on what works Address sexuality directly Utilize sexual response Exploratory mode Treat nervous system Prepare for flares
Sexual Ergonomics (Howard, 2010) Pleasure/ Pain Retraining (Howard, 2008) Conscious Embodiment Mindfulness (Kabat-Zinn, 2003) / sensate focus (Masters & Johnson, 1970) Voice Dialogue (Stone & Stone, 2000) / Body Dialogue (Stone, J.T.) Guided Exploration & Visualization Envisioning sacred space (Malan) Inner Body Visualization (Hartman & Fithian, 1972) Imagery methods effective in alleviating pain (Turk & Fernandez, 1989) Journaling (Epp) Boundary Setting Respectful Confrontation (Weston) Trauma Healing Somatic Experiencing (Levine, 2008)
Sexual Adjustment Additional Resources
Websites
www.Ergoerotics.com, www.SFSI.org, www.GoodVibes.com, www.Scarleteen.com www.SexualRehab.com, www.a-womans-touch.com Guide to Getting it On, Healing Painful Sex www.AASECT.org, www.americanboardorsexology.com, www.americancollegeofsexologists.org www.ISSWSH.org, www.AASECT.org, www.HermanWallace.org, www.sexscience.org Journal of Sexual Medicine, Journal of Sex Research Standard Practice in Sexual Medicine
Leveraging the Intersection between Sexuality & CPP in Treatment Design

International Pelvic Pain Societys Annual Meeting: Chicago October 20, 2012
Patient Handouts & Books

Sexuality Counselors & Educators
Continuing Professional Education
Heather S Howard, PhD, MPH
Professional Books & Journals

The Center for Sexual Health and Rehabilitation San Francisco, California 415.683.3231, Dr@HeatherHoward.com www.SexualRehab.com
plan to attend
IPPS 2013 Annual Fall Meeting October 17 19, 2013

The Peabody Orlando Orlando, Florida
S O C I E T Y ,
I N C.
Two Woodeld Lake 1100 E Woodeld Road, Suite 520 Schaumburg, IL 60173 Phone: (847) 517-8712 Fax: (847) 517-7229 Email: info@pelvicpain.org Website: www.pelvicpain.org

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Basics Course for General Gynecologists, Physical Therapists, Nurses and Residents Thursday, October 18, 2012 2012

Welcome to the 2012 IPPS Annual Fall Meeting

Stephanie Prendergast, MPT

Sawsan As-Sanie, MD, MPH

Georgine Lamvu, MD, MPH

International Pelvic Pain Society

7:00 a.m. 5:00 p.m.

International Pelvic Pain Society

International Pelvic Pain Society

7:00 a.m. 7:50 a.m.

6:00 a.m. 5:30 p.m.

International Pelvic Pain Society

International Pelvic Pain Society

International Pelvic Pain Society

International Pelvic Pain Society

International Pelvic Pain Society

Thank You to Our Promotional Partners

Thank You to Our 2012 Contributor KevMed, LLC

International Pelvic Pain Society

Thank You to Our Exhibitors

Thank You to Our 2012 Exhibitors

Thank You to Our 2012 Educational Grant Providers

International Pelvic Pain Society

2012 2013 Board of Directors

International Pelvic Pain Society

International Pelvic Pain Society

International Pelvic Pain Society

2012 IPPS Annual Fall Meeting Program Schedule

10:00 a.m. 5:30 p.m.

8:00 a.m. 8:05 a.m.

8:05 a.m. 8:35 a.m.

9:00 a.m. 9:05 a.m. 9:05 a.m. 9:25 a.m.

International Pelvic Pain Society

9:50 a.m. 10:00 a.m. 10:00 a.m. 10:20 a.m.

10:20 a.m. 11:00 a.m.

11:00 a.m. 11:05 a.m. 11:05 a.m. 11:35 a.m.

11:35 a.m. 11:40 a.m. 11:40 a.m. 12:10 p.m.

1:50 p.m. 1:55 p.m.

International Pelvic Pain Society

2:35 p.m. 2:40 p.m. 2:40 p.m. 3:10 p.m.

3:10 p.m. 3:20 p.m. 3:20 p.m. 3:40 p.m.

3:40 p.m. 4:20 p.m.

4:20 p.m. 4:25 p.m. 4:25 p.m. 5:00 p.m.

6:00 p.m. 9:00 p.m.

International Pelvic Pain Society

7:00 a.m. 7:00 p.m.

7:00 a.m. 5:30 p.m.

7:50 a.m. 8:00 a.m.

8:00 a.m. 8:10 a.m.

8:10 a.m. 9:05 a.m.

9:05 a.m. 9:45 a.m.

9:45 a.m. 10:25 a.m.

10:25 a.m. 10:45 a.m. 10:45 a.m. 11:15 a.m.

International Pelvic Pain Society

11:35 a.m. 11:55 a.m.

11:55 a.m. 12:15 p.m.

2:40 p.m. 3:10 p.m.

3:10 p.m. 3:25 p.m. 3:25 p.m. 3:55 p.m.

3:55 p.m. 5:10 p.m. 3:55 p.m. 4:25 p.m.

International Pelvic Pain Society

4:55 p.m. 5:10 p.m. 5:15 p.m. 7:00 p.m.

7:00 a.m. 7:50 a.m.